Psychopathology
Neurodevelopmental Disorders
The neurodevelopmental disorders involve developmental deficits that impair personal, social, academic, and/or occupational functioning and usually begin early in development (before the child starts school).
Intellectual Developmental Disorder (Intellectual Disability): For this diagnosis, the person must have (a) deficits in intellectual functioning as determined by the results of a clinical assessment and individualized, standardized intelligence testing; (b) deficits in adaptive functioning that cause a failure to meet developmental and socio-cultural standards for personal independence and social responsibility; and (c) an onset of deficits during the developmental period. With regard to intelligence testing, the DSM-5-TR notes that individuals with this disorder ordinarily obtain a score that is two or more standard deviations below the population mean on a standardized intelligence test. A specifier is used to indicate level of severity (mild, moderate, severe, or profound), which is based on adaptive functioning in conceptual, social, and practical domains and is useful for determining the amount of support the person needs. The cause of intellectual disability is known in 25 to 50% of all cases. Of cases with a known etiology, about 80 to 85% are due to prenatal factors (which includes chromosomal and other genetic causes), 5 to 10% are due to perinatal factors (e.g., asphyxia), and 5 to 10% are due to postnatal factors. Of the genetic causes, Down syndrome and Fragile X syndrome are the first- and second-most common causes, respectively. Note, however, that Down syndrome is a chromosome-related genetic disorder that is nearly always due to a chromosomal abnormality that is the result of an error during cell division. In contrast, Fragile X syndrome is the most common inherited genetic disorder and is due to the presence of a mutated gene on the X chromosome.
Autism Spectrum Disorder (ASD): The diagnosis of ASD requires the presence of (a) deficits in social communication and social interaction across multiple contexts and (b) restrictive and repetitive patterns of behaviors, interests, and activities. Deficits in social communication and interaction include impaired social-emotional reciprocity (e.g., little or no initiation of social interaction, no sharing of emotions, difficulty processing and responding to social cues); impaired nonverbal communication that is used for social interaction (e.g., atypical use of eye contact, facial expressions, and gestures); and impaired ability to develop, maintain, and understand relationships (e.g., atypical social interest, inappropriate approaches to others that seem aggressive or disruptive). Restrictive and repetitive behaviors, interests, and activities include stereotyped or repetitive motor movements, speech, or use of objects; insistence on sameness or inflexible adherence to routines; restricted or fixated interests that are abnormal in intensity or focus; and hyper- or hyporeactivity to sensory input. For the diagnosis, the onset of symptoms must be during the early developmental period. The prognosis for ASD is best when the person has an IQ over 70, functional language skills by age five, and an absence of comorbid mental health problems.
Associated features of ASD include intellectual and language impairments, self-injurious behaviors (e.g., head banging), motor abnormalities (e.g., clumsiness, walking on tiptoes), and disruptive/challenging behaviors. In addition, individuals with ASD often have impaired face recognition and emotion recognition, which have been identified as contributors to deficits in social relationships. In a study on face recognition, Dawson et al. (2002) compared the reactions of children 3- to 4-years of age with and without autism to novel and familiar faces and objects. While children without autism reacted differently to novel versus familiar faces and objects, children with autism reacted differently to novel and familiar objects but similarly to novel and familiar faces. With regard to emotion recognition, Fridenson-Hayo et al. (2016) found that children with autism had deficits in recognizing basic and complex emotions in all three expression modalities (face, voice, and body).
Reported prevalence rates for ASD in the United States and other countries vary: The global prevalence rate is about 1%, while the rate in the United States is higher at 3.2% (1 in 31) for children 8 years of age and 2.2% (1 in 45) for individuals ages 18 and older. ASD is diagnosed three to four times more often in males than females. In terms of etiology, research has confirmed that ASD is the result of both heredity and environmental factors. Family, twin, and adoption studies provide support for a genetic contribution. For example, a review of twin studies reports an average heritability estimate of 62% and concordance rates ranging from 59% to 84% for monozygotic twins and 3.5% to 29% for dizygotic twins. Environmental risk factors include birth before 26 weeks of gestation, exposure to certain drugs or teratogens (e.g., valproic acid) during prenatal development, and advanced parental age. Despite extensive research, a link between ASD and childhood vaccinations has not been established.
ASD has been linked to several brain and neurotransmitter abnormalities: Studies have found accelerated brain growth in children with ASD that begins at about 6 months of age and plateaus by the preschool years and that corresponds to a larger-than-normal head circumference and increased brain volume and weight during that period. Abnormalities have also been found in the cerebellum, corpus callosum, and amygdala. With regard to neurotransmitters, individuals with ASD often have lower-than-normal levels of serotonin in several areas of the brain but elevated levels of serotonin in the blood. One explanation for this difference is that blood serotonin enters the fetal brain during the early stages of development before the blood-brain barrier is fully mature, which causes reduced development of or damage to serotonergic neurons in the brain. Other neurotransmitters that contribute to ASD include dopamine, GABA, glutamate, and acetylcholine.
The primary goals for the treatment of children with ASD are to minimize the core symptoms of the disorder, maximize independence by promoting the acquisition of functional skills, and reduce or eliminate behaviors that may interfere with functional skills. With regard to nonpharmacological interventions, early intensive behavioral intervention (EIBI) is an evidence-based treatment that uses the principles and techniques of applied behavior analysis (ABA). An example is Lovaas’s (1987) method of EIBI, which involved providing young children with ASD with at least 40 hours per week of behavioral interventions and included using shaping and discrimination training to teach nonspeaking children to communicate verbally. Research evaluating the outcomes of EIBI have found that it has the greatest positive impact on intelligence and language acquisition and a smaller and less consistent impact on adaptive skills, social functioning, and severity of core ASD symptoms.
No medication has been found to be effective for the core symptoms of ASD, and medications are ordinarily prescribed for co-occurring psychiatric conditions and associated behaviors that cause distress but are not addressed by or haven’t been alleviated by nonpharmacological interventions. For instance, methylphenidate and other psychostimulants are used to alleviate symptoms of ADHD; SSRIs are used to treat depression and anxiety; and atypical antipsychotics (especially risperidone and aripiprazole) are used to reduce irritability and aggressive, self-injurious, and other disruptive behaviors.
Attention-Deficit/Hyperactivity Disorder (ADHD): ADHD involves a pattern of inattention and/or hyperactivity-impulsivity that has persisted for at least six months, had an onset before 12 years of age, is present in at least two settings, and interferes with social, academic, or occupational functioning. The diagnosis requires at least six symptoms of inattention and/or at least six symptoms of hyperactivity-impulsivity for individuals age 16 and younger and at least five symptoms of inattention and/or at least five symptoms of hyperactivity-impulsivity for individuals age 17 and older. Symptoms of inattention include does not listen when spoken to, fails to pay close attention to details, does not follow through on instructions, is easily distracted by extraneous stimuli, and is often forgetful in daily activities. Symptoms of hyperactivity-impulsivity include unable to engage in play or leisure activities quietly, often runs or climbs in inappropriate situations, talks excessively, and interrupts or intrudes on others. A specifier is used to indicate the subtype as predominantly inattentive presentation, predominantly hyperactive/impulsive presentation, or combined presentation. Children with ADHD have high rates of comorbidity. Although reported rates of specific comorbid disorders vary somewhat, most studies have found oppositional defiant disorder (ODD) to be the most common comorbidity. According to the DSM-5-TR, about half of children with the combined presentation also have ODD.
Surveys conducted in the United States have identified ADHD as the most prevalent diagnosed disorder among youth ages 3 to 17 years. With regard to gender, ADHD is two times more common in males than females during childhood, but the gender difference decreases somewhat in adulthood when the ratio of males to females is about 1.6:1. Estimates of the persistence of ADHD into adulthood vary, but there is evidence that the majority of children with ADHD continue to experience one or more core symptoms as adults. The studies have also found that symptoms change in adulthood: (a) The excessive motor activity associated with hyperactivity decreases and is replaced, for example, by an inability to relax or sit still, impatience, and a sense of restlessness. (b) Impulsivity decreases slightly and changes to include such behaviors as driving recklessly, abruptly quitting jobs and ending relationships, and overspending. (c) Inattention continues during adulthood and involves an inability to meet important deadlines, making careless mistakes, and procrastination, and it is most apparent for boring and tedious (versus novel or interesting) tasks.
ADHD has been linked to a number of brain abnormalities.Neuroimaging studies of children with ADHD have found that (a) impaired response inhibition, working memory, sustained attention, and other aspects of executive functioning are associated with abnormalities in the prefrontal cortex, striatum (caudate nucleus and putamen), and thalamus; (b) impaired temporal information processing (e.g., inability to perceive and organize sequences of events and anticipate when future events will occur) is associated with abnormalities in the prefrontal cortex and cerebellum; and (c) emotion dysregulation is associated with abnormalities in the prefrontal cortex and amygdala. The studies have also found that children with ADHD have reduced total brain volume with smaller-than-normal volumes in the prefrontal cortex, striatum, corpus callosum, and cerebellum, as well as reduced activity in these regions. With regard to neurotransmitters, low levels of dopamine and norepinephrine have most consistently been identified as contributors to the cognitive and behavioral symptoms of ADHD. For example, low levels of these neurotransmitters in the prefrontal cortex have been linked to impairments in impulse control, attention, and executive functioning.
A genetic contribution has been confirmed by family, twin, and adoption studies. For example, one review of the research reports an average heritability estimate derived from twin studies of 74% and concordance rates ranging from 62.8% to 79.3% for monozygotic twins and 21.2% to 39% for dizygotic twins. Because the concordance rate for monozygotic twins is less than 100%, this means that factors other than genetic inheritance contribute to this disorder. Several factors that may account for ADHD discordance have been identified: For example, there is evidence that twins diagnosed with ADHD had lower birth weights than their nonaffected co-twins, spent more time in an incubator following birth, and had a slower acquisition of motor skills.
The best treatment for ADHD depends, to some degree, on the person’s age. For example, guidelines prepared by the American Academy of Pediatrics recommend the following for children and adolescents: (a) Parent- and teacher-administered behavioral interventions are the treatment-of-choice for preschool children, with evidence-based parent training in behavioral management (PTBM) being the primary recommended intervention. Included in this category are the positive parenting program and parent-child interaction therapy (PCIT). Medication is prescribed only when behavioral interventions do not produce adequate improvement. (b) For elementary and middle-school children, the recommended treatment is a combination of medication and behavioral interventions at home and at school. (c) For adolescents, the recommendation is to prescribe medication with the adolescent’s assent and to combine medication with behavioral and instructional interventions when they are available. There is evidence that adolescents may benefit, for example, from behavioral therapy, motivational interviewing, mindfulness-based training, and classroom training. For adults, the first-line treatment is medication, but several psychosocial interventions have also been found to have beneficial effects, with cognitive behavior therapy having the strongest support. Note that, while ADHD in childhood has been linked to an increased risk for substance use problems in adolescence and adulthood, the research suggests this link is not due to treatment with a psychostimulant in childhood: A meta-analysis of the research conducted by Humphreys, Eng, and Lee (2013) found that children with ADHD who do and do not receive a psychostimulant drug are comparable in terms of rates of future substance-related problems. Based on their results, these investigators conclude that treatment of ADHD during childhood with a psychostimulant neither decreases nor increases the risk for later substance use disorders.
Tic Disorders: The DSM-5-TR defines a tic as a “sudden, rapid, recurrent, nonrhythmic motor movement or vocalization” (p. 93). Motor tics include eye blinking, facial grimacing, shoulder shrugging, and echopraxia, while vocal tics include throat clearing, barking, and echolalia. The DSM-5-TR distinguishes between three tic disorders: The diagnosis of Tourette’s disorder requires at least one vocal tic and multiple motor tics that may occur together or at different times, may wax and wane in frequency but have persisted for more than one year, and had an onset before 18 years of age. The diagnosis of persistent (chronic) motor or vocal tic disorder requires one or more motor or vocal tics that have persisted for more than one year and began before age 18. The diagnosis of provisional tic disorder requires one or more motor and/or vocal tics that have been present for less than one year and began before age 18. The onset of tics is typically between four and six years of age, and the severity of tics ordinarily peaks between 10 and 12 years of age. The tic disorders often co-occur with other psychiatric disorders, with ADHD being the most common comorbid disorder for Tourette’s disorder.
Tourette’s disorder has been linked to dopamine overactivity, a smaller-than-normal caudate nucleus, and heredity. Treatment may include an antipsychotic drug (e.g., haloperidol) and medication for comorbid conditions – e.g., serotonin for obsessive-compulsive symptoms and methylphenidate or clonidine for ADHD. Behavioral treatments include comprehensive behavioral intervention for tics (CBIT), which consists of psychoeducation, social support, and habit reversal, competing response, and relaxation training.
Communication Disorders: These disorders involve deficits in language, speech, and communication. Included in this category is childhood-onset fluency disorder (stuttering), which involves a disturbance in normal fluency and time patterning of speech that’s inappropriate for the person’s age and language skills, persists over time, and includes one or more of seven symptoms: sound and syllable repetitions, sound prolongations, broken words, audible or silent blocking, circumlocutions, words pronounced with excessive physical tension, monosyllabic whole-word repetitions. The onset is usually between two and seven years of age. Sixty-five to 85% of children recover from dysfluency, with the severity of symptoms at age eight being a good predictor of persistence or recovery. The treatment-of-choice is habit reversal training which incorporates several strategies including competing response training that, for this disorder, is regulated breathing.
Specific Learning Disorder: The diagnosis of this disorder requires difficulties related to academic skills as indicated by the presence of at least one of six symptoms that last for at least six months despite the use of interventions that address difficulties: inaccurate or slow and effortful word reading; difficulty understanding the meaning of what is read; difficulties with spelling; difficulties with written expression; difficulties mastering number sense, number facts, or calculation; and difficulties with mathematical reasoning. For the diagnosis, the person’s academic skills must be substantially below those expected for his/her age, interfere with academic or occupational performance or activities of daily living, have an onset during the school-age years, and not be better accounted for by another disorder or condition (e.g., uncorrected visual or auditory impairment). Specifiers are used to indicate subtype (with impairment in reading, with impairment in written expression, or with impairment in mathematics) and level of severity. About 5 to 15 percent of school-age children have a specific learning disability and approximately 80% of these children have a reading disorder (American Psychiatric Association, 2018). Of the reading disorders, dyslexia is the most common type; of the types of dyslexia, dysphonic dyslexia is most common. It involves difficulties connecting sounds to letters and is also known as dysphonetic, auditory, and phonological dyslexia (Healy, 2010; Keller & Goldberg, 2005). People with a specific learning disorder usually have an average to above-average IQ but elevated rates of other problems and disorders, with studies finding ADHD to be the most common comorbid psychiatric disorder (Khodeir, El-Sady, & Mohammed, 2020).
Schizophrenia Spectrum / Other Psychotic Disorders
The disorders in this category include brief psychotic disorder, schizophreniform disorder, schizophrenia, schizoaffective disorder, and delusional disorder. Also, like other DSM-5-TR diagnostic categories, this one includes “other specified” and “unspecified” designations that are used when a patient’s symptoms do not fully meet the diagnostic criteria for any specific disorder.
Brief Psychotic Disorder: The diagnosis of brief psychotic disorder requires the presence of one or more of four characteristic symptoms for at least one day but less than one month, with at least one symptom being delusions, hallucinations, or disorganized speech. The four characteristic symptoms are delusions, hallucinations, disorganized speech (e.g., derailment, tangentiality), and grossly disorganized or catatonic behavior. [The DSM-5 defines a delusion as “a false belief based on incorrect inference about external reality that is firmly held despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof of evidence to the contrary”. It defines an hallucination as “a perception-like experience with the clarity and impact of a true perception but without the external stimulation of the relevant sensory organ” and notes that hallucinations must be distinguished from illusions, which occur when “an actual external stimulus is misperceived or misinterpreted”.]
Schizophreniform Disorder: This diagnosis requires the presence of at least two of five characteristic symptoms for at least one month but less than six months, with at least one symptom being delusions, hallucinations, or disorganized speech. The five characteristic symptoms are delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, and negative symptoms (e.g., avolition, alogia, anhedonia).
Schizophrenia: The diagnosis of schizophrenia requires the presence of an active phase that lasts for at least one month and includes at least two of five characteristic symptoms, with at least one symptom being delusions, hallucinations, or disorganized speech. (The other two characteristic symptoms are grossly disorganized or catatonic behavior and negative symptoms). There must also be continuous signs of the disorder for at least six months that may include prodromal and/or residual phases in addition to the required active phase. Prodromal and residual phases consist of two or more characteristic symptoms in an attenuated form or negative symptoms only.
1. Etiology: Schizophrenia has been linked to genetic factors and neurotransmitter and brain abnormalities. With regard to genetic factors, research has confirmed that schizophrenia is not due to a single gene but is polygenic (like several other psychiatric disorders), which means it is the result of the effects of multiple genes. The studies have also confirmed that schizophrenia is highly heritable with twin, family, and adoption studies reporting heritability estimates ranging from 70% to 80%. Much of the evidence for a genetic contribution is provided by family studies which have found that, the greater the degree of genetic similarity, the greater the concordance rate (the likelihood that two people with shared genes will develop the same disorder). The concordance rates for first-degree relatives reported by Gottesman (1991) are frequently cited and are listed below. More recently, a review of the research found concordance rates of 42% to 48% for monozygotic twins and 4% to 11% for dizygotic twins.
Relationship to Person with Schizophrenia
Concordance Rate
Parent
6%
Biological sibling
9%
Child of one parent with schizophrenia
13%
Dizygotic (fraternal) twin
17%
Child of two parents with schizophrenia
46%
Monozygotic (identical) twin
48%
The contribution of genetics to schizophrenia has also been confirmed by studies investigating psychiatric outcomes for the adult offspring of discordant monozygotic and dizygotic twins (i.e., twin pairs in which only one twin has schizophrenia). These studies found that the offspring of discordant monozygotic twins had an increased risk for schizophrenia and schizophrenia-related disorders, with the risk being similar for the offspring of affected and non-affected twins. In contrast, for discordant dizygotic twins, the risk for offspring of affected twins was similar to the risk for offspring of monozygotic twins and was greater than the risk for offspring of non-affected twins. As noted by Pogue-Geile and Gottesman (2007), these results suggest that “discordant MZ twins have significant genetic liability that can be transmitted to their offspring even though they do not manifest it themselves”.
Neurotransmitters that have been linked to schizophrenia include dopamine, glutamate, and serotonin. According to the original dopamine hypothesis, schizophrenia is due to high levels of dopamine or hyperactivity of dopamine receptors. Evidence for this hypothesis is provided by research showing that amphetamines increase dopamine activity and produce schizophrenia-like symptoms, while drugs that decrease dopamine activity reduce or eliminate these symptoms. A revised version of the dopamine hypothesis predicts that the positive symptoms of schizophrenia are due to dopamine hyperactivity in subcortical regions of the brain (especially in striatal areas), while the negative symptoms are due to dopamine hypoactivity in cortical regions (especially in the prefrontal cortex).
Brain abnormalities associated with schizophrenia include enlarged ventricles and hypofrontality, which refers to lower-than-normal activity in the prefrontal cortex and is believed to contribute to the disorder’s negative and cognitive symptoms. One model of schizophrenia that’s consistent with the revised dopamine hypothesis described above implicates cortical and subcortical regions. It predicts that dysfunction in the temporal-limbic-frontal network causes the negative symptoms of schizophrenia as well as disinhibition in subcortical areas of the brain that, in turn, increases the release of dopamine in the striatum (caudate nucleus, putamen, and nucleus accumbens) and causes the positive symptoms.
2. Comorbidity: Common comorbid conditions include anxiety disorders, obsessive-compulsive disorder, and tobacco use disorder. With regard to the latter, the studies have found that about 70 to 85% of individuals with schizophrenia are tobacco users and, according to the DSM-5-TR, over half of individuals with this diagnosis meet the diagnostic criteria for tobacco use disorder.
3. Onset, Course and Prognosis: The psychotic symptoms of schizophrenia usually first appear between the late teens and early 30s, with the peak age of onset being in the early- to mid-20s for males and the late-20s for females. Psychotic symptoms often decrease with increasing age, while negative symptoms and cognitive symptoms persist. A better prognosis for schizophrenia is associated with female gender, an acute and late onset of symptoms, comorbid mood symptoms (especially depressive symptoms), predominantly positive symptoms, precipitating factors, a family history of a mood disorder, and good premorbid adjustment. In contrast, anosognosia (a lack of insight into or awareness of one’s disorder) is associated with non-adherence to treatment and an elevated risk for relapse. Patients whose family members are high in expressed emotion are also at increased risk for relapse. Expressed emotion refers to the emotional response of family members to a patient with schizophrenia or other mental disorder, and families high in expressed emotion are characterized by high levels of criticism and hostility toward and emotional overinvolvement with the patient.
The research has identified variations in the onset, course, and prognosis of schizophrenia across countries. For example, there’s evidence that patients living in non-Western developing countries are more likely than those living in Western industrialized countries to experience an acute onset of symptoms, a shorter course, and a higher rate of remission. The studies have also found that an “immigrant paradox” applies to schizophrenia, alcohol use disorder, and a number of other psychiatric disorders. It occurs when “newly arrived immigrants have better health outcomes than much more acculturated immigrants (with longer US residence) or even US born natives of the same ethnicity”.
4. Treatment: The treatment of schizophrenia is multimodal and includes psychosocial interventions, an antipsychotic drug, and adjunctive medications to treat comorbid disorders. Evidence-based psychosocial interventions include cognitive-behavior therapy for psychosis (CBTp), cognitive remediation for schizophrenia, acceptance and commitment therapy, assertive community treatment, family psychoeducation, illness self-management training, social skills training, and supported employment services. Antipsychotic drugs are divided into first-generation antipsychotics (FGAs), second-generation antipsychotics (SGAs), and third-generation antipsychotics (TGAs). The choice of a drug involves considering several factors including the drug’s likely benefits and side effects; its potential interactions with other drugs the patient is currently taking; and the patient’s preferences, past response to antipsychotic drugs, and health conditions that might be affected by the drug’s side effects. The SGA clozapine has been found to be the most effective antipsychotic for treatment-resistant schizophrenia which, as defined in the American Psychiatric Association’s Practice Guidelines for the Treatment of Patients with Schizophrenia (2021), occurs when “a patient’s symptoms have shown no response or partial or suboptimal response to two antipsychotic medication trials of at least 6 weeks each at an adequate dosage of medication”. Medication non-adherence is often a problem for patients with schizophrenia during all phases of the illness. There is evidence, however, that involvement of the patient’s family or other support system in the patient’s care increases medication adherence and decreases the risk for relapse. (Additional information about antipsychotic drugs is provided in the physiological psychology and psychopharmacology content summary.)
Finally, several multicomponent early interventions have been developed for individuals at high risk for schizophrenia or in the early stages of schizophrenia. An example is NAVIGATE, which is a team-based program that targets individuals experiencing their first episode of psychosis and includes family education, individual resiliency training, supported employment and education, and individualized medication treatment. Individualized resiliency training is based on CBTp and teaches patients the skills they need to manage their illness. For example, it helps patients process the precursors, triggers, and effects of their psychotic episodes; uses cognitive restructuring to help patients challenge self-stigmatizing beliefs; and teaches patients strategies that help them improve their psychological well-being by strengthening their positive feelings, thoughts, and behaviors.
Schizoaffective Disorder: The diagnosis of schizoaffective disorder requires concurrent symptoms of schizophrenia and a major depressive or manic episode for most of the duration of the illness, but with the presence of delusions or hallucinations for two or more weeks without mood symptoms.
Delusional Disorder: This diagnosis requires that (a) the person have one or more delusions for a duration of at least one month and (b) the person’s overall functioning has not been markedly impaired except for any direct effects of the delusion. The DSM-5-TR distinguishes between the following subtypes: (a) erotomanic (the person believes that another person is in love with him/her); (b) grandiose (the person believes he/she has great but unrecognized talent or insight); (c) jealous (the person believes his/her spouse or partner is unfaithful); (d) persecutory (the person believes he/she is being conspired against, spied on, poisoned, or maliciously maligned); and (e) somatic (the person’s delusion involves bodily functions or sensations).
Other Specified/Unspecified Schizophrenia Spectrum and Other Psychotic Disorders: The DSM-5-TR provides two diagnoses that can be used when a patient’s symptoms are similar to symptoms of diagnoses in this category but do not fully meet the criteria for a specific diagnosis: Other specified schizophrenia spectrum and other psychotic disorder is used when a clinician wants to indicate the reason why a patient’s symptoms do not meet the criteria for a more specific diagnosis. The DSM-5-TR lists several situations when this may occur – e.g., when the patient is experiencing persistent auditory hallucinations without any other symptoms or is experiencing attenuated psychosis syndrome which involves psychotic-like symptoms that are less severe or more transient than those associated with full psychosis. Unspecified schizophrenia spectrum and other psychotic disorder is used when a clinician chooses not to specify a reason why a patient’s symptoms do not meet the criteria for a specific diagnosis in this category (e.g., because currently available information is insufficient to assign a specific diagnosis).
Bipolar and Depressive Disorders
Diagnosis of the bipolar and depressive disorders involves considering a client’s current status and history in terms of three mood episodes: A manic episode is characterized by an abnormally and persistently elevated, expansive, or irritable mood and increased activity or energy for at least one week. It includes three or more characteristic symptoms (e.g., inflated self-esteem or grandiosity, decreased need for sleep, flight of ideas) and marked impairment in functioning, a need for hospitalization to avoid harm to self or others, and/or the presence of psychotic features. A hypomanic episode is characterized by an abnormally and persistently elevated, expansive, or irritable mood; increased activity or energy; and three or more symptoms of mania for at least four consecutive days. Symptoms are not severe enough to cause marked impairment in functioning or a need for hospitalization and do not include psychotic features. A major depressive episode is characterized by five or more characteristic symptoms with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities. Symptoms last for at least two weeks and cause significant distress and/or impaired functioning.
Bipolar Disorders: The bipolar disorders include bipolar I disorder, bipolar II disorder, and cyclothymic disorder. The diagnosis of bipolar I disorder requires at least one manic episode that may or may not have been preceded or followed by one or more major depressive or hypomanic episodes. The diagnosis of bipolar II disorder requires at least one hypomanic episode and at least one major depressive episode. The diagnosis of cyclothymic disorder requires numerous periods of hypomanic symptoms that do not meet the criteria for a hypomanic episode and numerous periods of depressive symptoms that do not meet the criteria for a major depressive episode. The minimum duration of symptoms for cyclothymic disorder is two years for adults or one year for children and adolescents.
1. Etiology of Bipolar Disorder: Bipolar disorder has been linked to heredity and environmental factors. Twin studies have established that it is highly heritable, with reported heritability estimates ranging from about 60% to 90%. These studies also report concordance rates that range from 40% to 80% for monozygotic twins and 5% to 30% for dizygotic twins, with some studies finding that rates are higher for female twins than male twins. Research that distinguishes between the heritability of bipolar I and bipolar II disorders is limited, but there is some evidence that it is greater for bipolar I disorder. Environmental risk factors include early parental loss; childhood maltreatment (especially emotional abuse); medical comorbidity (e.g., irritable bowel syndrome, asthma, migraine headache); cannabis, cocaine, and other substance use; and highly stressful life events.
2. Differential Diagnosis: It can be difficult to distinguish between bipolar I disorder and ADHD because they share several symptoms, including distractibility, irritability, and accelerated speech. Geller et al. (2002) propose that consideration of mania symptoms that do not overlap with symptoms of ADHD can help avoid over- or under-diagnosing bipolar disorder in children and adolescents. Their research found that the most manic-specific symptoms for youth 7 to 16 years of age were elation, grandiosity, flight of ideas/racing thoughts, decreased need for sleep, and hypersexuality (e.g., unusual interest in or preoccupation with sex, using sexually explicit sexual language, engaging in developmentally inappropriate sexual behavior). With regard to adults, Salvi et al.’s (2021) review of the research found that manic episodes are typically characterized by a euphoric, elevated, or irritable mood; increased self-esteem or grandiosity; distractibility caused by thought acceleration; and a decreased need for sleep, usually without physical discomfort. In contrast, ADHD in adults is characterized by a labile, dysphoric mood; reduced self-esteem; distractibility due to wandering (but not acceleration) of thoughts; and fatigue and discomfort after a loss of sleep. Studies on sexuality generally confirm that increased sexual activity is common for adults experiencing manic episodes. However, research is inconsistent with regard to ADHD: The results of some studies suggest that adult ADHD is not associated with increased sexual activity but is associated with higher rates of sexual disorders and greater involvement in risky sexual behaviors.
3. Treatment of Bipolar Disorder: Treatment usually consists of a combination of psychosocial interventions and pharmacotherapy. Evidence-based psychosocial interventions include psychoeducation, interpersonal and social rhythm therapy, cognitive-behavior therapy, and family-focused therapy (which is based on the assumption that high expressed emotion by family members can trigger relapse in the family member with this disorder). With regard to pharmacotherapy, lithium is usually most effective for “classic bipolar disorder” which is characterized by a low likelihood of mixed mood states and rapid cycling, long periods of recovery between episodes, and an onset between 15 and 19 years of age. In contrast, anticonvulsant drugs (e.g., carbamazepine, valproic acid) and second generation antipsychotic drugs are most effective for “atypical bipolar disorder,” which is characterized by mixed mood states, rapid cycling, a lack of full recovery between episodes, and an onset between 10 and 15 years of age. (Note that the distinction between classic and atypical bipolar disorder is not a DSM-5-TR categorization and that DSM-5-TR provides the specifier “with atypical features” for bipolar disorder that involves mood reactivity and at least two of the following: significant weight gain or increase in appetite, hypersomnia, leaden paralysis, interpersonal rejection sensitivity.)
Depressive Disorders: The depressive disorders include major depressive disorder (MDD), persistent depressive disorder, and disruptive mood dysregulation disorder. The diagnosis of major depressive disorder requires five or more symptoms of a major depressive episode for at least two weeks with at least one symptom being depressed mood or loss of interest or pleasure in most or all activities. The diagnosis of persistent depressive disorder requires a depressed mood with two or more characteristic symptoms (e.g., poor appetite or overeating, insomnia or hypersomnia, feelings of hopelessness) for at least two years in adults or one year in children and adolescents. The diagnosis of disruptive mood dysregulation disorder requires the presence for at least 12 months of (a) severe and recurrent temper outbursts that are verbal and/or behavioral, are grossly out of proportion to the situation or provocation, and occur three or more times each week; and (b) a persistently irritable or angry mood that is observable to others most of the day and nearly every day between outbursts. Note that, when patients meet the diagnostic criteria for MDD and persistent depressive disorder, both diagnoses are assigned, and the appropriate course specifier for persistent depressive disorder is recorded: with persistent major depressive episode; with intermittent major depressive episode, with current episode; or with intermittent major depressive episode, without current episode.
Specifiers provided in DSM-5-TR for MDD include with peripartum onset and with seasonal pattern: The specifier with peripartum onset applies when the onset of symptoms occurs during pregnancy or the four weeks after delivery. Up to 80% of women experience “baby blues” (sadness, irritability, anxiety) after the birth of their children, while a smaller percent experience symptoms that meet the criteria for MDD. Of those who do develop MDD, about 50% experienced the symptoms prior to delivery. Cognitive-behavioral therapy and interpersonal therapy are evidence-based psychotherapies for the prevention and treatment of peripartum depression. Antidepressants (especially sertraline) are also effective, but several factors must be considered before they are prescribed including the potential negative effects for the developing fetus and newborns who are being breast fed and the impact of untreated maternal depression on both the woman and her child. There is evidence that exercise reduces symptoms of peripartum depression, but the studies have produced inconsistent results about the magnitude of its effects due in part to differences in methodology: For example, the type of exercise varies from study to study, and some studies evaluate its effects as an adjunctive intervention while others have evaluated it as a stand-alone treatment. However, a meta-analysis of research comparing aerobic exercise alone to aerobic exercise with co-interventions found that exercise alone had a non-significant beneficial effect on depressive symptoms, while exercise with co-interventions was significantly more effective than the co-interventions alone.
The specifier with seasonal pattern applies when there’s a temporal relationship between mood episodes and time of year, which is usually winter. This disorder is also known as seasonal affective disorder (SAD), and its symptoms include hypersomnia, overeating, weight gain, and a craving for carbohydrates. It’s been linked to a lower-than-normal level of serotonin and a higher-than-normal level of melatonin, which is a hormone that plays an essential role in the sleep-wake cycle. SAD is often responsive to phototherapy which involves exposure to bright light that suppresses the production of melatonin.
During childhood, the rates of depression are similar for boys and girls; however, the rate for females increases in early adolescence while the rate for males remains fairly stable. Explanations for this gender difference incorporate the impact of biological and psychological factors. For example, there’s evidence that the increase of hormonal levels at puberty sensitizes females but desensitizes males to the stress of negative life events. The higher rate for females persists into adulthood, with female adolescents and adults having a rate that is 1.5 to 3 times higher than the rate for male adolescents and adults.
1. Etiology of Major Depressive Disorder: MDD has been linked to heredity; neurotransmitter, hormone, and brain abnormalities; and cognitive and behavioral factors. With regard to heredity, twin studies report heritability estimates ranging from about 30% to 50%, with most estimates being larger for females than males. In addition, the average reported concordance rates are 46% for monozygotic twins and 20% for dizygotic twins, with some studies finding that concordance rates are higher for female twins than male twins. There is also evidence that the personality trait of neuroticism explains a large proportion of the genetic contribution.
Studies looking at neurotransmitters have found that depression is related to low levels of serotonin, dopamine, and norepinephrine. Depression has also been associated with abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, which plays an important role in the body’s reaction to stress: Exposure to chronic stress (especially early in life) has been found to lead to persistent hyperactivity of the HPA axis and hypersecretion of cortisol, the primary stress hormone, which are associated with an increased risk for depression. In addition, neuroimaging studies have linked depression to structural and functional abnormalities in the prefrontal cortex, cingulate cortex, hippocampus, caudate nucleus, putamen, amygdala, thalamus, and several other areas of the brain. With regard to the prefrontal cortex, the studies have found that depression is associated with abnormally high levels of activity in the ventromedial prefrontal cortex (vmPFC) and abnormally low levels of activity in the dorsolateral prefrontal cortex (dlPFC) and that remission of depressive symptoms in response to psychotherapy or an antidepressant is associated with the opposite pattern – i.e., to decreased activity in the vmPFC and increased activity in the dlPFC.
Behavioral and cognitive explanations include Lewinsohn’s social reinforcement theory, Seligman’s learned helplessness model, and Beck’s cognitive theory: Lewinsohn’s (1974) social reinforcement theory describes depression as the result of a low rate of response-contingent reinforcement for social behaviors due to a lack of reinforcement in the environment and/or poor social skills. This results in social isolation, low self-esteem, pessimism, and other characteristics of depression that, in turn, further decrease the likelihood of positive reinforcement in the future. Seligman’s (1974) original version of the learned helplessness model links depression to repeated exposure to uncontrollable negative life events that results in a sense of helplessness, and a reformulated version stresses the role of a negative cognitive style that involves attributing negative life events to stable, internal, and global factors. The most recent revision of the model (referred to as hopelessness theory) describes a sense of hopelessness as the proximal and sufficient cause of depression which, in turn, is the result of exposure to negative events and a negative cognitive style. Beck’s (1974) cognitive theory attributes depression to a negative cognitive triad that consists of negative thoughts about oneself, the world, and the future.
2. Age and Cultural Factors: There’s evidence that risk factors for major depressive disorder are somewhat age-related. For example, for younger adults, the risk has been linked to genetics, stressful life events, and limitations in problem-solving and other cognitive abilities. In contrast, for older adults, chronic medical illness has been consistently identified as one of the strongest risk factors, especially when the illness decreases physical functioning and contributes to social isolation.
There’s also evidence that the experience and expression of major depressive disorder are related to age and cultural background. With regard to age, older adults are less likely than younger adults to refer to affective symptoms and more likely to refer to somatic symptoms, cognitive changes, and a loss of interest in usual activities. With regard to cultural background, members of some Latino, Mediterranean, Middle Eastern, Asian, and other non-Western cultures report a larger number of somatic symptoms than members of Western cultures who report a larger number of psychological symptoms. For example, Ryder and his colleagues (2008) compared Chinese and Euro-Canadian outpatients and found that the Chinese patients were more likely to emphasize somatic symptoms (e.g., appetite and sleep disturbances, headaches, heart palpitations), while Euro-Canadian patients were more likely to emphasize psychological symptoms (e.g., depressed mood, loneliness, hopelessness).
3. Comorbidity: Major depressive disorder often co-occurs with other psychiatric disorders. A survey of U.S. adults found that, among respondents with major depressive disorder, the largest percentage reported having a comorbid substance use disorder (especially alcohol use disorder) during their lifetimes followed by, in order, an anxiety disorder and a personality disorder. Depression is also associated with several sleep abnormalities including prolonged sleep latency (a longer time to fall asleep), reduced REM latency (a shortened time from sleep onset to REM sleep), reduced slow-wave (stages 3 and 4) sleep, and increased REM density (more rapid eye movements per unit of time). Finally, depression has been linked to coronary heart disease, stroke, diabetes, Parkinson’s disease, and a number of other medical conditions, with the relationship between depression and some medical conditions being bidirectional. For example, research has found depression to be independently predictive of an increased risk for myocardial infarction (a heart attack), which is a manifestation of coronary heart disease. There is also evidence that depression and anxiety are the psychiatric disorders that most commonly develop after a myocardial infarction, with most studies finding depression to be more common than anxiety.
4. Treatment of Major Depressive Disorder: The treatment of MDD consists of psychotherapy and/or pharmacotherapy. A meta-analysis of studies comparing the effects of psychotherapy alone, pharmacotherapy alone, and combined psychotherapy and pharmacotherapy for adults found that the combined treatment was more effective than either psychotherapy alone or pharmacotherapy alone in terms of both response and remission rates, with no significant differences between psychotherapy alone and pharmacotherapy alone. As noted above, MDD and substance use disorder are frequently comorbid, and the recommended intervention for patients with both disorders is a concurrent approach that addresses the two disorders simultaneously and consists of evidence-based behavioral or cognitive behavioral interventions and pharmacotherapy.
APA’s (2019) Clinical Practice Guideline for the Treatment of Depression Across Three Age Cohorts provides treatment recommendations for children and adolescents, adults, and older adults (ages 60 and over): (a) For children, the guideline states that there is insufficient evidence to recommend any particular psychosocial or pharmacological treatment. (b) For adolescents, it recommends cognitive-behavioral therapy (CBT) or interpersonal psychotherapy for adolescents (IPT-A) as a psychosocial intervention and fluoxetine as a first-line medication. However, it notes there is insufficient evidence to recommend either of these treatments (psychotherapy or fluoxetine) over the other. (c) For adults, the guidelines recommend that clinicians offer patients either psychotherapy or a second-generation antidepressant (an SSRI or SNRI) as the initial treatment. The psychotherapies it recommends are CBT, mindfulness-based cognitive therapy (MBCT), interpersonal therapy (IPT), behavioral therapy, psychodynamic therapy, and supportive therapy. For the initial treatment, the guidelines do not recommend one treatment option (psychotherapy or antidepressant) over the other or one of the psychotherapies over the others. The guidelines also suggest that the combination of CBT or IPT and an antidepressant is usually appropriate for patients with chronic or treatment-resistant depression but leave it up to the clinician and patient to decide if the combined treatment is desirable in other situations. (d) For older adults, the guideline recommends that clinicians offer patients either group cognitive-behavioral therapy (group-CBT) or the combination of IPT and a second-generation antidepressant. It also states that there is insufficient evidence for recommending self-guided bibliotherapy or life review therapy for older adults.
Several other interventions have some research support as effective treatments for depression: (a) The use of St. John’s wort is supported by studies showing that it has similar therapeutic effects as SSRIs have for mild and moderate depression as well as lower dropout rates and fewer side effects. However, St. John’s wort has not been shown to be effective for severe depression, and it interacts with certain other drugs. For example, taking St. John’s wort with an SSRI or other medication that increases serotonin levels can cause serotonin syndrome, and taking it with alprazolam (Xanax), bupropion (Wellbutrin), or certain statin or immunosuppressive drugs can reduce the effectiveness of those drugs. (b) Ketamine has been used as an anesthetic and analgesic since the 1960s and has also been found to be effective as a fast-acting treatment for treatment-resistant depression (TRD) and suicidal ideation. It exerts its therapeutic effects by increasing glutamate levels and is prescribed as a nasal spray (esketamine) that is used in conjunction with an oral antidepressant. Because of its potential for severe side effects, esketamine is self-administered under the supervision of a healthcare provider in a healthcare setting. (c) Electroconvulsive therapy (ECT) has been shown to have a high success rate when used to treat severe depression but is ordinarily used only when other treatments have not been effective or when the severity of symptoms requires a quick treatment response (e.g., when the individual is at high risk for suicide). An advantage of ECT is that, compared to other treatments, it has a higher response rate (a clinically meaningful reduction in symptoms), a higher remission rate (the absence or near absence of symptoms), and faster time to remission: Reported response and remission rates for ECT approach 80% and 70%, respectively, while response and remission rates for psychotherapy and pharmacotherapy are 30 to 60% and 25 to 45%, respectively. With regard to time to remission, ECT produces remission within 1 to 3 weeks compared to 6 to 10 weeks for IPT or CBT and 4 to 12 weeks for antidepressant medications. A disadvantage of ECT is that it causes both anterograde amnesia (an inability to form new memories after ECT) and retrograde amnesia (an inability to recall events that occurred before ECT): Anterograde amnesia usually resolves within a few weeks after the last ECT session. Retrograde amnesia affects recently acquired memories more than remote memories. It begins to resolve within weeks to several months after the last ECT session, with older memories returning before more recent ones. However, many patients experience persistent gaps in memory for events that occurred pre-ECT. Retrograde amnesia is more severe for bilateral placement of electrodes than for right unilateral placement and for a larger number of treatment sessions and less time between sessions. (d) Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive technique that uses a magnetic field to stimulate the left dorsolateral prefrontal cortex and is most often used as an intervention for treatment-resistant depression. A disadvantage of rTMS is that it has lower response and remission rates than does ECT. However, in contrast to ECT, rTMS does not require sedation or cause memory loss. (e) A meta-analysis of studies comparing telepsychology and face-to-face psychotherapy found that the two approaches had similar outcomes in terms of depressive symptom severity, quality of life, client satisfaction, and the therapeutic alliance. (f) A number of studies have evaluated the effectiveness of physical activity and exercise for reducing symptoms of depression. Based on the results of their systematic review and meta-analysis of the research, Pearce et al. (2022) conclude that physical activity reduces depressive symptoms even when activity is at levels lower than public health recommendations. In addition, research comparing the effectiveness of physical exercise, therapy, and antidepressants has provided some evidence that they can have comparable effects on the symptoms of mild to moderate depression and that adding exercise to therapy or antidepressants improves their effectiveness. There is also evidence that the positive effects of aerobic exercise on depression are due, at least in part, to its beneficial impact on areas of cognitive functioning (e.g., memory, executive functioning, reward processing) that are ordinarily impaired in individuals with this disorder.
Suicide in the United States: Research has identified a number of demographic characteristics that are associated with an increased risk for suicide and suicidality (suicidal ideation and suicide attempts):
(a) Data collected in 2022 by the Centers for Disease Control and Prevention found the following: The suicide rate for males was four times higher than the rate for females. For males, the highest suicide rate was for those ages 75 and older; for females, the highest rate was for those ages 45 to 64. For both males and females, suicide rates were highest for non-Hispanic American Indian/Alaskan Native individuals.
(b) Data collected by the U.S. Department of Veterans Affairs (2024) found that, in 2022, suicide rates among veterans were significantly higher than rates among non-veterans: Specifically, the rate per 100,000 was 34.7 for veterans and 17.1 for non-veterans.
(c) A number of studies have confirmed that the suicide rates of incarcerated and previously incarcerated individuals are higher than the rate for members of the general population. In addition, based on the results of their systematic review and meta-analysis of the research, Janca et al. (2023) conclude that the suicide rate for previously incarcerated individuals is higher than the rate for currently incarcerated individuals. These investigators also found that, in contrast to the general population in which men have higher rates of suicide than women, among previously incarcerated individuals, men and women have similar rates of suicide because the increased rate following release from incarceration is three times greater for women than for men. They conclude that this “may indicate that women released from incarceration are particularly vulnerable to suicide, because their rates of suicide are so high that they reach the same level as men released from incarceration”.
(d) There is evidence that suicide rates are higher for transgender than cisgender individuals, but it has been difficult to determine the specific difference in rates due to a lack of reliable data. However, a number of studies have found that transgender youth and adults have higher rates of suicidality. For example, data collected from nearly 30,000 patients at a community health center revealed that a larger proportion of transgender women reported suicidal ideation (23.6%) than did transgender men (17.4%), cisgender women (6.6%), and cisgender men (6.1%). In addition, the results of the U.S. Transgender Population Health Survey found that transgender adults reported lifetime rates of suicidal ideation and suicide attempts of 81% and 42%, respectively, while cisgender adults reported lifetime rates of 35% and 11%, respectively.
Anxiety Disorders and Obsessive-Compulsive Disorder
Anxiety Disorders: As described in DSM-5-TR, the disorders included in this category “share features of excessive fear and anxiety and related behavioral disturbances”. Data collected by the Global Burden of Disease Study indicate that the anxiety disorders are the most prevalent mental disorders worldwide. Risk factors for developing an anxiety disorder include exposure to stressful life events, the trait of behavioral inhibition, and having a parent with an anxiety disorder. With regard to the latter, there is evidence that children with anxious parents are nearly twice as likely to have anxiety problems than are children without anxious parents. A genetic contribution to these disorders is supported by family and twin studies reporting heritability estimates ranging from about 30% to 50% and concordance rates ranging from 12% to 26% for monozygotic twins and 4% to 15% for dizygotic twins.
1. Separation Anxiety Disorder: This disorder involves developmentally inappropriate and excessive fear or anxiety about being separated from attachment figures as indicated by at least three of eight symptoms – e.g., excessive distress when anticipating or experiencing separation from attachment figures; persistent reluctance to go to school, work, or other place away from home because of fear of separation from attachment figures; repeated complaints of physical symptoms when separation from a major attachment figure occurs or is anticipated. For the diagnosis, symptoms must last for at least four weeks in children and adolescents or six months in adults and cause significant distress or impaired functioning. Separation anxiety disorder often develops after exposure to a stressful event, such as parental divorce or the death of a relative or a pet.
School refusal is often a manifestation of separation anxiety disorder but, alternatively, may be due to social anxiety disorder or other disorder. Children with school refusal want to stay with their parents or other caregivers rather than go to school, and they complain of physical symptoms (e.g., headache, stomachache, nausea) and cry, plead, bargain, or exhibit panic symptoms when the time to go to school approaches.
The preferred treatment for separation anxiety disorder is ordinarily cognitive-behavior therapy (CBT) that includes psychoeducation, exposure, relaxation techniques, and cognitive restructuring, and there’s evidence that the effectiveness of CBT for children is increased when it’s combined with parent training. When the disorder involves school refusal, getting the child back to school is an initial treatment goal in order to reduce the risk for social isolation, academic failure, and other secondary impairments.
2. Specific Phobia: Specific phobia involves intense fear of or anxiety about a specific object or situation accompanied by avoiding the object or situation or enduring it with intense distress. For the diagnosis, fear or anxiety must be out of proportion to the actual danger posed by the object or situation, must be persistent (ordinarily lasting for at least six months), and must cause significant distress or impaired functioning. A specifier is used to indicate the type of phobia: animal (e.g., snakes, spiders); natural environment (e.g., lightening, heights); blood-injection-injury (e.g., seeing blood, having an invasive medical procedure); situational (e.g., elevators, bridges); other (e.g., situations that may cause vomiting, choking, or catching an illness). Specific phobia is about twice as common in girls than boys, although the rates differ somewhat for different phobic stimuli. Its onset is usually in childhood, with the mean age of onset being about 10 years of age.
Specific phobia has been linked to a number of factors including heredity, altered brain activity, and learning experiences. With regard to genetics, twin studies have produced moderate heritability estimates that vary somewhat for the different types of specific phobia but range from about 30% to 50%. Functional neuroimaging techniques have linked phobic responses to increased activity in the amygdala, insula, thalamus, dorsal anterior cingulate cortex (dACC), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC), which are responsible for emotion generation, and to reduced activity in the ventromedial prefrontal cortex (vPFC) and ventral anterior cingulate cortex (vACC), which are involved in emotion and fear regulation. Learning experiences are addressed by Mowrer’s (1947) two-factor theory, which attributes phobic reactions to a combination of classical and operant conditioning: Classical conditioning occurs when a previously neutral (non-anxiety arousing) object or event becomes a conditioned stimulus that elicits a conditioned response of anxiety after it has been paired with an unconditioned stimulus that naturally elicits anxiety. Operant conditioning then occurs when individuals learn that avoiding the conditioned stimulus allows them to avoid experiencing anxiety. In other words, their avoidance behaviors are negatively reinforced. As a result, the conditioned response of anxiety is not extinguished because individuals never have opportunities to experience the conditioned stimulus without the unconditioned stimulus.
The first-line treatment for specific phobia is exposure and response prevention (ERP) either alone or as a component of cognitive behavior therapy (CBT with ERP). The goal of ERP is to extinguish the conditioned anxiety response by exposing patients to feared objects or situations while preventing them from making their usual avoidance responses. There are two types of ERP, and both can be conducted in vivo or in imagination: Flooding involves immediately exposing a patient to the most feared object or situation until the patient’s anxiety subsides (i.e., is extinguished), while graded (graduated) exposure involves gradually exposing the patient to feared objects or situations, beginning with those that elicit less intense anxiety and progressing to those that elicit increasingly more intense anxiety. Research on ERP has found that in vivo exposure is more effective than exposure in imagination, that therapist-led exposure is more effective than self-directed exposure, and that virtual reality exposure may be as effective as in vivo exposure for some types of specific phobia including fear of heights (acrophobia), fear of flying, and fear of small animals. For some phobias, the effectiveness of ERP increases when it is combined with another intervention. For example, people with the blood-injection-injury subtype typically react to feared stimuli with a brief initial increase in heart rate and blood pressure that is followed by a decrease in heart rate and blood pressure, which causes them to faint. Therefore, exposure for this type of phobia is most effective when it’s combined with applied tension, which involves repeatedly tensing and relaxing the body’s large muscle groups to increase blood pressure and prevent fainting.
3. Social Anxiety Disorder (Social Phobia): Social anxiety disorder is characterized by a fear or anxiety reaction to at least one social situation in which the person may be exposed to scrutiny by others. For the diagnosis, the person must fear that exhibiting symptoms in the situation will be negatively evaluated and, as a result, either avoids the situation or endures it with intense fear or anxiety. In addition, fear or anxiety must be excessive for the actual threat posed by the situation, and fear, anxiety, and/or avoidance must be persistent (last for at least six months) and cause significant distress or impaired functioning. Cognitive behavior therapy and antidepressant medications (SSRIs and SNRIs) are first-line treatments for this disorder. Cognitive behavior therapy is an empirically supported treatment for children, adolescents, and adults and incorporates a number of techniques including cognitive restructuring and exposure. There is evidence that, for adults, guided internet-delivered cognitive behavior therapy is equivalent to face-to-face cognitive behavior therapy in terms of symptom reduction for this disorder and other anxiety disorders. The research has also found that school-based cognitive behavior therapy has beneficial effects for children and adolescents.
4. Panic Disorder: This disorder involves recurrent unexpected panic attacks with at least one attack being followed by one month or more of persistent concern about additional attacks or their consequences and/or a significant maladaptive change in behavior related to the attack. The DSM-5-TR defines a panic attack as “an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes” and that involves at least four of 13 symptoms: e.g., heart palpitations, sweating, nausea or abdominal distress, dizziness, fear of losing control or “going crazy,” fear of dying, paresthesia, derealization or depersonalization. Because symptoms of a panic attack are similar to those associated with hyperthyroidism, cardiac arrhythmia, and several other medical conditions, those conditions must be ruled out before this diagnosis is assigned.
The treatment of panic disorder often involves a comprehensive cognitive-behavioral intervention. An example is panic control treatment, which combines interoceptive exposure with relaxation and other techniques for controlling symptoms. (Interoceptive exposure involves deliberately exposing the person to the physical symptoms associated with panic attacks by, for example, having the person run in place, spin in a circle, or breathe through a straw.) Some antidepressants (e.g., imipramine) and benzodiazepines have been found useful for alleviating panic attacks, but they’re associated with a high relapse rate when used alone.
5. Agoraphobia: Agoraphobia involves marked fear or anxiety that occurs in at least two of five situations: using public transportation, being in open spaces, being in enclosed spaces, standing in line or being in a crowd, and being outside the home alone. For the diagnosis, the person must fear or avoid the situations due to concern that escape will be difficult or that help will be unavailable if he/she develops panic symptoms or other incapacitating or embarrassing symptoms. In addition, the person’s fear or anxiety must be excessive for the actual threat posed by the situations; the situations must almost always elicit fear or anxiety and be actively avoided, require the presence of a companion, or be endured with intense fear or anxiety; and the fear, anxiety, or avoidance must be persistent (typically lasting for at least six months) and cause significant distress or impaired functioning.
The first-line treatment for agoraphobia is in vivo exposure and response prevention. Graded exposure is most commonly used, but there’s evidence that intense (non-graded) exposure is also effective and may have better long-term effects. There’s also evidence that combining in vivo exposure with applied relaxation, breathing retraining, or cognitive techniques does not significantly improve outcomes and that the key contributor to the effectiveness of exposure is learning to tolerate high levels of fear and anxiety.
6. Generalized Anxiety Disorder: Generalized anxiety disorder (GAD) involves excessive anxiety and worry about multiple events or activities that occur on most days for at least six months. For the diagnosis, the person must find anxiety and worrying difficult to control, and symptoms must cause significant distress or impaired functioning and include at least three of the following (or at least one for children): restlessness, being easily fatigued, difficulty concentrating, irritability, muscle tension, sleep disturbance. Associated symptoms include sweating, nausea, headaches, dizziness, breathlessness, and visual disturbances (e.g., eye strain, blurry vision, tunnel vision, light sensitivity). In contrast to people with nonpathological anxiety, those with GAD feel unable to control their worrying, worry about a larger number of events, and are more likely to have associated somatic symptoms. The DSM-5-TR notes that the content of worries is age-related, with children and adolescents worrying most about catastrophic events and their competence in sports and school and older adults worrying most about their health and safety. Finally, in terms of lifetime prevalence, the most common comorbid disorder for GAD is major depressive disorder.
Worry is a central feature of GAD, and several explanations have been proposed to account for its function. According to cognitive avoidance theory, worry is a verbal-linguistic activity that elicits low levels of mental imagery and helps individuals with GAD avoid unpleasant imagery and the negative emotions and somatic arousal associated with that imagery. Support for this theory is provided by studies finding that individuals with GAD often claim that worry keeps them from engaging in more disturbing thoughts about feared events. The contrast avoidance model proposes that people with GAD engage in chronic worry to maintain a sustained state of negative emotions that allows them to avoid sudden shifts from a neutral or positive emotional state to a negative emotional state when faced with feared stimuli. Support for this model is provided by research showing that people with GAD are more disturbed than people without GAD when they experience emotional contrasts (i.e., rapid shifts from a neutral or positive mood to a negative mood). Finally, the intolerance of uncertainty model describes worry associated with GAD as being characterized by four factors: (a) Intolerance of uncertainty is a low tolerance for and strong reaction to ambiguity. (b) Negative problem orientation consists of poor problem-solving confidence and ability, especially in uncertain situations. (c) Positive beliefs about worry refers to the tendency to overestimate the advantages of worrying (e.g., to believe that worrying helps prevent bad things from happening and provides distraction from other disturbing thoughts). (d) Cognitive avoidance of mental images is based on Borkovec’s cognitive avoidance theory and refers to the use of coping strategies that facilitate the avoidance of threatening images. This model is supported by research confirming that the four factors distinguish people with GAD from those with other anxiety disorders.
Risk factors for GAD include a family history of an anxiety disorder; exposure to childhood trauma or chronic stress; and the temperament/personality traits of behavioral inhibition, harm avoidance, and neuroticism, which is also known as negative affectivity and is a risk factor for other anxiety disorders. In addition, neuroimaging studies have found that GAD is associated with abnormalities in the ventrolateral and dorsolateral prefrontal cortex, anterior cingulate cortex, posterior parietal cortex, amygdala, and hippocampus. For example, there’s evidence that GAD is associated with reduced connectivity between regions of the prefrontal cortex and anterior cingulate cortex and the amygdala, which suggests there is weak top-down control of amygdala reactivity.
The treatment of GAD ordinarily involves cognitive-behavior therapy (CBT) and/or pharmacotherapy, with some studies finding that CBT alone and CBT combined with pharmacotherapy are more effective than pharmacotherapy alone. In addition, studies investigating the effects of combining motivational interviewing as a pretreatment to CBT have generally found that the combination of interventions is more effective than CBT alone for reducing resistance to treatment, worry levels, and interpersonal problems. Finally, the first-line drugs for GAD are the SSRIs and SNRIs. In addition, buspirone may be prescribed as an adjunctive treatment when an antidepressant is only partially effective, and buspirone or a benzodiazepine may be prescribed as the sole medication when antidepressant drugs are not tolerated or are ineffective. Note that benzodiazepines are ordinarily used only for providing immediate short-term relief from acute anxiety because their long-term use can lead to the development of tolerance and physical dependence.
Obsessive-Compulsive and Related Disorders: Obsessive-compulsive disorder is included in the DSM-5-TR with body dysmorphic disorder and other disorders that share several diagnostic validators – e.g., symptoms, comorbidity, and treatment response.
1. Obsessive-Compulsive Disorder (OCD): OCD involves recurrent obsessions and/or compulsions that are time-consuming (consume more than one hour each day) and/or cause significant distress or impaired functioning: Obsessions are recurrent and persistent thoughts, urges, or images that the person experiences as intrusive and unwanted, that he/she attempts to ignore or suppress, and that usually cause marked anxiety or distress. Compulsions are repetitive behaviors or mental acts that the person feels driven to perform either in response to an obsession or according to rigidly applied rules. The goal of compulsions is to reduce anxiety or distress or prevent an undesirable situation from happening, but they’re excessive or not connected in a realistic way to their goal. Specifiers are used to indicate the person’s level of insight into the veracity of his/her beliefs and the presence of tics. Males have an earlier age of onset of this disorder than females do and, consequently, have a slightly higher prevalence rate than females in childhood, while females have a slightly higher prevalence rate than males in adulthood. Comorbidity is common, with the most frequent comorbid disorder being an anxiety disorder.
OCD has been linked to heredity and brain abnormalities: A genetic component has been confirmed by twin studies that report heritability estimates ranging from 27% to 57% for adults and 45% to 65% for children. Twin studies have generally found the concordance rate for monozygotic twins to be more than twice the size of the rate for dizygotic twins. For example, the DSM-5-TR reports concordance rates of 57% and 22% for monozygotic and dizygotic twins, respectively. Neuroimaging studies have identified several structural and functional abnormalities, including hyperactivity in the cortico-striato-thalamo-cortical (CSTC) pathway that links the orbitofrontal cortex and anterior cingulate cortex with areas of the basal ganglia (e.g., caudate nucleus, putamen, nucleus accumbens), the thalamus, and the amygdala and controls the execution of movement, habit formation, and reward.
The first-line therapy for OCD is exposure and response prevention (ERP) either alone or as a component of cognitive behavior therapy (CBT with ERP). ERP for OCD is also known as exposure with ritual prevention and involves exposing patients in vivo and/or in imagination to anxiety-arousing thoughts, objects, or situations and preventing them from engaging in ritualistic behaviors that are attempts to reduce anxiety. SSRIs are also considered a first-line treatment, and research comparing the effectiveness of ERP alone, an SSRI alone, and the combination of ERP with an SSRI for adults with OCD suggests that the combined treatment is most effective, at least in some circumstances – e.g., when an SSRI alone or ERP alone has been ineffective, the patient’s obsessive-compulsive symptoms are severe, or the patient has comorbid symptoms that are known to respond to antidepressants. In addition, there is evidence that combining motivational interviewing and CBT with ERP by providing motivational interviewing as a pretreatment may be more effective than CBT with ERP alone. Finally, a meta-analysis of research assessing the effectiveness of ERP and SSRIs for children and adolescents found that ERP delivered in-person or via telehealth are about equally effective and that ERP alone and ERP plus an SSRI are more effective than an SSRI alone.
2. Body Dysmorphic Disorder: This disorder involves a preoccupation with a perceived defect or flaw in physical appearance that’s not observable or appears to be minor to other people. For the diagnosis, the person must have performed repetitive behaviors or mental acts because of the defect or flaw (e.g., mirror checking, skin picking) at some time during the course of the disorder, and the person’s preoccupation must cause significant distress or impaired functioning. People with this disorder often seek medical treatment to correct the defect or flaw, and many have ideas or delusions of reference (i.e., believe that other people are mocking or taking special notice of them because of their physical appearance).
Trauma / Stressor-Related, Dissociative, and Somatic Symptom Disorders
Trauma- and Stressor-Related Disorders: All of the disorders in this category include exposure to a traumatic or stressful event as a diagnostic criterion.
1. Reactive Attachment Disorder: This disorder involves (a) a persistent pattern of inhibited and emotionally withdrawn behavior toward adult caregivers as demonstrated by a lack of seeking or responding to comfort when distressed and (b) persistent social and emotional disturbances that include at least two of the following: minimal social and emotional responsiveness to others; limited positive affect; unexplained irritability, sadness, or fearfulness when interacting with adult caregivers. For the diagnosis, there must be a history of extreme insufficient care that is believed to be responsible for the person’s symptoms, the onset of symptoms must have been before 5 years of age, and the person must have a developmental age of at least nine months.
2. Disinhibited Social Engagement Disorder: This disorder involves a persistent pattern of behavior that’s characterized by inappropriate interactions with unfamiliar adults as demonstrated by at least two of four symptoms: reduced or absent reticence in approaching or interacting with strangers, overly familiar behavior with strangers, diminished or absent checking with adult caregivers after being separated from them, willingness to accompany a stranger with little or no hesitation. The diagnosis also requires that the person has a history of extreme insufficient care that’s believed to be responsible for his/her symptoms and a developmental age of at least nine months.
3. Posttraumatic Stress Disorder (PTSD): The diagnostic criteria for PTSD differ slightly for adults, adolescents, and children over six years of age and children six years of age and younger. However, for individuals of all ages, symptoms must have lasted for more than one month, cause significant distress or impaired functioning, and be due to exposure to actual or threatened death, serious injury, or sexual violence. In addition, the symptoms for all age groups represent four types: intrusion (e.g., recurrent distressing memories of the event), persistent avoidance of stimuli associated with the traumatic event, negative changes in mood or cognition, and alterations in arousal and reactivity. Pre-trauma factors that increase the risk for developing PTSD include prior exposure to trauma, prior psychiatric disorder, negative affectivity, female gender, low education level, low socioeconomic status, lack of social support, and exposure to racial/ethnic discrimination.
PTSD has been linked to several brain abnormalities: Neuroimaging studies have linked it to a hyperactive amygdala and anterior cingulate cortex, a hypoactive ventromedial prefrontal cortex, and a reduced volume of the hippocampus, with some studies finding increased activity of the hippocampus and other studies finding decreased activity. In addition, there’s evidence that the ventromedial prefrontal cortex ordinarily inhibits activity of the amygdala but, in PTSD, reduced activity in the ventromedial prefrontal cortex reduces inhibitory top-down control of the amygdala, resulting in an exaggerated fear response. There’s also evidence of abnormalities in several neurotransmitters including increased levels and activity of dopamine, norepinephrine, and glutamate and decreased levels and activity of serotonin and GABA.
In terms of treatment, APA’s (2025) Clinical Practice Guideline for the Treatment of Posttraumatic Stress Disorder (PTSD) in Adults provides guidelines for both psychological and pharmacological treatments. Based on the results of research, the Guideline (a) recommends cognitive processing therapy (CPT), prolonged exposure (PE), and a trauma-focused cognitive behavioral therapy (CBT) as first-line treatments, and (b) suggests cognitive therapy (CT), eye movement desensitization and reprocessing (EMDR), and narrative exposure therapy (NET) as second-line treatments. The Guideline does not recommend any medication as a first-line treatment, but suggests the SSRIs fluoxetine, paroxetine, and sertraline and the SNRI venlafaxine as second-line treatments. Research confirms that these drugs are useful for treating the depression that often accompanies PTSD and may alleviate the core PTSD symptoms of re-experiencing, avoidance/numbing, and hyperarousal (Khouzam, 2013).
For patients with PTSD and comorbid substance use disorder (SUD), the Guideline recommends three integrated (concurrent) interventions: (a) treatment of PTSD and SUD using prolonged exposure (COPE) which consists of psychoeducation about PTSD and SUD, prolonged imaginal and in vivo exposure to trauma-associated stimuli for PTSD, and relapse prevention for SUD; (b) prolonged exposure for PTSD and treatment as usual for SUD; and (c) a trauma-focused cognitive behavioral therapy and treatment as usual for SUD. With regard to this comorbidity, Roberts et al. (2022) note that traditional interventions were sequential with the SUD being treated first. However, research clarifying the nature of the relationship between PTSD and SUD symptoms led to recognition that integrated treatments are likely to be more effective. Finally, note that single-session psychological debriefing, which is also known as critical incident stress debriefing, is not mentioned in the Guideline, but research has confirmed that it is not effective for PTSD and may actually worsen symptoms.
Finally, for children and adolescents, trauma-focused cognitive behavior therapy (TF-CBT) was initially designed for children and adolescents 3 to 18 years of age who have experienced sexual abuse but has subsequently been used to treat children and adolescents who have been exposed to other types of trauma. It incorporates family therapy, parenting skills training, and conjoint parent-child therapy and has been found effective not only for reducing symptoms of PTSD but also symptoms of depression, anxiety, and grief.
4. Acute Stress Disorder: Like PTSD, the diagnosis of acute stress disorder requires exposure to actual or threatened death, severe injury, or sexual violation. The person must also have at least nine symptoms from any of five categories (intrusion, negative mood, dissociative symptoms, avoidance, arousal), and symptoms must have lasted for three days to one month and cause significant distress or impaired functioning.
5. Prolonged Grief Disorder: The diagnosis of this disorder requires the death of a person close to the bereaved person (the patient) at least 12 months ago for adults and 6 months ago for children and adolescents. The grief response must include an intense yearning for the deceased person and/or preoccupation with thoughts about that person and three or more of eight symptoms nearly every day for at least the previous month: e.g., a marked sense of disbelief about the death, avoidance of reminders of the deceased person, emotional numbness, intense loneliness as a result of the death.
Dissociative Disorders: The DSM-5-TR describes the disorders in this category as involving “a disruption of and/or discontinuity in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behavior”.
1. Dissociative Amnesia: This disorder involves an inability to recall important personal information that cannot be attributed to ordinary forgetfulness and causes significant distress or impaired functioning. Amnesia takes one of the following forms, with localized amnesia being most common: localized (an inability to recall all events that occurred during a circumscribed period of time), selective (an inability to recall some events that occurred during a circumscribed period of time), generalized (a complete loss of memory for one’s entire life), systematized (a loss of memory for a specific category of information), and continuous (an inability to remember new events as they happen). A specifier is used to indicate if the disorder includes dissociative fugue, which is purposeful travel or purposeless wandering that’s associated with the loss of memory. Dissociative amnesia is often related to victimization or exposure to a traumatic event.
2. Depersonalization/Derealization Disorder: The diagnosis of this disorder requires persistent or recurrent episodes of depersonalization (a sense of unreality, detachment, or being an outside observer of one’s thoughts, actions, etc.) or derealization (a sense of unreality or detachment with regard to one’s surroundings) accompanied by intact reality testing and significant distress or impaired functioning.
Somatic Symptom and Related Disorders: These disorders involve physical symptoms and/or health-related concerns that cause significant distress or impaired functioning.
1. Somatic Symptom Disorder: This disorder involves one or more somatic symptoms that are distressing or cause a significant disruption in daily life and are accompanied by excessive thoughts, emotions, or behaviors related to the symptom(s) or associated health concerns as indicated by the presence of at least one of the following: disproportionate or persistent thoughts about the seriousness of the symptoms, a persistently high level of anxiety about health or symptoms, excessive time and energy spent on health concerns or symptoms. Specifiers are used to indicate if symptoms are mild, moderate, or severe, involve predominant pain, and are persistent (are severe, have caused marked impairment, and have lasted more than six months).
2. Illness Anxiety Disorder: This disorder involves a preoccupation with having a serious illness with no or mild somatic symptoms, excessive anxiety about health, and either excessive health-related behaviors or avoidance of health care. Symptoms must be present for at least six months, although the nature of the symptoms may vary over time.
3. Functional Neurological Symptom Disorder (Conversion Disorder): This disorder is characterized by one or more symptoms that involve a disturbance in voluntary motor or sensory functioning (e.g., paralysis, blindness). For the diagnosis, symptoms must be incompatible with any known neurological or medical condition and cause significant distress or impaired functioning. Specifiers are used to indicate symptom type, the course of the disorder (acute or persistent), and the presence or absence of a psychological stressor. Note that this disorder can involve psychogenic non-epileptic seizures (PNES) that resemble true epileptic seizures in terms of behavioral symptoms but are not accompanied by the brain electrical activity associated with epileptic seizures and that video EEG is often used to identify PNES. It involves simultaneously recording a person’s brain electrical activity with an EEG and overt behaviors on video. When the person’s seizure-like behaviors are due to PNES, the EEG pattern does not correspond to the behaviors because they are not being caused by abnormal brain electrical activity.
4. Factitious Disorder: The DSM-5-TR distinguishes between factitious disorder imposed on self and factitious disorder imposed on another. Individuals with factitious disorder imposed on self falsify or induce physical or psychological symptoms that are associated with a deception (e.g., ingestion of a drug to produce abnormal lab results). They present themselves to others as being ill or impaired and engage in the deception even when there’s no obvious external reward for doing so. Factitious disorder imposed on another has the same symptoms except that they’re induced in another person (often in a child by his/her mother).
Factitious disorder must be distinguished from malingering, which is included in the DSM-5-TR with Other Conditions That May Be a Focus of Clinical Attention. It involves an intentional production of physical or psychological symptoms for the purpose of obtaining a drug, financial compensation, or other external reward. According to the DSM-5-TR, “malingering is differentiated from factitious disorder by the intentional reporting of symptoms for personal gain … [while] the diagnosis of factitious disorder requires that the illness falsification is not fully accounted for by external rewards” (p. 369). The DSM-5-TR also states that malingering should be suspected whenever a person seeks a medical evaluation for legal reasons, there’s a marked discrepancy between the person’s symptoms and objective findings, the person is uncooperative with evaluation or treatment, and/or the person has antisocial personality disorder. The forced-choice method has been found useful for detecting malingering and involves presenting the person with test items that require the person to choose the correct answer from two or more alternatives. The use of this method is based on the assumption that people who are malingering will answer items incorrectly at a higher rate than would be expected by chance alone. For instance, when each item has two alternative answers (e.g., true or false), malingering is suggested when the person answers more than 50% of the items incorrectly.
Feigned memory loss associated with factitious disorder and malingering must be distinguished from genuine memory loss that’s due to traumatic brain injury or other condition: For people with genuine memory loss, the beginning and end of the amnestic period are gradual and hazy and these individuals often remember fragments of some events that occurred during that period. In contrast, for people with feigned memory loss, the onset and termination of the amnestic period are often sudden, and these individuals do not remember any events that occurred during this period. Also, in contrast to people with feigned memory loss, those with genuine memory loss often believe that hints or clues will help them recall their lost memories. Finally, several tests can be used to help detect malingering. For example, the Test of Memory Malingering (TOMM) was developed specifically to determine if an individual is feigning memory loss. It uses a forced-choice format that requires individuals to respond to items by indicating which of two images was presented to them just prior to testing. Individuals who are malingering perform significantly below chance level (below 50% correct), which indicates they deliberately chose wrong answers. Malingering is also suggested when individuals exhibit excessive impairment or an unexpected pattern of responding (e.g., a pattern that’s atypical for individuals with genuine impairment) on neuropsychological tests.
Feeding / Eating, Elimination, and Sleep-Wake Disorders
Feeding and Eating Disorders: The DSM-5-TR describes the disorders in this category as involving “a persistent disturbance of eating or eating-related behavior that results in the altered consumption or absorption of food and that significantly impairs physical health or psychosocial functioning”.
1. Pica: Pica involves persistent eating of non-nutritive, nonfood substances (e.g., paper, paint, coffee grounds) for at least one month that’s inappropriate for the person's developmental level and is not a culturally or socially acceptable practice. Pica can occur at any age, but it’s most common among children and has an elevated rate among pregnant women. It can lead to intestinal obstruction, lead poisoning, and other medical complications.
2. Anorexia Nervosa: This disorder involves a restriction of energy intake that causes a significantly low body weight for the person’s age, sex, developmental trajectory, and physical health. For the diagnosis, the person must have (a) an intense fear of gaining weight or becoming fat or engage in behavior that interferes with weight gain and (b) a disturbance in the way he/she experiences his/her weight or shape, self-evaluations that are unduly influenced by weight and shape, or a lack of awareness of the seriousness of his/her low weight. Specifiers are used to indicate type (restricting or binge-eating/purging), course (in partial remission or full remission), and severity, which is determined by the person’s current body mass index. Anorexia nervosa often co-occurs with depression or an anxiety disorder (especially obsessive-compulsive disorder), and there’s evidence that anxiety often precedes the onset of anorexia. Medical complications are usually the direct result of malnutrition and extreme weight loss, affect nearly all of the major organ systems, and can lead to death.
Anorexia nervosa is a life-threatening disease that often involves frequent relapses before a stable pattern of eating and weight maintenance is attained. It’s also one of the most difficult disorders to treat because people with this disorder often deny they have an eating problem and resist treatment. The prognosis for anorexia is generally considered to be poorer than the prognosis for bulimia nervosa, but there’s some evidence that long-term outcomes for the two disorders may be more similar than previously believed.
The initial treatment goals for anorexia are to restore the person to a healthy weight and address physical complications. Subsequent goals include (a) increasing the person’s motivation to participate in treatment; (b) providing the person with education about healthy nutrition; (c) helping the person identify and change beliefs, attitudes, and emotions that are contributing to the eating disorder; (d) treating psychological conditions that are contributing to the eating disorder (e.g., low self-esteem, impulse control problems); (e) enlisting family support and providing family therapy when appropriate; and (f) helping the person identify strategies for preventing relapse. Treatments with some research support include cognitive behavior therapy (CBT) for anorexia nervosa, enhanced cognitive-behavior therapy (CBT-E) for eating disorders, and family-based treatment (FBT) for anorexia nervosa: CBT for anorexia nervosa is a post-hospitalization intervention that is based on the assumption that “shape- and weight-related concerns engender dietary restriction and other extreme methods of weight control that maintain anorexic symptoms”. It employs behavioral strategies to establish regular eating patterns and eliminate frequent body-checking and cognitive strategies to identify and replace problematic thinking and enhance motivation. CBT-E is a transdiagnostic treatment which proposes that eating disorders share the same core psychopathology – i.e., excessive value given to physical appearance and weight. It is a personalized and flexible treatment that focuses on the factors that are maintaining the individual patient’s symptoms. Finally, FBT for anorexia nervosa is an outpatient intervention for adolescents who are medically stable. It consists of three phases: (1) Parents take charge of the adolescent’s nutritional rehabilitation and weight restoration with the help of the therapist, (2) control over eating is gradually returned to the adolescent, and (3) adolescent developmental issues are addressed and include establishing age-appropriate independence for the adolescent and healthy parent-child relationships. With regard to pharmacotherapy, the research has provided inconsistent results. For example, some (but not all) studies have found the antipsychotic olanzapine to be useful for fostering initial weight gain and the SSRI fluoxetine for improving weight maintenance. Because of the inconsistent findings about the effectiveness of these and other medications for treating anorexia, some experts recommend they be used only to treat comorbid symptoms such as depression and anxiety.
3. Bulimia Nervosa: This disorder involves recurrent episodes of binge eating that are accompanied by a sense of a lack of control, inappropriate compensatory behavior to prevent weight gain (e.g., self-induced vomiting, excessive exercise), and self-evaluation that’s excessively influenced by body shape and weight. For the diagnosis, binge eating and compensatory behavior must occur at least once a week for three months or more. Specifiers are used to indicate course (in partial or full remission) and severity, which is based on average number of episodes of inappropriate compensatory behavior per week. Like anorexia nervosa, bulimia nervosa frequently co-occurs with depression or anxiety, with anxiety sometimes preceding the eating disorder. Most people with this disorder are within the normal weight range or overweight, and medical complications are usually the result of compensatory behavior. For example, purging can cause dental erosion, caries, and other dental problems; gastroesophageal reflux, and dehydration, which causes an electrolyte imbalance that can result in heart arrhythmias and death.
The treatment of bulimia nervosa ordinarily consists of nutritional rehabilitation plus cognitive behavior therapy (CBT), enhanced cognitive-behavior therapy (CBT-E) for eating disorders, interpersonal therapy (IPT), or family-based treatment (FBT) for bulimia nervosa. CBT-E is a transdiagnostic intervention for eating disorders that is based on the assumption that these disorders share the same core psychopathology – i.e., excessive value given to physical appearance and weight. CBT, CBT-E, and IPT have comparable effects, but CBT and CBT-E are generally preferred because IPT takes longer to produce those effects. FBT for bulimia nervosa is similar to FBT for anorexia nervosa. It is also an outpatient intervention for adolescents and involves three phases. However, during the first phase, the focus is on disrupting the adolescent’s binging, purging, restrictive dieting, and other undesirable methods of weight control and establishing healthy eating. In addition, the nature of the phases differs somewhat because, in contrast to adolescents with anorexia, those with bulimia often experience their symptoms as ego-dystonic and are motivated to change: As a result, treatment is more collaborative, with the adolescent and parents working together to alter the adolescent’s undesirable food-related behaviors. Finally, with regard to pharmacological treatments, antidepressants (especially fluoxetine) have been found effective for alleviating comorbid depression and for reducing binge eating and purging in patients without depression.
4. Binge-Eating Disorder: The diagnosis of binge-eating disorder (BED) requires recurrent episodes of binge eating that involve eating an amount of food that is larger than what most people would eat during a similar period of time and in similar circumstances plus a sense of a lack of control over eating during episodes. For the diagnosis, the person must also (a) have at least three of five characteristics symptoms (eating more rapidly than usual; eating until uncomfortably full; eating large amounts when not feeling hungry; feeling alone due to embarrassment about one’s binge eating; feeling disgusted, depressed, or very guilty about one’s binge eating); and (b) have had episodes that occurred, on average, at least once a week for three months. Symptom severity (mild, moderate, severe, extreme) is determined by the number of episodes each week. BED is two to three times more common in women than in men and occurs in people who are normal weight, overweight, or obese. In contrast to people with bulimia nervosa, those with BED do not engage in recurrent inappropriate compensatory behaviors and usually have a better response to treatment. In addition, dieting often follows the onset of BED, while dysfunctional dieting often precedes bulimia nervosa. BED is associated with significant psychiatric comorbidity that is comparable to the comorbidity associated with bulimia nervosa and anorexia nervosa.
Cognitive-behavior therapy-enhanced (CBT-E) and interpersonal therapy (IPT) are evidence-based treatments for BED. However, while both treatments produce a significant reduction in binge eating, some studies have found CBT-E to be more effective. A number of studies have evaluated medications for treating BED, including SSRIs (fluoxetine, paroxetine, sertraline), the anti-seizure medication topiramate, and the CNS stimulant lisdexamfetamine. Most studies have found that medication alone is less effective than CBT and that combining CBT with medication is no more effective than CBT alone. Note that experts generally recommend focusing on binge-eating before or concurrently with weight loss when treating individuals with BED who are overweight or obese.
Elimination Disorders: The elimination disorders include enuresis, which involves repeated voiding of urine into the bed or clothing, with urination either occurring two or more times a week for at least three consecutive months or causing significant distress or impaired functioning. Urination is always or usually involuntary and is not due to substance use or a medical condition. For the diagnosis, the person must be at least five years old or the equivalent developmental level. A specifier is used to identify the subtype as nocturnal only, diurnal only, or nocturnal and diurnal. The most common treatment for nocturnal enuresis is the moisture alarm (also known as the bell-and-pad), which causes a bell to ring when a child begins to urinate while sleeping. The antidiuretic hormone desmopressin used alone also reduces or stops bedwetting in many cases, but it’s associated with a high risk for relapse when it’s discontinued.
Sleep-Wake Disorders: The DSM-5-TR describes these disorders as involving “dissatisfaction regarding the quality, timing, and amount of sleep … [with] resulting daytime distress and impairment”.
1. Insomnia Disorder: Insomnia disorder is characterized by dissatisfaction with sleep quality or quantity that’s associated with one or more of three symptoms: difficulty initiating sleep; difficulty maintaining sleep; early-morning awakening with an inability to return to sleep. For the diagnosis, the sleep disturbance must occur at least three nights a week, have been present for at least three months, occur despite sufficient opportunities for sleep, and cause significant distress or impaired functioning. There are three types of insomnia: sleep-onset (initial) insomnia that involves difficulty initially falling asleep, sleep maintenance (middle) insomnia that involves frequent or extended awakening during the night, and late insomnia that involves awakening in the early morning with an inability to return to sleep. Sleep maintenance insomnia is the most common single type, but the combination of the three types is most common overall. When retrospective subjective reports of people with this disorder about their sleep are compared to objective measures obtained during their sleep (e.g., polysomnography), subjective reports usually overestimate sleep latencies, overestimate time spent awake during the night, and underestimate total amount of sleep time.
Cognitive interventions for chronic insomnia include cognitive behavior therapy for insomnia (CBT-I) and cognitive therapy for insomnia (CT-I). CBT-I is generally considered the first-line treatment. It consists of multiple components that focus on processes that occur at night: (a) Stimulus control is used to strengthen the bedroom and bed as cues for sleep (e.g., going to bed only when tired and sleeping only in the bedroom). (b) Sleep restriction is used to improve sleep efficiency, which is the amount of time in bed that is spent sleeping. It involves restricting the amount of time in bed to the amount of time the person usually sleeps (as identified with a sleep diary) and then increasing the amount of time in bed as sleep efficiency increases. (c) Sleep hygiene training consists of providing education about behaviors that facilitate and interfere with sleep (e.g., creating a comfortable bedroom, limiting coffee consumption before bedtime, getting out of bed when unable to fall asleep for 20 minutes). (d) Relaxation training involves teaching the use of meditation, progressive muscle relaxation, and/or other techniques that facilitate a relaxed state. (e) Cognitive restructuring consists of strategies designed to identify and replace negative thoughts and beliefs that contribute to insomnia. CT-I is based on Harvey’s (2005) cognitive model of insomnia and focuses on reversing cognitive processes that occur at night and during the day: (a) sleep-related worry and rumination that cause physiological arousal and distress (e.g., “If I don’t fall asleep, tomorrow will be a horrible day”); (b) selective attention and monitoring for sleep-related threats (e.g., monitoring for fatigue and concentration problems during the day); (c) unhelpful beliefs about sleep (faulty assumptions about normal sleep and the consequences of inadequate sleep); (d) misperceptions about sleep and daytime deficits (e.g., discrepancies between subjective and objective reports of time awake and time asleep); and (e) sleep-related safety behaviors which are counterproductive coping strategies that are used to increase control over sleep but actually worsen insomnia by preventing disconfirmation of unhelpful beliefs (e.g., avoiding conversations about sleep, canceling evening social activities, frequently checking the time while trying to fall asleep, exercising or drinking alcohol before bedtime to promote sleep, trying to suppress disturbing thoughts and images at bedtime).
2. Narcolepsy: Narcolepsy involves attacks of an irrepressible need to sleep that causes sleep or daytime naps at least three times a week for three months or more. The diagnosis requires episodes of cataplexy (loss of muscle tone), hypocretin deficiency, or a rapid eye movement latency of 15 minutes or less as determined by nocturnal sleep polysomnography. Many people with narcolepsy have hypnagogic or hypnopompic hallucinations (vivid hallucinations just before falling asleep or just after awakening, respectively) and/or experience sleep paralysis when falling asleep or awakening. Cataplexy is often triggered by a strong emotion, so people with this disorder may attempt to control their emotions to prevent sleep episodes.
The treatment of narcolepsy involves a combination of behavioral strategies and medication. Behavioral strategies include establishing good sleep habits, taking daytime naps, and staying active. Medications are used to improve alertness and reduce cataplexy: Medications for alertness include modafinil and its newer form armodafinil, which increase dopamine levels, and amphetamines and other psychostimulants (e.g., methylphenidate), which increase dopamine levels and, to a lesser degree, serotonin and norepinephrine levels. The primary medication for cataplexy is an antidepressant (e.g., venlafaxine, fluoxetine, and clomipramine). In addition, sodium oxybate is useful for patients who do not respond to other treatments. It’s a derivative of a natural chemical in the brain and is taken at bedtime to improve deep sleep at night and reduce cataplexy and daytime sleepiness.
3. Non-Rapid Eye Movement Sleep Arousal Disorders: The non-rapid eye movement sleep arousal disorders include sleepwalking and sleep terrors, which involve recurrent episodes of incomplete awakening from sleep that usually occur during Stage 3 or 4 sleep in the first third of a major sleep period. Sleepwalking involves getting out of bed during sleep and walking about and may include sleep-related eating or sexual behavior, while episodes of sleep terror involve an abrupt arousal from sleep that usually starts with a panicky scream and is accompanied by intense fear and autonomic arousal (e.g., tachycardia, rapid breathing). The person is unresponsive to attempts to awaken or comfort him/her during a sleepwalking or sleep terror episode and, on awakening, has little or no memory of dream imagery and cannot recall the episode. Sleepwalking and sleep terrors occur most often in childhood and decrease in frequency with increasing age.
4. Nightmare Disorder: As described in the DSM-5-TR, nightmare disorder involves “repeated occurrences of extended, extremely dysphoric, and well-remembered dreams that usually involve efforts to avoid threats to survival, security, or physical integrity”. Nightmares usually occur during rapid eye movement (REM) sleep in the second half of a major sleep period. When awakened during a nightmare, the person is usually oriented and alert but may continue to experience a dysphoric mood.
Sexual Dysfunctions, Gender Dysphoria, and Paraphilic Disorders
Sexual Dysfunctions: The DSM-5-TR describes the disorders in this category as involving “a clinically significant disturbance in a person’s ability to respond sexually or to experience sexual pleasure”. Before a diagnosis of a sexual dysfunction is assigned, it must be determined that the person’s symptoms are not due to a nonsexual mental disorder, a serious relationship disturbance or other stressor, or the effects of a drug or medical condition. For all but one diagnosis, specifiers are provided to indicate the disorder’s onset (lifelong or acquired), extent (generalized or situational) and severity (mild, moderate, or severe). The exception is genito-pelvic pain/penetration disorder, which has specifiers only for onset and severity.
1. Erectile Disorder: For this diagnosis, the person must have at least one of three symptoms on 75 to 100% of all occasions of sexual activity: marked difficulty obtaining an erection during sexual activity, marked difficulty maintaining an erection until completion of sexual activity, marked decrease in erectile rigidity. Symptoms must have been present for at least six months and cause significant distress. An organic etiology can be ruled out if the person has spontaneous erections when not planning to engage in sexual activity, has morning erections, or has erections when masturbating or when with a sexual partner other than his usual partner.
Erectile disorder is treated with behavioral techniques and pharmacotherapy. Behavioral techniques focus on reducing performance anxiety and increasing sexual stimulation. For example, sensate focus was developed by Masters and Johnson (1970) as a method for reducing performance anxiety and is used to treat erectile disorder and other sexual dysfunctions. It consists of a series of activities for a couple that are designed to promote intimacy and reduce performance anxiety by having partners focus on pleasurable sensations associated first with non-sexual touching, then with sexual touching, and finally with sexual intercourse. Drugs used to treat erectile disorder include sildenafil citrate (Viagra), tadalafil (Cialis), and vardenafil (Levitra), which increase blood flow to the penis.
2. Premature (Early) Ejaculation: This disorder involves a persistent or recurrent pattern of ejaculation during partnered sexual activity within approximately one minute of vaginal penetration and before the person desires it. Symptoms must have been present for six months or more, occur during 75 to 100% of all occasions of sexual activity, and cause significant distress.
Treatment for premature ejaculation ordinarily includes sensate focus which, as noted above, is used to reduce performance anxiety, and the start-stop technique or pause-squeeze technique, which are used to help men learn to control ejaculation. There’s evidence that a low level of serotonin contributes to this disorder, and research has confirmed that an SSRI taken daily (especially paroxetine) can delay ejaculation for some men.
3. Genito-Pelvic Pain/Penetration Disorder: This disorder involves persistent or recurrent problems with at least one of the following: vaginal penetration during intercourse; marked vulvovaginal or pelvic pain during intercourse or penetration attempts; marked anxiety about vulvovaginal or pelvic pain before, during, or as the result of vaginal penetration; marked tensing of pelvic floor muscles during attempted vaginal penetration. For the diagnosis, symptoms must have a duration of six months or longer and cause significant distress. This disorder has been linked to a history of sexual and/or physical abuse and, for some women, has an onset after a history of vaginal infections. Interventions include relaxation training, sensate focus, a topical anesthetic, vaginal dilators, and Kegel exercises (which are useful for gaining control over pelvic floor muscles).
4. Female Orgasmic Disorder: The diagnosis of female orgasmic disorder (FOD) requires the presence of marked delay in, infrequency of, or absence of orgasm or markedly reduced intensity of orgasmic sensations on all or almost all occasions of sexual activity for at least 6 months. Cognitive behavioral techniques have been found effective for treating FOD, with directed masturbation being the most empirically supported technique (especially for lifelong FOD) and the first-line treatment. Treatment may also include sex education, sensate focus, anxiety reduction techniques, mindfulness training, and/or communication skills training.
Gender Dysphoria: This disorder involves a marked incongruence between one’s assigned gender and one’s experienced or expressed gender. For children with this disorder, the diagnosis requires at least six of eight symptoms that last for at least six months and cause significant distress or impaired functioning: e.g., a strong desire to be the other gender, a strong preference for wearing clothes of the other gender, a strong preference for toys and activities typically used or engaged in by the other gender, a strong preference for playmates of the other gender, a strong dislike of one’s sexual anatomy. For adolescents and adults, the diagnosis requires at least two of six symptoms that last for at least six months and cause significant distress or impaired functioning: e.g., a strong desire to be rid of one’s primary and/or secondary sex characteristics, a strong desire to be the other gender, a strong desire to be treated as the other gender, a strong conviction that one has feelings and reactions that are characteristic of the other gender.
The Dutch protocol and the gender-affirmative model are two approaches to the treatment of gender dysphoria (or, more generally, to the care of gender diverse youth). The Dutch protocol is based on the assumption “that gender dysphoria, or a transgender identity, persists into adolescence in only a small minority of people”. Consequently, for children under 12 years of age, it recommends “watchful waiting” accompanied by support for children and their families. Then, at the first signs of puberty, social transition and puberty-blocking drugs are started for children who are persistent in their gender dysphoria. This gives children time to further explore their gender identity and decide if they want to start cross-sex hormone therapy when they’re 16 years of age and undergo gender-affirming surgeries after they’re 18. The gender-affirmative model has become the most widely accepted approach and is based on the assumption that “a child of any age may be cognizant of their authentic identity and will benefit from a social transition at any stage of development”. Social transition is followed, as appropriate, by puberty blockers, cross-sex hormones, and surgeries; and, throughout the transition process, gender issues are addressed with youth and their families in a supportive and non-judgmental way. This model also assumes that (a) gender variations are not disorders; (b) gender presentations are diverse and vary across cultures; (c) gender is not always binary and may be fluid; and (d) if present, a child’s psychological problems are often secondary to negative interpersonal and cultural reactions to the child (e.g., transphobia, homophobia, sexism).
Research on the outcomes of gender confirmation surgery (also known as gender-affirming surgery) has generally found that it’s associated with a decrease in gender dysphoria, improved self-satisfaction, and a low incidence of regret. There’s also evidence that transgender male patients have somewhat more positive outcomes than transgender female patients do. Factors that have been linked to positive outcomes include careful diagnostic screening of individuals seeking surgery, psychological stability, adequate social support, and a lack of surgical complications.
Paraphilic Disorders: The DSM-5-TR defines a paraphilia as involving “intense and persistent sexual interest other than sexual interest in genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting human partners” and a paraphilic disorder as a paraphilia that “is currently causing distress or impairment to the individual or … has entailed personal harm, or risk of harm, to others”.
Treatments for paraphilic disorders combine cognitive-behavior therapy with other interventions including group therapy, marital therapy, and/or pharmacotherapy. Cognitive strategies include cognitive restructuring and empathy and skills training. Behavioral strategies are based on classical conditioning and include covert sensitization and orgasmic (masturbatory) reconditioning. Covert sensitization is a form of aversive counterconditioning that’s conducted in imagination and replaces the sexual arousal elicited by the paraphilic object or behavior with fear or other undesirable response. Orgasmic reconditioning involves instructing the person to switch while masturbating from fantasizing about the paraphilic object or behavior to fantasizing about a more appropriate object or behavior. Drugs used to treat severe forms of this disorder include gonadotropin-releasing hormones (e.g., Lupron) and antiandrogens (e.g., Depo-Provera). Although these drugs reduce sexual desire, they have serious side effects and a high risk for relapse as soon as they’re discontinued. SSRIs may be prescribed for individuals with less serious disorders to reduce the depression or compulsions that trigger paraphilic behavior.
1. Frotteuristic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months from touching or rubbing against a nonconsenting adult as manifested in fantasies, urges, and/or behaviors. For the diagnosis, the person must have acted on the urges with a nonconsenting person or experienced significant distress or impaired functioning as the result of the fantasies or urges.
2. Transvestic Disorder: Transvestic disorder involves cross-dressing for the purpose of sexual arousal for at least six months as manifested in fantasies, urges, and/or behaviors that cause significant distress or impaired functioning. Most men with this disorder identify themselves as heterosexual but may have had occasional sexual relations with men, especially when cross-dressed.
3. Pedophilic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months related to fantasies, urges, and/or behaviors involving sexual activity with a child or children 13 years of age or younger. The person must have acted on these urges or must have experienced significant distress or interpersonal problems because of them and must be 16 years of age or older and at least five years older than the child or children.
4. Fetishistic Disorder: This disorder involves recurrent and intense sexual arousal for at least six months in response to a nonliving object or specific non-genital body part with the arousal causing significant distress or impaired functioning.
5. Exhibitionistic Disorder: Exhibitionistic disorder involves recurrent and intense sexual arousal for at least six months from exposing one’s genitals to an unsuspecting person as manifested by fantasies, urges, or behaviors. For the diagnosis, the person must have acted on the urges with an unsuspecting person or experienced significant distress or impaired functioning as a result of sexual urges or fantasies. There are three subtypes: sexually aroused by exposing genitals to prepubertal children, to physically mature individuals, or to both prepubertal children and physically mature individuals. The diagnosis can be applied to individuals who either disclose information about their exhibitionistic fantasies, urges, or behaviors or deny them despite objective evidence to the contrary.
Disruptive, Impulse-Control, and Conduct Disorders
The disorders in this category involve “problems in the self-control of emotions and behaviors” and include oppositional defiant disorder, conduct disorder, and intermittent explosive disorder.
Oppositional Defiant Disorder: The diagnosis of oppositional defiant disorder (ODD) requires a recurrent pattern of an angry/irritable mood, argumentative/defiant behavior, and/or vindictiveness as evidenced by four or more characteristic symptoms that occur during interactions with at least one person who is not a sibling – e.g., often loses temper, is angry and resentful, often deliberately annoys others, often blames others for his/her mistakes or misbehavior. Symptoms have lasted for at least six months and have caused distress for the individual or others in the individual’s immediate social context or have a negative impact on the individual’s functioning. In young children, ODD is more common in boys than girls but, in older children and adolescents, it occurs about equally often in boys and girls. About 30% of children who have a diagnosis of ODD eventually receive a diagnosis of conduct disorder, with an early age of onset of symptoms being associated with a higher risk for conduct disorder.
There is no single optimal treatment for individuals with ODD, and the most effective treatment is multimodal and tailored to the age, symptoms, and comorbidities of the child or adolescent. Evidence-based psychosocial interventions are first-line treatments and are the same as those for other disruptive behavior disorders. These interventions are described in the section on treatments for conduct disorder.
Conduct Disorder: The diagnosis of conduct disorder (CD) requires a persistent pattern of behavior that violates the basic rights of others and/or age-appropriate social norms or rules as evidenced by the presence of at least three characteristic symptoms during the past 12 months and at least one symptom in the past six months. Symptoms represent four categories: aggression to people and animals, destruction of property, deceitfulness or theft, and serious violation of rules. Symptoms must have caused significant impairment in functioning. The diagnosis cannot be assigned to individuals over age 18 who meet the criteria for antisocial personality disorder. This disorder is more common in males than females and, although symptoms may occur during early childhood, they more often emerge between middle childhood and middle adolescence.
The DSM-5-TR provides specifiers for three subtypes: childhood-onset type for individuals who have at least one symptom before age 10; adolescent-onset type for individuals who exhibit no symptoms before age 10; and unspecified onset when the onset is unknown. The childhood-onset type is associated with a higher degree of aggressiveness and a greater risk for a future diagnosis of antisocial personality disorder and/or a substance-related disorder. It also provides specifiers for severity of the disorder (mild, moderate, and severe) that are based on the number of conduct problems and their consequences.
1. Etiology of Conduct Disorder: Conduct disorder has been linked to multiple factors including heredity, family experiences, and lower physiological reactions to stress. Evidence for the role of heredity is provided by family, twin, and adoption studies. For example, a frequently cited study of adult twin pairs obtained heritability estimates of 65% for men and 43% for women and concordance rates of 53% and 37% for male monozygotic and dizygotic twins, respectively, and 30% and 18% for female monozygotic and dizygotic twins, respectively. Research on family experiences has linked an increased risk for conduct disorder to physical and sexual abuse and neglect during childhood, harsh and inconsistent discipline, frequent changes in caregivers, and parental criminology and substance abuse. Finally, a low resting heart rate has been identified as a risk factor for this disorder, and several studies have found that, compared to healthy children, children with CD alone or CD with comorbid ADHD have lower physiological reactions to aversive stimuli as measured by self-reports, skin conductance, and heart rate. In addition, Fairchild and colleagues (2019) compared male adolescents with CD to adolescents without a psychiatric disorder and found that adolescents with CD did not experience the typical increase in cortisol level and cardiovascular response to a stressful procedure even though adolescents with and without CD reported similar increases in negative affect during the procedure. According to Fairchild et al., the discrepancy for youth with CD “between subjective and physiologic changes suggests poorer coordination between emotional and physiologic arousal”.
Moffitt (1993) distinguishes between two types of antisocial behavior that correspond to DSM-5’s childhood-onset and adolescent-onset CD, and she attributes the two types to different factors: Her life-course-persistent type involves a pattern of increasingly serious antisocial behaviors that begins in early childhood, continues into adulthood, and is consistent across situations. Moffitt describes this type as being due to a combination of neuropsychological deficits that affect the individual’s temperament, cognitive abilities, and other characteristics and an adverse child-rearing environment. In contrast, her adolescence-limited type is a temporary and situational type of antisocial behavior that’s due to a “maturity gap” between an adolescent’s biological and sexual maturity and his/her social maturity. For individuals with this type, antisocial behaviors are a way to attain mature status.
Moffitt’s description of the outcomes of life-course persistent and adolescent-limited types of conduct disorder are consistent with the DSM-5’s description of the course of the disorder. According to the DSM-5, for most individuals, conduct disorder remits by adulthood, and this is especially true for those whose symptoms have an onset in adolescence. In contrast, individuals whose symptoms begin in childhood have a worse prognosis and “an increased risk of criminal behavior, conduct disorder, and substance-related disorders in adulthood”.
2. Treatment of Conduct Disorder: Evidence-based psychosocial interventions are the first-line treatments for CD and other disruptive behavior disorders and can be categorized as child-focused, parent-focused, family-focused, or multimodal):
(a) Child-Focused Intervention: Problem-solving skills training (PSST) is for children and adolescents who have CD or another disruptive behavior disorder. It focuses on the cognitive processes that underlie children’s problematic behaviors and helps them accurately perceive the feelings of others, understand the consequences of their actions, and identify prosocial ways to resolve interpersonal problems and conflicts.
(b) Parent-Focused Interventions: Parent management training – Oregon model (PMTO) is for parents of children 2 to 18 years old. It is based on the assumption that children’s aggressive, antisocial, and other externalizing behaviors are the result of an escalating cycle of coercive interactions between children and their parents. PMTO helps parents replace coercive parenting practices with positive parenting that includes positive reinforcement, non-coercive discipline, setting limits, and monitoring children’s behaviors. Kazdin’s parent management training (PMT) is for parents of children 2 to 17 years old with oppositional, aggressive, and/or antisocial behavior. Training is based on the principles of operant conditioning and focuses on replacing antecedents and consequences that are maintaining problematic behaviors with antecedents and consequences that foster desirable behaviors. Research has confirmed that PMT has positive effects on child symptoms, parent symptoms, and family relationships and suggests that combining PMT with PSST is even more effective than either treatment alone for improving child and parent functioning. Parent-child interaction therapy (PCIT) is for parents of children 2 to 7 years old who have severe behavioral problems and is also an evidence-based intervention for children who have experienced or are at risk for experiencing maltreatment. PCIT focuses on altering negative parent-child interactions and consists of a child-directed interaction phase that focuses on enhancing the parent-child relationship and a parent-directed interaction phase that focuses on teaching parents effective disciplinary practices.
(c) Family-Focused Interventions: Functional family therapy (FFT) is an intervention for families that include a child 11 to 18 years old who has an externalizing behavior disorder and/or substance use problem or is at high risk for delinquency. It is based on the assumption that problematic behaviors within a family help regulate relational connections by fostering interdependence or independence and regulate relational hierarchies by creating power structures. The primary goal of therapy is to replace problematic behaviors with non-problematic behaviors that serve the same functions. Multidimensional family therapy (MDFT) is for families that include a member 11 to 21 years old who has a substance use disorder and comorbid internalizing or externalizing symptoms and/or delinquency. It incorporates elements of family systems theory, ecological theory, and developmental psychology. Its primary goals are to reduce or eliminate the adolescent’s substance use, aggression, and other symptoms and improve adolescent and family functioning by facilitating change in four interdependent domains: adolescent, parents, family interactions, and extrafamilial sources of influence.
(d) Multimodal Interventions: Multisystemic therapy (MST) is an intensive family and community-based intervention for adolescents 12 to 18 years of age who are at imminent risk for out-of-home placement due to antisocial behaviors, substance use problems, and/or serious psychiatric problems. It is based on Bronfenbrenner’s ecological theory and assumes that problematic behaviors are the result of multiple risk factors at individual, family, peer, school, and community levels and that interventions must be provided at all levels. Research investigating the effectiveness of MST has often included economically impoverished families, single-parent families, and African American and other racial/ethnic minority families and provide evidence that it is equally effective for these types of families. MST-CAN is a version of MST for families of abused and neglected children who are 6 to 17 years of age. Multidimensional treatment foster care (MTFC) is an alternative to residential care for children and adolescents who need intensive support due to child maltreatment, severe emotional disturbance, and/or juvenile delinquency. It involves developing a behavioral management plan that is tailored to the child and administered by a treatment team in the child’s home, school, and community. Children reside with highly trained and supervised foster parents while their biological parents receive the training and support they need for positive reunification.
Note that research investigating the effectiveness of Scared Straight programs as a prevention or intervention for conduct disorder have found that they tend to have harmful effects, with participation in these programs increasing the likelihood that juvenile offenders and at-risk juveniles will engage in criminal behaviors in the future. The studies have also found that confrontational “rap sessions” and nonconfrontational (educational) approaches have similar negative effects and that these programs may have even worse outcomes for seriously delinquent juveniles.
Intermittent Explosive Disorder: This disorder is diagnosed when the individual has had recurrent behavioral outbursts that are due to a failure to control aggressive impulses as manifested by one of the following: (a) verbal or physical aggression that occurs, on average, twice weekly for at least three months, with physical aggression not resulting in damage or destruction to property or physical injury to other people or animals. (b) three behavioral outbursts in a 12-month period that resulted in damage or destruction of property and/or physical injury to other people or animals. The diagnosis also requires that the level of aggressiveness must not be proportional to provocation or any precipitating social stressor and that outbursts must not be premeditated or committed to achieve a tangible outcome and must cause significant distress to the individual, impaired occupational or interpersonal functioning, or negative financial or legal consequences. In addition, the individual must be at least six years old or at the equivalent developmental level. The onset of this disorder is usually in childhood or adolescence.
Substance-Related and Addictive Disorders
This category includes substance-use and substance-induced disorders for 10 classes of substances: alcohol; caffeine; cannabis; phencyclidine and other hallucinogens; inhalants; opioids; sedatives, hypnotics, or anxiolytics; stimulants; tobacco; and other/unknown.
Substance-Use Disorders: The DSM-5-TR describes substance use disorders as involving “a cluster of cognitive, behavioral, and physiological symptoms indicating that the individual continues using the substance despite significant substance-related problems”. Substance use disorder can be diagnosed for all classes of substances except caffeine and are further described with specifiers to indicate the severity of the disorder (which is determined by the number of symptoms) and if the person is in early or sustained remission, on maintenance therapy, or in a controlled environment. For the diagnosis of all of these disorders, the person must have two or more characteristic symptoms within a 12-month period.
Substance-Induced Disorders: These disorders include substance intoxication, substance withdrawal, and substance/medication-induced mental disorders (e.g., substance-induced depressive disorder, anxiety disorder, major neurocognitive disorder, withdrawal delirium). In addition, hallucinogen-induced disorders include hallucinogen persisting perceptual disorder. The symptoms of some of these disorders are summarized below:
1. Alcohol Intoxication: This disorder involves problematic behavioral and psychological changes (e.g., inappropriate sexual or aggressive behavior, mood lability, impaired judgment) with at least 1 of 6 symptoms: slurred speech, incoordination, unsteady gait, nystagmus, impaired attention or memory, stupor or coma.
2. Alcohol Withdrawal: The diagnosis of this disorder requires at least two of eight symptoms that develop within several hours to a few days following cessation or reduction of heavy and prolonged alcohol use: autonomic hyperactivity, hand tremor, insomnia, nausea or vomiting, transient hallucinations or illusions, anxiety, psychomotor agitation, generalized tonic-clonic seizures.
3. Alcohol-Induced Major Neurocognitive Disorder: This diagnosis requires evidence of a significant decline in one or more cognitive domains that interferes with independence in everyday activities. A specifier is used to indicate if the disorder is the nonamnestic-confabulatory type or amnestic-confabulatory type. The latter type is also referred to as Korsakoff syndrome, which has been linked to a thiamine deficiency and involves anterograde and retrograde amnesia and confabulation.
4. Opioid Intoxication: This disorder involves significant problematic behavioral or psychological changes (e.g., initial euphoria followed by apathy or dysphoria and impaired judgment) plus pupillary constriction and the development of at least one of three symptoms during or shortly after opioid use: drowsiness or coma, slurred speech, impaired attention or memory. Opioid intoxication can occur with or without perceptual disturbances, which are hallucinations with intact reality testing or illusions in the absence of delirium. Opioids include opium, heroin, morphine, and codeine, which are derived from the opium poppy, and synthetic and partly-synthetic drugs, which include methadone, oxycodone, hydrocodone, and fentanyl.
5. Opioid Withdrawal: This diagnosis requires the development of at least three of nine symptoms following cessation of heavy and prolonged opioid use or administration of an opioid antagonist after opioid use: e.g., dysphoric mood, nausea or vomiting, muscle aches, diarrhea, yawning, fever, insomnia.
6. Stimulant Intoxication: Stimulant Intoxication is characterized by maladaptive behavioral and psychological changes (e.g., euphoria or affective blunting, hypervigilance, interpersonal sensitivity, anxiety or anger, impaired judgment) and the development of at least two of nine symptoms during or shortly after stimulant use: tachycardia or bradycardia, pupillary dilation, elevated or lowered blood pressure, perspiration or chills, nausea or vomiting, weight loss, psychomotor agitation or retardation, respiratory depression or cardiac arrhythmia, seizures or coma. Stimulant drugs include amphetamines, methamphetamines, and cocaine.
7. Stimulant Withdrawal: This diagnosis requires a dysphoric mood and at least two of five physiological changes that develop within a few hours to several days after cessation of prolonged stimulant use: fatigue, vivid and unpleasant dreams, insomnia or hypersomnia, increased appetite, psychomotor agitation or retardation.
8. Tobacco Withdrawal. This disorder involves at least four of seven symptoms that develop within 24 hours of abrupt cessation or reduction of the use of tobacco: irritability, anger or anxiety, impaired concentration, increased appetite, restlessness, depressed mood, insomnia. Note that the duration and severity of withdrawal symptoms vary for different levels of addiction but ordinarily peak 48 to 72 hours following cessation of nicotine use and then gradually wane over several weeks. Cravings for nicotine last longer than withdrawal symptoms and can be the cause of early and late relapses.
9. Hallucinogen Persisting Perception Disorder: This disorder involves reexperiencing at least one of the perceptual symptoms that were experienced while intoxicated with LSD or other hallucinogen, with symptoms causing significant distress or impairment. Visual disturbances (e.g., flashes of color, halos around objects) are most common. Episodes (“flashbacks”) are often very brief but may recur over days, weeks, months, or longer. Reality testing during episodes is intact (i.e., the person is aware that current symptoms are due to previous drug use).
Treatment of Substance-Related Disorders: The treatment of substance use disorders varies, depending on the type of substance(s), the severity of the disorder, the presence of comorbidities, and the person’s preferences. However, treatment ordinarily includes individual, family, and/or group interventions and medication. Evidence-based interventions include cognitive behavioral therapy, motivational interviewing, contingency management, family behavior therapy, the community reinforcement approach, personalized normative feedback, text messages, relapse prevention therapy, and 12-step facilitation. Research has generally found that combined interventions are most effective for substance use disorders. As an example, studies evaluating treatments for tobacco use disorder suggest that therapy (especially therapy that includes critical thinking skills training and social support) and medication (especially nicotine nasal spray and varenicline) are each effective when used alone but that the combination of therapy and medication is most effective. (Information about medications used to treat substance use disorders is provided in the physiological psychology and pharmacology content summary.)
1. Community Reinforcement Approach (CRA): The CRA is based on the principles of operant conditioning and “helps people arrange their lifestyles so that healthy, drugfree living becomes rewarding and thereby competes with alcohol and drug use”. Community reinforcement and family training (CRAFT) was derived from CRA but was designed for individuals who refuse to seek treatment for their substance abuse problems. Consequently, rather than focusing on the person with the substance use disorder (the identified patient), a CRAFT therapist works with a concerned significant other (CSO) who is a family member or close friend. The primary goals of CRAFT are to (a) help the CSO influence the identified patient to enter substance-use treatment, (b) teach the CSO procedures to help reduce the identified patient’s substance use, and (c) help the CSO make positive life changes that improve the CSO’s quality of life whether or not the identified patient enters treatment.
2. Voucher-Based Reinforcement Therapy (VBRT): VBRT is a type of contingency management that involves giving patients vouchers that can be exchanged for goods and services in the community when they achieve treatment goals (e.g., negative urine drug screens). Research has found that VBRT is effective as a stand-alone treatment for promoting abstinence for a number of substances, including cocaine, opiates, marijuana, and tobacco. However, some experts suggest that combining VBRT with another intervention may be the optimal approach. For example, in his summary of treatments for cocaine use disorder, Kampman (2019) points out that the studies have shown that VBRT is useful for promoting initial abstinence but that its effects fade when vouchers are discontinued. In contrast, cognitive-behavior therapy (CBT) is less useful for promoting initial abstinence but helps patients maintain abstinence following treatment because it provides them with coping skills they can continue to use post-treatment.
3. Personalized Normative Feedback (PNF): PNF is based on the assumption that, “if perceptions of the prevalence of a given behavior influence one’s own behavior … and one overestimates the prevalence of that behavior, then correcting this misperception should reduce the behavior”. Use of this intervention involves providing clients with information that allows them to compare the frequency of their own behavior and their perceived frequency for a typical person in their peer group to the actual average frequency for people in their peer group. For example, when using PNF to reduce a college student’s alcohol consumption, the student may be given three bar graphs: one that indicates the client’s frequency of drinking, another that indicates the client’s perceptions of a typical college student’s frequency of drinking, and another that indicates the actual average frequency of drinking of college students. PNF was initially developed as a brief stand-alone intervention for heavy-drinking college students in response to research which found that college students tend to over-estimate the amount and frequency of alcohol use of their peers and that this misperception is associated with higher levels of alcohol consumption. It has since been applied to other populations and other substance use disorders, gambling disorder, eating disorders, intimate partner violence, and other problematic behaviors and has been found to be effective both as stand-alone intervention and in combination with motivational interviewing or other interventions.
4. Text-Messages: Text messages have been found to be a useful intervention for several mental health conditions, including substance use disorders, schizophrenia, and affective disorders. When used as a mental health intervention, text messages serve four major functions: They provide appointment and medication reminders, health care information, support, and a means of self-monitoring. A number of studies have confirmed the effectiveness of text messaging as a smoking cessation intervention when used as a stand-alone treatment or in combination with other interventions: For example, Whittaker et al.’s (2019) meta-analysis of the research found that (a) text message smoking cessation interventions alone produced higher quit rates than did minimal smoking cessation support (e.g., general health advice provided by a clinician); (b) text messaging alone and other smoking cessation interventions alone (e.g., brief smoking cessation counseling, internet-based interactive smoking cessation program) produced similar quit rates; and (c) text messaging plus other smoking cessation interventions produced higher quit rates than did the other interventions alone.
5. Relapse Prevention Therapy (RPT): Marlatt and Gordon’s RPT is a cognitive-behavioral approach to relapse prevention. It describes substance addiction as a “learned habit pattern” and views lapses following a period of abstinence as being precipitated by a high-risk situation (e.g., a negative emotional state, interpersonal conflict, social pressure). It also proposes that a lapse is most likely to turn into a full-blown relapse when the person has poor coping skills, low self-efficacy, and high expectations about the positive effects of alcohol and responds to the lapse with an “abstinence violation effect” – i.e., with negative emotions, guilt, and a sense of personal failure. RPT utilizes cognitive and behavioral strategies that enable clients to recognize and deal more effectively with high-risk situations. Strategies include training in coping skills, enhancing self-efficacy, challenging myths about the positive outcomes of substance use, cognitive restructuring to view lapses as mistakes rather than the result of personal failure, and altering lifestyle factors that increase exposure or reduce resistance to high-risk situations.
6. Project MATCH: Project MATCH, a multisite clinical trial, compared the effectiveness of cognitive behavioral coping skills therapy, motivational enhancement therapy, and twelve-step facilitation for clients who had received a DSM-III-R diagnosis of alcohol dependence or abuse. It also evaluated the client-treatment matching hypothesis, which predicts that client outcomes can be improved by matching clients with certain characteristics to treatments most appropriate for those characteristics. Clients were randomly assigned to one of the three treatments, and clients in each group were categorized in terms of several characteristics (e.g., alcohol involvement, psychiatric severity, anger, and social support for drinking versus abstinence). Results indicated that, at one-year and three-year follow-ups, all three treatments had produced significant reductions in drinking, with twelve-step facilitation having a slight advantage over the other two treatments. The results also provided some support for the matching hypothesis. For example, at the three-year follow-up, clients whose social networks were supportive of drinking benefited most from twelve-step facilitation, while clients who were high in anger benefited most from motivational enhancement therapy.
Neurocognitive Disorders
This category includes delirium and mild and major neurocognitive disorders.
Delirium: The diagnosis of delirium requires (a) a disturbance in attention and awareness that develops over a short period of time (often hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity over the course of the day plus (b) at least one additional disturbance in cognition (e.g., a memory or language impairment). Symptoms must not be better explained by another pre-existing or evolving neurocognitive disorder and must not occur in the context of a severely reduced level of arousal (e.g., a coma). There must also be evidence that symptoms are the direct physiological consequence of a medical condition, substance intoxication or withdrawal, and/or exposure to a toxin.
Causes of delirium include a high fever, nutritional deficiency, electrolyte disturbance, renal or hepatic failure, head injury, and certain drugs and medications (e.g., alcohol, lithium, sedatives, anticholinergic drugs), and it’s most common in hospitalized older adults. Treatment involves addressing causal and contributing medical problems and reducing disorientation through environmental manipulation by, for example, providing sufficient lighting, reducing noise, and minimizing the number of visitors. In addition, haloperidol or other antipsychotic drugs may help reduce agitation and psychotic symptoms.
Major and Mild Neurocognitive Disorder: The core feature of major and mild neurocognitive disorder (NCD) is cognitive dysfunction that’s acquired rather than developmental. Major neurocognitive disorder is diagnosed when there’s a significant decline from a previous level of functioning in one or more cognitive domains (e.g., executive functioning, learning and memory, social cognition) that does not occur only in the context of delirium and that interferes with the person’s independence in everyday activities. Mild neurocognitive disorder is diagnosed when there’s a modest decline from a previous level of functioning in one or more cognitive domains that does not occur only in the context of delirium and that does not interfere with the person’s independence in everyday activities but may require greater effort or the use of compensatory strategies.
In the literature, a distinction is made between cortical, subcortical, and cortico-subcortical neurocognitive disorders. (a) Cortical neurocognitive disorders are primarily the result of damage to areas of the cerebral cortex. Memory loss is often the initial symptom of these disorders; other common symptoms are aphasia, agnosia, apraxia, poor insight, and impaired judgment. Included in this category are NCD due to Alzheimer’s disease and frontotemporal NCD. (b) The subcortical neurocognitive disorders are primarily the result of damage to the basal ganglia, thalamus, and brainstem. The primary symptoms are slowed cognitive processes, apathy, depression, and psychomotor retardation (e.g., dysarthric speech, gait disturbances). Included in this category are NCD due to Huntington’s disease, NCD due to Parkinson’s disease, NCD due to HIV infection, and some forms of vascular NCD. (c) The cortico-subcortical neurocognitive disorders involve damage in the connections between cortical and subcortical areas of the brain, with symptoms depending on the specific areas that are affected. This category includes some types of vascular NCD, NCD with Lewy bodies, and Creutzfeldt-Jakob disease, which is a type of NCD due to prion disease.
1. Neurocognitive Disorder Due to Alzheimer’s Disease: This disorder accounts for about 60 to 80% of all cases of NCD (Jalbert, Daiello, & Lapane, 2008). It’s diagnosed when the person’s symptoms (a) meet the criteria for mild or major NCD, (b) have an insidious onset and gradual progression of impairment in one or more cognitive domains that does not interfere with daily activities for mild NCD and two or more cognitive domains that interfere with daily activities for major NCD, (c) meet the criteria for the probable or possible form of the disorder, and (d) are not better explained by another disorder. For major NCD, the diagnosis of probable Alzheimer’s disease requires evidence of a causative genetic mutation from genetic testing or family history and/or evidence of a decline in memory and learning and at least one other cognitive domain, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology. When these criteria are not met, the diagnosis of possible Alzheimer’s disease is assigned. For mild NCD, the diagnosis of probable Alzheimer’s disease requires evidence of a causative genetic mutation from genetic testing or family history, while the diagnosis of possible Alzheimer’s disease is assigned when there’s no evidence of a causative genetic mutation but there’s evidence of a decline in memory and learning, a steadily progressive and gradual decline in cognition, and no evidence of a mixed etiology. Prevalence rates for Alzheimer’s disease are affected by gender and race/ethnicity: Reported prevalence rates indicate that, overall, the rate for women is greater than the rate for men, although this difference may be due to the fact that women live longer than men do. Also, when considering gender and age, it is not clear that women have higher rates than men of the same age. With regard to race, among adults ages 65 and older, Black Americans have both the highest prevalence and incidence rates followed by, in order, Hispanic and White Americans. The DSM-5-TR notes that the onset of symptoms is most often from 70 to 89 years of age and that an early onset form of the disorder in individuals ages 49 through 59 is often related to known chromosomal mutations. It also states that “younger individuals are more likely to survive the full course of the disease, while older individuals are more likely to have medical comorbidities that affect the course and management of the illness” (p. 692).
The diagnosis of Alzheimer’s disease can be definitively confirmed only with a brain biopsy or an autopsy of the brain after death (Khan, 2016). However, a brain biopsy is rarely done because of the discomfort and risks associated with this procedure. Therefore, an in vivo clinical diagnosis requires the presence of characteristic symptoms as well as elimination of other explanations for the symptoms. Eliminating alternative explanations involves obtaining information from a variety of sources including a family history, physical and neurological exams, laboratory tests, neuroimaging (e.g., CT scan, MRI, FDG-PET),, mental status evaluation, and neuropsychological testing. Note that several techniques are used to identify Alzheimer’s disease in research settings (e.g. molecular imaging, cerebrospinal fluid protein tests, and genetic risk profiling) but are not routinely used for clinical diagnosis.
The term “pseudodementia” is sometimes used to describe depression that has prominent cognitive symptoms. Unlike people with Alzheimer’s disease, people with pseudodementia usually respond well to treatment, and they have an abrupt onset of symptoms, exaggerate their cognitive problems, have moderate memory loss and symptoms of melancholia and anxiety, and often say “I don’t know" in response to assessment questions. In contrast, those with Alzheimer’s disease have an insidious onset of symptoms, minimize or deny their cognitive problems, have severe memory impairment, and symptoms of apathy and avolition, and often respond to assessment questions with wrong answers (Ahmed & Takeshita, 1997; Taylor, 1999).
a. Etiology of Alzheimer’s Disease: Alzheimer’s disease has been linked to chromosomal, neurotransmitter, and brain abnormalities (Turkington & Mitchell, 2010). Several genetic variants have been identified as risk factors, including the ApoE4 variant on chromosome 19. Neurotransmitter abnormalities include reduced acetylcholine (ACh) and excessive glutamate, which are both known to be involved in learning and memory. The hallmark brain abnormalities of Alzheimer’s disease are amyloid plaques and neurofibrillary tangles, which disrupt cell-to-cell communication. Both are due to a build-up of proteins that occurs with normal aging but is more pervasive in individuals with Alzheimer’s disease. Extracellular amyloid plaques consist of clumps of beta-amyloid protein, which is formed from the breakdown of a larger protein known as amyloid precursor protein (APP). Intracellular neurofibrillary tangles are created by an abnormal accumulation of tau protein that results in the formation of threads that join to form tangles. Amyloid plaques and neurofibrillary tangles are first evident in medial temporal lobe structures (which include the entorhinal cortex, amygdala, and hippocampus) and, as the disease progresses, they appear in the frontal and parietal lobes and eventually throughout the cortex. There’s also evidence that the locus coeruleus (an area in the brain stem) is the first area of the brain to be affected by Alzheimer’s disease and shows abnormalities before the appearance of symptoms (Mather & Harley, 2016). Note that neuronal loss in the locus coeruleus has also been linked to neurocognitive disorder with Lewy bodies and neurocognitive disorder due to Parkinson’s disease (Brunnstrom, Friberg, Lindberg, & Englund, 2011). Finally, studies have found that a rapid deterioration in the sense of smell during a period of normal cognition predicts the subsequent development of mild cognitive impairment or Alzheimer’s disease, with greater olfactory loss being associated with greater cognitive impairment. These studies have also shown that deterioration in the sense of smell is related to structural changes in areas of the brain that are involved in olfactory processing and are known to be affected by Alzheimer’s disease (e.g., entorhinal cortex, amydgala, hippocampus) (e.g., Murphy, 2019; Pacyna et al., 2023).
b. Factors Associated with Alzheimer’s Disease: As noted in the DSM-5-TR, an increased risk for Alzheimer’s disease has been linked to several factors including low educational status, obesity, and hearing loss. Down Syndrome is also a risk factor: Standard trisomy 21 is the most common type of Down syndrome and is caused by an extra chromosome 21, which means that people with this disorder have an extra gene for the amyloid precursor protein (APP) gene. Because of the extra APP gene, amyloid begins to accumulate in the brains of people with Down syndrome in their late teens to early 20s and increases their risk for early-onset Alzheimer’s disease. Finally, Alzheimer’s disease has been linked to the Big Five personality traits: Terracciano et al. (2021) compared scores obtained by participants in the Baltimore Longitudinal Study of Aging on the Revised NEO Personality Inventory with the results of their positron emission tomography (PET) scans. They found that participants who obtained high scores on neuroticism and low scores on conscientiousness had more deposits of amyloid and tau (the hallmarks of Alzheimer’s disease) than did participants who obtained low scores on neuroticism and high scores on conscientiousness.
c. Stages of Alzheimer’s Disease: The average duration of Alzheimer’s disease from symptom onset until death varies from person to person but is usually about 8 to 10 years. The progression of symptoms also varies somewhat but can be described as involving three stages (Cohan, 2012; Hammond, 2012; Turkington & Mitchell, 2010): The early stage lasts for about 2 to 4 years and involves short-term memory loss (which is usually the first symptom), anomia (difficulty recalling names of familiar people and objects), personality changes (often indifference and loss of spontaneity), anxiety or depression, impaired attention and concentration, poor judgment, and disorientation to time and space. The middle stage lasts for 2 to 10 years and is characterized by increasing short-term memory loss, long-term memory loss, labile mood, irritability, increasing disorientation, delusions and hallucinations, wandering and pacing, perseveration (repetitive speech and actions), loss of impulse control, impaired speech, disrupted sleep patterns, problems with normal daily activities (e.g., bathing, grooming, dressing), and sundowning (increased confusion, agitation, and restlessness in the late afternoon or evening). The late stage lasts for 1 to 3 years and involves severely deteriorated cognitive functioning, severe disorientation, apathy, severely impaired communication, agitation and aggression, decreased appetite, urinary and fecal incontinence, loss of basic motor skills and most or all self-care skills, abnormal reflexes, seizures, and frequent infections.
d. Treatment of Alzheimer’s Disease: There’s no cure for Alzheimer’s disease, but there are treatments that can temporarily reduce specific symptoms. Cholinesterase inhibitors and memantine are used to reduce or stabilize memory loss, confusion, and other cognitive symptoms. Cholinesterase inhibitors include donepezil and rivastigmine and delay the breakdown of ACh, while memantine is an NMDA receptor antagonist and regulates glutamate activity. In addition, donanemab was recently approved by the FDA to slow the progression of early-stage Alzheimer’s disease. It is an intravenous infusion that is delivered every four weeks and exerts its effects by targeting and reducing amyloid plaques in the brain. Treatment often includes cognitive and behavioral interventions to improve cognitive functioning and reduce problematic behaviors and, as appropriate, antidepressants to alleviate depression and irritability, anxiolytics to reduce anxiety and restlessness, and antipsychotics to reduce behaviors that are related to mania or psychosis or pose a danger to self or others. Support, skills training, and other interventions for caregivers are also important. They not only benefit the caregivers but also reduce the likelihood that caregivers will place the family member with Alzheimer’s disease in a nursing home, which is desirable because remaining at home is associated with better patient outcomes (e.g., Mittelman, Haley, Clay, & Roth, 2006).
2. Neurocognitive Disorder with Lewy Bodies: This disorder is due to the build-up in certain areas of the brain of Lewy bodies, which consist of an abnormal protein. It’s diagnosed when the individual meets the criteria for major or mild NCD and has the required number of core and suggestive features for the probable or possible forms of the disorder, and symptoms have an insidious onset and a gradual progression. The core features are fluctuating cognition with variations in attention and alertness, recurrent visual hallucinations, and symptoms of parkinsonism that develop after the cognitive symptoms. Suggestive features are symptoms of rapid eye movement sleep behavior disorder and severe neuroleptic sensitivity. For probable NCD, the person must have at least two core features or one core feature and one suggestive feature; for possible NCD, the person must have one core feature or one or both suggestive features.
Note that one difference between NCD with Lewy bodies and NCD due to Alzheimer’s disease is that, in the former, the prominent early cognitive symptoms are deficits in complex attention and visuospatial and executive functions while, in the latter, the prominent early cognitive symptoms are deficits in learning and memory. Also, the main difference between NCD with Lewy bodies and NCD due to Parkinson’s disease is the sequence of the onset of motor and cognitive symptoms: Motor symptoms precede cognitive symptoms in NCD due to Parkinson’s disease, while cognitive symptoms precede (or, in some cases, are concurrent with) motor symptoms in NCD with Lewy bodies.
3. Vascular Neurocognitive Disorder: This disorder is diagnosed when the individual meets the criteria for major or mild NCD; symptoms are consistent with a vascular etiology as suggested by a temporal relationship between the onset of symptoms and a stroke or other cerebrovascular event or by a prominent decline in complex attention and executive functioning; and there’s evidence of cerebrovascular disease from the individual’s history, a physical exam, or neuroimaging. Its prognosis and course depend on the cause and may involve an acute onset with partial recovery, a stepwise decline, or a progressive course with fluctuations in symptom severity and plateaus that vary in duration. Prevention and intervention efforts target risk and causative factors, which include hypertension, heart disease, diabetes mellitus, obesity, high cholesterol, and heavy cigarette smoking.
4. Neurocognitive Disorder due to HIV Infection: The diagnosis of this disorder requires the presence of symptoms that meet the criteria for major or mild NCD plus evidence of infection with the human immunodeficiency virus. Symptoms are characteristic of those associated with damage to subcortical areas of the brain and include forgetfulness, impaired attention and concentration, cognitive slowing, psychomotor retardation, clumsiness, tremors, apathy, and social withdrawal.
5. Neurocognitive Disorder due to Prion Disease: This disorder is diagnosed when the individual’s symptoms meet the criteria for major or mild NCD, symptoms have an insidious onset followed (in most cases) by a very rapid progression of impairment, and symptoms include motor features associated with prion disease or there’s biomarker evidence of the disease (e.g., characteristic lesions on an MRI). The most common type is Creutzfeldt-Jakob disease (CJD). It’s characterized by a rapid progression of symptoms that often meet the criteria for major NCD in as few as six months. Symptoms include confusion and disorientation, impaired memory and judgment, and other neurocognitive deficits; ataxia, myoclonus, chorea, and other prominent motor symptoms; and psychiatric symptoms that may include apathy, anxiety, and/or mood swings. There are several types of CJD: Sporadic CJD is most common and has an unknown etiology, familial CJD is inherited, and acquired CJD can be due to consuming infected meat (variant CJD) or transmission during a blood transfusion or other medical procedure (iatrogenic CJD).
6. Frontotemporal Neurocognitive Disorder: Frontotemporal NCD is the most common cause of early-onset NCD (i.e., of onset prior to 65 years of age). Its diagnosis requires the presence of symptoms that (a) meet the criteria for major or mild NCD; (b) have an insidious onset and gradual progression; (c) do not include a significant impact on learning and memory or perceptual-motor functioning, especially in the early stages; and (d) meet the criteria for the behavioral or language variant. The behavioral variant is most common and involves prominent declines in social cognition and/or executive abilities (e.g., socially inappropriate behaviors, deficits in organizing and planning) plus three or more of the following behavioral and personality symptoms: behavioral disinhibition; apathy and inertia; loss of sympathy or empathy; perseverative, stereotyped, or compulsive/ritualistic behaviors; hyperorality and dietary changes (e.g., overeating, preference for sweet foods). The language variant is characterized by a prominent decline in language that involves deficits in speech production, word finding, object naming, grammar, or word comprehension. [Note that the language variant is often referred to in the literature as primary progressive aphasia (PPA), which consists of three subtypes: semantic (impaired comprehension of written and spoken language), agrammatic/nonfluent (incorrect grammar and effortful, hesitant speech), and logopenic (impaired repetition of phrases and sentences and difficulty finding the right word).] Finally, although frontotemporal NCD and NCD due to Alzheimer’s disease have similar symptoms in their later stages, their prominent symptoms differ substantially in the early stages: Personality and behavioral changes (e.g., socially inappropriate behaviors, lack of concern for others) or aphasia and other language deficits are the prominent initial symptoms of frontotemporal NCD. In contrast, memory impairment is prominent in the early stages of Alzheimer’s disease and, initially, does not interfere with social behaviors.
7. Neurocognitive Disorder Due to Another Medical Condition: This diagnosis is assigned when the individual’s symptoms meet the diagnostic criteria for major or mild NCD and there is evidence that the symptoms are a pathophysiological consequence of a medical condition. As noted in the DSM-5-TR, the course of this disorder “progresses in a manner that is commensurate with progression of the underlying medical condition” (p. 730). Some NCDs caused by a medical condition are irreversible but, when the medical condition is treatable, the NCD may improve or not progress. For example, NCDs due to hypoxia, infections, endocrine disorders, normal-pressure hydrocephalus, poisoning, or nutritional deficiencies are potentially reversible.
Personality Disorders
The DSM-5-TR describes personality disorders as involving “an enduring pattern of inner experience and behavior that deviates markedly from the norms and expectations of the individual’s culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment” (p. 733). The personality disorders are divided into three clusters: Cluster A disorders involve odd or eccentric behaviors and include paranoid, schizoid, and schizotypal personality disorders. Cluster B disorders involve dramatic, emotional, or erratic behaviors and include antisocial, borderline, histrionic, and narcissistic personality disorders. Cluster C disorders involve anxiety and fearfulness and include avoidant, dependent, and obsessive-compulsive personality disorders.
Several studies have assessed the relationship between the DSM personality disorders and the Big Five personality traits. Based on their meta-analysis of the research, Saulsman and Page (2004) concluded that (a) openness to experience does not have a strong relationship with any of the personality disorders; (b) conscientiousness has strong relationships with some personality disorders; (c) neuroticism, extraversion, and agreeableness have the greatest number and magnitude of strong relationships with the personality disorders; and (d) neuroticism has the most positive relationships with the personality disorders, while agreeableness has the most negative relationships.
With one exception, a diagnosis of a personality disorder can be assigned to a person under the age of 18 when symptoms have been present for at least one year. The exception is antisocial personality disorder, which cannot be assigned to people under 18 years of age.
1. Paranoid Personality Disorder: This diagnosis requires a pervasive pattern of distrust and suspiciousness that involves interpreting the motives of others as malevolent as indicated by at least four of seven symptoms: suspects without sufficient reason that others are exploiting, harming, or deceiving him/her; is preoccupied with unjustified doubts about the loyalty and trustworthiness of others; is reluctant to confide in others; reads demeaning content into benign remarks or events; persistently bears grudges; perceives attacks on his/her character and reputation and is quick to react with anger or a counterattack; is suspicious without justification about the fidelity of his/her spouse or sexual partner.
2. Schizoid Personality Disorder: This disorder involves a pervasive pattern of detachment from social relationships and a restricted range of emotional expression in interpersonal settings with at least four of seven symptoms: doesn’t desire or enjoy close relationships, almost always chooses solitary activities, has little or no interest in sexual relationships, takes pleasure in few activities, lacks close friends or confidents other than first-degree relatives, appears to be indifferent to praise or criticism, is emotionally cold or detached or has flat affect.
3. Schizotypal Personality Disorder: A diagnosis of schizotypal personality disorder requires a pervasive pattern of social and interpersonal deficits involving acute discomfort with and reduced capacity for close relationships, distortions in cognition and perception, and eccentricities in behavior as indicated by at least five of nine symptoms: exhibits ideas of reference, has odd beliefs or magical thinking that influence behavior, has bodily illusions and other unusual perceptions, exhibits odd thinking and speech, is suspicious or has paranoid ideation, has inappropriate or constricted affect, has peculiarities in behavior and appearance, lacks close friends or confidents other than first-degree relatives, has excessive social anxiety that doesn’t diminish with familiarity. Note that schizotypal personality disorder shares a lack of close relationships with several other personality disorders including schizoid and avoidant personality disorders. However, the reasons for the lack of close relationships differ: Individuals with schizotypal personality disorder may express unhappiness about their lack of friends but say they’re uncomfortable around other people and act in ways that suggest a lack of interest in developing close relationships (e.g., they usually interact with others only when necessary). In contrast, people with schizoid personality disorder have a limited desire for and do not derive pleasure from close relationships, while individuals with avoidant personality disorder desire close relationships but avoid them because they fear being criticized or rejected by others.
4. Antisocial Personality Disorder: This disorder involves a pervasive pattern of disregard for and violation of the rights of others since 15 years of age that involves at least three of seven symptoms: fails to conform to social norms with respect to lawful behaviors, is deceitful, is impulsive and fails to plan ahead, is irritable and aggressive, has a reckless disregard for the safety of self and others, is consistently irresponsible, has a lack of remorse. In addition, the person must be at least 18 years of age and have a history of conduct disorder before 15 years of age. This disorder is chronic, but its symptoms (especially involvement in criminal behavior) often become less severe or remit by the fourth decade of life. Psychiatric comorbidity is common for people with antisocial personality disorder. The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-III; Goldstein et al., 2017) found that, for individuals with this disorder, a substance use disorder was the most common lifetime comorbid disorder followed by, in order, a mood disorder, borderline personality disorder, and an anxiety disorder.
Antisocial personality disorder is one of the most difficult disorders to treat because people with this disorder don’t believe they have a problem and rarely seek treatment voluntarily. In addition, no intervention has received consistent empirical support for its effectiveness in reducing the disorder’s core characteristics. However, there’s some evidence that cognitive-behavioral interventions (especially group interventions) may be helpful for reducing re-offending rates and that contingency management that provides reinforcement for desirable behaviors and pharmacological treatment may be helpful for reducing comorbid substance use disorders (National Collaborating Centre for Mental Health, 2010).
5. Borderline Personality Disorder: A diagnosis of this disorder requires a pervasive pattern of instability in interpersonal relationships, self-image, and affects, and marked impulsivity as indicated by at least five of nine symptoms: engages in frantic efforts to avoid abandonment, has a pattern of unstable and intense interpersonal relationships that involve fluctuations between idealization and devaluation, has an identity disturbance that involves a persistent instability in sense of self, is impulsive in at least two areas that are potentially self-damaging, has made recurrent suicide threats or gestures or engages in self-mutilating behavior, exhibits affective instability, experiences chronic feelings of emptiness, exhibits inappropriate intense anger, has transient stress-related paranoid ideation or severe dissociative symptoms. Borderline personality disorder typically has an onset in late adolescence with symptoms being most severe in early adulthood. However, many individuals subsequently experience a decrease in symptom severity, and there’s evidence that up to 75% no longer meet the full criteria for the diagnosis by age 40 (Paris & Zweig-Frank, 2001).
A commonly used treatment is Linehan’s (1993) dialectical behavior therapy (DBT), which is a type of cognitive-behavior therapy. It’s based on the assumption that borderline personality disorder is due to emotion dysregulation, which is the result of a combination of biological and environmental factors. DBT consists of three components: Group skills training focuses on increasing the client’s emotion regulation, distress tolerance, relationship effectiveness, and mindfulness. The primary goals of individual psychotherapy are increasing skills and decreasing suicidal and other life-threatening behaviors, therapy-interfering behaviors, and quality-of-life interfering behaviors. Therapy-interfering behaviors (TIBs) interfere with the progress of therapy and include being late for therapy sessions, not completing homework, and frequently threatening to quit therapy. Quality-of-life interfering behaviors interfere with the ability to maintain a life worth living and include relationship problems and financial and housing crises. Intersession coaching is also known as telephone coaching and (a) helps clients generalize skills to real-world situations and environments and deal with crises and (b) provides opportunities to make repairs to the therapeutic relationship. A therapist consultation team is often described as a fourth component of DBT. It is a peer consultation team that DBT therapists participate in for the purpose of helping them maintain the motivation and skills they need to continue to be effective therapists.
6. Histrionic Personality Disorder: This disorder involves a pervasive pattern of excessive emotionality and attention seeking with at least five of eight symptoms: is uncomfortable when not the center of attention, is inappropriately sexually seductive or provocative when interacting with others, has rapidly shifting and shallow emotions, consistently uses physical appearance to gain attention, exhibits speech that is excessively impressionistic and lacking in detail, shows an exaggerated expression of emotion, is easily influenced by others, considers relationships to be more intimate than they are. As noted in the DSM-5-TR, histrionic and antisocial personality disorders share several features – e.g., “a tendency to be impulsive, superficial, excitement seeking, reckless, seductive, and manipulative” (American Psychiatric Association, 2022, p. 759). However, people with histrionic personality disorder have exaggerated emotions and are manipulative in order to gain nurturance, while those with antisocial personality disorder engage in antisocial behaviors and are manipulative to gain power or material gratification. In addition, Hamburger et al. (1996) propose that histrionic and antisocial personality disorders share psychopathy as their underlying trait but that this trait is moderated by biological sex so that psychopathy is manifested in different ways by men and women: “Specifically, given high levels of psychopathy, males will be more likely to exhibit features of ASPD than females, and females will be more likely to exhibit features of HPD than males” (p. 44). However, subsequent research has not been very supportive of Hamburger et al.’s hypothesis, and some investigators suggest that gender biases in the diagnosis of the two disorders (rather than biological sex) explain why antisocial personality disorder is more often diagnosed in men and histrionic personality disorder is more often diagnosed in women (e.g., Cale & Lilienfeld, 2002).
7. Narcissistic Personality Disorder: A diagnosis of narcissistic personality disorder requires a pervasive pattern of grandiosity, a need for admiration, and a lack of empathy as indicated by at least five of nine symptoms: has a grandiose sense of self-importance; is preoccupied with fantasies of unlimited success, power, beauty, and love; believes he/she is unique and can be understood only by special or high-status people; requires excessive admiration; has a sense of entitlement; is interpersonally exploitative; lacks empathy; is often envious of others or believes others are envious of him/her; exhibits arrogant behaviors and attitudes.
8. Avoidant Personality Disorder: This diagnosis requires a pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation with at least four of seven symptoms: avoids occupational activities that involve interpersonal contact due to fear of criticism, disapproval, or rejection; is unwilling to get involved with people unless certain of being liked; shows restraint in intimate relationships due to fear of being ridiculed; is preoccupied with concerns about being criticized or rejected in social situations; is inhibited in new relationships because of feelings of inadequacy; views self as socially inept, unappealing, or inferior to others; is usually reluctant to engage in new activities because they may be embarrassing.
9. Dependent Personality Disorder: This disorder involves a pervasive and excessive need to be taken care of that leads to submissive and clinging behavior and a fear of separation as indicated by at least five of eight symptoms: has difficulty making everyday decisions without advice and reassurance from others, needs others to assume responsibility for most areas of his/her life, avoids disagreeing with others due to fear of losing support or approval, has difficulty doing things alone, goes to excessive lengths to obtain nurturance and support, feels uncomfortable or helpless when alone, urgently seeks another relationship for care and support when a close relationship ends, is unrealistically preoccupied with fears of being left to care for him/herself.
10. Obsessive-Compulsive Personality Disorder: The diagnosis of this disorder requires a pervasive pattern of preoccupation with orderliness, perfectionism, and mental and interpersonal control that severely limits flexibility, openness, and efficiency as indicated by at least four of eight symptoms: is preoccupied with details, rules, and schedules so the major point of an activity is lost; shows perfectionism that interferes with task completion; is excessively devoted to work and productivity to the exclusion of leisure activities and friendships; is overly conscientious, scrupulous, and inflexible about morality, ethics, or values; is unable to discard worn-out or worthless objects even when they don’t have sentimental value; is reluctant to delegate work to others unless they’ll do it his/her way; adopts a miserly spending style toward self and others; shows rigidity and stubbornness. As noted in the DSM-5-TR, obsessive-compulsive personality disorder and obsessive-compulsive disorder share similar names, but only obsessive-compulsive disorder involves true obsessions and compulsions.