Neuro Final

What is ADHD?

developmental disorder characterized by a persistent pattern of inattention and hyperactivity and impulsivity that interferes with functioning or development. Symptoms must appear before age 12 and manifest in multiple settings.

Theory of Mind

the ability to attribute mental states to others, to know that other individuals are separate selves with their own points of view and feelings

Comorbidity

when disorders coexist, presence of two or more disease/medical condition in patients

How does ADHD differ between children and adults?

• Children: More physical hyperactivity and impulsivity.

• Adults: More internal restlessness, disorganization, and difficulty with sustained focus.

Rate of Cycling

frequency in which people with bipolar disorder switch from a state of mania/hypomania to

depression

What are the three subtypes of ADHD according to DSM-5?

1. Inattentive Type

2. Hyperactive/Impulsive Type

3. Combined Type

Stimming

A stereotypie seen in individuals with autism or ADHD, this includes flapping of arms, bouncing legs, bouncing, etc., can be dangerous to the individual

What are the symptoms of the inattentive type of ADHD?

• Easily distracted by external stimuli or irrelevant thoughts.

• Often loses things necessary for tasks (e.g., keys, glasses).

• Difficulty sustaining focus during tasks or conversations.

• Makes careless mistakes and overlooks details.

• Poor time management, often misses deadlines.

• Avoids tasks requiring sustained mental effort (e.g., reports).

Monoamine

a neurotransmitter that contains one amino group connected to an aromatic ring by a two-carbon

chain

What are the symptoms of the hyperactive/impulsive type of ADHD?

• Fidgets or taps hands/feet; squirms in seat.

• Talks excessively and interrupts conversations.

• Runs or climbs inappropriately.

• Difficulty waiting their turn, e.g., in lines.

• Always "on the go," as if driven by a motor.

Alerting Network

comprised of interactions between frontal, parietal cortex, and thalamus, supports attention,

weaker in individuals in ADHD

What is the prevalence of ADHD worldwide?

• Approximately 7.6% of children, with a male-to-female ratio of 3:1.

• Adult ADHD prevalence is ~2.5%, with persistence in ~30-50% of childhood cases.

How does culture impact ADHD diagnosis?

• Hyperactivity may not be pathologized in non-academic or less structured societies.

• Academic-focused cultures might diagnose ADHD more frequently due to higher sensitivity to inattentiveness.

What genetic factors contribute to ADHD?

• Heritability is up to 80%. - might be an overestimate

• Associated genes: Dopamine transporter (DAT1) and D4 dopamine receptor.

• Overlap with Autism Spectrum Disorder genes.

What are environmental risk factors for ADHD?

• Prenatal exposure to smoking or alcohol.

• Perinatal hypoxia (low oxygen levels at birth).

• No clear evidence links sugar or food additives as direct causes.

What brain regions are implicated in ADHD?

• Frontal lobe: Impaired executive function.

• Mesocorticolimbic system: Reduced dopamine activity, affecting reward processing.

• alerting network is weak for people with ADHD

What is the "Dual Pathway Model"?

A theory suggesting ADHD arises from impairments in:

1. Executive functioning (frontal lobe).

2. Reward sensitivity (dopaminergic pathways).

What medications are used to treat ADHD?

• Stimulants (70-90% efficacy):

  • Methylphenidate.

  • Amphetamines (Adderall).

  • d-amphetamine

• Non-stimulants: Atomoxetine, guanfacine.

How do stimulant medications work in ADHD?

They increase dopamine and norepinephrine availability in the prefrontal cortex, improving attention and impulse control.

What is schizophrenia?

A chronic psychotic disorder characterized by disruptions in thought processes, perceptions, emotional responsiveness, and social interactions.

What are the three symptom categories of schizophrenia?

• Positive symptoms - symptoms that go beyond normally occurring experiences: Hallucinations, delusions, disorganised speech.

• Negative symptoms - characterised by a deficit or absence in normal behaviour: Apathy, social withdrawal, emotional flatness.

• Cognitive symptoms - characterised by erratic changes in speech, motor behaviour and emotions: Impaired attention, memory, and problem-solving.

What types of delusions are common in schizophrenia?

• Persecutory (belief of being targeted).

• Grandiose (inflated sense of self-importance).

• Erotomanic (belief someone is in love with them).

What are hallucinations in schizophrenia?

False sensory experiences, most commonly auditory (e.g., hearing voices).

What genetic factors increase schizophrenia risk?

• First-degree relatives have ~10% risk.

• Monozygotic twins: 48% concordance.

• Dizygonic twins: 50% concordance

• Associated genes: Dopamine regulation, glutamate NMDA receptor genes.

What are the key points of schizophrenia diagnosis

• Individuals must have at least one of the delusions, hallucinations or disorganised speech

• diminished level of function

• long-lasting symptoms

• not due to drugs or some medical conditions

• diagnosed in late adolescent and early adulthood

• Symptoms decrease with age

what are perinatal factors of schizophrenia

Fatal exposure to influenza and other viruses like desease may subtly damage the fetal brain in a way that causes symptoms of schizophrenia later in life

What is the "two-hit hypothesis"?

Schizophrenia is caused by genetic vulnerability ("first hit") combined with perinatal stressors or environmental triggers ("second hit").

What brain changes are seen in schizophrenia?

• Enlarged ventricles (brain tissue loss).

• Reduced hippocampal volume and dendritic spine density in the prefrontal cortex.

• Reduced dendritic spine density

• Abnormal synaptic pruning during adolescence.

What is hypofrontality?

Reduced activity in the prefrontal cortex, associated with negative and cognitive symptoms. - associated with schizophrenia

How is dopamine dysregulated in schizophrenia?

• Excess dopamine in subcortical areas causes positive symptoms.

• Deficient dopamine in the prefrontal cortex contributes to cognitive deficits.

What are antipsychotics and how do they work?

• First-generation: Chlorpromazine- affects ay neurotransmitters but mosty dopamine (D2 receptor blockers).

• Second-generation: Clozapine, risperidone (affect dopamine and serotonin pathways).

Antipsychotic’s reduce psychotic symptoms without producing too much sedation

What is PET

Position emission Tomology is an imaging techinque that detects changes in blood flow by measuring changes in the uptake of oxygen and glucose

• good temporal solution for schizophrenia

What is Major Depressive Disorder (MDD)?

A mood disorder characterized by persistent feelings of sadness, hopelessness, and a lack of interest or pleasure in activities.

What are the DSM-5 diagnostic criteria for MDD?

At least 5 of the following symptoms present for 2 weeks, with at least one being either depressed mood or loss of interest:

• Depressed mood most of the day.

• Significant weight loss or gain.

• Insomnia or hypersomnia.

• Psychomotor agitation or retardation.

• Fatigue or loss of energy.

• Feelings of worthlessness or excessive guilt.

• Diminished ability to think or concentrate.

• Recurrent thoughts of death or suicide.

What is the prevalence of depression?

• 1 in 6 individuals will experience depression in their lifetime.

• Women are diagnosed at twice the rate of men, potentially due to hormonal, psychosocial, and cultural factors.

What comorbidities are common with depression?

Anxiety disorders, substance use disorders, cardiovascular diseases, and chronic pain conditions.

What is the monoamine hypothesis of depression?

Depression is linked to deficits in monoamine neurotransmitters (serotonin, norepinephrine, dopamine).

How does the HPA axis contribute to depression?

Chronic stress dysregulates the HPA axis, causing hypercortisolemia and hippocampal damage.

How does depression affect the hippocampus?

• Reduced hippocampal volume due to decreased neurogenesis.

• Prolonged untreated depression leads to greater hippocampal shrinkage.

What evidence challenges the monoamine hypothesis?

• Lowering monoamine levels in healthy individuals doesn’t cause depression.

• Antidepressants alter neurotransmitter levels within days, but symptom relief takes weeks.

What are the main classes of antidepressants?

• SSRIs (e.g., fluoxetine): Block serotonin reuptake.

• SNRIs (e.g., venlafaxine): Block serotonin and norepinephrine reuptake.

• MAOIs: Inhibit monoamine oxidase, preventing breakdown of monoamines.

How does psychotherapy help depression?

• Cognitive Behavioral Therapy (CBT): Identifies and changes negative thought patterns.

• Interpersonal Therapy (IPT): Focuses on improving relationships and social skills.

What are the two main types of bipolar disorder?

• Bipolar I: Full manic episodes, often with depressive episodes.

• Bipolar II: Hypomanic episodes (less severe than mania) and major depressive episodes.

What is cyclothymia?

A milder form of bipolar disorder with periods of hypomanic symptoms and depressive symptoms that do not meet full criteria for major episodes.

What are the symptoms of mania?

• Inflated self-esteem or grandiosity.

• Decreased need for sleep.

• Increased talkativeness or pressured speech.

• Racing thoughts or flight of ideas.

• Distractibility.

• Increased goal-directed activity or psychomotor agitation.

• Excessive involvement in risky activities.

How do depressive episodes differ in bipolar disorder?

Similar to MDD, but depressive episodes in bipolar disorder may occur more suddenly and be interspersed with periods of normal mood or hypomania.

What are the leading neurobiological theories of bipolar disorder?

• Dopamine Dysregulation: Mania linked to hyperdopaminergia; depression to hypodopaminergia.

• BDNF Theory: Reduced brain-derived neurotrophic factor impairs neuroplasticity during mood episodes.

• Mitochondrial Dysfunction: Increased oxidative stress and cell death may underlie neurodegeneration.

What medications are used to treat bipolar disorder?

• Mood Stabilizers: Lithium (gold standard), valproate.

• Antipsychotics: Quetiapine, aripiprazole.

• Antidepressants: Used cautiously to avoid triggering mania.

What are the risks of treating bipolar disorder with antidepressants alone?

Antidepressants can trigger manic episodes or rapid cycling if not combined with mood stabilizers.

What are the DSM-5 categories of anxiety disorders?

• Generalized Anxiety Disorder (GAD).

• Panic Disorder.

• Specific Phobias.

• Social Anxiety Disorder.

• Separation Anxiety Disorder.

How is fear distinct from anxiety?

• Fear: Immediate response to a present threat; activates the sympathetic nervous system.

• Anxiety: Anticipatory worry about future threats; characterized by hypervigilance.

What are the symptoms of GAD?

• Excessive worry about various aspects of life.

• Restlessness or feeling on edge.

• Muscle tension.

• Difficulty concentrating.

• Sleep disturbances.

What brain regions are implicated in GAD?

• Increased prefrontal cortex (PFC) activity (overthinking).

• Reduced amygdala function.

What are the diagnostic criteria for panic disorder?

• Recurrent, unexpected panic attacks with symptoms such as heart palpitations, sweating, trembling, shortness of breath.

• Persistent concern about additional attacks or their implications.

What role does the amygdala play in panic disorder?

Overactivation of the amygdala triggers an exaggerated fear response even in the absence of a true threat.

What are common pharmacological treatments for anxiety?

• SSRIs: First-line treatment for GAD, social anxiety, and panic disorder.

• Benzodiazepines: increase inhibitory signalling in brain and cause relaxation - agonist of GABA receptors

• Beta-blockers: treat autonomic symptoms of panic/anxiety

What are non pharmacological treatments for anxiety disorders

• CBT: Challenges distorted thoughts; uses interoceptive exposure for panic attacks (e.g., hyperventilation) to reduce fear.

• EMDR: Trauma therapy involving memory recall with eye movements or audio tones (controversial).

What is Cognitive Behavioral Therapy (CBT)?

A psychotherapeutic approach that challenges distorted cognitions and introduces relaxation techniques to manage anxiety.

What is Autism Spectrum Disorder (ASD)?

neurodevelopmental disorder characterized by challenges with social communication, restricted interests, and repetitive behaviors. Symptoms vary in severity, leading to the term "spectrum."

Why is ASD considered a "spectrum"?

Symptoms range widely in type and severity, with individuals experiencing varying levels of impairment in social, communication, and behavioral domains.

What are the three core areas of difficulty in ASD?

• Social Communication: Difficulty understanding social cues, emotional reciprocity, and forming relationships.

• Repetitive Behaviors: Repetitive actions, insistence on routines, or intense focus on specific topics.

• Restricted Interests: Narrow, intense interests that dominate attention.

What are common symptoms of ASD in early childhood?

• Delayed speech or language development.

• Limited eye contact.

• Preference for solitary play.

• Intense reactions to sensory stimuli (e.g., noise, textures).

How do ASD symptoms evolve over time?

Some symptoms, like repetitive behaviors, may become less pronounced with age, but social and communication challenges often persist.

What are examples of repetitive behaviors in ASD?

• Hand-flapping.

• Rocking back and forth.

• Echolalia (repeating phrases or words).

What is hyper- or hypo-sensitivity in ASD?

• Hyper-sensitivity: Overreaction to sensory input (e.g., loud sounds, bright lights).

• Hypo-sensitivity: Underreaction or seeking sensory input (e.g., spinning objects).

How is ASD diagnosed?

Diagnosis is based on DSM-5 criteria, focusing on deficits in social communication and restricted/repetitive behaviors. Symptoms must:

• Be present in early developmental stages.

• Cause significant impairment in daily functioning.

What are levels of severity in ASD according to DSM-5?

• Level 1: Requires support (difficulty initiating social interactions).

• Level 2: Requires substantial support (marked deficits in verbal/nonverbal communication).

• Level 3: Requires very substantial support (severe deficits in communication and behavior).

What is the role of developmental screenings in ASD diagnosis?

Tools like the M-CHAT (Modified Checklist for Autism in Toddlers) identify potential ASD symptoms for early intervention.

What is the prevalence of ASD?

• Global prevalence: ~1 in 54 children.

• Boys are diagnosed 4 times more often than girls.

Why is ASD less frequently diagnosed in girls?

Girls may mask symptoms better, or present differently, often focusing intensely on social-related interests (e.g., relationships).

How early can ASD symptoms be detected?

Symptoms may emerge as early as 12-18 months, with reliable diagnosis possible by age 2.

What are the genetic factors associated with ASD?

• Heritability is high (~80-90%).

• Specific genes: Chromosomal abnormalities, SHANK3, and genes regulating synaptic function.

What environmental factors increase ASD risk?

• Advanced parental age.

• Prenatal factors: Maternal infection, exposure to valproate, or poor nutrition.

• Birth complications, including low birth weight and prematurity.

What is the "gut-brain axis" in ASD?

The gut microbiome's role in modulating immune and neurological functions; dysbiosis (imbalance) is often linked to ASD.

What structural changes in the brain are associated with ASD?

• Accelerated brain growth in early life (macrocephaly in some).

• Abnormal cortical organization and connectivity.

• Reduced volume in areas like the amygdala and corpus callosum.

What is the role of the amygdala in ASD?

Amygdala abnormalities contribute to difficulties in processing emotions and social cues.

How does synaptic dysfunction relate to ASD?

Dysregulation in synaptic formation and pruning (e.g., excess synapses in some regions) impacts neural communication.

What neurotransmitters are implicated in ASD?

• GABA: Imbalances in inhibitory signaling.

• Glutamate: Disruptions in excitatory signaling.

What are common non-pharmacological interventions for ASD?

• Applied Behavioral Analysis (ABA): Reinforces desired behaviors.

• Speech and Occupational Therapy: Enhances communication and motor skills.

• Social Skills Training: Builds peer interaction skills.

What pharmacological treatments are used for ASD?

Medications for associated symptoms (not core symptoms):

• SSRIs for anxiety or depression.

• Risperidone or aripiprazole for irritability and aggression.

Why is early intervention important for ASD?

Early therapies (before age 3) capitalize on neural plasticity, leading to better long-term outcomes in communication and social skills.

What is the relationship between ASD and intellectual disability?

~31% of individuals with ASD have intellectual disabilities, but many show strengths in specific areas like memory or pattern recognition.

What are common strengths observed in individuals with ASD?

• Exceptional memory and attention to detail.

• High proficiency in structured, rule-based activities.

• Strong logical reasoning and pattern recognition.

• Intense focus on special interests.

What are the key features of ADHD

signs of ADHD can be minimal or absent when individuals is under close supervision, receiving frequent reward or doing something interesting which makes it challenging to diagnose

What are 1st degree biological relatives

1st degree relatives share 50% of their genetics like sibling and parents

What is addiction?

A syndrome marked by a loss of control over a reward-seeking behavior, such as drug use, resulting in significant impairment in life.

How is addiction related to the brain’s reward system?

Addiction hijacks the brain’s mesocorticolimbic dopamine system, leading to exaggerated dopamine release in response to drugs, which reinforces compulsive use

What is the mesocorticolimbic dopamine system?

• Composed of the ventral tegmental area, nucleus accumbens, hippocampus and prefrontal cortex

• Responsible for detecting rewards and reinforcing behaviors.

How do addictive drugs affect dopamine levels?

They cause supraphysiological dopamine release in the NAc, far exceeding levels seen with natural rewards, leading to compulsive drug-seeking.

What is the "teaching signal" in addiction?

Dopamine release during unexpected rewards strengthens the association between the drug and its pleasurable effects.

What is drug tolerance?

A phenomenon where larger doses are needed to achieve the same effect due to reduced receptor sensitivity.

What are common withdrawal symptoms?

• Alcohol: Tremors, seizures, delirium tremens.

• Opioids: Muscle aches, sweating, nausea, diarrhea.

• Cannabis: Irritability, sleep disturbances, decreased appetite.

What are the main components of cannabis?

• THC: Psychoactive, responsible for the "high."

• Cannabidiol (CBD): Non-intoxicating, modulates THC effects.

How does THC work in the brain?

THC mimics anandamide, binding to CB1 receptors in the brain, reducing neurotransmitter release and causing euphoria.

What are common psychological effects of cannabis?

• Impaired attention and short-term memory.

• Altered time perception.

• Anxiety or paranoia at high doses

What is PTSD?

A trauma-related disorder characterized by intrusive memories, avoidance, cognitive changes, and hyperarousal following exposure to a traumatic event.

What are common causes of PTSD?

• Exposure to war.

• Physical or sexual assault.

• Natural disasters.

• Life-threatening events.

What are the key DSM-5 diagnostic criteria for PTSD?

1. Trauma exposure: Direct experience, witnessing, or learning about a traumatic event.

2. Intrusion symptoms: Flashbacks, nightmares

3. Persistent avoidance of stimuli associated with the event

4. Negative alterations in cognitions and mood associated with the event,

5. alterations in arousal and reactivity associated with traumatic
   events: Hypervigilance, irritability, sleep disturbances.

Prevalence of PTSD

More prevalence in females

projected lifetime risk is 9.2%

What is the fear circuitry of PTSD

• Medial Prefrontal Cortex
  (mPFC) appraises threat

• If threat exists, signals to
  amygdala/HPA

• Amygdala signals to
  hippocampus (learn about
  context) and hypothalamus
  (activates brainstem response
  to fear)