Mood Disorders and Suicide Unit

Overview of Mood Disorders

• Mood disorders involve extreme alterations in emotion—ranging from deep depression to intense, unrealistic euphoria. 

• Normal mood states may occur between episodes, although sometimes mixed symptoms can be present within a single episode. 

• Two main categories:

  • Unipolar depressive disorders: Only depressive episodes are experienced.  

  • Bipolar disorders: Both depressive and manic (or hypomanic) episodes occur.  Normal mood states may occur between episodes, although sometimes mixed symptoms can be present within a single episode.

Depressive Episode

• Definition: Markedly depressed mood or loss of interest in once pleasurable activities for at least 2 weeks.  

• Additional symptoms: 

  • Changes in sleep and appetite  

  • Feelings of worthlessness or guilt  

  • Difficulty concentrating  

  • Recurrent thoughts of death or suicidal ideation  

• These episodes represent the most common form of mood disturbance.

Manic and Hypomanic Episodes

• Manic Episodes:  

 – Abnormally and persistently elevated, euphoric, or expansive mood lasting at least 1 week (or any duration if hospitalization is needed).  

 – Accompanied by three (or four if mood is only irritable) additional symptoms such as:  

  • Inflated self-esteem or grandiosity  

  • Decreased need for sleep  

  • More talkative or pressured speech  

  • Flight of ideas or racing thoughts  

  • Distractibility  

  • Increase in goal-directed activity or psychomotor agitation  

  • Excessive involvement in high-risk activities  

• Hypomanic Episodes:  

 – Similar symptoms to mania, but less severe, lasting at least 4 days, with no marked impairment or need for hospitalization.

Epidemiology and Prevalence 

Unipolar Depression (Major Depressive Disorder):

 – Lifetime prevalence nearly 17%; 12-month prevalence about 7% (NCS-R data)  

 – Women are approximately twice as likely as men to experience major depression.  

Bipolar Disorder: 

 – Lifetime risk estimated at about 1%  

 – No significant gender differences in prevalence 

DSM 5 Criteria for Manic Episodes

Criterion A: Distinct period of abnormally and persistently elevated, expansive, or irritable mood plus increased energy or activity for at least 1 week.  

• Criterion B: During this period, at least three (or four if only irritable) of the following symptoms must be present:  

 – Inflated self-esteem or grandiosity  

 – Decreased need for sleep  

 – More talkative or pressured speech  

 – Flight of ideas or racing thoughts  

 – Distractibility  

 – Increased goal-directed activity or psychomotor agitation  

 – Excessive involvement in risky activities  

• Criterion C: The disturbance causes marked impairment or necessitates hospitalization.  

• Criterion D: Not attributable to substance use or another medical condition.

DSM 5 Criteria for MDD

Core Requirement: Presence of a major depressive episode without any history of manic or hypomanic episodes.  

• Key Symptoms (at least five during a 2-week period):  

 – Depressed mood most of the day  

 – Markedly diminished interest or pleasure  

 – Significant weight change or appetite disturbance  

 – Sleep disturbances (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 suicidal ideation  

• The symptoms must represent a change from previous functioning and cause significant distress or impairment.

Specifiers for MDD – Psychotic Features

 With Melancholic Features:  

 – Early morning awakening, depression worse in the morning, psychomotor changes, loss of appetite/weight, excessive guilt.  

• With Psychotic Features:  

 – Presence of delusions or hallucinations (usually mood-congruent).  

• With Atypical Features: 

 – Mood reactivity (mood brightens in response to positive events) plus two or more symptoms (e.g., weight gain, hypersomnia, leaden paralysis, sensitivity to rejection).  

• With Catatonic Features:  

 – Motoric immobility, including mutism and rigidity.  

• With Seasonal Pattern:  

 – Recurrent depressive episodes occurring at the same time each year with full remission in other seasons.

Persistent Depressive Disorder (Dysthymia)

Definition: Depressed mood most of the day, on most days, for at least 2 years (1 year for children/adolescents)  

• Additional Symptoms: At least two of the following: poor appetite/overeating, insomnia/hypersomnia, low energy, low self-esteem, poor concentration, feelings of hopelessness.  

• Key Characteristic: Intermittent periods of normal mood (lasting a few days to a few weeks, but never more than 2 months).  

• Clinical Note: Despite intermittent normal moods, the chronic nature of persistent depressive disorder often results in outcomes as impaired as those seen in MDD.

Other Forms of Depression 

• Double Depression:

 – Co-occurrence of persistent depressive disorder and intermittent major depressive episodes.  

• Premenstrual Dysphoric Disorder: 

 – Symptoms appear in the final week before menses and improve soon after onset.  

 – Key symptoms include affective lability, irritability/anger, depressed mood, or marked anxiety.  

• Postpartum Blues:  

 – Common in new mothers (and occasionally fathers), with symptoms like mood lability, crying, sadness, and irritability occurring in up to 50–70% within 10 days of childbirth and typically subsiding on their own.

Biological and Genetic Casual Factors

• Biological Influences:  

 – Diseases and drugs can affect mood (an idea dating back to Hippocrates and the notion of “black bile”).  

• Genetic Influences:  

 – Family studies show a 2–3 times higher prevalence of mood disorders among blood relatives of affected individuals.  

 – Twin studies suggest 31–42% of variance in liability to MDD is genetic (up to 70–80% for severe or recurrent cases).  

 – Research on candidate genes (e.g., the serotonin-transporter gene and its alleles) provides mixed results but indicates a genetic contribution.  

• Environmental Contributions:  

 – A significant portion of risk is attributable to nonshared environmental factors (unique individual experiences).

Neurochemical Factors of Depression 

• Since the 1960s, researchers have proposed that depression may arise from disruptions in the balance of neurotransmitters.  

• Early focus on monoamines (norepinephrine and serotonin) led to the monoamine theory: depression may result from a depletion of these neurotransmitters at key receptor sites.  

• Possible mechanisms include impaired synthesis, increased degradation, or altered receptor functioning.  

• Later findings revealed that some patients show increased norepinephrine activity, and only a minority with depression have lowered serotonin levels (often those with high suicidal ideation).  

• Antidepressants increase neurotransmitter availability

Genetics and Gene Environment Interactions

• Research on the 5-HTT gene (serotonin-transporter) examined allelic variations: s/s, s/l, and l/l.  

• Studies (e.g., Caspi et al., 2003) found that individuals with s/s alleles who experienced four or more stressful life events were twice as likely to develop a major depressive episode compared to l/l individuals.  

• Similar findings were observed for those with severe childhood maltreatment.  

• These results support a diathesis–stress model, though later quantitative reviews have challenged the interaction.

Endocrine Dysregulation- The HPA Axis

• The hypothalamic–pituitary–adrenal (HPA) axis regulates cortisol release in response to stress.  

• Elevated cortisol is observed in 20–40% of outpatients and 60–80% of hospitalized patients with depression.  

• In about 45% of patients with serious depression, dexamethasone fails to suppress cortisol levels (the “dexamethasone nonsuppressor” phenomenon).  

• Prolonged cortisol elevations can lead to memory impairments, cognitive difficulties, and cell death in the hippocampus.

Additional Endocrine and Immune System Factors 

The hypothalamic–pituitary–thyroid axis:  

 – Hypothyroidism is often associated with depression.  

 – Approximately 20–30% of depressed patients with normal thyroid levels show dysregulation of this axis.  

 – Administration of thyrotropin-releasing hormone can improve symptoms in some treatment-resistant cases.  

• Immune system dysregulation:  

 – Depression is linked with activation of the inflammatory response system and increased production of proinflammatory cytokines (e.g., interleukin, interferon).

Neurophysiological & Neuroanatomical Influences

 EEG studies reveal an asymmetry in prefrontal cortex activity: depressed individuals show lower left-hemisphere activity and higher right-hemisphere activity.  

• PET and MRI research have found:  

 – Decreased volume in regions of the prefrontal cortex (orbital and dorsolateral)  

 – Reduced hippocampal volume, possibly due to prolonged cortisol exposure  

 – Abnormalities in the anterior cingulate cortex and increased amygdala activation, which may relate to biased attention toward negative stimuli.

Circadian Rhythms & Seasonal Factors 

Circadian (24-hour) rhythms regulate sleep, appetite, and social interactions.  

• Abnormalities in these rhythms are commonly observed in depression.  

• Seasonal affective disorder (SAD) is linked to the total quantity of available light; most patients become depressed in the fall/winter and normalize in spring/summer.  

• Light therapy may help reestablish normal biological rhythms in affected individuals.

Sleep Disturbances in Depression

Normal sleep involves five stages (Stages 1–4 of non-REM and REM sleep).  

• Depressed patients frequently experience:  

 – Difficulty falling asleep and maintaining sleep  

 – Early morning awakening  

 – A shortened latency to the first REM period (often 15–20 minutes sooner than normal)  

 – Increased amounts of REM sleep in early cycles and reduced deep sleep

• Such sleep changes are particularly pronounced in patients with melancholic features.

Stressful Life Events and Depression

Severe stressful events (e.g., loss of a loved one, major economic or health crises) often precipitate a major depressive episode.  

• Distinction between independent life events (e.g., natural disasters) and dependent life events (those partly generated by the person’s behavior).  

• Research indicates dependent life events may play a stronger role in triggering depression.  

• Chronic stress—ongoing for several months (e.g., poverty, marital discord)—is associated with increased risk for the onset, maintenance, and recurrence of depression.

Psychological Factors

Stressful life events, personality traits (e.g., neuroticism), and negative cognitive styles all contribute to depression.  

• Cognitive vulnerabilities (such as dysfunctional beliefs) may be activated by stressful events, triggering depressive symptoms.  

• These psychological factors may also be mediated by underlying biological changes (e.g., hormonal imbalances).

Psychodynamic Theories of Depression 

 Freud’s “Mourning and Melancholia” (1917) noted similarities between depression and the symptoms of mourning.  

• Freud and Abraham proposed that depression involves the regression to an earlier developmental stage and the introjection of the lost object, leading to anger turned inward.  

• Emphasis on both real losses and symbolic losses (e.g., failure in school or relationships) as triggers for depression.

Cognitive Theories- Brecks Model 

Aaron Beck (1967) argued that negative automatic thoughts often precede mood symptoms.  

• Central to his model are dysfunctional beliefs or depressogenic schemas.  

• The model highlights the “negative cognitive triad”:  

 – Negative views about the self (“I’m worthless”)  

 – Negative views about the world (“No one loves me”)  

 – Negative views about the future (“It’s hopeless because things will always be this way”)  

• Cognitive biases (e.g., all-or-none thinking, selective abstraction, arbitrary inference) serve to maintain these negative thoughts.

Learned Helplessness and Reformulated Helplessness Theories 

Seligman’s learned helplessness model (1974, 1975) originated from animal studies showing that uncontrollable shocks lead to passivity and depressive symptoms.  

• In humans, exposure to uncontrollable negative events may lead to a sense of helplessness that parallels these findings.  

• The reformulated helplessness theory emphasizes that the attributions people make about negative events (internal, stable, global) determine their vulnerability to depression.

The Hopelessness Theory of Depression 

The hopelessness theory (Abramson et al., 1989) posits that a pessimistic attributional style, in combination with negative life events, leads to a state of hopelessness that triggers depression.  

• Research indicates that individuals with a pessimistic style are at increased risk for both first-onset and recurrent depressive episodes.  

• Longitudinal studies have demonstrated that high-risk individuals (those with negative attributions and dysfunctional beliefs) are significantly more likely to develop depression.