Comprehensive Study Guide on Psychological Disorders and Biological Etiology

DSM-5 Diagnostic Classification and Changes

• The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), published by the American Psychiatric Association, is the primary clinical text used to diagnose major mental disorders based on specific symptom patterns.

• While previous editions grouped disorders under broad umbrellas like "mood disorders," the DSM-5 has moved toward more distinct categorizations.

• Mood Disorder Classification Changes:

  • Depression (Major Depressive Disorder) and Bipolar Disorder are now treated as two separate, distinct categories rather than being grouped together as "mood disorders."

• Anxiety Disorder Classification Changes:

  • Previously, any disorder where anxiety was a major symptom was grouped under the anxiety umbrella.

  • Generalized Anxiety Disorder (GAD) and Panic Disorder remain classified under Anxiety Disorders.

  • Post-Traumatic Stress Disorder (PTSD) has been moved to a separate category titled "Trauma and Stressor-Related Disorders."

• Clinical vs. Biological Perspective:

  • While clinical classification has become more complex and separate, the underlying biological etiological pathways and understanding provided in academic texts remain correct despite these organizational shifts.

Major Depressive Disorder (MDD)

• Major Depression is characterized by several clusters of clinical symptoms that must be present for diagnosis:

  • A persistent sad, depressed mood.

  • Anhedonia: The loss of interest and pleasure in usual activities and hobbies (e.g., no longer enjoying movies or social interactions).

  • Changes in sleep patterns: This can manifest as either insomnia (difficulty falling asleep) or hypersomnia (excessive sleep).

  • Changes in appetite and weight: Depression can lead to either significant weight gain or weight loss.

  • Psychomotor and Energy Changes: Great fatigue, tiredness, and a general loss of energy.

  • Negative Self-Concept: Persistent feelings of worthlessness and a low view of oneself.

  • Cognitive and Suicidal Symptoms: Difficulty in concentration and recurrent thoughts of death or suicide.

• Biological Factors in Depression:

  • Genetics: Sharing genetic material with a parent who has depression creates a predisposition; studies of twins indicate a moderate degree of heritability, though no single "depression gene" has been identified.

  • Immune System: Research indicates increased activity in the immune system, often triggered by high stress, trauma, or poor diet.

  • Brain Activity Asymmetry:

    • Depressed individuals often show decreased activity in the left hemisphere.

    • Increased activity is noted in the right prefrontal cortex.

    • In contrast, non-depressed individuals show a relationship between a happy mood and increased activity in the left prefrontal cortex.

• Biochemistry: The Monoamine Hypothesis:

  • Asserts that depression results from low levels of the neurotransmitters norepinephrine ($NE$) and serotonin ($5-HT$), collectively known as monoamines.

  • These monoamines are essential for the functioning of the hypothalamus, which regulates sleep, appetite, sex, and motor behavior.

  • The specific balance between the two is uncertain, but low levels correlate with the reduction in physical drives associated with MDD.

Pharmacological Treatments for Depression

• Tricyclic and Bicyclic Antidepressants:

  • Mechanism of Action: These drugs block the reuptake or reabsorption of serotonin or norepinephrine by the presynaptic neuron by fitting into the reabsorption channels. This increases the availability of neurotransmitters at the synapse, thereby increasing neurological activity.

  • Tricyclics (e.g., Tofranil, Elavil, Senequin): Block reuptake of both serotonin and norepinephrine.

  • Bicyclics (e.g., Prozac, Zoloft): Known as Selective Serotonin Reuptake Inhibitors (SSRIs) because they typically only block serotonin reuptake.

  • Side Effects: Tricyclics can cause considerable weight gain. Both groups may cause dry mouth, constipation, urinary retention, blurred vision, heart palpitations, hypotension (low blood pressure), drowsiness, and sexual dysfunction (e.g., delayed orgasm).

• Monoamine Oxidase Inhibitors (MAOIs):

  • Function of MAO: Monoamine oxidase is an enzyme that destroys excess neurotransmitters at the synapse to keep it "clean."

  • Mechanism: MAOIs (e.g., Marplan, Nardil) inhibit this enzyme, reducing catabolism (breakdown) of monoamines so more are available for transmission.

  • Dietary Restrictions: MAOIs can cause fatally high blood pressure if combined with foods high in tyramine (e.g., unpasteurized cheese, aged meats, wines, some beers) or drugs like stimulants and decongestants.

  • Clinical Use: Usually reserved for patients who do not respond to other antidepressants and are often administered in hospital settings where diet is supervised.

• Electroconvulsive Therapy (ECT):

  • Usage: Reserved for severe depression unresponsive to therapy/medication or for patients at extreme risk of suicide.

  • Procedure: An electrical current of $70-150\,V$ is passed through the skull for $0.1-1.0\,\text{second}$ to induce a convulsion lasting $45-60\,\text{seconds}$.

  • Preparation: Patients receive a strong sedative and a muscle relaxant to prevent injury and induce sleep. Oxygen is provided post-convulsion due to carbon dioxide buildup.

  • Efficacy and Risks: Effective in about $70\%$ of cases. Side effects include headaches and memory loss. It carries a mortality risk of approximately $1$ in $1,000$ patients.

Bipolar Disorder and Seasonal Variations

• Bipolar Disorder (Formerly Manic Depression):

  • Defined by two extremes or "polarities" of mood: depression and mania.

  • Mania Symptoms: Intense excitement, restless activity, rapid speech (talkativeness), flight of ideas (racing thoughts), decreased need for sleep, inflated self-esteem (grandiosity), distractibility, and excessive involvement in risky activities (e.g., reckless spending or gambling).

  • Bipolar I Disorder: Characterized by full-blown episodes of mania.

  • Bipolar II Disorder: Characterized by milder manic phases called hypomania, often presenting as agitation or anxiety.

  • Biological Basis: Associated with a larger than normal amygdala. Biochemistry suggests a "dysregulation" of neurotransmission: high levels of neurotransmitters during mania and low levels during depression.

  • Treatment: Lithium salts are the primary treatment, effective in $80\%$ of cases. Lithium moderates norepinephrine levels. It requires constant blood monitoring because high levels are poisonous. Side effects include thirst, frequent urination, tremors, and dizziness.

• Major Depressive Disorder with Seasonal Pattern (SAD):

  • Depression that recurs during specific seasons, most often winter.

  • Most prevalent near the poles where winter nights are long; unheard of in the tropics.

  • Treatment: Exposure to very bright lights ($2,500\,\text{lux}$) for an hour or more daily, particularly in the morning. This likely affects serotonin synapses and circadian rhythms.

Schizophrenia: Symptoms and Clinical Presentation

• Schizophrenia involves major disturbances in thought, emotion, and behavior. Patients often have no realization that their behavior is unusual.

• Positive Symptoms (Excesses of behavior):

  • Delusions: False beliefs held despite contrary evidence. Includes delusions of persecution (spying/hurting), identity (believing one is famous), and thought interference (thoughts being broadcast or placed by external sources).

  • Hallucinations: Sensory experiences without reality. Auditory hallucinations (harsh/critical voices) are most common, but can also be visual, olfactory (smell), or tactile.

  • Disorganized Speech: Incoherent speech that lacks narrative structure because thoughts are not connected.

• Negative Symptoms (Deficits/Lacking behaviors):

  • Poverty of Speech: Reduced amount of speech that is vague and repetitive.

  • Flattened Affect: Limited emotional expression, vacant staring, flaccid facial muscles, and toneless voice.

  • Anhedonia: Inability to experience pleasure.

• Diagnostic Timing: Symptoms must be present for at least one month according to the DSM-5 and must significantly impact social or occupational functioning.

Etiology and Biochemistry of Schizophrenia

• Neurodevelopmental Factors:

  • Genetics: Lifetime risk is $1.5\%$. Having a sibling with schizophrenia increases risk $6-10 \times$. An identical twin with the disorder increases risk by $50\%$.

  • Prenatal/Neonatal Insult: Poor maternal nutrition, premature birth, low birth weight, and delivery complications (excessive bleeding/prolonged labor).

  • Season of Birth Effect: People born in winter have a slightly higher risk, possibly due to maternal influenza infections in the autumn during crucial brain development stages.

• Brain Structure Abnormalities:

  • Enlarged Ventricles: CAT and MRI scans show enlarged brain cavities, indicating atrophy (death) of surrounding brain tissue.

  • Limbic System: Abnormalities in the hippocampus, amygdala, and basal ganglia.

• Biochemical Hypotheses:

  • Dopamine Hypothesis: High levels of dopamine activity cause positive symptoms. This is supported by the fact that dopamine-reducing drugs alleviate symptoms, while dopamine-increasing drugs (like cocaine) worsen them.

  • Glutamate Hypothesis: Suggests low levels of glutamate, particularly in the prefrontal cortex, contribute to the disorder.

Pharmacological Treatment of Schizophrenia

• Antipsychotic Drugs (Neuroleptics):

  • Phenothiazines (Older Class): e.g., Thorazine, Stelazine. They block dopamine receptors. Side effects include dry mouth, blurred vision, and extrapyramidal symptoms (tremors, shuffling gait, muscular rigidity). Prolonged use can cause tardive dyskinesia (involuntary lip smacking/sucking).

  • Atypical Neuroleptics (Newer Class): e.g., Clozaril. These block fewer dopamine receptors and are more selective, targeting tracts leading to the frontal and temporal lobes while sparing motor tracts. They also increase serotonin, which inhibits dopamine activity.

• Limitations: Drugs provide management but not a cure, are mostly effective for positive symptoms, and do not work for all patients ($80\%$ efficacy for Thorazine).

Anxiety-Related Disorders: GAD, Panic, and PTSD

• Generalized Anxiety Disorder (GAD):

  • Persistent anxiety (lasting at least $6\,\text{months}$) not linked to a specific object. Physical symptoms include sweating, pounding heart, and dry mouth (autonomic hyperactivity).

  • Biochemistry: Due to low levels of GABA (gamma-aminobutyric acid). Low GABA leads to high neurological arousal.

  • Treatment: Benzodiazepines (e.g., Valium/diazepam) which increase GABA activity in the amygdala and hypothalamus.

• Panic Disorder:

  • Brief periods of intense, spontaneous anxiety and physical symptoms (shortness of breath, choking, chest pain) lasting about $10\,\text{minutes}$.

  • Biochemistry: Linked to low GABA and overly sensitive respiratory control centers in the brainstem.

  • Treatment: Antidepressants (Tricyclics/Bicyclics) are effective because they increase serotonin, which inhibits the respiratory control center and prevents "false alarms."

• Post-Traumatic Stress Disorder (PTSD):

  • Criteria: Exposure to a traumatic event involving threatened death/injury. Symptoms include re-experiencing (flashbacks/dreams), avoidance of stimuli, psychic numbing (detachment), and heightened arousal (startle response).

  • Biological Findings: Possible sensitization of the brainstem and amygdala involving dopamine. Research suggests individuals who develop PTSD often have a smaller than average hippocampus from the start.