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Psychopathology: Biological Bases of Behavioral Disorders

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Psychopathology: Biological Bases of Behavioral Disorders

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    1. Psychopathology: Biological Bases of Behavioral Disorders Mental Disorders: SZ, Depression, BPD Anxiety Disorders: General, PTSD, OCD Infectious proteins (prions)

    3. History of Schizophrenia (SZ) Syphilis and psychosis Emil Kraepelin – “dementia praecox” Eugen Blueler – Schizophrenia (split brain) Core symptom – dissociative thinking Kurt Schneider Positive symptoms: hallucinations, delusions, excited motor behavior Negative symptoms: slow and impoverished thought and speech, emotional and social withdrawal, blunted affect

    4. Heritability of SZ 50% MZ twin concordance / 17% DZ 6-17% first-degree relatives Adoptions studies Greater prevalence among biological relatives Mode of transmission complex Genetic component Spread across all but 8 of 23 chromosomes Gene for ACH, NMDA, GABA and ACh receptor regulation, COM-T (DA regulation) Environmental stressor(s)

    5. Anatomy of SZ Ventricular enlargement Disoriented hippocampal cells Degree R2 with severity of symptoms 2nd trimester exposure to influenza / temperature of gestating fetus Early cell development Regional anatomical abnormalities Adolescent SZs loose more gray matter and at faster rate Shrinkage of cerebellar vermis Thicker corpus callosum Abnormal fetal cell migration to prefrontal cortex Functional maps Frontal cortex hypofrontality – in general and in response to WISC Antipsychotics alleviate Neurochemical changes Amphetamine psychosis Typical antipsychotics (D2 antagonists – high density in SZ) Atypical antipsychotics (5-HT2A antagonists) Glutamate hypothesis – PCP-induced SZ, NMDA antagonist

    6. Depression Prolonged unhappy mood; loss of interests, energy and appetite; age of onset (typical) ~40 yr, hereditary component Bipolar Disorder younger age of onset; cycles of mania and depression lithium effective therapy 2-3 times more common in women 80% of suicides – depressed individuals Lower 5-HT (contributes to depression in PD) Higher cortisol levels (contributes to Cushing’s Disease)

    7. Functional Maps / Neurochemistry of Depression Increased frontal cortex & amygdala activity Decreased parietal and posterior temporal cortex activity Monoamine theory Decreased 5-HTergic and noradrenergic activity Antidepressants Restore monoamine levels ECT Drugs that deplete monoamines exacerbate depression

    8. Depression and Adrenal Function Increased cortisol HPA axis unresponsive to feedback Dexamethasone suppression test fails Decreased neurotrophic factors (BDNF – 5-HT and NE agonist increase)

    9. Depression and Gender 2-fold difference (women v. men) Psychosocial Social discrimination, low self assertion/ esteem & depression Learned-helplessness Endocrine physiology – no strong evidence Before menstruation Contraceptive pill use Following childbirth Menopause Amish women and men show same prevalence Alcohol banished – men in typical US society mask depression w/ alcohol consumption?

    10. Depression and Sleep Decreased stages 3 and 4 SWS Increased stages 1 and 2 SWS Shortened REM onset / REM bouts more rigorous REM sleep deprivation improves depression

    11. Physiological Markers and Treatment for Anxiety Disorders Temporal lobe abnormalities Increased parahippocampal basal activity High oxygen metabolism Anxiolytics – pharmacotherapy Most common class - benzodiazepines

    12. Post Traumatic Stress Disorder Traumatic experience Witnessing, participating in mass killings Severe abuse Fear conditioning and behavioral sensitization Previously neutral stimuli evoke response Autonomic Fear, trembling Vivid memories Evoked by stressful circumstances

    13. Treatment for PTSD - I Cognitive-behavioral therapy (CBT) Work with cognition to change emotions Exposure therapy through imagery Flooding (“all-at-once” confrontation) Desensitization (gradual exposure) Learning coping skills Group Treatment Sharing “traumatic narrative” Sharing coping mechanisms

    14. Obsessive Compulsive Disorder Obsessions or compulsions Intrusive thoughts – compelled to act on Insight Time-consuming Treatment CBT Exposure Pharmacotherapy Tricyclics (increaase monoamine) SSRIs (increase 5-HT)

    15. Prions, Mad Cows and Creutzfeldt-Jakob Disease Normal protein takes on new, abnormal shape - prions Induces other proteins to fold as well Leads to brain degeneration Bovine spongiform encephalopathy (BSE, mad cow disease Creutzfeldt-Jakob Disease – ingested cows with BSE in Britons Treatment experimental / early stages of investigation and effective treatment

    16. Take Home Message Psychobiological approaches to understanding and treating psychiatric decline Schizophrenia Depression Anxiety Disorders Mad Cow Disease

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