psychiatric treatment


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psychiatric treatment

  1. 1. Psychiatric disorders dr shabeel pn
  2. 2. Disorders of Mind & Brain <ul><li>Mind and brain are two sides of one coin; disorders of the mind are disorders of the brain. </li></ul><ul><li>Particular clusters of symptoms (syndromes) tend to occur together in various different mental illnesses </li></ul><ul><li>The ways in which symptoms cluster together tells us something about the structure of the human mind and brain </li></ul>
  3. 3. Anatomy of psychiatric disorders <ul><li>Contemporary psychiatry implicates neurotransmitters rather than anatomy. </li></ul><ul><ul><li>Schizophrenia :: dopamine </li></ul></ul><ul><ul><li>Depression :: serotonin </li></ul></ul><ul><li>To some degree, this may reflect the popular treatments – neurotransmitters specific to brain regions. </li></ul>
  4. 4. Major symptom clusters <ul><li>Reality distortion </li></ul><ul><li>Disorganization </li></ul><ul><li>Psychomotor poverty </li></ul><ul><li>Psychomotor excitation </li></ul><ul><li>Depression </li></ul><ul><li>Euphoria </li></ul><ul><li>Anxiety </li></ul>
  5. 5. Reality distortion <ul><li>Mismatch between representation of reality in individual’s mind and representation supported by objective evidence </li></ul><ul><li>Hallucinations and delusions </li></ul><ul><ul><li>Tend to occur together </li></ul></ul><ul><ul><li>Tend to respond similarly to dopamine blocking medication </li></ul></ul>
  6. 6. <ul><li>Hallucination : perception with quality of a sensory perception but nor derived form stimulation of a sense organ </li></ul><ul><ul><li>Individual usually falsely attributes perception’s origin to external world </li></ul></ul><ul><li>Delusion: fixed belief derived by erroneous inference or unjustified assumption that cannot be accounted for by culture or religion </li></ul>
  7. 7. Delusions <ul><li>Delusions usually false but the key issue is lack of rational grounds and fixity. </li></ul><ul><li>Ability to engage in logical deduction about other issues is usually intact; certain ideas seem exempted from the need for logic. </li></ul><ul><li>Non-psychotic distortions of reality (eg in OCD or in non-psychotic depression) reflect biased thinking but are less resistant to debate </li></ul>
  8. 8. Psychotic Reality Distortion <ul><li>Can occur in schizophrenia, mania, psychotic depression, brain injury or degeneration </li></ul><ul><li>Themes: persecution; alien control, religion, grandiosity, guilt </li></ul><ul><li>Influenced by culture, but some themes are common across cultures </li></ul>
  9. 9. Reality distortion in schizophrenia <ul><li>Characteristic forms (but not present in every case) </li></ul><ul><ul><li>Delusions of alien influence over thought, volition, action, affect, bodily function –characteristic </li></ul></ul><ul><ul><li>Third person auditory hallucinations </li></ul></ul><ul><li>Less specific but common forms: </li></ul><ul><ul><li>Persecutory delusions (52%), delusions of reference (50%) </li></ul></ul><ul><ul><li>Second person auditory hallucinations </li></ul></ul>
  10. 10. Affective psychosis <ul><li>Mood disorder with psychotic features is diagnosed if psychotic illness is dominated by mood symptoms unless there is reality distortion without substantial mood symptoms for at least two weeks </li></ul><ul><li>Delusions and hallucinations are usually mood congruent (eg guilt, worthlessness, critical voices with depressed mood; grandiose delusions and self-reinforcing halluciations in mania) </li></ul><ul><li>Reality distortion shows similar response to antipsychotic medication irrespective of diagnosis </li></ul>
  11. 11. Neuropsychological correlates of reality distortion <ul><li>Reality Distortion can occur in absence of general defect in reasoning. </li></ul><ul><li>Defective internal monitoring of self-generated mental activity (Frith & Done 1989; Mlakar et al, 1994) </li></ul><ul><li>Jumping to conclusions – the bead test (Huq et al, 1988) </li></ul><ul><li>Patients with persecutory delusions tend to attribute negative outcomes to external causes (Bentall, 1994) </li></ul>
  12. 12. Regional cerebral activity and reality distortion <ul><li>Early SPECT studies reported over-activity in medial temporal lobe (eg Musalek et al 1989) </li></ul><ul><li>More recent PET studies demonstrate overactivity in left parahippocamapl gyrus and hippocampus (Liddle et al 1992; Silbwersweig et al, 1995) </li></ul>Liddle et al, 1992
  13. 13. Neurochemistry and pharmacology of reality distortion <ul><li>Antipsychotic drugs that block dopamine D2 receptors decrease reality distortion </li></ul><ul><li>Dopamine agonists (eg amphetamine, cocaine) exacerbate delusions and hallucinations </li></ul><ul><li>Amphetamine produces greater increase in intra-synaptc dopamine in schizophrenia than in healthy individuals (Laruelle et al 1996) </li></ul>
  14. 14. Pharmacology of reality distortion <ul><li>Serotonin = 5-hydroxytryptamine, or 5-HT </li></ul><ul><li>5HT2 receptor agonists such as LSD (which reduce 5HT signalling via autoreceptors) are hallucinogenic </li></ul><ul><li>Glutamatergic blockers (eg ketamine) can also produce reality distortion </li></ul>
  15. 15. Hypothesis for generation of reality distortion <ul><li>Episodic memories rely on context for evaluation and validation; semantic memories (eg Paris is capital of France) do not require contextual validation </li></ul><ul><li>Neural circuits in hippocampus generate a ‘validation’ signal when a mental event (eg an episodic memory) fits its context promoting consolidation of the memory </li></ul><ul><li>Aberrant hippocampal firing might reinforce incidental thoughts irrespective of context and allow consolidation without need of contextual validation – delusion formation </li></ul><ul><li>Internal speech might be processed without context thereby becoming detached from internal source- hallucinations </li></ul><ul><li>Dopamine hyperactivity might reinforce the effect of hippocampal overactivity via the striato-thalamo-cortical feed back loops which mediates the hippocampal signal (This might be blocked by antipsychotic drugs) </li></ul>
  16. 16. Disorganization syndrome <ul><li>Disjointed thought, emotion, behaviour </li></ul><ul><li>Formal thought disorder, inappropriate affect, bizarre behaviour </li></ul><ul><li>Speech shows ‘looseness of associations’, ‘derailment’, replies can be tangential or incoherent </li></ul><ul><li>Occurs in schizophrenia (a core feature); mania (less commonly); frontal lobe damage. </li></ul><ul><li>Severity of disorganization is strong predictor of poor occupational and social function </li></ul>
  17. 17. Neuropsychological correlates of disorganization <ul><li>Core executive processes, especially the selection between competing mental events. Poor Stroop performance (Liddle & Morris, 1991);Errors of commission in CPT (Frith et al 1992) </li></ul><ul><li>Abnormal spreading of semantic and phonological associations (Spitzer et al 1994) </li></ul>
  18. 18. Regional cerebral activity and disorganization Liddle et al, 1992
  19. 19. Regional cerebral activity and disorganization <ul><li>PET study (Liddle et al 1992): </li></ul><ul><ul><li>increased activity in medial frontal cortex/anterior cingulate & thalamus; </li></ul></ul><ul><ul><li>decreased activity in ventral prefrontal cortex, insula, temporoparietal junction </li></ul></ul><ul><li>SPET studies (Ebmeier et al 1993; Yuasa et al, 1995) </li></ul><ul><ul><li>replicate finding of increased activity in medial prefrontal cortex/ anterior cingulate (ACC) </li></ul></ul><ul><li>ACC strongly engaged in response selection, eg in Stroop task </li></ul>
  20. 20. Psychomotor poverty and excitation <ul><li>Psychomotor poverty: </li></ul><ul><ul><li>Poverty of speech </li></ul></ul><ul><ul><li>Flat affect, anhedonia </li></ul></ul><ul><ul><li>Decreased voluntary activity </li></ul></ul><ul><li>Psychomotor excitation </li></ul><ul><ul><li>Pressure of speech </li></ul></ul><ul><ul><li>Excited or irritable mood </li></ul></ul><ul><ul><li>Motor hyperactivity </li></ul></ul>Abnormalities of the rate at which the mind generates thoughts, feelings and actions
  21. 21. Psychomotor poverty & excitation: context <ul><li>Psychomotor poverty </li></ul><ul><ul><li>Schizophrenia (negative symptoms) </li></ul></ul><ul><ul><li>Retarded depression </li></ul></ul><ul><ul><li>Frontal lobe injury or degeneration </li></ul></ul><ul><ul><li>Basal ganglia degeneration (eg Parkinson’s disease </li></ul></ul><ul><li>Psychomotor excitation </li></ul><ul><ul><li>Mania </li></ul></ul><ul><ul><li>Acute schizophrenia </li></ul></ul><ul><ul><li>Basal ganglia degeneration eg Huntingtons’ disease </li></ul></ul>
  22. 22. Neuropsychological correlates of psychomotor poverty <ul><li>Associated with </li></ul><ul><ul><li>impaired memory, </li></ul></ul><ul><ul><li>Abstraction </li></ul></ul><ul><ul><li>Initiation and planning of activity </li></ul></ul><ul><ul><ul><li>Decreased verbal fluency (Liddle & Morris, 1992; Norman et al 1997) </li></ul></ul></ul><ul><ul><ul><li>Increased RT in choice RT tasks (Ngan & Liddle, 2000) </li></ul></ul></ul>
  23. 23. Regional cerebral activity and psychomotor poverty Liddle et al, 1992
  24. 24. Psychomotor poverty and brain structure <ul><li>In schizophrenia; some studies report psychomotor poverty is associated with ventricular enlargement (Lewis, 1990) </li></ul>
  25. 25. Neurochemistry & pharmacology of psychomotor poverty <ul><li>Dopamine metabolism decreased (van Praag & Korf, 1971) </li></ul><ul><li>Stimulants can reduce apathy (Marin et al 1995) </li></ul><ul><li>Dopamine blocking antipsychotics can exacerbate psychomotor poverty (van Putten et al, 1990) </li></ul>
  26. 26. Neurochemistry & pharmacology of psychomotor excitation <ul><li>Drugs that promote dopaminergic neurotransmission (eg amphetamine) produce psychomotor excitation in healthy people (Jaobs and Silverstone, 1986) </li></ul>
  27. 27. Depression & Elation <ul><li>Depression </li></ul><ul><ul><li>Low mood disproportionate to circumstances </li></ul></ul><ul><ul><li>Sad facial expression, voice, posture </li></ul></ul><ul><ul><li>Anhedonia </li></ul></ul><ul><ul><li>Cognitive distortions –negative bias, including low self-esteem, guilt, hopelessness, suicidal thought </li></ul></ul><ul><ul><li>Somatic symptoms (loss of sleep, appetite, libido etc) </li></ul></ul><ul><ul><li>Sometimes associated with psychomotor poverty </li></ul></ul><ul><li>Elation </li></ul><ul><ul><li>Euphoric mood </li></ul></ul><ul><ul><li>Animated expression </li></ul></ul><ul><ul><li>Elevated self-esteem and optimism </li></ul></ul><ul><ul><li>Decreased need for sleep </li></ul></ul><ul><ul><li>often associated with psychomotor agitation </li></ul></ul>
  28. 28. Mood disorders <ul><li>Depression can occur in </li></ul><ul><ul><li>Major depressive disorder (15-20% of pop) </li></ul></ul><ul><ul><li>Bipolar affective disorder (2% of pop) </li></ul></ul><ul><ul><li>Brain injury or degeneration </li></ul></ul><ul><ul><li>Drug induced mood disorder </li></ul></ul><ul><ul><li>Schizophrenia (depression in >50% of cases) </li></ul></ul>
  29. 29. Neuropsychological correlates of depression <ul><li>Processing bias, preferential recall or attention to negative material (Gotlib, 1991) </li></ul><ul><li>Decreased speed of processing (Weingartner et al, 1981) </li></ul><ul><li>Impaired declarative memory (Zakzanis et al, 1998) </li></ul>
  30. 30. Brain structure and mood disorders <ul><li>Decreased grey matter in (sub-genual) anterior cingulate cortex in bipolar disorder and in major depression (Drevetts et al 1997) </li></ul><ul><li>Decreased hippocampal volume associated with duration of illness (Sheline et al, 1996). Possibly due to damage by elevated cortisol during acute episodes </li></ul>
  31. 31. Regional cerebral activity and depression <ul><li>decreased activity in lateral prefrontal cortex resolves as symptoms resolve (Baxter et al 1989). </li></ul><ul><li>overactivity in anterior cingulate during acute episodes (Mayberg et al, 1998) </li></ul><ul><li>evidence underactivity in anterior cingulate and medial prefrontal cortex in those prone to relapse and also in cases that respond poorly to treatment (Bench et al, 1992) </li></ul>
  32. 32. Regional cerebral activity associated with elation <ul><li>Global increase in regional brain activity during manic episodes (elation + psychomotor excitation) (Baxter et al 1985) </li></ul>
  33. 33. Regional cerebral metabolism in bipolar disorder (Baxter et al 1985) <ul><li>Depression </li></ul><ul><li>Mania </li></ul><ul><li>Depression </li></ul>
  34. 34. Neurochemistry and pharmacology of mood disorders <ul><li>Depression </li></ul><ul><ul><li>Depression is decreased by drugs that enhance monoamine neurotransmission eg SSRIs such as fluoxetine (Prozac) & SNRIs such as venlafaxine – this suggests that serotonin and noradrenaline neurotransmission is under-active in depression, but evidence is inconclusive </li></ul></ul><ul><ul><li>Cortisol regulation is disrupted– maybe this is the core biochemical abnormality </li></ul></ul><ul><li>Elation </li></ul><ul><ul><li>Associated with increased dopamine neurotransmission </li></ul></ul>
  35. 35. Bipolar affective disorder <ul><li>Genetic influence </li></ul><ul><ul><li>High concordance of bipolar affective disorder in monozygotic twins between 0.67 and 0.85 (Glahn et al. 2004)-indicate environmental factors must have a role to play. </li></ul></ul><ul><ul><li>Occurs around the world at a consistent prevalence, suggests alleles have been present for a long time. </li></ul></ul><ul><li>Why does this gene survive? Does it pose a benefit. As an analogy, sickle cell trait can lead to illness but is recessive and helps resistantance to malaria. </li></ul><ul><ul><li>In low doses the symptoms of hypomania could be advantageous: increase in energy, faster thoughts, less sleep. </li></ul></ul><ul><ul><li>Rates of mood disorders elevated among creative individuals (Richards and Kinney, 1989; Jamison, 1989) </li></ul></ul><ul><ul><li>Individuals with bipolar traits more likely to be leaders within social groups (Gardner, 1982) </li></ul></ul>
  36. 36. Anxiety <ul><li>Feeling of unease, dread, fear together with symptoms reflecting over-activity on the sympathetic nervous system </li></ul><ul><ul><li>Generalised anxiety disorder </li></ul></ul><ul><ul><li>Panic disorder - brief dramatic episodes </li></ul></ul><ul><ul><li>Specific phobias eg fear of spiders </li></ul></ul><ul><ul><li>Agoraphobia - fear of public places </li></ul></ul><ul><ul><li>Post-traumatic stress disorder </li></ul></ul><ul><ul><li>Obsessive-compulsive disorder </li></ul></ul><ul><li>Anxiety disorders frequently coexist, and are often associated with depression </li></ul>
  37. 37. Regional cerebral activity associated with anxiety <ul><li>Provocation of anxiety produces activation of frontal, limbic and paralimbic cortex in patients and in healthy people </li></ul>
  38. 38. Pharmacology of anxiety <ul><li>Benzodiazepines (which promote GABA activity) – effective anxiolytics but addictive </li></ul><ul><li>Antidepressants are also effective anti-anxiety drugs </li></ul>
  39. 39. Concepts of schizophrenia <ul><li>Characteristic symptoms </li></ul><ul><ul><li>Positive – presence of abnormal mental activity </li></ul></ul><ul><ul><ul><li>Reality distortion </li></ul></ul></ul><ul><ul><ul><li>Disorganization </li></ul></ul></ul><ul><ul><li>Negative – diminution of normal mental activity </li></ul></ul><ul><ul><ul><li>Psychomotor poverty </li></ul></ul></ul><ul><li>Many other symptoms: psychomotor excitation; depression </li></ul><ul><li>Onset tends to occur early in adult life </li></ul><ul><li>Deterioration in function (variable in degree) </li></ul>
  40. 40. Reality distortion <ul><li>Delusions </li></ul><ul><ul><li>*Thought insertion, withdrawal, broadcast </li></ul></ul><ul><ul><li>*Control – made will, made acts, made affect </li></ul></ul><ul><ul><li>*Somatic passivity </li></ul></ul><ul><ul><li>*Delusional perception </li></ul></ul><ul><ul><li>Persecution etc </li></ul></ul><ul><li>Hallucinations </li></ul><ul><ul><li>*Third person auditory (commenting, discussing); Audible thought </li></ul></ul><ul><ul><li>Second person auditory </li></ul></ul><ul><ul><li>Olfactory, visual, tactile </li></ul></ul><ul><li>* Schneider’s first rank symptoms </li></ul>
  41. 41. Age of onset 10 20 30 40 50 years From Jennen-Steinmetz et al 1997
  42. 42. Characteristic time course 1 st acute epidsode prodrome relapse residual phase relapse
  43. 43. ICD 10 diagnostic criteria <ul><li>At least one strongly characteristic symptom </li></ul><ul><ul><li>Schneiderian first rank symptom (eg 3 rd person hallucination; delusion of control.) </li></ul></ul><ul><ul><li>Persistent bizarre delusion </li></ul></ul><ul><li>OR two less characteristic symptoms </li></ul><ul><ul><li>Other hallucinations </li></ul></ul><ul><ul><li>Formal thought disorder </li></ul></ul><ul><ul><li>Catatonia </li></ul></ul><ul><ul><li>Negative symptoms </li></ul></ul><ul><li>Duration: at least one month </li></ul><ul><li>Exclusion of affective psychosis; exclusion of overt brain disease, or drug toxicity </li></ul>
  44. 44. Aetiology : predisposing factors <ul><li>Genes </li></ul><ul><ul><li>twin concordance: MZ 45%, DZ 12-15% </li></ul></ul><ul><ul><li>adoption: risk is determined by biological parent </li></ul></ul><ul><li>Intra-uterine insult </li></ul><ul><ul><li>Maternal viral infection </li></ul></ul><ul><ul><li>Maternal starvation </li></ul></ul><ul><ul><li>Maternal stress </li></ul></ul><ul><li>Birth complications </li></ul>
  45. 45. Aetiology: precipitating factors <ul><li>Stress </li></ul><ul><li>Drug abuse- </li></ul><ul><ul><li>amphetamine, cocaine, </li></ul></ul><ul><ul><li>marihuana etc </li></ul></ul>
  46. 46. Brain structure in schizophrenia <ul><li>Ventricular enlargement (but effect size is only 0.6 – therefore most cases in nromal range) </li></ul><ul><li>Loss of grey matter in many brain regions, most marked in medial temporal lobe and thalamus </li></ul>
  47. 47. Cognitive deficits in schizophrenia <ul><li>Executive function, attention, memory (e.g. Green, 1998) </li></ul><ul><li>Variation over time and between patients is complex, symptoms tend to be worse during acute episodes, but also present during remission </li></ul>
  48. 48. Pharmacology <ul><li>Typical antipsychotics: eg chlorpromazine; haloperidol: block dopamine - alleviate reality distortion, disorganization and excitation </li></ul><ul><li>Atypical antipsychotics: block dopamine + other transmitters (eg serotonin). Slightly greater efficacy against positive symptoms; moderate effect on negative symptoms, small improvment in cognition </li></ul>
  49. 49. Bipolar mood disorder <ul><li>Depressive episode </li></ul><ul><ul><li>Depressive syndrome </li></ul></ul><ul><ul><ul><li>Sad mood, anhedonia </li></ul></ul></ul><ul><ul><ul><li>Negative thoughts, hopelessness, suicidality </li></ul></ul></ul><ul><ul><ul><li>Guilt (can be delusional) </li></ul></ul></ul><ul><ul><ul><li>Somatic symptoms </li></ul></ul></ul><ul><ul><li>often accompanied by: </li></ul></ul><ul><ul><li>Psychomotor poverty (retarded depression) </li></ul></ul><ul><ul><li>or </li></ul></ul><ul><ul><li>Psychomotor excitation (agitated depression) </li></ul></ul><ul><li>Manic episode </li></ul><ul><ul><li>Psychomotor excitation </li></ul></ul><ul><ul><ul><li>Elation or irritability </li></ul></ul></ul><ul><ul><ul><li>Pressure of speech </li></ul></ul></ul><ul><ul><ul><li>Overactivity, reduced need for sleep </li></ul></ul></ul><ul><ul><li>often accompanied by: </li></ul></ul><ul><ul><li>Grandiose reality distortion </li></ul></ul><ul><ul><ul><li>Grandiose delusions </li></ul></ul></ul><ul><ul><ul><li>Mood congruent hallucinations </li></ul></ul></ul>
  50. 50. Aetiology of bipolar disorder <ul><li>Genetics </li></ul><ul><li>Concordance for affective disorders is 67% in monozygotic twins and in 20% in dizygotic twins (Bertelson et al., 1977), genetic factors for unipolar depression related by partially distinguishable </li></ul>
  51. 51. <ul><li>Ventricular enlargement (e.g. Pearlson & Veroff, 1981) usually less marked than in schizophrenia </li></ul><ul><li>Decreased grey matter in anterior cingulate (Drevets et al., 1997) </li></ul>Anatomy of bipolar disorder
  52. 52. Pharmacology of bipolar disorder <ul><li>Antipsychotics (which block dopamine): effective in treating psychomotor excitation and reality distortion during acute episodes of mania </li></ul><ul><li>Mood stabilizers (eg Lithium, and various anticonvulsants) </li></ul><ul><li>Antidepressants have a limited role as they promote mania </li></ul>
  53. 53. Psychopathy <ul><li>A personality disorder (enduring throughout adult life) with two main groups of features: </li></ul><ul><ul><li>Callous disregard for others (Lack of empathy; lying; manipulative; glib; shallow affect; lack of remorse or guilt) </li></ul></ul><ul><ul><li>Impaired regulation of behaviour (impulsivity, irresponsibility; need for stimulation) </li></ul></ul>
  54. 54. Aetiology of psychopathy <ul><li>Genes </li></ul><ul><ul><li>Concordance for antisocial personality disorder is 51% in monzygotic twins and 22% in dizygotic twins </li></ul></ul><ul><li>Brain injury: </li></ul><ul><ul><li>damage to frontal lobes in infancy can lead to psychopathy </li></ul></ul><ul><ul><li>Frontal damage in adulthood can produce pseudopsychpathy – impaired behavioural regulation without callousness (Phineas Gage) </li></ul></ul><ul><li>Adverse social circumstances ? </li></ul>
  55. 55. Cognition and information processing in psychopathy <ul><li>Psychopaths do not show widespread cognitive impairments (Hart et al., 1990), but there is evidence of orbital frontal cortex dysfunction (Lapierre et al., 1995) </li></ul><ul><li>Reaction time to affect-laden words reduced in healthy people but not psychopaths in lexical decision task (Williamson et al, 1991); less limbic activation while processing affect laden words (Kiehl et al 2001) </li></ul><ul><li>Abnormal ERPs for response inhibition (Kiehl et al., 2000) and target detection (Kiehl et al 1999) </li></ul>
  56. 56. Psychopaths exhibit a large fronto-central negativity during stimulus detection tasks that is also present in patients with anterior temporal lobe lesions (Kiehl et al., 1999) Kiehl et al. Yamaguchi & Knight (1993) Johnson (1989) 400 800ms 500 1000ms Parietal lobe damaged patients Temporal lobectomy Temporal lobe damaged patients Psychopaths Controls Controls Nonpsychopaths