1 / 36

Schizophrenia

Schizophrenia. “A Slow Fire Burning” Dr C Christie. General. Schizophrenia is a major psychotic disorder Chronic debilitating illness Devastating effects on all aspects of patient’s life Comprehensive and continuous lifelong treatment Heterogeneous disorder Variation in presentation

tiffany
Télécharger la présentation

Schizophrenia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Schizophrenia “A Slow Fire Burning” Dr C Christie

  2. General • Schizophrenia is a major psychotic disorder • Chronic debilitating illness • Devastating effects on all aspects of patient’s life • Comprehensive and continuous lifelong treatment • Heterogeneous disorder • Variation in presentation • Clinical diagnosis • No single symptom pathognomonic of 295

  3. 3 Symptom clusters • Positive symptoms – hallucinations and delusions • Disorganised thought, behaviour and speech • Negative symptoms • Affective flattening, alogia, anhedonia and avolition

  4. History • Kraeplin (1856 – 1926) termed dementia precox (early onset of cognitive decline) • Bleuler (1857 – 1939) used term schizophrenia. • Schism between thought, emotion and behaviour • Does NOT mean split personality

  5. DSM IV A. Characteristic symptoms (2 or more) Delusions, hallucinations, disorganised speech Grossly disorganised or catatonic behaviour Negative symptoms B. Social/occupational dysfunction C. Duration: 6 months D. Exclude schizoaffective and mood disorder E. Exclude GMC and substances F. Exclude pervasive developmental disorder (autism)

  6. Disorganised Paranoid Catatonic Undifferentiated Residual Subtypes

  7. Epidemiology • 1% prevalence • Risk increased if first degree relatives have the disorder • Risk increased if person is single, industrialised nation, in lower SE class, urban, problems in utero, perinatal problems, born in winter, recent stressful life event

  8. Males Present at earlier age Peak in early 20’s Poorer premorbid personality and social adjustment Females Peaks in late 20’s and 30’s Better prognosis Fewer admissions, shorter length of stay Age and Sex. M = F

  9. Mortality and morbidity • Mortality twice that of general population • Suicide high, 50% attempt • 10 -15% successful • Higher risk of dying a violent death • GMC present needs to be vigorously diagnosed and treated

  10. Substance Abuse • Co-morbidity of substance abuse and schizophrenia very common • 30 – 50% alcohol abuse • 15 – 25% cannabis • Nicotine!

  11. Genetics • Sibling of schiz patient 8% • Dizygotic twin 12% • Child of one schiz parent 12% • Both parents with schiz 40% • Monozygotic twin 47%

  12. Cultural and socioeconomic • Found in all cultures and socio-economic groups • In developing countries prognosis and outcome better • Related to stronger family/social support • Homelessness and 295 linked • Downward drift and deinstitutionalisation

  13. Biological factors/ structural • Changes in limbic system, basal ganglia and frontal cortex • Enlarged lateral and third ventricles • Reduction in cortical volume • Cytoarchitextural abnormalities of amygdala,hippocampus and parahippocampal gyrus

  14. Neuroimaging • Abnormal PET scans,shows deranged glucose utilisation/cerebral blood flow when challenged with psychological task, hypoactivity of frontal lobes and intellectual testing may show deficits • Is 295 a neurodevelopmental disorder only manifesting later in life with microanatomical cortical dysgenesis?

  15. Neurochemistry • Neurochemical abnormalities central • Models have been hypothesised using drug induced psychotic models • Dopamine hypothesis: hyperdopaminergia is main protagonist • Drugs that reduce firing of mesolimbic dopamine neurons have antipsychotic effect • Drugs that stimulate dopamine increase psychosis

  16. Neurochemistry • Hypothesis revised • Low prefrontal dopamine causes deficit, negative symptoms • Excessive dopamine activity in mesolimbic dopamine neurons cause positive symptoms

  17. Dopamine AND serotonin • Atypical neuroleptics act as 5HT2 and Dopamine antagonists • 5HT2a, 5HT2c antagonism, 5HT1a agonism • Cholinergic, muscarinic, GABA and glutamate mediated actions modulate antipsychotic drug action

  18. Clinical features/Acute phase • Behaviour and appearance – normal, perplexed, sudden behavioural changes • Speech – vague, concrete, bizarre, pressure, poverty, word salad, neologisms • Range of affect – blunted • Auditary hallucinations common • Voices often derogatory and refer to patient in 3rd person • Delusions • Insight is reduced

  19. Chronic Phase • Psychotic symptoms may be less severe • Symptoms persist in attenuated form • Negative symptoms may predominate

  20. Delirium Schizophreniform disorder Schizoaffective disorder Delusional disorder Brief psychotic disorder Bipolar mood disorder Substance induced psychotic disorder Psychosis secondary to GMC – TLE, epilepsy

  21. Course and prognosis • 10 -15% have a good prognosis • 20 – 30% lead reasonably normal lives • 40 – 60% poor outcome with chronic deteriorating course • Paranoid subtype best prognosis • Disorganised subtype worst prognosis

  22. Course and prognosis • Symptoms begin in adolescence • May have prodrome diagnosed in retrospect • Each relapse followed by deterioration • Positive symptoms may become less severe over time • Psychosis is toxic for the brain!

  23. Later onset Female gender Absent family hx Marriage Good pre-morbid personality and psychosocial adjustment Obvious precipitant Positive symptoms Good support systems Mood symptoms with family history of mood disorder Good prognostic indicators

  24. Management • Involve family and patient in active collaboration using integrated approach with pharmacologic, psychotherapeutic, psychosocial and rehabilitative measures • Need comprehensive and continuous treatment • At present NO CURE

  25. General goals of treatment • Decrease frequency, severity and psychosocial consequences of episodes • Maximise psychosocial functioning • Establish and maintain therapeutic alliance • Monitor patient status at regular intervals

  26. Thorough initial workup • Rule out conditions that mimic 295 • Identify co-morbid conditions that complicate diagnosis and treatment • Establish baseline for monitoring course of illness and response to treatment

  27. Acute phase management • HOSPITALISE IF: • Poses a threat to self or others • Unable to care for self • Co-morbidity • First episode • Substance abuse • May need involuntary hospitalisation

  28. Antipsychotics • Biological treatment the mainstay • Typical antipsychotics – high potency – haloperidol, low potency – chorpromazine • Atypical antipsychotics – clozapine, respiridone, olanzipine, quetiapine. Useful for negative symptoms, poor responders and patients prone to side effects • Choice of drug depends on age, physical status, co-existing medical problems

  29. Drug treatment • 60% of patients on antipsychotics for 6 weeks improve • If meds of well patient stopped 75% relapse in 6 – 24 months • First episode patients – 40 – 60% relapse during the year after episode if not on medication

  30. Duration of treatment - debate • First episode: 1 – 2 years of maintenance • Multiple episodes: minimum of 5 years • Violent or aggressive behaviour or suicide attempts need indefinite treatment

  31. Psychosocial treatment • Become ill during critical career forming years • Psychosocial interventions need to be integrated with psychopharmacological treatments • Focus on improving social functioning in the hospital, community, at home and at work

  32. Rehabilitation • Programmes emphasise social skills training and vocational training • NB for community based treatment • Cognitive remediation can assist recognition and treatment of cognitive impairments • Distractibility, memory problems, lack of vigilance, limitations in planning and decision making

  33. Individual psychotherapy • Supportive, reality orientated individual therapy • Individual and groups • Teach coping and problem solving skills • Psychotherapy is not a substitute for medication and is helpful once antipsychotics have started working

  34. Families • Grief with no end • Teach family to recognise early signs of relapse • Psycho education to help families deal with disease profile • Blame should not be placed on patient for pathology • Families who are highly critical or overprotective can increase relapse

  35. Families • Group therapy enhances problem solving, goal planning, social interactions and medication and side effect management • A lot more could be done for schizophrenics in our society!

  36. References • Kaplan and Sadock’s Synopsis of Psychiatry eighth edition. pp 456 - 491 • APA guidelines. Practice guideline for the treatment of patients with Schizophrenia. Am Jnl Psychiatry 154: 4 April 1997 (supplement) • Carpenter WT, Buchanan RW. Schizophrenia. New England journal of Medicine. Vol 80, March 1983 • Schizophrenia focus. The Lancet. Vol 346. Sept 9, 1995.

More Related