abpsy-l6-05-06

Introduction to psychosis: Schizophrenia as disease : 

Introduction to psychosis: Schizophrenia as disease Week six

Aims of lecture : 

Aims of lecture Main aim: to examine biological, psychological and social evidence on the cause(s) of schizophrenia Descriptive aims: To indicate what it’s like… To introduce official diagnosis. To explore medical/disease models and psychological (critical/cognitive) perspectives. To introduce recent developments in psychology and examine the conceptual framework of the symptom approaches.

Definition of psychosis : 

Definition of psychosis Gross impairment in reality testing - the person makes incorrect inferences concerning external reality, makes improper evaluations of the accuracy of his or her thoughts and perceptions and continues to make errors in the face of contrary evidence. Classic symptoms include hallucinations, severe regressive behaviours…and markedly incoherent speech

History of Schizophrenia : 

History of Schizophrenia Kraepelin (1898) “Dementia Praecox” A general mental deterioration from an early age. Bleuler (1911) - “Schizophrenia”. A loosening or splitting of the association of ideas so that thinking becomes disordered. The splitting between thinking and emotion leads to inappropriate ideas (Lintner, 1989). 1% population diagnosed today. Age of onset, from adolescence to mid-thirties (DSM-IV). Rare cases found in 5-6 year olds. Median age of onset is mid-20s for men and late 20s and early 30s for women

Positive and Negative symptoms : 

Positive and Negative symptoms Schneider – first rank symptoms are believed to be key features in diagnosis Positive symptoms: Excesses: disorganised speech, hallucinations, delusions (65%) and bizarre behaviour. Negative symptoms: Behavioural deficits, avolition (apathy) Alogia (speech poverty) Anhedonia (like a depression) Flat affect (Outward lifelessness - not a true reflection of inward feelings). Asociality Disorganised.

DSM IV (1994) – Diagnostic criteria : 

DSM IV (1994) – Diagnostic criteria At least six months of disturbance + one month of active phase: two of the following for a period of one month. 1) delusions 2) hallucinations 3) disorganised speech 4) disturbed or catatonic. Mood disordered, substance abuse and general medical condition patients must be excluded Other disorders: Schizophreniform and brief psychotic disorder.

Categories of schizophrenia in DSM-IV : 

Categories of schizophrenia in DSM-IV Disorganised: (disorganised speech, neologisms and periods of unrestrained laughter and crying fits). Incontinence, lack of personal hygiene. Catatonic: Motor activity and behaviour predominantly impaired. (a rarer form). Paranoid: Persecutory delusions, grandiosity, ideas of reference. They remain emotionally responsive and are more alert and verbal. Undifferentiated Type I and II: whether positive (I) or negative (II) symptoms predominate.

Diagnostic considerations : 

Diagnostic considerations Subtypes have little predictive validity (information about treating or predicting the course of the illness). Considerable overlap among the subtypes Most schizophrenics show mixed symptoms (Andreasen & Olsen, 1982). Concern over presence of symptoms in bi-polar disorder (one-third). (Goodwin & Jamison, 1992)

Vital Statistics : 

Vital Statistics Similar cross cultural rates (0.5-1.7%). Course and outcome are more favourable in developing countries (59% recovery in Mauritius and 34% in London). Despite early pessimism, longitudinal data suggests up to two-thirds recover. Higher rate in men than women (2-3times higher). Recovery is more likely in women. Social and familial support has significant impact on recovery and outcome. (Barrowclough & Tarrier, 1994.)

Key major theories : 

Key major theories Biological aspects. Stress vulnerability model. Psychological. Pharmacological. Social and community interventions. Psycho-social (cognitive, family, existential).

Three ‘facts’ that support a biologically based illness : 

Three ‘facts’ that support a biologically based illness ‘Schizophrenia’ is equally frequent in all countries. The brain of ‘schizophrenics’ are abnormal There is a genetic predisposition to ‘schizophrenia’

Cause of the symptoms are biological : 

Cause of the symptoms are biological The definition of schizophrenia is a valid description of an underlying illness Biological processes represent ‘primary’ causes of disturbance

DISEASE MODELS : 

DISEASE MODELS Discontinuity and discrete disease entities – classic ‘lesion’ notion of disease – demonstrable pathophysiology and a discrete cause. Systemic diseases: Continuum of normal functioning describing dimensions of vulnerability. Full blown disease as interaction between exogenous and endogenous factors (as in hypertension- related diseases) (Claridge, 1988).

Schizophrenia and heredity – axiom or hypothesis? : 

Schizophrenia and heredity – axiom or hypothesis? Family studies Twin studies Adoption studies

General medical model I: Genetics and biology : 

General medical model I: Genetics and biology Schizophrenia is a phenotype – defined by behaviour Two parents = 40% (deviant environment?)Twin studies (MZ concordance rate - 45-50%: DZ - 14%)Adoption studies support genetic factors (Heston, 1966). Negative symptoms have a stronger genetic component than positive symptoms of schizophreniaParent studies: (Lintner, 1989). Heston, 1966: One parent = 16% risk: General risk = 1% of population Chen et al (1999) Eye-tracking (frontal and temporal lobes) Tiernari, Wynne & Moring et al (1994) suggest that vulnerability to illness may be raised or lowered according to status of interactions between the individuals and family

General medical model II:Brain abnormalities : 

General medical model II:Brain abnormalities Post-mortem studies: Structural problems in: Temporal-limbic area – Long term medication Hippocampus & Amygdala (Benes 1992). CT/MRI: Enlarged ventricles and wasted brain tissue (Suddath, 1990). Low metabolic rates in the prefrontal cortex - involved in speech production and problem solving. Significant reduction in 5HT-2 receptors in pre-frontal cortex. Serotonergic under activity leads to failure of dopamine inhibition. Not specific to schizophrenia (Reider, 1983) Fetal infection (prefrontal development occurs late in adolescence).

Neurotransmitters and pharmacological research : 

Neurotransmitters and pharmacological research Dopamine hypothesis (amphetamines can induce psychotic states). Neuroleptics block dopaminergic neurones (Johnstone et al, 1978). Catecholamines: Sensitive receptors rather than excess dopamine (D2 & D4). Mesocortical dopamine pathway: from prefrontal cortex to limbic area Question over role of neuroleptic medication (Birchwood & Jackson, 2001). Ohouha et al, 1993: serotonergic underactivity and increased dopaminergic activity – serotonin and regulation – more studies

Brain anatomy : 

Brain anatomy Enlarged ventricles – Reveley founds percentages ranging from 6-60% (Reveley, 1985) – not specific to schizophrenia – found in manic patients Twin studies reveal environmental influences (Suddath, 1990) Measurement of discordant twins Reduction of grey matter and decreased metabolic rates in the prefrontal cortex (Buchanan, 1998) Neuropsychological testing, CT and fMRI scans

General medical model III: Neuroleptic medication (psychopharmacological evidence) : 

General medical model III: Neuroleptic medication (psychopharmacological evidence) Only 16% of first-episodes benefited from neuroleptics compared to placebo (Crow et al, 1986). Many schizophrenics are resistant (Nasrallah et al, 1979). Patients do just as well with minimal anti-psychotic medication if backed up with other care (Soteria-project, Mosher, 2003) Negative symptoms particularly resistant. Low-doses have been recommended with accompanied prodromal identification.

General medical model IV:Bio-chemistry, brain structures. : 

General medical model IV:Bio-chemistry, brain structures. All bio-chemical evidence suggests no unilateral trait like symptomatology. Extreme variability in bio-chemical activity. Conceptually, it is parsimonious to think of biological factors etc. as contributing to individual’s vulnerability to develop schizophrenia.

Stress vulnerability models : 

Stress vulnerability models Stress-vulnerability (Zubin, Leff, Lopez). Life-events and Expressed Emotion work. Work on relapse, accumulation of stress and EE). HPA axis – hyper secretion of cortisol – dopamine activity increase Above are risk factors not causes. Social anthropological data (Murphy, 1978; Waxler, 1979): Role assignment Alienation Toleration/ family support Labelling theory

High Risk Studies : 

High Risk Studies Fish et al (1992) Fine motor control and co-ordination in mid-childhood Erlenmeyer-Kimling (1987) Attention and information processing Ingraham et al (1995) Locus of control Tienari et al (1994) Evidence of familial disturbance in adoptive families affected only those children from biological parents with schizophrenia

Psychological perspectives:Psychotic traits in general population : 

Psychological perspectives:Psychotic traits in general population Schizoptyal personality disorder and the diathesis stress model. The existence of psychotic characteristics as traits widely distributed in the general population (Claridge, 1993). ‘Cognitive’ (aberrant thinking and perception) and ‘affective’ anhedonia and general cognitive disorganisation associated with anxiety - paranoid ideation (Faily and Venables, 1986). Hearing voices is fairly common (up to 40% in US samples).

Summary : 

Summary Schizophrenia is a functional diagnosis A cause for schizophrenia has never been found – risk factors have been identified What does the high degree of variation in symptoms and prognosis indicate?