F20-F29 ; ETIOLOGYBIOLGICAL THEORIESLEARNING THEORIESCOGNITIVE THEORIES

TANIYA THOMAS11699014

1ST MSC CLINICAL PSYCHOLOGY

DISCOVER THROUGH…Schizophrenia , an introduction

Risk factorsBiological etiology and theories

Learning theoriesCognitive theoriesSummary and conclusion

IDENTIFY

Dementia precox (1899)

Differentiated from manic depressive illness

EMIL KRAEPELIN

IDENTIFY

Schizophrenia Identified four

fundamental symptoms and accessory symptoms

4 A’s

EUGENE BLEULER

Just brush up Schizophrenia – the gain of function as well as the loss of

function ( Tamminga C.A, Kaplan & Sadock,2009)

Distortion in perception, emotion, thinking, cognition and behavior (Ruiz, Sadock & Sadock, 2015)

Disturbs the most basic function that give a normal person a feeling of individuality, uniqueness and self direction (ICD-10,2007)

Onset is usually before 25 years, persists throughout the life and affects persons of all economic classes. (Ruiz, Sadock & Sadock, 2015)

RISK FACTORS1) Gender and age2) Reproductive factors3) Infection and birth season4) Substance abuse5) Socio economic and cultural

factors

BIOLOGICAL ETIOLOGY

1. GENETIC THEORIES OF SCHIZOPHRENIAFAMILY STUDIESTWIN STUDIES ADOPTION STUDIES

2. BIO CHEMICAL THEORY OF SCHIZOPHRENIADOPAMINE HYPOTHESISSTRESS DIATHESIS MODELVIRAL HYPOTHESIS

3. NEURODEVELOPMENTAL THEORIESBRAIN STRUCTURE AND ENLARGED VENTRICLESABBERANT CONNECTIVITYALTERED SYNAPTIC CIRCUITY

FAMILY STUDIES Schizophrenia DO run in the

family 1st systematic study by Ernst

Rudin An individual's FDR (parents,

siblings and off springs) share, on an average, 50% of his genes while his second degree relatives (grandparents, aunts, uncles and grand children) share, on an average,25% of the genes.

FAMILY STUDIES(Continues….) Hirsch and Leff made an extensive review of studies which

supports the following hypotheses:

1.More parents of schizophrenics are psychiatrically disturbed than parents of normal children and more of the mothers are schizoid.

2.There appears to be a link between allusive thinking in schizophrenics and their parents.

3.The parents of schizophrenics show more conflict and disharmony than the parents of other psychiatric patients.

4.The parents of schizophrenics show more abnormalities in their communications.

EVIDENCES Pope HG Jr, Jonas J, Cohen B, Lipinski JF(1982) , studied 199

FDR and they could not find any significant relationship between genetic component and prevalence of schizophrenia.

Kender (1985) studied the morbidity risk for psychiatry illnesses among 62 schizophrenic patients and he found that the morbid risk of schizophrenia is significantly greater(18 times more) in relatives of schizophrenia

Wolyniec(1992) studied the morbidity risk in the families of male and female schizophrenics and reported that the relatives of female schizophrenics are more prone to develop schizophrenia than males.

TWIN STUDIES

TWIN STUDIES Hypothesis- the genes really did make a difference

and that familial aggregation of schizophrenia was not simply due to shared family environment

Gottesman and Shields(1972) MZ (N=22) 58% morbid risk DZ(N= 33) 12% morbid risk

TWIN STUDIES The major question that arises is whether

schizophrenia in a MZ twin, with an unaffected co-twin, represents a sporadic or a non-genetic `phenocopy' of the illness.

The results of the study by Gottesman II, Shields J (1976) in Danish sample would argue against this.

Individual differences in the evoking environments and the timing of the genetic activation during the intrauterine and early postnatal periods may have differential effects on the genome.

ADOPTION STUDIES

•Kety SS, Rosenthal D, Wender PH, Schulsinger F, Jacobsen B(1972)

•Studied Danish Population

•3 groups

•Found that biological offsprings had higher rate of schizophrenia than adopted

Gottesman (1991)

1) Both parents = 46% risk

2) One schizophrenic parent = 16% risk

3) If a sibling has schizophrenia = 8% risk

4) If a grandparent has schizophrenia = 5% risk

5) If the identical twin of one parent hasschizophrenia = 17% risk.

BIO CHEMICAL THEORY OF

SCHIZOPHRENIA

DOPAMINE HYPOTHESIS Abnormally high dopamine activity

Neuroleptics control positive symptoms by reducing dopamine activity

L-Dopa, a dopamine pre-cursor (usually given to Parkinson’s patients), brings on schizophrenic symptoms in clinically normal people

the increase of dopamine in meso-cortical dopamine pathway could improve negative ,cognitive and affective symptoms of Schizophrenia.(Gordana Rubeša, Lea Gudelj & Natalija Kubinska, 2011)

STRESS DIATHESIS MODEL

combines the insights gained from biological and environmental approaches.

schizophrenics inherit a vulnerability to the disorder which makes them overly sensitive to their social environment

stressful life events, family dysfunction, trauma

VIRAL HYPOTHESIS

Schizophrenia gene? infants are infected

during the prenatal period, more particularly during late pregnancy or shortly after birth and only manifest symptoms many years later.

NEURODEVELOPMEAL THEORIES

ALTERED SYNAPTIC CIRCUITY

Continues…

Cortical neurons from subjects with schizophrenia exhibit:

(1) smaller somal volume, (2) decreased spine density, (3) decreased dendritic length, and (4) decreased terminals (as demonstrated by

decreased presynaptic markers) postmortem findings contribute to the

hypothesis that schizophrenia stems from altered synaptic circuitry. 

BRAIN STRUCTURE

reduced brain weight; enlarged ventricles; abnormalities in the cortex and hippocampus.

left amygdale is generally smaller than the right in normal people but the same size in schizophrenics. (Tom Burns, Harrison P, Cown P, 2012)

ABERRANT CONNECTVITY Abnormal connectivity in

neural circuits and brain regions(Tom Burns, Harrison P, Cown P, 2012)

Arises developmentally Studied by MRI scan Given cognitive tasks to

assess

LEARNING THEORIES

LABELLING THEORYSOCIAL LEARNING THEORY

LABELLING /FAULTY LEARNING

SOCIAL LEARNING THEORY

SOCIAL LEARNING THEORY Family environment Learning through observation and modeling Ullman and Krasner (1969) observed mental health nurses in

their interactions with patients and concluded that staff actually reinforce schizophrenic behaviour by giving more attention to these patients.

Expressed emotion (EE)- way in which family speaks reflects criticism, hostile feelings, emotional over involvement or over concern. (trying to recover)

Suffer relapse if living in families with high Expressed emotions.

COGNITIVE THEORY

FRITH MODEL HEMSLEYS THEORY ZIMBARDO’S A RATIONAL PATH TO

MADNESS

FRITH MODEL Faulty attention system unable to distinguish between actions that are brought

about externally or generated internally. For Frith this accounts for the positive symptoms of

schizophrenia, such as hallucinations, delusions and disorganised speech.

Divided into 3 cognitive processes1. in ability to do willed actions2. Inability to regulate action3. Inability to monitor belief

HEMSLEYS THEORY Linked to memory and perception Focus on unimportant and

irrelevant factors Schemes overloaded Internal thoughts not recognized •Internal thoughts are often not

recognized as arising from memory and so are thought to be from an external source and experienced as auditory hallucinations

ZIMBARDOS A RATIONAL PATH TO MADNESS

Due to denial of sensation by others, a few people conclude that they hide truth

Eventually avoid all feedback

Strengthen the believe of persecution

REFERANCES Ahuja, N., (2011). A short textbook of psychiatry (7th edn.). New Delhi: Jaypee

Brothers  Sadock, B.J., Sadock, V.A., & Kaplan, H.I., (2015).Kaplan and Sadock's Synopsis

of   Psychiatry Behavioural Sciences/Clinical Psychiatry (11th edn.). Philadelphia: Wolters  Kluwer

World Health Organization. (1992). The ICD-10 classification of mental and behavioural disorders: Clinical descriptions and diagnostic guidelines. Geneva: World Health Organization

Hirsch SR, Leff JP. Abnormalities in parents of schizophrenics. London, Oxford UniversityPress, 1975.

Pope HG Jr, Jonas J, Cohen B, Lipinski JF. Failure to find evidence of schizophrenia in firstdegree relatives of schizophrenic probands. American Journal of Psychiatry, 1982; 139:826-828.

Kendler KS, Catherine CM, Kenneth LD. Psychiatric illness in first degree relatives ofpatients with paranoid psychosis, schizophrenia and medical illness. British Journal ofPsychiatry, 1985; 147: 524-531

Wolyniec PS, Pulver AE, McGrath JA, Tam D. Schizophrenic gender and familial risk.Journal of Psychiatric Research, 1992; 26 (1): 17-27.

Wender PH, Rosenthal D, Kety SS, Schulsinger F, Weiner J. Cross fostering: A researchstrategy for clarifying the role of genetic and experimental factors in the etiology ofschizophrenia. Archives of General Psychiatry, 1974; 30: 121-128.

REFERENCES

Gottesman II, Shields J. Schizophrenia and genetics: A twin study. Vantage Point. New York, Academic Press, 1972; 17-33.

Gottesman II, Shields J. A critical review of recent adoption, twin and family studies of schizophrenia: Behavioural genetics perspectives. Schizophrenia Bulletin, 1976; 2: 360-398.

Gordana Rubeša, Lea Gudelj & Natalija Kubinska: ETIOLOGY OF SCHIZOPHRENIA AND THERAPEUTIC OPTIONS Psychiatria Danubina, 2011; Vol. 23, No. 3, pp 308–315

(Tom Burns, Harrison P, Cown P .(2011), shorter textbook of psychiatry .(6th edi.). , london: oxford university press.