Schizophrenia 2009 (2)

8/6/2019 Schizophrenia 2009 (2)

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SCHIZOPHRENIA DUE

TO BIOLOGICAL AND

PSYCHOSOCIAL

FACTOR


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SCHIZOPHRENIA

a chronic, debilitating mental disordercharacterized by periods of loss oftouch with reality (psychosis), however7-15% have only one episode and full

remissionusually involves repeated psychoticepisodes and a chronic, downhill courseover years

persistent disturbances of thought,

behavior, appearance, and speech;abnormal affect;social withdrawal.often stabilizes in midlife.


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SYMPTOMS OF SCHIZOPHRENIA

Positive - things additional to expectedbehavior and include delusions, hallucinations,agitation, and talkativeness.

Negative - things missing from expectedbehavior and include lack of motivation, socialwithdrawal, flattened affect, cognitivedisturbances, poor grooming, and poor (i.e.,impoverished) speech content.


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DIAGNOSTIC CRITERIA OF

SCHIZOPHRENIA

Positive Symptoms

Delusions paranoia,grandiosity

Experiences of control believe under control of alienforce.

Auditory hallucinations bizarre, unreal perceptions,usually auditory.

Disordered thinking thoughts have been inserted orwithdrawn from the mind.

Negative symptoms

Affective flattening reduction in range andintensity of emotionalexpression, including facial

expression, tone of voice etc

Alogia lessening speechfluency

Avolition reduction or

inability to take part in goaldirected behaviour.

Diagnosis requires 1 monthof two or more positivesymptoms.


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SCHIZOPHRENIA

A. Two (or more) of the following symptoms, eachpresent for a significant portion of time during a 1-month period (or less if successfully treated):

1. Delusions

2. Hallucinations

3. Disorganized speech (e.g., frequent derailment orincoherence)

4. Grossly disorganized or catatonic behavior

5. Negative symptoms, i.e., affective flattening, alogia,or avolition

Note: Only one Criterion A symptom is required ifdelusions arce bizzare or hallucinations consist of avoice keeping up a running commentary on the person'sbehavior or thoughts, or two or more voices conversingwith each other.

DSM-IV


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SCHIZOPHRENIA

C. Duration: Continuous signs of thedisturbance persist for at least 6 months..

During these prodromal or residual periods,the signs of the disturbance may hemanifested by only negative symptoms or twoor more symptoms listed in Criterion A presentin an attenuated form (e.g., odd beliefs,unusual perceptual experiences).

D. Schizoaffective and Mood Disorderexclusion

DSM-IV


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SCHIZOPHRENIA

E. Substance/general medical conditionexclusion

F. Relationship to a PervasiveDevelopmental Disorder. If there is ahistory ofAutistic Disorder or anotherPervasive Developmental Disorder, theadditional diagnosis of Schizophrenia ismade only if prominent delusion, or

hallucinations are also present for atleast a month (or less if successfullytreated).

DSM-IV


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TYPES OF SCHIZOPHRENIA:

Disorganized schizophrenia

Catatonic schizophrenia

Paranoid schizophrenia

Undifferentiated schizophrenia


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ETIOLOGY OF

SHIZOPHRENIA


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Experts now agree that schizophrenia developsas a result of interplay between biologicalpredisposition (for example, inheriting certaingenes) and the kind of environment a person

is exposed to. These lines of research are converging: brain

development disruption is now known to bethe result of genetic predisposition andenvironmental stressors early in development

(during pregnancy or early childhood), leadingto subtle alterations in the brain that make aperson susceptible to developingschizophrenia.


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Environmental factors later in life (during earlychildhood and adolescence) can either damagethe brain further and thereby increase the riskof schizophrenia, or lessen the expression ofgenetic or neurodevelopmental defects anddecrease the risk of schizophrenia.

In fact experts now say that schizophrenia(and all other mental illness) is caused by a

combination of biological, psychological andsocial factors, and this understanding ofmental illness is called the bio-psycho-socialmodel.


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The Path to Schizophrenia -

The diagram above shows how

biological, genetic and

prenatal factors are believed to

create a vulnerability to

schizophrenia. Additional

envronmental exposures (for

example, frequent or ongoing

social stress and/or isolation

during childhood, drug abuse,

etc.) then further increase the

risk or trigger the onset of

psychosis and schizophrenia.

Early signs of schizophrenia

risk include neurocognitive

impairments, social anxiety

(shyness) and isolation and

"odd ideas"


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.

FAMILY STUDIES: DATA

Relation to index case % with schizophrenia

Spouse 1

Grandchildren 2.84

Nieces/nephews 2.65

Children 9.35

Siblings 7.30

Dizygotic twins 12.08Monozygotic twins 44.30

(100% identical)

(Gottesman, McGuffin, and Farmer, 1987).


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TWIN STUDIES

rates as low as 11.0%13.8% amongmonozygotic twins, and 1.8%4.1%among dizygotic twins,

however. In the "Pairs of Veteran Twins"study, for example, 338 pairs wereschizophrenic with only 26 pairsconcordant, and it was concluded in onereport: "the role of the suggestedgenetic factor appears to be a limitedone; 85 percent of the affectedmonozygotic pairs in the sample werediscordant for schizophrenia".


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ADOPTION STUDIES:

Adoption studies have also indicated asomewhat increased risk in those with a parentwith schizophrenia even when raised apart.

Studies suggest that the phenotype is genetically

influenced but not genetically determined; thatthe variants in genes are generally within therange of normal human variation and have lowrisk associated with them each individually; andthat some interact with each other and withenvironmental risk factors; and that they maynot be specific to schizophrenia


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By studying children of schizophrenic mothersreared in adoptive parental homes,environmental factors are eliminated.


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HESTON (1966): FOLLOW-UP STUDY

Examined 47 people born (1915-1945) toschizophrenic mothers in a mental hospital.

Babies separated from their mothers at birth &reared by foster or adoptive parents.

Fifty control Ss selected were also examined.


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SS WERE FOLLOWED UNTIL 1964.

Assessment included: clinicalinterviews,

Each S was examined by twopsychiatrists & Heston.

None of the control Ss were diagnosed

with schizophrenia, whereas 16.6% ofchildren born to schizophrenicmothers were diagnosed withschizophrenia.


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B. BIOCHEMICAL BASIS:

Particular focus has been placed upon the function ofdopamine in the mesolimbic pathway of the brain

The dopamine hypothesis: there is an excess of dopamine

in the schizophrenic brain.

Based on idea that drugs used to treat schizophrenia, reducedopamine.

Evidence for this theory includesfindings that the potency

of many antipsychotics is correlated with their affinity

to dopamine D2 receptors and the exacerbatory effects of adopamine agonist(amphetamine) and a dopamine beta

hydroxylase inhibitor (disulfiram) on schizophrenia


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PROBLEM WITH DOPAMINE THEORY:

A major metabolite of dopamine (homovanillicacid (HVA) has not been found in greateramounts in patients with schizophrenia.

Schizophrenics may have more dopaminereceptors, not dopamine in brain.


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POSTMORTEM STUDIES:

On schizophrenics, show their brains havemore dopamine receptors than aged-matchedcontrols.

Pet Scans have confirmed this.


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DOPAMINE PATHWAYS:

Excess dopamine activity relevant toschizophrenia is localized in the mesolimbicpathway.

Antipsychotics alleviate positive symptoms byblocking dopamine receptors there & therebylowering activity in this neural system.


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PROBLEMS WITH DOPAMINE

HYPOTHESIS:

1. Despite fact that antipsychotics work on blocking

D2 receptors right away, there is a delay in the relief

of positive symptoms.

2. Antipsychotics dont show therapeutic effects until

dopamine receptor activity is below normal.

3. Other neurotransmitters may be involved.

E.g, Serotonin.


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b. Serotonin hyperactivity is implicated inschizophrenia because hallucinogens thatincrease serotonin concentrations causepsychotic symptoms and because some

effective antipsychotics, such as clozapin,have anti-serotonergic-2 (5-HT2) activity.

c. Glutamate is implicated inschizophrenia because antagonists of theN-methyl-D-aspartate (NMDA) subtype ofglutamate receptors (e.g., phencyclidine)increase and agonists of NMDA receptorsalleviate psychotic symptoms


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C.ANATOMY AND PATOLOGY

With the advent of neuroimaging techniques in

the 1960s, it became possible to document what

many had long suspected: that schizophrenia was

associated with brain abnormalities.

The earliest reports, based on computerized axial

tomography, showed that patients had enlarged

brain ventricles, especially increased volume of

the lateral ventricles (Dennert & Andreasen

1983).


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As new imaging techniques were developed,these findings were replicated, and additionalabnormalities were detected (Henn & Braus1999).

Magnetic resonance imaging (MRI) revealeddecreased frontal, temporal, and whole-brainvolume (Lawrie & Abukmeil 1998).

More fine-grained analyses demonstratedreductions in the size of structures such as thethalamus and hippocampus.

In fact, of all the regions studied, thehippocampus is one that has most consistentlybeen identified as distinguishing schizophreniapatients from healthy controls (Schmajuk 2001).


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D. INFECTIONS

Numerous viral infections, in utero or inchildhood, have been associated with anincreased risk of later developingschizophrenia

Schizophrenia is somewhat more common inthose born in winter to early spring, wheninfections are more common


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E.OBSTRETRIC EVENTS

It is well establishedthat obstetric complications or events areassociated with an increased chance of thechild later developing schizophrenia, althoughoverall they constitute a non-specific riskfactor with a relatively small effect

One epidimiological finding :

a.Women who were pregnant during the Dutch

famine of 1944, where many people wereclose to starvation (experiencing malnutrition)had a higher chance of having a child whowould later develop schizophrenia.


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b. Studies ofFinnish mothers who werepregnant when they found out that theirhusbands had been killed during the WinterWar of 19391940 have shown that theirchildren were significantly more likely todevelop schizophrenia when compared withmothers who found out about their husbands'death after pregnancy, suggesting that

maternal stress may have an effect c. born in winter or spring


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PSYCHOSOCIAL (ENVIRONMENT) FACTOR IN

SCHIZOPHRENIA


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it Is important to understand that whenschizophrenia researchers talk about"environment" they have a very broad definitionthat basically includes everything other than"genes" or genetic factors.

whereas the typical person might think of their"environment" as their house, or theirneighborhood - scientists trying to understand thefactors that influence the development ofschizophrenia define environment to includeeverything from the social, nutritional, hormonal

and chemical environment in the womb of themother during pregnancy, up to the socialdynamics and stress a person experiences, tostreet drug use, education, virus exposure, vitaminuse, and much, much more.


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word "environment" used when talking aboutthe causes of schizophrenia - another way tothink of it is "everything other than genes". Itsbasically the same as when people talk about"nature vs. nuture" - what they are saying is"genes vs. environment".


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A.PSYCHOANALYSISAPPROACH

Freud (1924)

Schizophrenia is the result of:

Regression to a pre-ego stage.

Attempts to re-establish ego control.

Ego = driven by the reality principle whichworks to satisfy the ID in realistic ways.Makes the child accommodate to thedemands of the environment.


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REGRESSION TO A PRE-EGO STAGE.

If a schizophrenics world is harsh, e.g. cold anduncaring parents, a child may regress back toa developmental stage before the ego wasproperly formed, before the child haddeveloped realistic awareness oftheexternal world.

Schizophrenia is seen as an infantile state,positive symptoms ofdelusions ofgrandeurreflect this condition.

Whereas auditory hallucinations reflect apersons attempt to re-establish ego control

control of reality.


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B.BEHAVIOURAL EXPLANATIONS

Explain schizophrenia as a consequence offaulty learning.

If a child receives little or no socialreinforcement early on in life (parental

disinterest), the child will attend toinappropriate and irrelevant environmentalcues e.g. sound of a word instead ofmeaning.

Result childs verbal or other behaviouralresponses will become bizarre and thosewho observe the child's behaviour will eitheravoid it or respond erratically thereforereinforcing the bizarre behaviour.

This cycle will eventually deteriorate into apsychotic state.


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C.FAMILY THEORY

Schizophrenigenic mother

double-bind

Communication deviance (excessive

vagueness/blurring -attack children/double-bind)

Another measure of disturbed familycommunication is expressed emotion-measured : critical comments by the relativeabout the patient, hostility toward the patient,emotional overinvolvement. Some researchsuggests high EE may play a role in course ofschizophrenia.


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FAMILY RELATIONSHIPS

Bateson et al argued Childs ability to respondis incapacitated by the contradictions.

Prolonged exposure to these interactionsprevents the development of a coherentconstruction of reality.

Which in the long run manifests itself as

schizophrenic symptoms, e.g. flattened effect,delusions, hallucinations, incoherent thinkingand speaking and some cases paranoia.


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FAMILY RELATIONSHIPS

Expressed emotion:

Negative emotion or a high degree ofexpressed emotion (EE) is associated with

schizophrenia.

EE = a family communication style thatinvolves criticism, hostility, and emotionalover-involvement.

Linzen et al 1997 found a patient returning toa family with high EE is 4 times more likely torelapse.


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EXPRESSED EMOTION RESEARCH

SUPPORT

Kalafi and Torabi 1996 studied the rateof relapse in schizophrenics in Iran.

Found: High prevalence ofEE in Iranianculture (overprotective mothers andrejecting fathers) was one of the maincauses of relapse.

Conclusion: Negative emotional climate(environment) in families seems toarouse patients and leads to stressbeyond his or her coping methods.


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D.DOUBLE BIND THEORY

Created by Gregory Baetson

Hipoethic family

A double bind is a dilemma

in communication in which an individual (orgroup) receives two or more conflictingmessages, with one message negating theother.

This creates a situation in which a successfulresponse to one message results in a failedresponse to the other, so that the person willbe automatically wrong regardless ofresponse.


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The nature of a double bind is that the personcannot confront the inherent dilemma, andtherefore can neither comment on the conflict, norresolve it, nor opt out of the situation.

creating a situation in which the victim couldn'tmake a comment or "metacommunicativestatement" about their dilemma would (in theory)escalate their mental anxiety and potentially causea crisis.

Children who receive contradictory messages fromtheir parents are more likely to developschizophrenia.


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SOCIOCULTURAL FACTORS Social Labelling

Scheff (1999) promoted the labelling theory ofschizophrenia.

Theory states social groups create the concept of psychiatric

deviance by constructing rules for group members to follow.

Thus the symptoms of schizophrenia are seen as deviating(going against) from the rules that we attribute to normalexperience or behaviour.

Therefore those who display unusual behaviour areconsidered deviant and the label schizophrenic may beapplied which becomes a self fulfilling prophecy thatpromotes the development of other symptoms ofschizophrenia (Comer 2003).


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SCHIZOPHRENIA TREATMENT

Pharmacologic:

- traditional antipsychotics [dopamine-2 (D2)-receptor antagonists] first generation ofantipsychotic medication

- atypical antipsychotic agents second generationof antipsychotic medication

- Because of their better side-effect profiles, theatypical agents are now first-line treatments.


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SCHIZOPHRENIA TREATMENT

Psychosocial treatments:

- Psychotherapy: individual, family, and group

- Psychoeducation with activity of patients or

enhancing motivation to the treatment- Social support


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CONCLUSION

Neither the biological nor the environmental(psycho-social) categories is completelydeterminant, and there is no specified amount ofinput that will ensure someone will or will notdevelop schizophrenia

Moreover, risk factors may be different fordifferent individuals - while one person maydevelop schizophrenia due largely to a strongfamily history of mental illness (e.g. a high level ofgenetic risk), someone else with much less geneticvulnerability may also develop the disease due to a

more significant combination ofprepregnancyfactors, pregnancy stress, other prenatalfactors, social stress, family stress orenvironmentalfactors that they experience during theirchildhood, teen or early adult years

Schizophrenia 2009 (2)

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