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SCHIZOPHRENIA DUE TO BIOLOGICAL AND PSYCHOSOCIAL FACTOR

SCHIZOPHRENIA
a

chronic, debilitating mental disorder characterized by periods of loss of touch with reality (psychosis), however 7-15% have only one episode and full remission usually involves repeated psychotic episodes and a chronic, downhill course over years persistent disturbances of thought, behavior, appearance, and speech; abnormal affect; social withdrawal. often stabilizes in midlife.

SYMPTOMS OF SCHIZOPHRENIA
Positive - things additional to expected behavior and include delusions, hallucinations, agitation, and talkativeness. Negative - things missing from expected behavior and include lack of motivation, social withdrawal, flattened affect, cognitive disturbances, poor grooming, and poor (i.e., impoverished) speech content.

DIAGNOSTIC CRITERIA OF
SCHIZOPHRENIA
Positive Symptoms Delusions paranoia, grandiosity

Experiences of control believe under control of alien force. Auditory hallucinations bizarre, unreal perceptions, usually auditory. Disordered thinking thoughts have been inserted or withdrawn from the mind.

Negative symptoms Affective flattening reduction in range and intensity of emotional expression, including facial expression, tone of voice etc

Alogia lessening speech fluency Avolition reduction or inability to take part in goal directed behaviour. Diagnosis requires 1 month of two or more positive symptoms.

DIAGNOSTIC CRITERIA OF SCHIZOPHRENIA


A. Two (or more) of the following symptoms, each present for a significant portion of time during a 1month period (or less if successfully treated): 1. Delusions 2. Hallucinations 3. Disorganized speech (e.g., frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior 5. Negative symptoms, i.e., affective flattening, alogia, or avolition Note: Only one Criterion A symptom is required if delusions arce bizzare or hallucinations consist of a voice keeping up a running commentary on the person's behavior or thoughts, or two or more voices conversing with each other.

DSM-IV

DIAGNOSTIC CRITERIA OF SCHIZOPHRENIA


C. Duration: Continuous signs of the disturbance persist for at least 6 months.. During these prodromal or residual periods, the signs of the disturbance may he manifested by only negative symptoms or two or more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences). D. Schizoaffective and Mood Disorder exclusion

DSM-IV

DIAGNOSTIC CRITERIA OF SCHIZOPHRENIA


Substance/general medical condition exclusion F. Relationship to a Pervasive Developmental Disorder. If there is a history of Autistic Disorder or another Pervasive Developmental Disorder, the additional diagnosis of Schizophrenia is made only if prominent delusion, or hallucinations are also present for at least a month (or less if successfully treated).
E.

DSM-IV

TYPES OF SCHIZOPHRENIA:
Disorganized

schizophrenia

Catatonic

schizophrenia

Paranoid

schizophrenia schizophrenia

Undifferentiated

ETIOLOGY

OF SHIZOPHRENIA

Experts now agree that schizophrenia develops as a result of interplay between biological predisposition (for example, inheriting certain genes) and the kind of environment a person is exposed to. These lines of research are converging: brain development disruption is now known to be the result of genetic predisposition and environmental stressors early in development (during pregnancy or early childhood), leading to subtle alterations in the brain that make a person susceptible to developing schizophrenia.

Environmental factors later in life (during early childhood and adolescence) can either damage the brain further and thereby increase the risk of schizophrenia, or lessen the expression of genetic or neurodevelopmental defects and decrease the risk of schizophrenia. In fact experts now say that schizophrenia (and all other mental illness) is caused by a combination of biological, psychological and social factors, and this understanding of mental illness is called the bio-psycho-social model.

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"

A.GENETIC FAMILY STUDIES:


Relation

DATA
% with schizophrenia 1 2.84 2.65 9.35 7.30 12.08 44.30

to index case

Spouse Grandchildren Nieces/nephews Children Siblings Dizygotic

twins Monozygotic twins


(100% identical)

(Gottesman,

McGuffin, and Farmer, 1987).

TWIN STUDIES
rates

as low as 11.0%13.8% among monozygotic twins, and 1.8%4.1% among dizygotic twins, however. In the "Pairs of Veteran Twins" study, for example, 338 pairs were schizophrenic with only 26 pairs concordant, and it was concluded in one report: "the role of the suggested genetic factor appears to be a limited one; 85 percent of the affected monozygotic pairs in the sample were discordant for schizophrenia".

ADOPTION STUDIES:
Adoption studies have also indicated a somewhat increased risk in those with a parent with schizophrenia even when raised apart. Studies suggest that the phenotype is genetically influenced but not genetically determined; that the variants in genes are generally within the range of normal human variation and have low risk associated with them each individually; and that some interact with each other and with environmental risk factors; and that they may not be specific to schizophrenia

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

HESTON (1966): FOLLOW-UP STUDY

Examined 47 people born (1915-1945) to schizophrenic 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.

SS WERE FOLLOWED UNTIL 1964.


Assessment

included: clinical

interviews,

Each S was examined by two psychiatrists & Heston.


None

of the control Ss were diagnosed with schizophrenia, whereas 16.6% of children born to schizophrenic mothers were diagnosed with schizophrenia.

B. BIOCHEMICAL BASIS:
Particular focus has been placed upon the function of dopamine 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, reduce dopamine. 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 a dopamine agonist(amphetamine) and a dopamine beta hydroxylase inhibitor (disulfiram) on schizophrenia

PROBLEM WITH DOPAMINE THEORY:


A major metabolite of dopamine (homovanillic acid (HVA) has not been found in greater amounts in patients with schizophrenia. Schizophrenics may have more dopamine receptors, not dopamine in brain.

POSTMORTEM STUDIES:

On schizophrenics, show their brains have more dopamine receptors than aged-matched controls. Pet Scans have confirmed this.

DOPAMINE PATHWAYS:

Excess dopamine activity relevant to schizophrenia is localized in the mesolimbic pathway. Antipsychotics alleviate positive symptoms by blocking dopamine receptors there & thereby lowering activity in this neural system.

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. Antipsychotics dont show therapeutic effects until dopamine receptor activity is below normal.

2.

3.

Other neurotransmitters may be involved. E.g, Serotonin.

b. Serotonin hyperactivity is implicated in schizophrenia because hallucinogens that increase serotonin concentrations cause psychotic symptoms and because some effective antipsychotics, such as clozapin, have anti-serotonergic-2 (5-HT2) activity. c. Glutamate is implicated in schizophrenia because antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (e.g., phencyclidine) increase and agonists of NMDA receptors alleviate psychotic symptoms

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).

As new imaging techniques were developed, these findings were replicated, and additional abnormalities were detected (Henn & Braus 1999). Magnetic resonance imaging (MRI) revealed decreased frontal, temporal, and whole-brain volume (Lawrie & Abukmeil 1998). More fine-grained analyses demonstrated reductions in the size of structures such as the thalamus and hippocampus. In fact, of all the regions studied, the hippocampus is one that has most consistently been identified as distinguishing schizophrenia patients from healthy controls (Schmajuk 2001).

D. INFECTIONS

Numerous viral infections, in utero or in childhood, have been associated with an increased risk of later developing schizophrenia Schizophrenia is somewhat more common in those born in winter to early spring, when infections are more common

E.OBSTRETRIC EVENTS
It is well established that obstetric complications or events are associated with an increased chance of the child later developing schizophrenia, although overall they constitute a non-specific risk factor with a relatively small effect One epidimiological finding : a.Women who were pregnant during the Dutch famine of 1944, where many people were close to starvation (experiencing malnutrition) had a higher chance of having a child who would later develop schizophrenia.

b. Studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 19391940 have shown that their children were significantly more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy, suggesting that maternal stress may have an effect c. born in winter or spring

PSYCHOSOCIAL (ENVIRONMENT) FACTOR IN SCHIZOPHRENIA

it Is important to understand that when schizophrenia researchers talk about "environment" they have a very broad definition that basically includes everything other than "genes" or genetic factors. whereas the typical person might think of their "environment" as their house, or their neighborhood - scientists trying to understand the factors that influence the development of schizophrenia define environment to include everything from the social, nutritional, hormonal and chemical environment in the womb of the mother during pregnancy, up to the social dynamics and stress a person experiences, to street drug use, education, virus exposure, vitamin use, and much, much more.

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

A.PSYCHOANALYSIS APPROACH
Freud

(1924) Schizophrenia is the result of: to a pre-ego stage. Attempts to re-establish ego control.
Regression Ego

= driven by the reality principle which works to satisfy the ID in realistic ways. Makes the child accommodate to the demands of the environment.

REGRESSION TO A PRE-EGO STAGE.


If

a schizophrenics world is harsh, e.g. cold and uncaring parents, a child may regress back to a developmental stage before the ego was properly formed, before the child had developed realistic awareness of the external world. is seen as an infantile state, positive symptoms of delusions of grandeur reflect this condition.

Schizophrenia

Whereas

auditory hallucinations reflect a persons attempt to re-establish ego control control of reality.

B.BEHAVIOURAL
Explain

EXPLANATIONS

schizophrenia as a consequence of faulty learning. If a child receives little or no social reinforcement early on in life (parental disinterest), the child will attend to inappropriate and irrelevant environmental cues e.g. sound of a word instead of meaning. Result childs verbal or other behavioural responses will become bizarre and those who observe the child's behaviour will either avoid it or respond erratically therefore reinforcing the bizarre behaviour. This cycle will eventually deteriorate into a psychotic state.

C.FAMILY THEORY
Schizophrenigenic mother double-bind Communication deviance (excessive vagueness/blurring -attack children/doublebind) Another measure of disturbed family communication is expressed emotionmeasured : critical comments by the relative about the patient, hostility toward the patient, emotional overinvolvement. Some research suggests high EE may play a role in course of schizophrenia.

FAMILY RELATIONSHIPS

Bateson et al argued Childs ability to respond is incapacitated by the contradictions. Prolonged exposure to these interactions prevents the development of a coherent construction of reality. Which in the long run manifests itself as schizophrenic symptoms, e.g. flattened effect, delusions, hallucinations, incoherent thinking and speaking and some cases paranoia.

FAMILY RELATIONSHIPS
Expressed emotion: Negative emotion or a high degree of expressed emotion (EE) is associated with schizophrenia.

EE = a family communication style that involves criticism, hostility, and emotional over-involvement. Linzen et al 1997 found a patient returning to a family with high EE is 4 times more likely to relapse.

EXPRESSED EMOTION RESEARCH


SUPPORT
Kalafi

and Torabi 1996 studied the rate of relapse in schizophrenics in Iran. High prevalence of EE in Iranian culture (overprotective mothers and rejecting fathers) was one of the main causes of relapse.

Found:

Conclusion:

Negative emotional climate (environment) in families seems to arouse patients and leads to stress beyond his or her coping methods.

D.DOUBLE BIND THEORY Created by Gregory Baetson Hipoethic family A double bind is a dilemma in communication in which an individual (or group) receives two or more conflicting messages, with one message negating the other. This creates a situation in which a successful response to one message results in a failed response to the other, so that the person will be automatically wrong regardless of response.

The nature of a double bind is that the person cannot confront the inherent dilemma, and therefore can neither comment on the conflict, nor resolve it, nor opt out of the situation. creating a situation in which the victim couldn't make a comment or "metacommunicative statement" about their dilemma would (in theory) escalate their mental anxiety and potentially cause a crisis. Children who receive contradictory messages from their parents are more likely to develop schizophrenia.

SOCIOCULTURAL FACTORS

Social Labelling Scheff (1999) promoted the labelling theory of schizophrenia. 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 normal experience or behaviour. Therefore those who display unusual behaviour are considered deviant and the label schizophrenic may be applied which becomes a self fulfilling prophecy that promotes the development of other symptoms of schizophrenia (Comer 2003).

SCHIZOPHRENIA TREATMENT
-

Pharmacologic: traditional antipsychotics [dopamine-2 (D2)receptor antagonists] first generation of antipsychotic medication atypical antipsychotic agents second generation of antipsychotic medication Because of their better side-effect profiles, the atypical agents are now first-line treatments.

SCHIZOPHRENIA TREATMENT
-

Psychosocial treatments: Psychotherapy: individual, family, and group Psychoeducation with activity of patients or enhancing motivation to the treatment Social support

CONCLUSION

Neither the biological nor the environmental (psycho-social) categories is completely determinant, and there is no specified amount of input that will ensure someone will or will not develop schizophrenia Moreover, risk factors may be different for different individuals - while one person may develop schizophrenia due largely to a strong family history of mental illness (e.g. a high level of genetic risk), someone else with much less genetic vulnerability may also develop the disease due to a more significant combination of prepregnancy factors, pregnancy stress, other prenatal factors, social stress, family stress orenvironmental factors that they experience during their childhood, teen or early adult years

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