about four times more likely to relapse than a patient returning to a family with low EE (
Linszen et al.,1997).
In a study of the relapse rates among schizophrenics In Iran,
Kalafi and Torabi (1996)
found that the
high prevalence of EE in Iranian culture
(overprotective mothers and rejective fathers) was one of the
main causes of schizophrenic relapses
. It appears that the negative emotional climate in thesefamilies arouses the patient and leads to stress beyond his or her already impaired coping mechanisms,thus triggering a schizophrenic episode.
The labelling theory of schizophrenia, popularised by
states that social groups constructrules for members of their group to follow. The symptoms of schizophrenia (e.g. hallucinations and
delusions, and bizarre behaviour) are seen as deviant from the rules we ascribe to ‘normal’
If a person displays these unusual forms of behaviour, they are considered
deviant, and the label ofschizophrenic may be applied. Once this diagnostic label is applied it becomes a self-fulfillingprophecy that promotes the development of other symptoms of schizophrenia (Comer, 2003)
Brown and Birley (1968)
reported that life events play an important role inprecipitating episodes of schizophrenia. They found that about
50% of people experience stressful life eventsin the 3 weeks prior to a schizophrenic episode, while only 12% reported one in the weeks prior to that.
Acontrol sample reported a low and unchanging level of stressful life events over the same period, suggesting thatit was the life events that triggered the relapse.
unlike retrospective studies, which study events in the past, prospective studies monitorthe
presence or absence of stressful life events prospectively (i.e. in the future). Hirsch et al. (1996)
71 schizophrenic patients over a 48 week period
. it was clear that life events made a significantcumulative contribution in the
12 months preceding relapse
rather than having a more concentrated effect inthe period just prior to the schizophrenic episode (as suggested by the retrospective studies).
no research evidence
to support Freud’s specific ideas concerning schizophrenia, except that
subsequent psychoanalysis have claimed, like him, that disordered family patterns are the cause of thisdisorder. For example,
or familieswho are rejecting, overprotective, dominant and moralistic, as important contributory influences in thedevelopment of schizophrenia.
Studies have shown that
parents of schizophrenic patients do behave differently
from parents ofother kinds of patients, particularly in the presence of disturbed offspring (
Oltmanns et al., 1999
this is as likely to be a consequence of their children’s problems as a cause.
There is much evidence of a physical basis for the cognitive deficits associated with schizophrenia, forexample, research by
Meyer-Lindenberg et al. (2002),
which found a link between excess dopamine in
the prefrontal cortex, and working memory. The suggestion that ‘madness’ is a consequence of
disbelieving others receives curious support from a recent suggestion for treatment.
Yollowlees et al. (2002)
have developed a machine that produces virtual hallucinations, such ashearing
the TV tell you to kill yourself, or one person’s face morphing into another. The intention is to
show schizophrenics that their hallucinations are not real. As yet there is no evidence that this willprovide a successful treatment.
Life events and schizophrenia
Not all evidence supports the role of life events. For example,
van Os et al. (1994)
between life events and the onset of schizophrenia. Patients were not more likely to have had a majorstressful life event in the
3 months preceding the onset of their illness
. In a prospective part of the