Rethinking schizophrenia
At the end of the 19th century the German psychiatrist Emil Kraepelin (1856–1926) took the then unitary concept of psychosis and divided it into two distinct forms, which he called manic-depressive psychosis and dementia praecox. The first of these conditions was a progressive illness that
might exhibit itself in episodes spread over the years but eventually
ended in recovery and restoration of the previous personality. The second
was a mental disorder characterised by dissociation, intellectual and
affective in particular, which later became known as schizophrenia.
Recently, more than a century after Kraepelin first recognised the condition,
it has been suggested that the concept of schizophrenia may be scientifically
meaningless, since its precise pathophysiology and cause are unknown.
However, an editorial in the 20 January 2007 issue of the BMJ argues
that, although the condition may defy strict diagnosis, the term “schizophrenia” is
still a useful one.
Among the symptoms of schizophrenia are delusions, hallucinations, disorganised
speech and behaviour, along with negative symptoms such as lack of motivation.
The evidence is that these symptoms are all manifestations of brain pathology.
Comparisons with normal controls show detectable abnormalities in brain
structure and function. It seems clear also that there is a genetic basis
to vulnerability to schizophrenia.
A mistaken diagnosis can lead to the wrong treatment and brand the patient
as having a mental illness without justification. For example, a toxic
psychosis induced by a drug such as phencycyclidine may lead to lengthy
and unnecessary treatment with antipsychotic drugs. Only if the symptoms
continue for a substantial period after the patient has ceased to take
the suspected drug is a diagnosis of schizophrenia now allowed.
In order to minimise the stigma associated with schizophrenia, it has
been suggested that it be renamed “integration disorder” or “dopamine
dysregulation disorder”. This might help to relieve the concern
of relatives that the disorder might cause undue fear in people who associate
with the sufferer, with the result that the individual rather than the
illness is blamed for the condition.
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