Secondary Schizophrenia (43 page)

ing excitotoxic glutamate release resulting in suppression of seizures. Although small doses of adenosine
can exert an inhibitory action on the release of exci-

Implications for a neurobiological

tatory neurotransmitters such as glutamine, inhibition
of release of inhibitory neurotransmitters requires very
understanding of schizophrenia

high concentrations of adenosine. Cerebral adenosine
None of these hypotheses may individually provide
levels have been found to increase substantially dur-the neurobiological explanation for the antagonism
ing seizures. It can be hypothesized that during kin-between seizures and psychopathology in a proportion
dling, these doses are small and sufficient to exert
of patients. However, it seems possible, even likely, that
an inhibitory action on excitatory neurotransmitters
these varied mechanisms are closely interlinked.

resulting in seizure suppression. In a FN situation
Various brain regions also have been implicated.

108

wherein there is a sudden cessation of seizures, the
For example, reduced cortical inhibition has been
Chapter 7 – Understanding the pathophysiology of schizophrenia

implicated as being responsible for the defective sen-extent a predilection for this region of interest. That
sory gating observed in schizophrenia, leading to hal-patients with temporal lobe epilepsy appear to have
lucinations
[26, 27]
. Although this “excessive neuronal
a greater predilection for FN makes this a region of
noise” is primarily in the thalamus, it is noteworthy
interest for neurobiological study.

that this structure has extensive neuronal connections
FN is thus a useful clinical model for further study
with other regions of the brain, including the cortex,
of the antagonism between epilepsy and psychopathol-limbic system, and the cerebellum.

ogy, the psychoses in particular. Those who special-There is also today a convergence of evidence
ize in epilepsy neuropsychiatry do not regard it as an
pointing to the temporal lobe, especially the mesial
uncommon phenomenon, rather one that has putative
temporal structures, as a region of interest in the gen-importance as a clinical research tool that can facil-esis of schizophrenia. A substantial body of MRI liter-itate our understanding of psychopathology. Perhaps
ature has demonstrated mesial temporal involvement
the antagonistic relationship that fostered a successful
in this condition
[28]
. Further, we know from basic
treatment paradigm – ECT – will also lead eventually
science research that the neurobiological changes that
to viable neurobiological models of psychopathology
underlie this condition demonstrate to a considerable
and thereby to advances in treatment.

109

Organic Syndromes of Schizophrenia – Section 3

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111

Section 3

Organic syndromes of schizophrenia:

8 Substance-inducedpsychosis:anoverview

Jagadisha Thirthalli, Vivek Benegal, and Bangalore N. Gangadhar
Facts box

Substance use disorders and psychotic disorders
r

are both mental health problems of considerable pub-Although different substances consistently
lic health significance. Not only do they coexist in a
produce or exacerbate psychotic symptoms
substantial proportion of patients, but also they may
in patients with primary psychosis, they
share a common neurobiological substrate. Knowl-differ in their psychotogenic properties in
edge about the conditions that influence this conjunc-

“healthy” individuals.

tion is of obvious clinical importance – acute man-r
Individuals with substance use/dependence
agement and rehabilitation depend on their accurate
are five times more likely to experience
evaluation. Studying these conditions is also of great
clinically significant delusions and/or
heuristic value because the construction of these con-hallucinations than nonusers.

ditions has the potential to reveal valuable clues about
r
Cohort studies suggest that the rate of
the etiopathogenesis of both substance use disorders
schizophrenia is increased in chronic
and “functional” psychotic disorders. Circumstances
cannabis users.

in which there is coexistence of the two conditions
r
Alcohol use may worsen psychotic symptoms
vary. Traditionally, the diagnostic debate has focused
or increase risk of relapse, but it is not
on two different sequential presentations – whether
considered to “cause schizophrenia.”

a person with a primary psychotic disorder conser
quently abuses substances or, conversely, whether a
Brief amphetamine-induced psychosis is well
person with primary substance abuse experiences psy-documented. Chronic heavy use also
chotic symptoms. If the onset of the two conditions
predisposes to psychosis.

r

is clearly separated by a considerable time gap, then
Schizophrenic brains may be sensitized to
the one that occurs first may be argued as the pri-the effects of psychotogenic drugs.

r

mary, and the other, secondary. However, this is not an
Evidence suggests that in some individuals,
absolute truism. For instance, it is known that patients
genetic vulnerability combined with drug
with schizophrenia have subtle behavioral changes
abuse can bring about psychosis.

several months prior to the onset of positive symp-r
Nosological status of substance-induced
toms. This may sometimes lead to interpersonal dif-psychoses (SIP) and causal role of substances
ficulties and the breaking up of relationships. If the
in causing schizophrenia remain
individual develops frank psychosis following this, it
controversial.

may be construed as a reaction to this “life event” even
though he/she has developed psychosis as part of its
natural history. In fact, in this case the life event is a