GENETIC FACTORS
Most genetic studies have focused on immediate
families (i.e., parents, siblings, offspring) to exam-
ine whether schizophrenia is genetically transmit-
ted or inherited. Few have focused on more distant
relatives. The most important studies have cen-
tered on twins; these findings have demonstrated
that identical twins have a 50% risk for schizo-
phrenia, whereas fraternal twins have only a 15%
risk (Cancro & Lehman, 2000). This finding indicates
that schizophrenia is at least partially inherited.
Other important studies have shown that chil-
dren with one biologic parent with schizophrenia have
a 15% risk; the risk rises to 35% if both biologic parents
have schizophrenia. Children adopted at birth into a
family with no history of schizophrenia but whose bio-
logic parents have a history of schizophrenia still re-
flect the genetic risk of their biologic parents. All these
studies have indicated a genetic risk or tendency for
schizophrenia, but genetics cannot be the only factor:
identical twins have only a 50% risk even though their
genes are 100% identical (Cancro & Lehman, 2000).
NEUROANATOMIC AND
NEUROCHEMICAL FACTORS
With the development of noninvasive imaging tech-
niques such as CT scans, magnetic resonance imag-
ing (MRI), and positron emission tomography (PET)
in the past 25 years, scientists have been able to study
the brain structure (neuroanatomy) and activity
(neurochemical) of people with schizophrenia. Find-
ings have demonstrated that people with schizophre-
nia have relatively less brain tissue and cerebrospinal
fluid than people who do not have schizophrenia
(Flashman et al., 2000); this could represent a failure
in development or a subsequent loss of tissue. CT
scans have shown enlarged ventricles in the brain
and cortical atrophy. PET studies suggest that glu-
cose metabolism and oxygen are diminished in the
frontal cortical structures of the brain (Fig. 14-1).
The research consistently shows decreased brain vol-
ume and abnormal brain function in the frontal and
temporal areas of persons with schizophrenia. This
pathology correlates with the positive signs of schiz-
ophrenia (temporal lobe) such as psychosis and the
negative signs (frontal lobe) such as lack of volition
or motivation and anhedonia. It is unknown if these
changes in the frontal and temporal lobes are the re-
sult of a failure of these areas to develop properly or
if a virus, trauma, or immune response has damaged
them. Intrauterine influences such as poor nutrition,
tobacco, alcohol and other drugs, and stress also are
being studied as possible causes of the brain pathol-
ogy found in people with schizophrenia (Buchanan &
Carpenter, 2000).
Neurochemical studies have consistently demon-
strated alterations in the neurotransmitter systems of
the brain in people with schizophrenia. The neuronal
networks that transmit information by electrical sig-
nals from a nerve cell through its axon and across
synapses to postsynaptic receptors on other nerve cells
seem to malfunction. The transmission of the signal
across the synapse requires a complex series of bio-
chemical events. Studies have implicated the actions
of dopamine, serotonin, norepinephrine, acetylcholine,
glutamate, and several neuromodulary peptides.
Currently the most prominent neurochemical
theories involve dopamine and serotonin. One promi-
nent theory suggests excess dopamine as a cause.
This theory was developed based on two observations.
First, drugs that increase activity in the dopaminer-
gic system, such as amphetamine and levodopa, some-
times induce a paranoid psychotic reaction similar to
schizophrenia (Egan & Hyde, 2000). Second, drugs
blocking postsynaptic dopamine receptors reduce psy-
chotic symptoms; in fact, the greater the ability of
the drug to block dopamine receptors, the more ef-
fective it is in decreasing symptoms of schizophrenia
(O’Connor, 1998).
More recently, serotonin has been included
among the leading neurochemical factors affecting
schizophrenia. The theory regarding serotonin sug-
gests that serotonin modulates and helps to control
excess dopamine. Some believe that excess serotonin
itself contributes to the development of schizophre-
nia. Newer atypical antipsychotics such as clozapine300 Unit 4 NURSINGPRACTICE FORPSYCHIATRICDISORDERS
Genetic studies