Secondary Schizophrenia (77 page)

pedigrees (OR 0.75, CI 0.10 to 5.93), but a fourfold
review suggested a trend toward focal lesions affecting,
increase in families with two or more first-degree rel-in particular, the frontal and temporal lobes. Although
atives affected with schizophrenia (OR 4.27, CI 1.40 to
65% cases reported positive findings on CT/MRI, no
13.0). The authors did not, however, test for interac-brain region emerged as being necessarily affected in
tion effects to confirm that this difference was greater
patients with SLP, however, in closed, head injury, the
than a chance effect. In the Sachdev and colleagues
lack of involvement of specific brain regions becomes
[15]
study, it emerged that the most significant risk
difficult to prove. Similarly, laterality has not emerged
factor for SLP-TBI was a genetic vulnerability to psy-as a significant factor in the development of psychosis,
chosis as reflected in the family history, even though
although a suggestion has been made that left tempo-this was present in only a fraction of patients. Family
ral lesions may be more common in those who develop
history has been used as a marker of genetic predis-SLP
[15].

position for schizophrenia and other psychiatric disorders. For schizophrenia, the lifetime risks of psy-

Is there a specific cognitive syndrome underlying the

chosis reported for first-degree relatives have varied
development of SLP following TBI?

from 3.1 to 16.9%
[28].
The Sachdev and colleagues
[15]
finding of 24% risk in first-degree relatives, com-Cognitive deficits have the potential of providing con-pared to 3% for controls, is therefore high, even if
tinuity between the brain damage of TBI and the
an upward reporting bias in the SLP group is con-development of psychosis. If the cognitive deficits of
sidered as a factor. In a study of schizophrenia sec-SLP-TBI patients resemble those seen in schizophre-ondary to a variety of neurological disorders, Feinstein
nia and differ from the deficits seen in TBI patients
and Ron
[29]
found a positive family history in only
who do not develop psychosis, an argument relating
3.8%. In epilepsy patients with chronic SLP, the risk of
to their specificity can be supported. The difficulty is
schizophrenia in first degrees was reported by Slater
that what constitutes core deficits in schizophrenia is
and Glithero
[30]
to be no higher than the general pop-still in dispute, although attention, memory, and exec-ulation. It is possible that head injury brings out a vul-utive deficits are broadly recognized as being charac-nerability to schizophrenia due to genetic or other fac-teristic. In the study by Sachdev and colleagues
[15],

tors in at least some patients. Further, Malik and col-SLP-TBI subjects were more likely to have abnormal-leagues
[14]
reported that in those with a family his-ities on measures of verbal and nonverbal memory
tory of schizophrenia, TBI before 10 years was related
and frontal-executive functioning, when compared to
with an earlier age of onset of schizophrenia.

TBI subjects without psychosis. However, they also
tended to have more of a disturbance in language and
parietal lobe functioning, suggesting a diffuse impair-Relationship with epilepsy?

ment in neuropsychological functioning in compari-A varying percentage of patients, depending on the
son with the non-SLP group. In the other review
[5]

location and severity of injury, will have seizures dur-mentioned earlier, 88% of cases reported impairments
ing the acute period after the trauma. Post-traumatic
on neuropsychological testing. The most common
epilepsy, with repeated seizures and the requirement
impaired function was memory, followed by execu-for anticonvulsant medication, occurs in approxi-tive and visuospatial functions. Clearly, more work is
mately 12%, 2%, and 0.8% of patients with severe,
necessary to establish the salience and specificity of
moderate, and mild head injuries, respectively, within
some neurocognitive deficits in the development of
5 years of the injury
[31].
The rate of epilepsy
SLP.

reported by Fujii and Ahmed in their review of SLP-TBI was 34%, which is an over-representation
[32].

Are TBI patients who develop SLP predisposed to

On the other hand, in the case-control study pre-

psychosis due to some pre-existing vulnerability?

sented by Sachdev and colleagues
[15],
the SLP sub-The cohort studies mentioned earlier are informa-jects had a nonsignificantly lower epilepsy rate, and
tive on this question. In the study by Corcoran and
epilepsy in these patients was well-controlled, unlike
192

Chapter 13 – Schizophrenia-like psychosis and traumatic brain injury

those TBI patients who were not psychotic who had
medication-resistant epilepsy. These authors specu-

Conclusion and future directions

lated that epileptic seizures might in some way be
SLP is a relatively uncommon psychiatric consequence
protective against the development of psychosis. An
after brain injury. The epidemiological literature on
interesting observation from the Fujii and Ahmed
[5]

the association between SLP and TBI is considerable,
review was that SLP patients with epilepsy were less
but a definitive longitudinal study has never been con-likely to have delusions than those without epilepsy.

ducted. The two Scandinavian studies
[11, 12]
present
the best current evidence for the association and support only a marginally increased risk, if at all. The
Is age of TBI important?

risk may be significantly greater, however, in those
The schizophrenia literature suggests that brain injury
with a genetic vulnerability to schizophrenia. It is also
early in childhood may be more important in rela-possible that TBI may exacerbate pre-existing psy-tion to the risk for schizophrenia
[7, 8]
because it is
chosis. Whether an individual in the prodrome of a
likely to disrupt normal neurodevelopment. The SLP-schizophrenic illness has an altered risk of having a
TBI literature does not consistently support this con-TBI is not certain from the data.

clusion, however, and head injury in these individuals
When it does develop, the clinical presentation of
occurred across a wide age span, including child-the psychosis following TBI has considerable overlap
hood, adolescence, and adulthood. The Wilcox and
with primary schizophrenic disorder, with a promi-Nasrallah
[9]
and Gureje and colleagues
[10]
stud-nence of persecutory and other delusions, auditory
ies, designed specifically to examine the effect of head
hallucinations, and a dearth of negative symptoms.

injury in childhood, reported a strong association with
The interval between TBI and the onset of SLP is
SLP. In the Canadian study of multiply affected fam-very variable. The onset is often gradual, with a sub-ilies, injury <10 years was over-represented in the
acute or chronic course. More severe and diffuse
schizophrenia cases (OR 2.34, CI 1.03 to 5.36). How-brain injury, especially one that involves the temporal
ever, in the large Swedish case control study
[12],

and frontal lobes, is the most prominent risk factor,
the small increase in incidence of nonschizophrenic,
and EEG and neuroimaging abnormalities are often
nonaffective psychosis occurred only in those with
present. The presence of epilepsy does not appear
injury during adolescence or later. In the Sachdev
to increase the risk of SLP and could possibly be
and colleagues
[15]
study, childhood injury was not
protective.

over-represented.

The interaction of TBI with genetic risk factors for
schizophrenia is worthy of further examination, and
this should include the study of candidate genes impli-Birth trauma and schizophrenia
cated in schizophrenia. Detailed studies of SLP-TBI
The proposal that pregnancy and birth complications
patients with newer imaging techniques, combined
are associated with an increased risk of schizophrenia
with electrophysiology, should enable us to better
has been extensively studied and is generally accepted
understand the nature of brain injury that is associ-despite some controversy
[7].
In a cohort study men-ated with the development of psychosis. These patients
tioned earlier, Wilcox and Nasrallah
[9]
concluded that
must also be examined for neurobiological and neu-childhood head trauma at less than 5 years of age was
ropsychological abnormalities commonly associated

more likely to have occurred in schizophrenic patients.

with schizophrenia to determine the relative contribu-Gureje and colleagues
[10],
in another retrospective
tions of a diathesis and brain injury toward the genesis
study, also found an association between childhood
of SLP.

brain trauma and schizophrenia. The markers used
What are the implications of the conclusion for
to indicate these perinatal insults include low birth
medicolegal practice? Although the evidence for the
weight, prematurity, preeclampsia, prolonged labor,
association is not overwhelming, as noted earlier, the
hypoxia, and fetal distress
[33].
The overall effect of
possibility that TBI might make a contribution toward
perinatal accidents when calculated is small, increas-the development of schizophrenia, especially in vul-ing risk of disease by only 1%. The evidence only points
nerable individuals cannot be dismissed. Medicolegal
to an association and not causality.

determination must therefore occur on an individual
193

Organic Syndromes of Schizophrenia – Section 3

basis, after considering the premorbid status of the
The level of evidence needed for medicolegal purposes
individual, the nature of the TBI, the psychologi-is different from that required for scientific inquiry,
cal trauma and social factors related to the injury,
and it may be possible that some injuries could be
neuropsychological and anatomical deficits from the
compensable, at least partially, due to the subsequent
injury, and the nature of the psychosis that follows.

development of SLP.

194

Chapter 13 – Schizophrenia-like psychosis and traumatic brain injury

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