Secondary Schizophrenia (79 page)

198

Chapter 14 – Cerebrovascular disease and psychosis

Table 14.1
Selected case reports and case series of psychotic symptoms associated with cerebrovascular lesions
Author

Psychotic symptoms

Lesion location

Berthier and Starkstein,

Complex visual hallucinations associated

Extensive right fronto-temporo-parietal ischemic infarct
1987 [1]

with sporadic auditory and tactile

hallucinations.

Reduplicative paramnesia

Kumral and ¨

Ozt ürk, 2004

Paranoid (jealousy or persecutory) or

Lesions involving most frequently the right posterior
[6]

somatic delusions in a selected series of 15

temporoparietal cortex, although lenticular, thalamic,
patients

and medullar lesions were also observed

Rabins et al., 1991 [8]

Unspecified delusions and hallucinations in

Right hemisphere lesions involving one or more of the
a select series of 5 patients. Subjects met

following structures: frontal, temporal, parietal, and
DSM-III criteria for the diagnosis of

occipital cortices or caudate, putamen, and internal
schizophrenia or schizophreniform disorder

capsule

Filley et al., 1999 [27]

Delusion of jealousy

Extensive diffuse and symmetric confluent white-matter
changes on MRI associated with small infarcts in the
centrum semiovale and left thalamus (CADASIL)

Nagaratnam and O’Neile,

Tactile hallucinations and delusions of

Left temporo-occipital ischemic stroke

2000 [28]

parasitic infestation

Cerrato et al., 2001 [29]

Musical hallucinations

Hemorrhagic lesion involving the left putamen and
internal capsule

Beniczky et al., 2002 [30]

Complex visual and tactile hallucinations

Right medial occipital ischemic infarct

Suzuki et al., 2003 [31]

Auditory hallucinations (commanding and

Bilateral hippocampi lesions (more prominent on the left)
derogatory voices)

ffytche DH et al., 2004 [32]

Complex visual hallucinations (written

Bilateral temporo-occipital ischemic lesion (more
sentences and people)

extensive in the right hemisphere)

Predescu et al., 2004 [33]

Auditory hallucinations and paranoid

Bilateral mesencephalo-thalamic ischemic lesion (more
delusions

extensive in the left hemisphere)

Narumoto et al., 2005 [34]

Delusion of persecution

Bilateral caudate ischemic infarct (head of caudate)
Nye and Arendts, 2002 [35]

Episodic olfactory hallucinations

Hemorrhagic lesion to the left uncus

Mechanisms leading to

capsule (1 case). These 5 patients with poststroke psychosis were compared with 5 stroke patients who were
poststroke psychosis

within 2 years of the patient’s age and whose strokes
Kumral and ¨

Oztürk
[6]
found that delusional ideation
were in a similar brain region. Neurological findings
was predominantly associated with right posterior
were similar for both groups, except that seizures were
temporoparietal lesions in a selected series of 15

more frequent in those with psychosis (3/5 vs. 0/5).

stroke patients. However, as outlined in
Table 14.1,

However, there was no significant association between
delusions and hallucinations may also arise in associa-the onset of seizures and of hallucinations. Robinson
tion with lesions to the left cerebral cortex and subcor-

[9]
compared these 5 psychotic subjects with a con-tical structures. Rabins and colleagues
[8]
described
secutive series of 301 people with acute stroke lesions
a series of 5 patients who developed psychotic symp-assessed for other psychiatric disorders. Patients with
toms shortly after a stroke (a few hours after the stroke
psychotic symptoms were significantly older and had
in 2 cases, within several days in another 2 cases,
higher frequency of family history of psychiatric dis-and 2 months poststroke in the remaining patient).

orders than stroke patients without psychosis. Finally,
All patients had right hemisphere lesions involving
4/5 patients with poststroke psychosis had cortical
the frontal operculum and parietal cortex (1 case),
lesions, as compared to 42% of the unselected stroke
basotemporal and occipital cortex (1 case), fronto-group. On the other hand, there were no differences
temporoparietal cortex (1 case), occipital cortex (1

in lesion volume between the poststroke psychotic
case), and head of the caudate, putamen, and internal
patients, the lesion-matched controls, or the overall
199

Organic Syndromes of Schizophrenia – Section 3

stroke population. There were no significant between-

(VaD). As a consequence, little is known about the
group differences in measures of cortical atrophy, but
prevalence and characteristics of psychotic symptoms
patients with poststroke psychosis had significantly
among these patients. Ballard and O’Brien
[11],
in
more severe subcortical atrophy (as determined by
their review of the available literature, identified eleven
frontal horn and third ventricle-to-brain size ratios)
cross-sectional studies (mostly of clinical samples).

than stroke patients without psychosis. Starkstein and
They described a wide variation in the reported preva-colleagues
[3]
suggested that the reason poststroke
lence of delusions and hallucinations: 9–70% (total
psychosis is uncommon is that several factors may be
number of patients included in these studies
=
288).

required to produce psychotic symptoms: right hemi-For example, a retrospective analysis of data collected
sphere lesion involving the temporo-parieto-occipital
as part of the assessment of 92 patients with VaD and
junction in combination with seizures, genetic vulner-92 with AD in the Tyneside Hospital, UK, found psy-ability, and subcortical atrophy probably preceding the
chotic symptoms in 42 patients (45.6%) with VaD.

brain lesion.

Visual and auditory hallucinations were observed in 20

The mechanism of secondary hallucinosis after

(21.7%) and 7 (7.6%) people with VaD, whereas delu-peduncular lesions is even less well known. L’Hermitte
sions and misidentification syndromes were recorded
[2]
suggested that disturbance of the wake/sleep cycle
for 33 (35.9%) and 21 (22.8%) patients. The frequency
in association with attentional deficits and a tendency
distribution of psychotic symptoms in people with AD

to confabulate may play an important role. Stark-was similar to VaD.

stein and colleagues
[3]
considered that secondary
In the largest community-based study available to
hallucinosis could be a “release phenomenon” sec-date, Lyketsos and colleagues
[12]
observed delusions
ondary to damage to reticular activating brainstem
and hallucinations in 5 (8.1%) and 8 (12.9%) of their
pathways and that the presence of primary sensory
62 patients with VaD. All subjects were assessed with
deficits could be an important predisposing factor.

the Neuropsychiatric Inventory and were part of a
Levine and Finklestein
[10]
reported that promi-large community-based study (Cache County Study)
nent hallucinations, delusions, and agitation might
[12].
There was no obvious association between the
be associated with right temporoparietal strokes or
presence of psychotic symptoms and the severity of
trauma.

the dementia, as measured by the Clinical Dementia
There are no systematic studies comparing patients
Rating. In a later publication
[13],
this same group
with secondary hallucinations and patients with sec-described the types of psychotic symptoms present
ondary hallucinosis, and it is unclear whether these
among these patients. They included the belief that
entities are independent phenomena or are symp-others were stealing (4/59) or planning to abandon
toms of the same syndrome. Starkstein and col-

them (2/59), that intruders were living in their house
leagues
[3]
compared patients with secondary hal-

(3/59), that people were not who they claimed to be
lucinations reported in the literature with patients
(3/59), that their house was not their real home (2/59),
with secondary hallucinosis. They found that patients
or that media figures were in the home (1/59). The fre-with secondary hallucinations had a higher frequency
quency distribution of these beliefs was similar to that
of visual and auditory phenomena, delusions, and
observed among patients with AD. Hallucinations in
depression when compared to those with hallucinosis.

the form of audible voices (4/58), talking to people who
On the other hand, sensory deficits (mainly hemi-were not there (5/58) and seeing things others could
anopia) were significantly more frequent in patients
not see (5/59) were also reported. Again, subjects with
with secondary hallucinosis. Finally, there were no sig-VaD and AD had a similar frequency distribution of
nificant between-group differences in the frequency of
hallucinations.

confusional states.

There is debate as to whether the psychotic symptoms associated with dementia correlate with the
severity of the cognitive impairment. Tentative evi-Vascular dementia and psychosis
dence suggests that delusional ideation is more likely
Compared to Alzheimer’s Disease (AD) and demen-to arise in people with moderate dementia, whereas
tia with Lewy bodies (DLB), few clinical and epidemi-hallucinations may be more prevalent amongst those
ological investigations have explored the association
with severe cognitive impairment
[14, 15].
How-

200

between psychotic symptoms and vascular dementia
ever, it remains unclear whether psychosis in VaD is
Chapter 14 – Cerebrovascular disease and psychosis

associated with the disruption of particular neuronal
Conclusion

networks or simply represents a nonspecific response
Cerebrovascular disease has been associated with
associated with dementia.

behavioral changes, including psychosis, for decades, if
not centuries. Surprisingly, however, systematic information on this topic remains sparse and, on the
Cerebrovascular disease in delusional

whole, inconclusive. After stroke, the onset of psychotic symptoms is uncommon and the development
disorder and schizophrenia

of typical schizophrenic symptoms rare. Preliminary
Schizophrenia and delusional disorder with late onset
evidence suggests that lesions to the right temporo-have been associated with a variety of structural brain
parietal-occipital cortex are more likely to be found in
abnormalities compared to healthy controls, including
association with psychosis, although strokes in almost
increased ventricular-to-brain ratio, third ventricu-all other areas of the brain have been observed in
lar enlargement, generalized cerebral cortical atrophy,
association with psychotic symptoms. It is also impor-smaller superior temporal gyrus, and greater white-tant to note that most stroke patients never experi-matter disease burden
[16].
The purported changes in
ence delusions or hallucinations, even when the stroke
white-matter tracts have attracted a great deal of atten-affects the right temporoparietal-occipital cortex.

tion and led to the suggestion that the onset of psy-There is also limited evidence about the associa-chotic symptoms in later life might be partly medi-tion between psychosis and vascular dementia. The
ated by cerebrovascular pathology
[17].
However, find-reported prevalence of psychotic symptoms in peo-ings from studies using MRI are far from conclu-ple with vascular dementia and Alzheimer’s Disease
sive. To date, four studies reported greater burden
is similar
[13, 14]
, and it might be argued that it is
of white-matter disease among patients than controls
not so much the vascular pathology but the disrup-

[18, 19, 20, 21]
, with another four studies observing
tion of neuronal networks associated with dementia
no obvious difference between these groups
[22, 23,

that leads to the expression of delusional ideation and
24, 25].