I N T E R N A T I O N A L J O U R N A L OF G E R I A T R I C PSYCHIATRY, VOL.

2: 83-90 (1987)

LATE PARAPHRENIA: NEUROPSYCHO-

LOGICAL IMPAIRMENT AND STRUCTURAL
BRAIN ABNORMALITIES ON COMPUTED
TOMOGRAPHY
MOHSEN N A G U I B , ” MRCPsych, DPM A N D R A Y M O N D LEVY, FRCPsych, FRCP, PhD
Section of Old Age Psychiatry, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, CIK

SUMMARY
Forty-three patients with ‘late paraphrenia’ were subjected to detailed clinical and psychological assessment and
computed tomography (CT). The paraphrenics had significantly larger lateral cerebral ventricles and greater
cognitive deficits than a group of 40 age-matched normal volunteers. Group comparisons within the patients,
between those with particularly large ventricular brain ratio (VBR) (equal or more than two standard deviations
above the control mean) and the rest of the group, showed that the extent of ventricular enlargement had no direct
bearing on the clinical presentation of the paraphrenic syndrome. The results suggest that ventricular enlargement
may have preceded the onset of overt symptoms by a period of years and probably served as a non-specific risk
factor for the development of the disorder. The unimodal distribution of VBR values suggests that paraphrenia, at
least at a brain structural level, is a unitary condition. It also indicates the presence of subcortical pathology which
might be in part responsible for the cognitive dysfunction elicited.

KEY woms-Paraphrenia psychological impairments, C A T scan, Abnormalities

INTRODUCTION zophrenia had variable degrees of increased

Kraeplin (1919), who first introduced the term
paraphrenia to describe patients with late onset
paranoid delusions and hallucinations, considered
that intellectual functions and memory were not
impaired in this disorder. He believed that the
later age of onset of florid symptoms and the
failure to progress -in the majority of cases -to
defect states set paraphrenia apart from dementia
praecox. The two conditions were presumed to be
free from any morbid anatomical brain changes
and permanent cognitive impairment. However,
there is now a growing body of knowledge which
suggests that at least in chronic schizophrenia
there are morphological brain changes, neurop-
sychoiogical deficits and neurological symptoms.
Structural brain abnormalities were first de-
scribed in pneumoencepholographic studies
(Moore et al., 1933; Matthews and Booker, 1972)
which showed that patients with chronic schi-
*Now at St Mary’s Hospital Medical School and St Charles
Hospital. Exmoor Street. London WIO
ventricular size and/or sulcal enlargement. These
are usually interpreted as evidence for central and
surface cerebral atrophy respectively. Similar
results have been demonstrated using CT scan-
ning (Johnstone et al., 1976; Kingsley and
Trimble, 1978; Weinberger et al., 1979a, b, 1982).
Patients with chronic schizophrenia are almost
invariably reported to perform poorly on various
neuropsychological tests (Klonoff et al., 1970;
Watson et al., 1968; Golden et al., 1980). On the
basis of their test performance alone they are
frequently indistinguishable from patients with
organic brain damage (Golden e f af., 1978;
Watson, 1971). Furthermore, a number of studies
have reported the presence of motor disorders
and other features suggestive of neurological
dysfunction in unselected groups of psychiatric
patients and particularly those with severe and
chronic forms of schizophrenia (Rogers, 1985;
Pollin et al., 1966; Rochford et af., 1970).
In the case of schizophrenia of late onset Hi!l
(1956) stated that: ... ‘in the involutional period
of life organic cerebral factors usually act as
precipitants of the psychosis and inevitably

0885-6230/87/02008W8$05 .OO Received 28 November 1986

01987 by John Wiley & Sons, Ltd Accepted 2 December 1986
84 M . NAGUIB AND R. LEVY
determine an unfavourable progress’. While Kay
and Roth (1961) found a pathological degree of
cerebral degeneration -which they postulated to
be related to the onset of late paraphrenia - in
5% of their cases, Post (1966), aiming to estimate
the contribution made by cerebral disease to the
causation of paranoid and paraphrenic syn-
dromes, judged that about 26% of his patients
had an associated cerebral disease. Herbert and
Jacobson (1967) found specific E E G abnormali-
ties in over half the patients studied, but they
considered these to be age related. Similarly,
Maggs and Turton (1956) in a survey of EEGs in
people over the age of 60 suffering from delusions
found the same number of specific abnormalities
as in normal controls. There is a great deal of
controversy in the literature about the relevance
of organic cerebral disease to the genesis of late
paraphrenia. Whilst Fish (1960) in his Edinburgh
Series of senile paranoid states found organic
factors to be very important, other authors
tended to place greater emphasis on elements like
social isolation, personality traits and sensory
defects.
In the present study, we have attempted to
investigate the role of these factors in the
causation of paraphrenia. We report here the
results of CT investigations and the neuropsycho-
logical assessment. E E G findings will be given in
a separate report.
SUBJECTS AND METHODS
The subjects consisted of 43 patients suffering
from late paraphrenia who were hospital inpa-
tients, outpatients or day patients. Thirty-nine
subjects were current patients of the Joint
Hospital and five came from other sources. The
control group consisted of 40 normal elderly
volunteers who were living independently in the
community and who showed no evidence of
dementia or psychiatric disorder. They were
matched for age and sex. The latter were derived
from Age Concern centres, local day centres and
Salvation Army Homes for elderly officers. Both
groups were broadly comparable in terms of their
previous occupational status.
The diagnosis of paraphrenia was first estab-
lished by the consultant psychiatrist in charge of
the case, but before being included in the study
patients were required to fulfill the following
criteria (Naguib et al., 1987). (1) The presence of
fantastic, persecutory or grandiose delusions,
delusions of reference with or without hallucina-
tions; (2) the absence of a primary affective
disorder; (3) intellectual capacity in keeping with
that of normal ageing; (4) the phenomena
occurred in the setting of clear consciousness; (5)
the first onset of symptoms was at or over the age
of 60; (6) absence of a history or physical signs of
cerebrovascular accidents, neurological disorders
or alcoholism.
Clinical data
In addition to obtaining detailed personal and
demographic data all subjects were assessed
using:
1. The Geriatric Mental State Schedule (GMS)
(Copeland et al., 1976).
2. The Mental Test Score (MTS) (Hodkinson,
1973), a test of memory and orientation.
3. The Digit Copying Test (DCT) (Kendrick,
1965), a test of psychomotor speed and
concentration.
4. The Digit Symbol Substitution Sub-Test
(DST) of the WAIS (Wechsler, 1955). Scores
on this test probably reflect a variety of
functions including both psychomotor speed
and learning ability. The learning component
may be dependent on both visuo-spatial
discrimination and memory (Glosser et al.,
1977).
Radiological data
CT scans were obtained using the EM1 CT 1010
head scanner. A minimum of eight cuts were
made parallel to the orbito-meatal line. Each slice
represented a thickness of 10 mm. The two slices
showing the biggest lateral ventricular areas were
chosen and the ventricular-brain ratio (VBR) was
determined using a planimeter. The largest value
is given here for both groups. A linear measure of
the maximum width of the frontal horns of the
lateral ventricles to the maximum intenral dia-
meter of the skull (bifrontal-intracranial ratio)
was also determined for each subject.
RESULTS
These concern comparisons between paraphre-
nics and normal controls.
1. Age. Both groups were well matched for age
 LATE PARAPHRENIA
Table 1. Psychological tests and CT measurements
Paraphrenia
n = 43
Mean f SD
Age 75.27f 6.29
Mental Test Score (MTS) 28.48f 4.03
Digit Copying Test 59.62 f 32.96
Digit Symbol Substitution Test 9.93 f 7.03
(DST)
Ventricular-brain ratio 13.09f 4.34
( V W
Bifrontal-intracranial 32.09k 6.39
ratio
~~
f-test (two-tailed).
(paraphrenics 75.85 k 8.6 vs controls 75-28
k 6-2).
2. Sex. The female to male ratio was somewhat
higher in the paraphrenic group as compared
to the controls (37/6 vs 31/9). 5.
3. Sensory defects. Sixteen (37%) of the para-
phrenics were ‘socially deaf‘ while this was so
in only two (5%) of the normal controls. Three
(7%) paraphrenics had variable degrees of
visual impairment and four (10%) of the
controls had similar defects.
4. Psychological tests. When compared with the
normal controls paraphrenics performed less
well on all tests. The differences were signifi-
cant for the MTS (p<O.OOl) and the DCT 6.
(p < 0.002). The DST differences were in the
same direction but were not significant.
Results are given in Table 1. Subjects who
were visually impaired have been excluded
from the analysis of the DCT and DST.
Although there was a highly significant cor-
relation between scores on neuropsychological 7.
tests and measures of cerebral atrophy (VBR
and bifrontal-intracranial ratio) in the normal
control group, amongst the paraphrenics no
such significant associations emerged. There
were also no significant correlations between
performance on the neuropsychological tests
or the measures of cerebral atrophy and the 8.
duration of illness. Scores on psychological
tests showed a non-significant association, with
the presence of hearing impairment (MTS,
p < 0.06; DCT, p < 0.07). Statistically signifi-
cant correlations were found between scores
85
Normals Significance
n = 40 level
Mean k SD
75.85f 8.64 N.S.
31.72t 3.08 p<O.OOI
93.59 k 30.86 p < 0.002
11.52 f 3.22 N.S.
9.75f 4.35 p<O.O01
31.91 f 4.33 N.S.
on the MTS and GMS symptom factors
‘depression’, ‘memory impairment’, ‘retarded
speech’ and ‘disorientation’. Results are given
in Table 2.
Radiological data. Patients with paraphrenia
differed significantly from normal controls on
planimetric measures of cortical atrophy VBR
(p < 0.001). The same trend was seen for the
bifrontal-intracranial ratio although it did not
reach significance level. Results are given in
Table 1. There were no significant correlations
between VBR (or bifrontal-intracranial ratio)
and the various symptoms elicited by the GMS
(see Table 2).
Distribution of Mental Test Score and ven-
tricular-brain ratio by age decade. The VBR
values increased with age in both paraphrenics
and normal controls indicating greater degree
of cerebral atrophy. This was paralleled by a
similar fall in MTS scores for both groups
(Table 3).
Six patients had VBR values equal to or more
than two standard deviations above the con-
trols’ mean (18.45). Those subjects did not
differ from the rest of the patient group in age,
age of first onset, duration of illness or its
severity, the presence of positive or negative
symptoms, or in MTS, DCT and DST scores.
The mean duration of paraphrenia was 47
months with a range of 3-240. An arbitrary
duration of two years was taken to divide the
patients into a group with a relatively acute
form of the illness ( N = 15) and one with a
more chronic form ( N = 27).
Table 2. Intercorrelation of clinical, psychological and CT variables

GMS FACTORS

Paraphrenia months 1 1.00

Memory/orientation 2 -0.04 1 .00
Digit copying 3 -0.14 0.51*** 1.00
Digit symbol 4 -0.15 0.48 * * * 0.31% I.00
Depression 5 0.04 -0.32* 0.12 -0.30* 1 40
Anxiety 6 0.30* 0.15 0.03 0.009 0.20 1 .oo
Memory impaired 7 -0.004 -0.7 I * * * * -0.5 I**** -0.20 0.13 -0.22 1.00
Retarded speech 8 -0.04 -0.31* 0.13 0.12 0.38* -0.06 0.32** 1.00
Disorientation 9 0.12 -0.31* -0.09 -0.13 0. I3 -0.12 0.44** * 0.51**** 1 .00
Insight impaired 10 0.37** 0.08 0.07 0.03 -0.12 -0.31 -0.14 -0.13 -0.22 1.00
11 -0.01 -0.04 - ().'j6*il '? :v
Paranoid delusions 0.30 0.09 -0.21 -0.06 -0.17 0.01 0.43*** 1.00
Visual hallucination 12 -0.07 0.05 0.50*** 0.10 0.18 ().37*:i- * -0.25* -0.05 -0.09 -0.03 -0.19 1.00
Auditory hallucination 13 0.16 0.16 - 0.0 1 -0.06 0.05 0.06 -0.10 0.21 0.02 -0.09 -0.02 -0.16 1.00
VBR 14 0.11 -0.16 0.25 0.07 0.05 -0.02 0.08 -0.06 0.11 0.008 -0.21 0.19 0.07 1.00
Bifron tal-intracranial 15 0.01 -0.16 -0.08 -0 4 2 0.01 0.07 0.20 -041 0.20 -0.10 -0.12 -0.05 0.17 0.75*'" 1.00
ratio
1 2 3 4 5 6 7 8 9 10 11 12 I? 14 15

* p < 0.05
* * p <0.01
* * * p < 0.005
* * * * p < 0.00 1
 LATE PARAPHRENIA 87

Table 3. Distribution of Mental Test Score and ventricular-brain

ratio by age decade

Age decade MTS VBR

Paraphenia Controls Paraphrenia Controls

6&69 30.00 ? 3.4 33.22 f 1.3 11.46 f 4.3 6.33 f 2.3

70-79 29.07 f 3.4 32.00 f 3.4 12.96 f 3.7 10.38 f 4.9
80-89 26.30 f 4.8 29.75 f 3.01 14.04 f 3.8 11.12 f 3.6

The two subgroups did not significantly differ on
any of the psychological or radiological indices
(VBR 12.6 vs 13-3; MTS 28.2 vs 28.6; DCT 58.0
vs 60.8; DST 10.7 vs 9-2).
DISCUSSION
This investigation demonstrated for the first time
that patients with late paraphrenia had lateral
cerebral ventricles which were larger than those
of an age-matched normal control group. This
was associated with a mild but appreciable
impairment on a number of psychological tests.
Whilst the degree of ventricular enlargement was
much less than that reported in patients with
dementia (Jacoby and Levy, 1980; Naguib and
Levy, 1982), it was of a similar magnitude to that
seen in elderly depressives (Jacoby and Levy,
1980). Similar results have been found in younger
patients with schizophrenia (Johnstone et al.,
1976; Weinberger et al., 1979a, 1982; Tanaka et
al., 1981; Okasha and Madkour, 1982; Nasrallah
et al., 1982).
This finding appears to challenge the widely
held belief that structural brain abnormalities do
not occur in paraphrenia and raises a number of
interesting questions. Does ventricular enlarge-
ment precede or follow the development of the
condition? Is there a causal connection between
the two? What bearing does ventricular enlarge-
ment have on the type of clinical presentation
seen? Is the cognitive impairment a direct result
of ventricular enlargement or does it reflect some
other illness-related variables?
The answers to many of these questions must
remain inferential. The lack of correlation be-
tween ventricular enlargement and duration of
illness suggests that ventricular enlargement may
have preceded the development of late paraphre-
nia. Further supporting evidence for this view was
the lack of significant difference in VBR between
subjects with a relatively short history and those
who had been ill for more than two years. VBR
values were in fact normally distributed in the
patient group which, cannot be meaningfully
subdivided in terms of ventricular size.
The role of medication is somewhat unclear. Of
10 patients who were drug-free some showed
ventricular enlargement. The same is true for
younger patients with schizophrenia. Abnormal
ventricles were found by pneumoencephalogra-
phy in patients who had never received neurolep-
tics (Huber, 1957; Asano, 1967). More recently
Johnstone et al. (1976, 1978) using CT techniques
also found enlarged ventricles in patients who had
never received phenothiazines.
Institutionalization and its long-term effects
have been suggested as causes of ventricular
enlargement. The lack of correlation between
ventricular size and duration of illness refutes this
proposition in this patient group. Moreover,
Weinberger et al. (1979b) studying patients with
schizophrenia found that neither duration of
illness nor length of hospitalization correlated
with ventricular size.
Our own data and those reported in most
studies in schizophrenia, notably that of Weinber-
ger et al. (1982), support the notion that
ventricular enlargement may precede the de-
velopment of the psychosis both in young patients
and in late life. Large ventricles probably serve as
a non-specific risk factor for later development of
paraphrenia in vulnerable individuals. This is
consistent with the notion of a multifactorial
genetic-environmental continuum of liability
(Reich et al., 1972), with paraphrenics having a
smaller genetic loading as compared with schi-
zophrenics and requiring more environmental
events before manifesting the disorder (Naguib et
al., 1987). The additive effects of various
environmental events such as ventricular enlarge-
88 M . NAGUIB A N D R . LEVY
ment (which might be an expression of past or
present cerebral insult), prolonged social isola-
tion, longstanding sensory defects, superimposed
on an abnormal personality of paranoid or
schizoid type may lead to the psychosis becoming
overt for the first time late in life. This view is
supported by a report by Reveley et a / . (1984),
who studied schizophrenia in twins’ birth and
found that later age of onset was associated with a
negative family history and enlarged cerebral
ventricles. The latter, they suggested, may be just
one non-specific indicator of cerebral pathology
necessary to produce psychiatric illness in those
with a low genetic predisposition. Preexisting
cerebral abnormalities were also reported by Kay
and Roth (1961) and McClelland et al. (1966) in
relation to late paraphrenia. Furthermore, Davi-
son and Bagley (1969) who examined the role of
focal CNS lesions in producing psychosis pointed
out that there was a lapse of some six years (with
a range of 0-31 years) between the development
of the lesion and the onset of psychiatric
symptoms.
The evidence also suggested that the degree of
ventricular enlargement appeared to have n o
direct bearing on the presentation of the clinical
syndrome. There was no difference between
those with particularly large VBRs and the rest on
any of the clinical or psychological parameters.
This accords with the views of Nasrallah et al.
(1983) studying young and middle aged patients.
However, other investigators attempting to iden-
tify variables which appear to be differentially
associated with enlarged ventricles have reported
associations between increased ventricular size
and chronic schizophrenia, the presence of
neuropsychological impairment, negative symp-
toms, poor premorbid adjustment and poor
response to neuroleptic drugs (Johnstone et al.,
1978; Crow, 1980; Weinberger et al., 1980).
As in the studies of dementia (Jacoby and
Levy, 1980; Naguib and Levy, 1982a,b), we
found that the memory and orientation test
correlated with the greatest number of variables,
confirming its clinical value. The negative correla-
tions between GMS factors ‘depression’ and
‘retarded speech’ with scores on the memory and
orientation test confirm the observation that
depression andlor depressive symptoms which are
prominent features of paranoid disorders may
produce cognitive change. It seems likely that the
relationship between Digit Copying Test and the
GMS factor ‘visual hallucination’ is a chance
finding in a large matrix.
Patients with paraphrenia have historically
been considered to show little or no intellectual
deterioration. The finding of a significant cogni-
tive impairment amongst those in this study is
important and interesting. The significant rela-
tionship between measures of brain atrophy and
those of psychological impairment in the normal
control group and their gradual progression with
advancing age indicate that the two processes are
a feature of normal ageing (Barron et al., 1976;
Wood, 1982). The lack of such correlation in the
patient group may signify that other variables
such as psychotic experiences, hearing impair-
ment, medication, lack of motivation or other
related difficulties may account for more of the
variance in the patient group.
These results merit further investigation. Fu-
ture studies should exploit the greater resolution
of more advanced CT scanners. PET scanning
may provide valuable dynamic information about
cerebral function and magnetic resonance imag-
ing (MRI) may provide greater information about
possible changes in white matter. In the mean-
time a follow-up study is likely to yield useful
information about the prognostic significance of
the changes reported.
ACKNOWLEDGEMENTS
We would like to thank Dr Klaus Bergmann, Dr
George Stein and D r Marisa Silverman for
allowing us to study their patients. We are also
most grateful to D r Felix Post, Professors Alwyn
Lishman and Brice Pitt and Dr Robin Jacoby for
reading earlier drafts and making constructive
suggestions and the staff of the neuroradiology
department of the Maudsley Hospital for patient-
ly carrying out the scans. The work was supported
by a grant from the Special Health Authority of
the Bethlem Royal Hospital and the Maudsley
Hospital.
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