INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, VOL.

6 103-109 (1991)

LATE-ONSET PARANOIA: DISTINCT FROM

PARAPHRENIA?
ALASTAIR J. FLINT,* SANDRA L. R I F A T ~ AND M. ROBIN EASTWOOD$
*Assistant Professor of Psychiatry, The Toronto Hospital, Edith Cave11 Wing, 399 Bathurst Street, Toronto,
Ontario, MST 2.27. Canada
?Research Scientist, Section of Epidemiology and Biostatistics, Clarke Institute of Psychiatry, 250 College Street,
Toronto, Ontario, MST 1R8, Canada
$Professor of Psychiatry and Preventive Medicine and Biostatistics, Clarke Institute of Psychiatry, 250 College Street,
Toronto, Ontario, M5T lR8, Canada

SUMMARY
Using Kraepelin’s distinction between paraphrenia and paranoia, 2 1 patients with late paraphrenia were compared
with 12 with late-onset paranoia. The paranoia group had significantly more clinically unsuspected (silent) cerebral
infarction on CT brain scan and was less responsive to antipsychotic medication. The results suggest that cerebral
organicity, especially stroke, is an important risk factor for late-onset paranoia and may contribute to a relatively
poor prognosis.

KEY woaos-Late paraphrenia, paranoia, organic delusional syndrome, stroke, CT scan, prognosis.

Emil Kraepelin (1919) introduced the term para-
noia to describe a chronic illness characterized by
well-organized delusions, with an absence of hallu-
cinations, formal thought disorder, or personality
deterioration. He differentiated this from para-
phrenia, which, in addition to delusions, had hallu-
cinations, and paranoid dementia praecox which
followed a deteriorating course.
Since then, the nosology of paranoia and para-
phrenia has been controversial. ICD-9 (1978) dis-
tinguishes paranoia from paraphrenia and
paranoid schizophrenia, and employs Kraepelin’s
definition. DSM-111-R (APA, 1987), however, does
not include paraphrenia in its classification. Its
category Delusional Disorder, characterized by
well-systematized delusions, makes allowance for
the presence of non-prominent hallucinations,
thereby blurring the boundary between Kraepelin’s
concepts of paranoia and paraphrenia.
Available evidence suggests that chronic, non-
hallucinatory, deluded states, although rare, d o
exist and are distinct from schizophrenia (Kendler,
1980, 1982; Kendler and Tsuang. 1981; Winokur,
1977). However, the nosological status of para-
phrenia is less certain. Mayer-Gross (1932) fol-
lowed Kraepelin’s original group of paraphrenics
Requests for reprints to first author
and found that 38% eventually deteriorated to
schizophrenia with the development of prominent
thought disorder and personality disintegration.
After that, the concept of paraphrenia fell into dis-
favour until revived by Roth (1955) to describe a
group of elderly individuals with what he con-
sidered to be late-onset schizophrenia. Whether
paraphrenia and late-onset schizophrenia are
synonymous remains a matter of debate. Some
authors believe that late paraphrenia is schizo-
phrenia (Graham, 1982), others suggest that the
two disorders are different yet lie on a continuum
(Munro, 1982), while a third group believes that
paraphrenia is heterogeneous, with only some
individuals meeting schizophrenia criteria (Fish,
1960; Holden, 1987).
A lack of diagnostic criteria has also contributed
to the controversial status of late paraphrenia.
Roth (l955), Kay and Roth (1961) and Post (1966)
considered the presence of hallucinations to be
optional, thereby failing to differentiate between
paranoia and paraphrenia. In fact, 11-20% of their
cases did not have hallucinations. Recent studies
of late paraphrenia have continued to include sub-
jects with delusions but no hallucinations (Naguib
and Levy, 1987), despite the body of evidence sup-
porting paranoia as a distinct entity.

0885-623019 11020103-07$05.00 Received 26 October 1989

0 1991 by John Wiley & Sons, Ltd Accepted 12 January 1990.
104 A. J. FLINT, S. L. RIFAT, M . R. EASTWOOD
All previous studies of paranoia have specifically
excluded individuals 60 years of age or older.
Therefore, the purpose of this study was to examine
the concept of paranoia beginning in old age and
determine whether it differed from strictly defined
late paraphrenia.
METHOD
All new cases, 60 years of age and over, presenting
to the Clarke Institute of Psychiatry, a tertiary care
facility, between 1972 and 1987 and meeting ICD-8
diagnoses 295,297, and ICD-9 diagnoses 295,297,
298.3/4/8, were located through the Institute’s com-
puterized database. Charts were reviewed and
patients were admitted to the studv if thev fulfilled
following criteria:
the presence of delusions, with or without
hallucinations, of at least three months’
duration
no personality deterioration
absence of affective disorder (ICD-9 296,300.4)
absence of dementia or delirium (ICD-9 290-
294)
first onset of symptoms at age 60 years or over
no previous history of psychosis
absence of a history or physical examination
findings of neurological disorder, including
cerebrovascular disease
Those with delusions and hallucinations fulfilled
Kraepelin’s (1919) and ICD-9’s (297.2) definition
of paraphrenia, and those with delusions without
hallucinations met Kraepelin’s and ICD-9’s (297.1)
definition of paranoia and Kendler’s (1980) and
Winokur’s (1977) definition of delusional disorder.
The study population consisted of 33 patients
who were given routine physical examination,
blood work, neuropsychological testing, audio-
logical and ophthalmological assessment if hearing
and eyesight were impaired, and an EEG. Sixteen
subjects, seen from 1980 onwards, had a routine
CT brain scan. This reflected the growing interest
in structural brain changes of schizophrenic-like
illnesses, as well as the increased availability of CT
scans. Subjects who were scanned were not selected
on the basis of clinical findings. All scans were
obtained using the 8800 GE scanner. The EEG was
reported by a neurologist and scans by a neuro-
radiologist blind to the nature of the study.
Data on each case were collected as follows:
(a) Demographic andsocial data Age, sex, marital
status, social isolation (defined as having no
regular contact with at least one or more friends
or family members)
Clinical features Type and duration of
delusion, type of hallucination (if present),
presence of loosened associations, sensory
deficits, cerebrovascular risk factors (hyper-
tension, ischaemic heart disease, congestive
heart failure, cardiac arrhythmia, peripheral
vascular disease, carotid bruits)
Investigations EEG, CT brain scan
Treatment Dose (in mg chlorpromazine equi-
valents) and duration of antipsychotic medica-
tion, presence of dose-limiting side-effects,
presence of non-compliance, treatment
response
Response to treatment was defined as (1) full-
complete resolution of delusions without relapse
while on medication; (2) partial--either complete
resolution of delusions but with relapse while on
medication, or, improvement in, but incomplete
resolution of, delusions while on medication; ( 3 )
nil-no improvement in delusions while on medi-
cation, despite at least a one-month trial of anti-
psychotic at maximum tolerated dose.
Following the collection of data on each subject,
the sample was divided into two groups-those
with delusions and hallucinations (paraphrenia
group; N = 21) and those with delusions and no
hallucinations (paranoia group; N = 12).
Contrasts between groups on categorical vari-
ables were conducted using the chi-square pro-
cedure where the number of subjects was
sufficiently large and Fisher’s exact test where the
total number was less than 25. Contrasts between
groups on continuous variables (eg age, treatment
duration, treatment dose) were conducted using the
t-test for differences between group means.
Reported probability values from two-tailed tests
of significance and t-tests were conducted using
pooled variance estimates. All statistical tests were
carried out using the computer software Statistical
Package for Social Sciences (SPSS-X, 1986).
RESULTS
Total sample description
Characteristics of the total sample are shown in
Table 1.
Strikingly, of the 16 patients with CT scans, five
showed evidence of ‘silent’ (clinically unsuspected)
cerebral infarction. All affected patients had
 LATE-ONSET PARANOIA: DISTINCT FROM PARAPHRENIA? 10s

subcortical (mostly basal ganglia) or frontal lobe although there was a trend for the paraphrenics
infarctions, with one patient in addition having a to be younger, more often female, never married,
left parieto-occipital infarct. Twenty-one per cent and socially isolated. There were no significant
of the group had EEG abnormalities, usually non- differences on any of the clinical variables.
specific slowing. Of the 16 patients undergoing CT brain scan,
the paranoia group had significantly more cerebral
Table 1. Total sample description infarction (p = 0.003) and there was a trend to-
wards more EEG abnormalities 0, = 0.17).
N=33 '%
Paraphrenics responded to treatment more often
Demographickociul (p = 0.024), although there was no difference
Age ( y r P 73.1(9.5) between groups on other treatment variables.
Female 27 82 Within-group comparisons were made with regard
Currently married 6 18 to treatment response. Of the 21 paraphrenics, 18
Never married 7 21 responded to treatment. As expected, non-
Widowed 18 55 responders had shorter courses of treatment
Divorced 2 6
(p = 0.04) but did not differ from responders on
Socially isolated 17 52
Never married x isolated 5 29 other treatment variables or age. Five of the 12
Clinical features patients with paranoia responded, but could not
Delusions (persecutory) 33 100 be distinguished from the seven non-responders.
Delusions (other) 9 27
Duration of delusions (months)* 27.6(29.3)
Hallucinations 21 64 Contrast of subjects with and without brain
Loosened associations I 3 infarction
Visual impairment 11 33
Hearing impairment 14 42 Since the paranoia and paraphrenia groups dif-
Cerebrovascular risk factors 12 36
fered with regard to cerebral infarction, compar-
Investigations
Cerebral infarction? 5/16 31
ison of patients with and without infarction on CT
EEG abnormality 7 21 brain scan ( N = 16) was conducted (Table 3).
Treatment Patients with infarction were significantly less
Dose (CPZ equiva1ents);l 2 3 3 154) isolated (p = 0.005) and were more likely to have
Duration (months)* 10.2(15.5) married (p = 0.12).
Side-effects(dose-limiting) 19 58 There were trends in the predictable direction
Non-compliance 8 24 on cerebrovascular risk factors and EEG abnorma-
Response lities. Bearing in mind that dementia had been
Nil 10 31 excluded on the basis of neuropsychological test-
Partial 12 36
ing, mean Mini Mental State (Folstein et ul., 1975)
Full 11 33
~
scores, conducted routinely from 1980 onwards,
* Values represent means (standard deviations). were 26.3 in the infarction group and 27.4 in those
i Data based on 16 patients undergoing CT brain scan. without infarction. Thus, the presence of cerebral
infarction was not associated with significant cog-
Sixty-nine per cent of the group demonstrated ni tive impairment .
partial or full response to treatment. Treatment Response to treatment was significantly worse
duration varied, ranging from one month to 60 among those with infarction (p = 0.02), although
months, with a mean of 10.2 months. The treatment non-compliance and presence of side-effectsdid not
distribution for the group tends towards the shorter differ between groups. The infarction group
duration, since antipsychotic medication was not received significantly less antipsychotic (1 10 mg
persisted with if individuals did not show a chlorpromazine equivalents) than the patients
response over several months. without infarction (205 mg chlorpromazine equiva-
lents) (p = 0.05). Although comparison of treat-
Contrast qf paranoia and paruphreniu groups ment responders versus non-responders within the
cerebral infarction group was limited by the small
There were no statistically significant differences numbers, there were no differences in age or treat-
on demographic or social factors (Table 2) ment variables.
106 A. J . FLINT, S. L. RIFAT, M . R . EASTWOOD

Table 2. Contrast of paranoia and paraphrenia groups

Paranoia Paraphrenia p-Value
N = 12 N=21

Demographic/sociul
Age W * 75.3( 1 1.3) 71.8(8.2) 0.32
Female 8 19 0.22
Never married 1 6 0.35
Socially isolated 4 13 0.22
Clinicalfeatures
Delusions (persecutory) 12 21 1.OO
Delusions (other) 2 7 0.53
Duration of delusions (months)* 21.9(28.5) 30.8(29.9) 0.41
Hallucinations 0 21 <0.001
Loosened associations 0 1 1 .oo
Visual impairment 5 6 0.70
Hearing impairment 5 9 1 .00
Cerebrovascular risk factors 6 6 0.39
Investigations
Cerebral infarction? 414 1/12 0.003
EEG abnormality 5 2 0.17
Treatment
Dose (CPZ equivalents)* 250(203) 226( 122) 0.67
Duration (months)* 8.8(17.4) 11.1 (14.6) 0.69
Side-effects (dose-limiting) 6 13 0.76
Non-compliance 2 6 0.73
Response
Partiallfull 5 18 0.024
*Values represent means (standard deviations).
t Data based on 16 patients undergoing CT brain scan.

DISCUSSION in control populations of similar age (Roberts et

This study confirms that paranoia, as defined by
Kraepelin and others, can begin in old age, and
suggests that it differs from paraphrenia.
Two findings differentiate the two disorders-the
presence of clinically unsuspected cerebral infarc-
tion, as detected by CT brain scan, and treatment
response. The data suggest that these two findings
are related.
Even after excluding all patients with a history
and examination findings of neurological disorder,
3 1% of the sample scanned had evidence of cerebral
infarction. However, this finding was contributed
to by the presence of infarction in all patients with
paranoia, compared with only 8% of paraphrenics.
It is recognized that not all subjects underwent CT
brain scan, but even if the remainder of the para-
noia group had normal scans (which is unlikely
since those being scanned were unselected) the
prevalence in this group would still be 33%. This
compares with a 2% prevalence of silent infarction
al., 1988; Jacoby et al., 1980).
Most lesions were subcortical or in the frontal
lobes. This is consistent with previous findings that
lesions affecting limbic and subcortical structures
are associated with the highest frequency of
delusions (Davison, 1983; Cummings, 1985). How-
ever, since evidence of stroke was an exclusion
criteria for this study, there may have been a bias
towards excluding individuals with cortical infarc-
tion, which tends to be clinically apparent.
Although causality cannot be proven, the very
high frequency, and location, of infarction in the
paranoia group implies that cerebrovascular injury
may be an important risk factor for this disorder
in the elderly. This is consistent with previous
hypotheses on the development of paranoia in
younger populations. A number of authors have
commented on the apparently low genetic risk for
paranoia (Kendler, 1980;Watt, 1985) and have pro-
posed that other factors, especially cerebral organ-
icity, may play a significant aetiological role
 LATE-ONSET PARANOIA: DISTINCT FROM PARAPHRENIA? 107

Table 3. Contrast of subjects with and without brain infarction

Infarction No infarction p-Value
N=5 N = 11
Demographidsocial
Age (yr)* 82(7.2) 74(8.8) 0.10
Female 4 9 1.00
Never married 0 5 0.12
Socially isolated 0 9 0.005
Clinicalfeatures
Delusions (persecutory) 5 11 1.oo
Delusions (other) 0 4 0.25
Duration of delusions (months)* 24.6(27) 35.3(33) 0.54
Hallucinations 1 11 0.003
Loosened assocations 0 0 1.oo
Visual impairment 3 3 0.30
Hearing impairment 3 6 1 .oo
Cerebrovascular risk factors 4 3 0.11
In vestiga fions
Cerebral infarction 5 0 <0.001
EEG abnormality 3 2 0.25
Treatment
Dose (CPZ equivalents)* 1 lO(62.8) 205(90.7) 0.05
Duration (months)* 3.2(2.2) 10.9(10.9) 0.15
Side-effects (dose-limiting) 5 8 0.30
Non-compliance 0 3 0.30
Response
Partial/full 2 11 0.02
*Values represent means (standard deviations).

(Munro, 1988). In studies of broadly defined ‘late
paraphrenia’, up to 20% of subjects had evidence
of stroke (Kay and Roth, 1961; Post, 1966; Miller
and Lesser, 1988). Unfortunately, in all these
studies the presence of hallucinations was con-
sidered optional. As a result, it is not known how
many of the subjects in fact had paranoia, rather
than paraphrenia.
In previous studies of late paraphrenia, abnor-
mal premorbid personality, a tendency not to
marry, and prolonged social isolation have been
regarded as aetiologically important (Graham,
1982).In our study, all of those with cerebral infarc-
tion had married and none were isolated, whereas
only 55% of subjects without infarction had ever
married and 80% were socially isolated. The
paucity of social risk factors for the infarct group,
therefore, lends further support to the hypothesis
that stroke, when present, is a potent mechanism
in the pathognesis of late-onset paranoia. This con-
trasts with Kraepelin’s (1919) and Kay and Roth’s
(1961) formulation that the single greatest risk for
developing paranoia is a premorbid paranoid
personality.
For the overall sample, response to treatment
was similar to that found by Post (1966) and Rabins
et al. (1984). However, in this study, when groups
were compared, 58% of those with paranoia
showed no response to treatment compared with
only 14% of paraphrenics. Since there were no dif-
ferences between these groups in terms of age and
treatment variables, it is hypothesized that factors
intrinsic to the disorder led to worse treatment
response. The contribution of cerebral organicity
to poor prognosis is supported by the finding of
worse response in the infarction subgroup. Post
(1966), Leuchter and Spar (1985), and Holden
(1987) all found a significantly worse outcome in
late-onset paranoid patients with organicity com-
pared to those without.
One possible reason why cerebral infarction
might have contributed to worse response is sug-
gested by the difference in neuroleptic dose between
the infarction and non-infarction subgroups. Maxi-
mum dose of antipsychotic medication was dictated
by either remission of symptoms or the production
of dose-limiting side-effects. Although the fre-
quency of troublesome side-effects was the same
108 A. J. FLINT, S. L. RIFAT, M . R. EASTWOOD
in both groups, they first appeared at a significantly
lower dose in the infarction group, implying that
the brains of these people were more vulnerable
to the unwanted effects of medication. Had this
group tolerated a higher dose of antipsychotic
medication they might well have shown greater
symptomatic improvement.
However, other, as yet unknown, factors must
also have contributed to worse response in para-
noia, since, overall, both paranoia and paraphrenia
groups tolerated equivalent doses of medication
with similar frequencies of side-effects.
Although this study was retrospective, the
patients are comparable to those described in pre-
vious studies of late-onset ‘paraphrenia’. In
addition, data on each patient were collected and
tabulated before contrasts between groups were
made, thereby effectively making the procedure
blind. One-half of the patient population did not
have CT scans, and although those scanned were
not a selected group, the numbers for analysis were
small. Therefore, our conclusions about the role
of organicity in late-onset paranoia are tentative
and preliminary. However, the study does
emphasize that paranoia in the elderly can arise
in association with cerebral infarction without con-
comitant cognitive impairment. In this context,
cases would be more correctly diagnosed as
‘organic delusional syndrome’ (APA, 1987).
ACKNOWLEDGEMENTS
We would like to thank Dr Ken Shulman, Dr
Adrian Grek and Dr Sandra Black for their helpful
comments on the manuscript, and Sheila Hood and
Rav Sandhu for their secretarial assistance.
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