Organic delusions: phenomenology, anatomical correlations, and review.

J L Cummings BJP 1985, 146:184-197. Access the most recent version at doi: 10.1192/bjp.146.2.184

Reprints/ permissions You can respond to this article at Downloaded from

To obtain reprints or permission to reproduce material from this paper, please write to permissions@rcpsych.ac.uk http://bjp.rcpsych.org/cgi/eletter-submit/146/2/184 http://bjp.rcpsych.org/ on September 23, 2011 Published by The Royal College of Psychiatrists

To subscribe to The British Journal of Psychiatry go to: http://bjp.rcpsych.org/site/subscriptions/

British Journal of Psychiatry (1985), 146, 184197

Organic Delusions:
Phenomenology, Anatomical Correlations, and Review
JEFFREYL. CUMMINGS Summary: metabolic Organic delusions are common, but have received little systematic processes and in disorders affecting the limbic system and basal

study. Review of the literature reveals that they occur most commonly in toxic ganglia. A prospective study of 20 consecutive patients with organic delusions revealed four general types of false beliefs: simple persecutory delusions, complex persecutory delusions, grandiose delusions, and those associated with
specific neurological defects (anosognosia, reduplicative paramnesia). Simple delusions responded best to treatment, and complex delusions were more resistent. Acting on delusional beliefs was not unusual, and treatment of the delusions was an important aspect of management of the patient.
Delusions occur in the course of a wide variety of disorders that disturb brain function; false beliefs may be the sole manifestation of central nervous system (CNS) dysfunction or they may co-exist with dementia, delirium, or hallucinations. Although the occurrence of delusions in neurological disor ders is well known, their characteristics have
received little systematic study. Predisposing fac tors, natural history, response to therapy and the

Psychoses with delusional beliefs are particularly common among the extrapyramidal disorders in cluding Huntington's disease, Wilson's disease, Parkinson's disease, Sydenham's chorea, idiopathic calcification of the basal ganglia, and the spinocerebellar degenerations. Dewhurst et a! (1969) reported that 50% of patients with Huntington's disease were deluded at the time of admission. Bromberg (1930) and Fairweather
(1947) noted a high incidence of delusions in

anatomical correlates of delusional syndromes remain largely unknown. This report presents preliminary conclusions based on a review of the literature and findings in 20 prospectively studied patients. Correlations between the anatomical loci of lesions and the characteristics of the associated delusions are emphasised. The literature review is presented first, followed by descriptive information concerning the 20 delusional patients. Five repre sentative cases are described, and a tentative pathophysiology of paranoid delusions proposed.

Literature Review
Table I presents a tabulation of organic disorders

in which delusions have been recorded. A large number of metabolic disturbances, including sys temic illnesses, endocrinopathies, deficiency states, inflammatory disorders, and drug and metal intoxi cations have induced delusional syndromes; in
many cases the delusions were one manifestation of

an acute confusional state but in a few, were the presenting or sole indication of the disorder. They were commonly persecutory and, where recovery was commented on, they usually resolved when the underlying condition was recognised and treated. A diverse group of structural disorders of the central nervous system (CNS) has also been associated with organic delusions (Table I).

patients with post-encephalitic parkinsonism, and Francis & Freeman (1984) and Cummings et a! (1983) described an association between schizo phrenia-like illnesses with delusions and idiopathic basal ganglia calcification. Epileptic foci located in the temporal-limbic regions produce schizophrenia-like psychoses (Slater et al, 1963; Toone, 1981; Trimble, 1981) and within this group psychotic behaviour is more common among patients with left-sided lesions. Delusions are also common in non-epileptic struc tural disorders affecting the limbic system. Herpes encephalitis has a predilection for involvement of the temporal lobe, and frequently presents as an organic psychosis with delusions (Rennick et a!, 1973). Hillbom (1960) found that post-traumatic psychoses were also highly correlated with tempo ral lobe injuries and that left temporal lesions were more likely to be associated with psychoses than right-sided damage. Neoplasms and cerebrovascu lar lesions reported to induce delusions have likewise tended to involve temporal lobe or subcortical structures (White & Cobb, 1955; Gal, 1958; Vaillant, 1965; Trimble & Cummings, 1981; Levine & Finklestein, 1982; Peroutka eta!, 1982). Delusions are less common among disorders such as Alzheimer's disease and Pick's disease, where
184

ORGANIC DELUSIONS:

PHENOMENOLOGY, ANATOMICAL CORRELATIONS, AND REWEW

TABLE I

185

Principal organic disturbances producing Disorder affecting CNS function References

delusions References

Disorder affecting CNS function

Metabolic Disorders Systemic illness uraemia dialysis dementia hepatic encephalopathy pancreatic encephalopathy hyponatraemia porphyria
hypercalcaemia

CNS disorders Extrapyramidal disturbances

Schreiner,959 1 idiopathic Parkinson's

Burks et al, 1976;

Chokroverty et al, 1976

disease post-encephalitic Parkinson's disease Huntington's disease Syndenham's chorea Wilson's disease spinocerebellar degenerations idiopathic basal ganglia calcification carbon monoxide poisoning

Crow ci al, 1970; Mindham, 1970

Bromberg, 1930; Fairweather,947 1

Read etal, 1967 Rothermich & von Haam,

1941 Burnell Foster, & 1972

Roth, 1945
Weizmanetal, 1979

Dewhurst ci al, 1969; McHugh & Folstein,

1975 Hammes, 1922 Beard,1959; Gysin& Cooke, 1950 Keddie,1969 Francis,979; 1 Cummings etal, 1983

hypoglycemia Endocrinopathies Addison'sdisease

Cushing's disease hypothyroidism hyperthyroidism hypoparathyroidism hyperparathyroidism

Nash, 1983 Cleghorn, 1951; Gorman & Wortis, 1947 Spillane, 1951 Asher. 1949; Sanders, 1962 Bursten, 1961 Green & Swanson, 1941 Fitz & Hallman, 1952
Wijsenbecketal, 1964; Hanna, 1970

Davison & Bagley, 1969 Rennick ci al, 1975 Keddie, 1965; Still, 1958 Raymond & Williams. 1948
Goldhammer ci al, 1972

CNSinfections
herpes encephalitis other acute viral
encephalitides

panhypopituitarism
Deficiencytates s Thiamine(Wernicke Korsokoff syndrome) B12 folate

niacin Inflammatory disorders systemic lupus erythematosus temporal arteritis Drug intoxication
antiparkinsonian drugs

Cutting, 1978a Bowman, 1935; Smith 1960 Strachan & Henderson, 1967 Sydenstrtcker, 1948 MacNeill ci al, 1976; Stern &

Jakob-Creutzfeldt disease cerebral malaria syphilis trypanosomiasis Diseases affecting myelin multiple sclerosis metachromatic leucodystrophy adrenoleukodystrophy
Marchiafava-Bignami

Blocker ci al, 1968 Dewhurst, 1969 Nash, 1983 Geocaris, 1957;

Langworthycial, 1941

Robbins,1960
Grant & McMenemey, 1966 Goodwin, 1971; Hausner, 1980; Moskovitz etal, 1978;
Serby,1978 antituberculous drugs antimalarials, anticonvulsants anticholinergics, antidepressants Nash, 1983 antihypertensive drugs Remick etal, 1981; Paykel etal, 1982

Be.ttsci al, 1968; Muller

cial, 1969 Powell ci al, 1975

disease Miscellaneous
hydrocephalus

Freeman, 1980
Price & Tucker, 1964;
Rice& Gendelman, 1973; Reveley& Reveley,1983

hallucinogens

Cohen & Ditmar, 1963; Ames, 1958; Jefferson & Marshall, 1981 Beamish & Kiloh. 1960; Askevold, 1959 Adler ci al, 1980 Adler ci al, 1980 Nash, 1983 Perkins, 1955 Vroom&Greer,1972 Schenk & Stolk, 1967 Abd el Naby & Hassanein,
1965 Grunfeld & Hinostroza, 1964

temporal lobe epilepsy

post-traumatic encephalopathy neoplasms (temporal lobe,

Slater ci al, 1965; Toone,

1981;Trimble, 981 1

Hillbom, 1960; Nasrallah

cial, 1981

Miscellaneous drugs amphetamines cimetidine disulfiram corticosteroids, benzodiazepines, digitalis

deep hemispheric) cerebrovascular disease

Gal, 1958; White & Cobb, 1955 Levine & Finkelstein, 1982;Vaillant, 1965;

Trimble& Cummings,
Alzheimer's disease Pick's disease Leber's hereditary optic
atrophy, cerebral lipido

pentazocine
bromide

Metal toxicity mercury arsenic manganese

thallium

1981, Peroutka ci al, 1982 Goodman, 1953; Larson etal, 1963 Bouton, 1940; Malamud & Boyd, 1944)

sis, Niemann-Pick's disease, cerebral anoxia,

phenylketonuria

Davison & Bagley, 1969

186

JEFFREY L. CUMMINGS
TABLE II

Specific delusions and their reported organic causes Delusion Reported etiology Reference Thisreport

Schneiderianfirst-rank
symptoms (delusions of

Metabolic disorders
hepatic encephalopathy hypothyroidism

thought control)

DeFine Olivenus & Roder, 1970

This report

CNS disorders idiopathic basal ganglia calcification post-traumatic encephalopathy temporal lobe neoplasm post-encephalitic parkinsonism temporal lobe epilepsy encephalitis cerebrovascular disease (limbic)
hydrocephalus

Nasrallahci al, 1981

Gal, 1958
Bromberg, 1930; Menninger, 1926

Slatereial, 1963
Misra& Hay, 1970

Trimble & Cummings, 1981 Reveley & Reveley, 1983

Capgras syndrome

Systemic illnesses B12deficiency hepatic encephalopathy pneumonia, malnutrition, diabetic encephalopathy

hypothyroidism pseudohypoparathyroidism

Zuckereial, 1981 This report; Pies, 1982 MacCallum, 1973 Madakusira & Hall, 1981
Hayeial, 1974

CNS disorders intracerebral hemorrhage post-traumatic encephalopathy right hemisphere dysfunction

Hayman & Abrams, 1977 Alexander ci al, 1979; Weston & Whitlock, 1971
Quinn, 1981

temporallobeepilepsy,
post-encephalitic parkinsonism, following varicella encephalitis migraine Frgoli syndrome
lntcrmctamorphosis syndrome Delusional ealousy j (Othello syndrome) temporallobeepilepsy
cerebral dysrhythmia

Chawla & Virmani, 1977 Rudnick, 1982 MacCallum. 1975

Christodoulou, 1976

Huntington'sisease d encephalitis

Malliaras et al, 1978 This report Keddie, 1965

Shepherd, 1961

Delusions ofinfestation Lycanthropy

(werewolfism)
Heutoscopy(thedouble:

CNS neoplasms. Alzheimer's disease, multiple sclerosis, epilepsy Parkinson's disease, general paresis, drug intoxication B12an iron deficiency toxic psychoses LSD intoxication, primary degenerative dementia migraine toxic psychoses. encephalitis, post-traumatic encephalopathy, intracranial hemorrhage

Mooney, 1965 Pope, 1970

Wilson, 1952

Surawicz & Banta. 1975 Damas Mora ci al, 1980; Christodoulou, 1978 Damas Mora ci al, 1980 Lovett Doust & Christie. 1978

doppelganger) de Clerambault's syndrome

toxic psychosis epilepsy mcningioma

pathological changesprimarilynvolve i thecerebral neocortex. Larson eta! (1963) found that only 18% of 377 Alzheimer's disease patients manifested delusions, and these are uncommon in the course of Pick's disease (Bouton, 1940; Malamud & Boyd, 1940). Thus, delusions are a more conspicuous feature of disorders associated with limbic and subcortical dysfunction and there is a tendency for
left-sided lesions to produce schizophrenia-like

illnesses more frequently than right-sided injuries. Davison & Bagely (1969), in their extensive review,

also concluded that schizophrenia-like illnesses with hallucinations and delusions were more com mon among patients with temporal-limbic or diencephalic dysfunction. Table II presents specific types of delusional beliefs that have been reported in association with organic conditions. These specific delusions show the same association with toxic-metabolic processes and structural disorders affecting limbic and deep hemispheric regions that was observed for paranoid delusions in general. Thus, Schneiderian first-rank

ORGANIC DELUSIONS:

PHENOMENOLOGY, ANATOMICAL CORRELATIONS, AND REVIEW

187

symptoms
broadcasting,

involving

thought

insertion,

thought

TABLE III

and thought

blocking,

as well as delu

Organic causesof secondary mania

sions of external influence have been reported with hypothyroidism (De Fine Olivanus & Boder,

1970), with a variety of extrapyramidaldisorders,

and with limbic dysfunction produced by traumatic, hydrocephalalic, epileptic, and infectious processes. Capgras syndrome, the delusion that significant

people have been replaced by identical-appearing

imposters, has been observed in a number of organic psychoses including systemic illnesses such as vitamin B12 deficiency (Zucker et a!, 1981), hepatic encephalopathy (Pies, 1982), diabetes (MacCallum, 1973), hypothyroidism (Madakusira & Hal, 1981), and pseudohypoparathyroidism (Hay et a!, 1974). Focal CNS disorders producing the Capgras syndrome have more often involved the right than the left hemisphere. Alexander eta!, (1979) considered the combination of bilateral frontal and right temporal lobe lesions to be aetiologically significant, and Hayman & Abrams (1977) and Quinn (1981) also suggested that right hemispheric dysfunction was of primary impor tance in producing the Capgras syndrome. Two disorders that share features with the Capgras syndrome, the Frgolisyndrome (where the patient identifies his persecutors in several persons, the persecutor being accused of changing faces, like an actor), and intermetamorphosis syndrome (the delusion that people have taken on the physical appearance of others) have been observed in epileptic disorders (Christodoulou, 1976; Milliaras eta!, 1978). In most cases, bilateral EEG abnormal ities were present. Delusions of infestation, lycanthropy (were wolfism), heutoscopy (the false belief that one has a double), and the de Clerambault syndrome (erotomania or the delusional belief that one is secretly loved by another) have been reported in a small number of patients with toxic-metabolic, epileptic, or structural CNS disorders (Christodoulou, 1978; Damas Mora et a!, 1980; Lovett Doust & Christie, 1978; Pope, 1970; Surawicz & Banta, 1975; Wilson, 1952). Delusional jealousy (delusions concerning infidelity of one's spouse or the Othello syndrome) may be one of a number of manifestations of paranoid psychosis, or may occur as a monosymptomatic delusional belief. It has been reported in patients with metabolic disturbances and in a variety of CNS disorders including extrapyramidal syndromes, neoplasms, Alzheimer's disease, encephalitis, multiple sclero sis, and epilepsy (Keddie, 1965; Mooney, 1965; Shepherd, 1961).

CNS disorders Neoplasms hypothalamic teratoma parasagittal meningioma diencephalic glioma craniopharyngioma brainstem tumour metastatic tumours subtemporal bone tumour Extrapyramidal syndromes Huntington's disease Postencephalitic Parkinson's
disease

Alpers, 1937 Oppler, 1950 Stern & Dancey, 1942 Malamud, 1967 Oyewumi & Lapierre, 1981 Jamieson & Wells, 1979 Bourgeois & Campagne, 1967 McHugh & Folstein, 1975
Bromberg, 1930

Wilson's disease infections general paresis viral encephalitis Miscellaneous subarachnoid haemorrhage
and temporal lobe injury

Pandy ci a!, 1981 Mapelli & Bellelli, 1982 Steinberg et al, 1972; Weisert Hendrie, 1977

Rosenbaum & Barry, 1975;

Cohen& Niska
post-traumatic encephalopathy temporal lobe epilepsy Pick's disease
Kleine-Levin syndrome

Hillbom & Kaila, 1951 for-Henry, 1969 Neumann, 1949

Jeffries & Lefebvre, 1973 Cameron & Landau, 1980

Klinefelter's syndrome
hemidecorticectomy
trauma

Forrest, 1982 Cohn eta!, 1977

Jampala & Arams, 1983

stroke multiple sclerosis

Drugs levodopa

Kemp eta!, 1977 Lin & Ziegler, 1976; Ryback & Schwab, 1971
Waters& Lapierre, 981 1

sympathomimetics, steroids, isoniazid, procarbazine. bromide, stimulants (cocaine), amphetamines, bromocriptine procyclidine hydralazine phencyclidine cimetidine baclofen Systemic Conditions uraemia and haemodialysis dialysis dementia hyperthyroidism pellagra carcinoid syndrome B12deficiency

Krauthammer & Klerman,

1978

McEvoy, 1981; Jeffersonnd a Vlissides etal,1978; Brook &

Cookson, 1978 Coid & Strang, 1982 Paykel ci a!, 1982 Rosen. 1977 Hubain eta!, 1982 Arnold et a!, 1980 Cooper. 1967 Jack eta!, 1983 Jefferson & Marshall, 1981; Villani & Weitzel. 1979
Spivak& Jackson, 1977 Lehmann, 1966

Goggans. 1983

Grandiose delusions occur primarily in organic psychosyndromes associated with secondary mania (Table III). Disorders of the CNS recorded as

188
TABLE IV

JEFFREY L. CUMMINGS
Delusions associated with neurological deficits

DelusionsAetiologyReferenceDenial

of blindnessBilateral 1957;(Anton's
syndrome)cerebral Peripheral

posteriorBergman,
artery blindness &

occlusion 1945Denial with dementia or

MacKenzie, 1957
Redlich &

Dorsey,

deliriumSymonds 1978hemiparesis(parietal insultCutting, ofHemispheric lobe)ReduplicationHemispheric

eta!,of insultWeinstein lobe)1954ReduplicativePost-traumaticBenson body(parietal eta!,paramnesiaencephalopathy Fisher, Cerebrovascular disease1976; 1982

producing

manic

behaviour

tend

to involve

the

perihypothalamic areas (hypothalamic, diencephalic glioma, post-encephalitic

sonism), basal ganglia (Huntington's

teratoma, parkin
Wil

disease,

son's disease), or the frontal lobe (general paresis, Pick's disease, meningiomata, trauma). The few reported lateralised lesions associated with secon dary mania have nearly all involved diencephalic structures on the right side (Cohen & Niska, 1980; Forrest, 1982; Flor-Henry, 1969; Jamieson & Wells, 1979; Oppler, 1950; Rosenbaum & Barry, 1975; Stern & Dancey, 1942). Reports of metabolic and toxic causes of secondary mania have included agents that modify monoaminergic neurotransmit ter function (levodopa, sympathomimetics, isonia zid, stimulants) as well as uraemia, hyperthyroi dism, pellagra, B12 deficiency and the carcinoid syndrome Table IV presents organic delusions uniquely associated with specific neurological defects. De
nial of illness is a delusional Denial syndrome in which and the of

on the involved side (Weinstein eta!, 1954). Denial of weakness and delusional limb reduplication have been associated primarily with parietal lobe lesions. A final neurological delusion is reduplicative par amnesia, a state in which the patient believes that he is simultaneously in two geographical locations; the delusion is usually transient, occurs during recovery from an acute cerebral lesion, and has been associated with right parietal or combined right parietal and bilateral frontal dysfunction (Benson eta!, 1976; Fisher, 1982). Tables I to IV present lists of structural and metabolic disorders associated with organic delu sions, and demonstrate the variety of organic processes producing delusional psychosyndromes. Such lists, however, are not exhaustive; are likely to contain an unrepresentative number of cases with dramatic clinical presentations; and are based on case descriptions that often lack essential clinical information. In many reports, descriptions of the delusions were inadequate, and there was often no discussion of a possible history of psychiatric disturbance, predisposing genetic background, re sponse to treatment, or associated clinical features. A prospective study of patients with organic delusions was therefore undertaken to examine these issues.

Prospective

Study

Definitions and se!ection of patients The term organic' used as a generic term to was signify disordersssociated a withidentifiable struc tural changes in the brain (degenerative disorders, trauma, tumours, strokes, etc.) or brain dysfunc tion secondary to systemic toxic and metabolic disturbances. This usage is consistent with DSM III (1980) terminology, but has the unfortunate impli cation that idiopathic psychiatric disorders are not organically mediated, in spite of considerable pharmacological and clinical evidence to the con trary. Despite this limitation, the term organic' has practical utility when understood to denote tradi tionally recognised structural and metabolic disor ders affecting CNS function. Delusions were defined in accordance with DSM III (1980), and also met the more specific criteria proposed by Jaspers (1963) as false beliefs that: (a) are firmly held; (b) are impervious to incontrovert ible proof to the contrary; (c) are impossible or are not endorsed by members of the individual's culture or sub-culture. Criteria were chosen to limit the prospective portion of the study to patients whose delusions could be confidently attributed to their brain

patient
obvious

will not admit to physical deficits despite

dysfunction. of blindness

hemiparesis are the most well-established syn dromes. Most patients with denial of blindness (Anton's syndrome) have cerebral blindness secon dary to bilateral occipital lobe lesions (Bergman, 1957; Symonds & MacKenzie, 1957), but blindness produced by lesions in the anterior visual pathways may be denied by patients who are demented or in acute confusional states (Redlich & Dorsey, 1945). Denial of hemiparesis is most commonly described with right hemispheric lesions, but may occur with lesions in either hemisphere (Cutting, 1978b). A related phenomenon is delusional reduplication of body parts, wherein a patient with unilateral weakness believes that multiple limbs are present

ORGANIC DELUSIONS:

PHENOMENOLOGY, ANATOMICAL CORRELATIONS, AND REVIEW

TABLE V

189

Clinical characteristics of twenty patients with organic delusions Patient 1 2 3 4 5 6 7 8 9 10 11 Age 64 71 75 83 77 86 74 60 64 64 62 Sex F M M F M M M M M M M MMSE Score' 9 13 9 14 14 13 17 28 28 26 19 Hallucinations Diagnosis Delusions Persecutory, simple

None None None None None

Visual

Alzheimer's disease Alzheimer's disease Alzheimer's disease Alzheimer's disease Multi-infarct dementia Multi-infarct dementia Multi-infarct dementia Hepatic encephalopathy Idiopathic Parkinson's disease Post-encephalitic Parkinson's disease Post-traumatic encephal opathy with partial
complexseizuresleft (

Persecutory, Persecutory, jealousy Persecutory, Persecutory,

transient simple; delusional simple simple

None None
None Auditory Auditory

Persecutory, simple Persecutory, simple Persecutory; ideas of reference;

first rank symptoms Persecutory, rigidly systematized Persecutory, first rank symptoms Persecutory; first rank symptoms

12

34

17

None

13
14

56
78

M
M

30
28

Auditory Visual

sided EEG abnormalities) Post-traumatic encephal opathy (right temporo parietal injury) Idiopathic calcification of the basal ganglia Chromophobe adenoma
with partial complex

Persecutory complex; reduplicative paramnesia Persecutory complex; first-rank

symptoms Persecutory; delusional jealousy

seizures (bilateral EEG

15 16 17 18 19 20 69 59 59 40 69 68 F M M M M M 24 None None Auditory Auditory None abnormalities) Hepaticencephalopathy Huntington'sisease d Huntington'sisease d Status-post encephalitis Multi-infarct dementia with bilateral

23

Refused
24 7

Capgras syndrome Delusional jealousy Grandiose (with hypomania) Grandiose (with mania)
Denialofblindness

None

Left-hemispheric infarction

Denial of hemiparesis and aphasia

*MMSE score mini-mental state examination score (Folstein eta!, 1975).

dysfunction. All patients first experienced delu

sions or other evidence of psychosis simultaneously with, or after the onset of, an identified disorder

affecting brain function. All patients were free of

any past history of psychiatric disturbance and a family history of neuropsychiatric illness was

The first 20 consecutive patients referred for neurobehavioural evaluation, and meeting the above stipulations, formed the study group. Each subject's mental state was evaluated by means of an interview and mental status examination, and was quantitatively assessed with the Mini-Mental State

present only in the three individuals suffering from

inherited neurobehavioural disorders (two with Huntington's disease and one with idiopathic calcification of the basal ganglia). In those patients

Examination (MMSE) (Folstein et a!, 1975). Char

acteristics of the delusions, including complexity, extension, duration, and response to treatment were carefully explored with the patient and, when

with dementia or amnesia, delusions were distin guished from confabulation by requiring that
endorsement of the false beliefs be stable for several days. Hallucinations were either entirely absent or comprised only a minor part of the clinical

possible, with a family member. Patients were

studied with clinical, laboratory, and radiological procedures to ensure the accuracy of clinical

diagnosis. Patients identified as suffering from

dementia of the Alzheimer's type met DSM III criteria proposed by

symptomatology.
screened

Each

patient
and those

was carefully
exhibiting a

(1980) criteria for primary degenerative dementia,

as well as the more stringent tia was diagnosed

for depression

depressed
neurovegetative

affect,

depressed

mood,

or

Cummings & Benson (1983); multi-infarct demen

on the basis of appropriate

signs of depression

were excluded.

190

JEFFREY L. CUMMINGS

historical and physical findings and of a high score

dementia

(Cases 57).The average MMSE score

on the Hachinski Ischaemia Scale (Hachinski et a!,

1975; Rosen
patients had

for the group with simple delusions was 12.7 (range

et a!, 1980); Huntington's

choreiform movements,

disease

917). patients were in the early or mid-phases All

of their dementing illnesses; no patients were observed who showed evidence of delusions in the
late stages of dementia. The four patients with

intellectual

impairment, and a family history of similar distur bances; idiopathic Parkinson's disease was identi fled by tremor, rigidity, and bradykinesia in the absence of neuroleptic treatment, and post-en cephalitic parkinsonism was indicated by a history of encephalitis, early onset of parkinsonian fea tures, and asymmetric neurological signs; the
patient with idiopathic calcification of the basal

Alzheimer's disease represented 15% of patients with dementia of the Alzheimer type examined during the period of study; the three patients with multi-infarct dementia represented 27% of patients
with vascular dementia seen during the same

period.
Complex delusions occurred in patients with hepatic encephalopathy (Case 8); Parkinson's dis ease (Cases 9, 10), post-traumatic encephalopathy

ganglia serum
patients

had

radiological and

evidence

of extensive levels;
appearance

intracranial calcification, in the presence of normal

calcium
had

phosphorus
of sudden

stroke
of

a history

(Cases 11,12), idiopathic calcification of the basal

ganglia (Case 13), and after surgery for a

neurological deficits and findings on computerised tomography (CT) consistent with hemispheric in farction; post-traumatic and post-neurosurgical
patients had the appropriate historical antecedents;

chromophobe

adenoma (Case 14). Patients with

these complex persecutory beliefs had an average MMSE score of 25 (range 1730).

and hepatic encephalopathy was identified by appropriate laboratory evaluations showing hepatic dysfunction.

Schneiderian first-rank symptoms were noted in

patients with hepatic encephalopathy post-encephalitic Parkinson's disease (Case 8), (Case 10),

Results
The principal clinical features of the patients with organic delusions are summarised in Table V. and five cases illustrating variations of organic delusions are described below. The average age of the
patients at the time of onset of the delusions was 63.7 years. The mean MMSE score was 17; seven

post-traumatic
idiopathic

encephalopathy

(Case 11), and

calcification

of the basal ganglia (Case

13). Delusional monosymptomatic

jealousy occurred as a delusion in one patient with

Huntington's disease (Case 6), and Capgras syn drome was the major delusional belief present in Case 15 with hepatic encephalopathy. Two patients with complex delusions (one with post-traumatic

patients had MMSE scores above 23 (the cut-off value for normal performance) and 12 scored in the impaired range (1 patient refused to answer the MMSE questions). Five patients had auditory hallucinations and two had visual hallucinations. Four general types of delusions were observed in the study population: (1) simple persecutory delu sions, (2) complex persecutory delusions, (3) grandiose delusions, and (4) delusions related to specific neurological deficits. Simple persecutory delusions consisted of elementary, loosely struc tured, usually transient beliefs, such as believing that possessions or money were being stolen or that one's spouse was unfaithful. Complex delusions were characterised by a more complicated and intri cate structure, rigidity, and stability and were sup ported by substantial, though distorted, confirm atory' observations. Schneiderian first-rank symp toms of schizophrenia (Hamilton, 1976) and mono symptomatic delusions such as Capgras syndrome were included among the complex delusions. Simple delusions were encountered in patients

encephalopathy

and one with a chromophobe

adenoma) had partial complex seizures as a result of their brain injuries. In both cases, seizures were present for several years before psychiatric symp toms appeared. Grandiose delusions were observed

only in patients with secondary mania including one with Huntington's disease (Case 17) and one who
had had encephalitis (Case 18).

Delusions associated with specific neurological

conditions included reduplicative paramnesia in one patient with post-traumatic encephalopathy (Case 12), denial of blindness in a patient with bilateral occipital lobe infarctions (Case 19); and

denial of hemiparesis and aphasia in a patient with

an acute left hemispheric infarction (Case 20). Action on the delusional beliefs was not uncom mon. Several patients began striking out at spouses they believed to be unfaithful, others telephoned police that they were being watched or threatened,

and some adopted exaggerated security measures.

Complex delusions were most likely to lead to

misguided actions, but even simple delusions were

disruptive to family or nursing home routines. Response of the delusional beliefs to treatment was

suffering from dementia of the Alzheimer type (Cases 14) and in patients with multi-infarct

ORGANIC DELUSIONS:

PHENOMENOLOGY, ANATOMICAL CORRELATIONS, AND REVIEW

191

variable. Simple delusions usually improved after treatment with low doses of neuroleptic drugs and both patients with hepatic encephalopathy im
proved as their metabolic disturbances resolved. One patient with post-traumatic encephalopathy,

Though no treatment of the delusions was instituted,

the false beliefs spontaneously diminished after several

months.
Case 9: Parkinson's disease and levodopa therapy with at

one

with delusions

following

removal

of a

complex delusions.
This patient had the onset of parkinsonian symptoms

chromophobe Huntington's

adenoma, and one with disease all benefited from treatment

with neuroleptic agents. One patient with post

traumatic encephalopathy, one with post-encepha litic parkinsonism, and one with idiopathic calcification of the basal ganglia showed little response to neuroleptics. One patient (Case 12) with post-traumatic psychosis and reduplicative paramnesia had a dramatic and rapid spontaneous recovery, several months after the accident that initiated his psychotic behaviour. Of the two patients with secondary mania, one failed to improve with either neuroleptics or lithium, and

the age of 49. Complete neurological evaluation was unrevealing, and his condition was diagnosed as
idiopathic Parkinson's disease. Tremor, rigidity and bradykinesia progressed, and after two years, he was

begun on levodopa. He remained ambulatory and mdc pendent, with increasing doses of levodopa, but his symptoms gradually worsened. At the age of 58, he became increasingly suspicious of business associates,
neighbours, and doctors. He thought that street lights

were focussed on him, that he was being followed, and that others were talking about him. He believed there was
a plot to steal his house and that his doctors were intentionally misleading him into thinking that he suffered from Parkinson's disease. There was no history of encephalitis or other neurological illness and no family history of neuropsychiatric disturbances. On examination

one left hospital before treatment could be started.

The individual with denial of blindness had had the syndrome for several years at the time of evalua tion, and did not improve during the period of observation. The patient with denial of hemiparesis

he was alert, attentive, and orientated.

Recent and

remote memory, calculations, and abstracting ability were intact. His language was unremarkable. He generated a

and aphasia had gradual spontaneous resolution of

the anosognosia, and recognised his remaining deficits several weeks after onset of his infarction. Case Reports
Case 1: Alzheimer's disease with simple delusions. This 64 year-old right-handed woman was referred for evaluation of progressive intellectual deterioration. Five years prior to admission, she became increasingly forget ful, got lost in familiar surroundings, and gradually lost the ability to care for herself. She had shown paranoid ideation early in the course of her illness and became increasingly suspicious of the motives of friends and family members. After transfer to a nursing home, she

word list of only eight animals in one minute (normal 12

18/minute) and had difficulty reproducing the three

dimensional aspects of complex constructions. His affect

was flattened and his psychomotor speed slowed. He achieved a score of 28/30 on the MMSE. Neurological

examination revealed poor convergence movements of

the eyes and a mask-like facies. He had slow, hypophonic speech and a tremor of the tongue. There was cogwheel rigidity of both upper limbs, a paucity of spontaneous

movement, stooped posture, and intermittent resting tremor of the arms. He was treated with thioridazine, but the delusions persisted.
Case 15: Hepatic encephalopathy with Capgras syndrome

This patient was a 69 year-old, right-handed woman, who became frankly delusional, believing that she was being had long history of alcohol abuse. Three years prior to pursued by men and that she was in imminent danger of admission, she developed ascites. pedal oedema, ataxia, being raped, robbed, or killed. She failed to recognise her and confusion. Hepatic encephalopathy was diagnosed, own reflection in mirrors and believed that that woman and she improved with a course of diuretics and low was following her and stealing her possessions. On protein diet. After discharge, she became convinced that examination, the patient was disorientated as to time and her husband had been replaced by an identical-appearing location. She had a fluent aphasia, with poor namingand imposter. She was begun on a low dose of haloperidol, mildly impaired comprehension. Moderate deficits in which led to resolution of the Capgras symptom. After calculation, abstraction, and constructions were evident, two years, she stopped the haloperidol, the Capgras and judgement was poor. She had limited insight into her delusion returned, and she was referred for further evaluation. situation and displayed no mood disturbance. She

achievedan MMSEscore of 9 and a HachinskiIschaemia Scalescore of 4 (consistentwith degenerative dementia).

There were no abnormalities on the basic neurological
examination or the general physical evaluation. An EEG

Except for the alcoholism, there was no history of

psychiatric illness and no family history of neuropsych iatric disturbance. On examination, the patient was alert and orientated to location but did not know the date. Her digit span was five forwards and three backwards. Language comprehension and repetition and confronta tion naming were normal. She named nine animals in one

revealed slowing of the background rhythm, while CT demonstrated moderate ventricular dilation and widening of the cortical sulci, Routine laboratory studies with assessments ofliver thyroid and functions werenormal. minute. Recent and remote memory were moderately

192
impaired. abstraction and she made minor and three-dimensional

JEFFREY L. CUMMINGS errors in addition, constructions. Her

demonstrated bilateral posterior cerebral artery infarc

tions and generalised cerebral atrophy.

MMSEscore was 24/30and her mood waseuthymic. She

believed that her husband had been replaced by a'series of imposters, who belonged to an organisation that was interested in confiscating her house and car. Her neuro logical examination revealed mildly increased limb tone,

Discussion
The 20 patients
sional beliefs in

reported
association

here manifested
with a variety

delu
of

diminished coordination, psychomotor slowing, and pos tural tremor. Laboratory studies showed decreased serum
albumin and elevated serum ammonia. Haloperidol was begun and the Capgras delusion promptly disappeared.

neurological disorders. Most of them had structural

CNS lesions, as would be expected referred to a neurological consultation for patients service, but

the review of the literature

demonstrates

that

After commencing a low-protein diet, she was maintained without neuroleptics with variable control of the delu sional beliefs.
Case 18: Huntington's disease with mania.

delusions also occur with many toxic and metabolic

disorders. Several observations were made that help to characterise organic delusions and to
distinguish them from delusions associated with idiopathic psychoses. Patients with more severe neuropsychological impairment showed simple,

This patient

recreationdirector, who had a gradualonset of

was a 59 year-old,

right-handed

former

choreiform movements nine years prior to admission. A few months before admission, he developed grandiose delusions, believing that he had special powers, could

loosely held, persecutory beliefs that were often

transient. Intellectual patients was indicated deterioration in these by MMSE scores in the

control the Federal Bureau of Investigation and several

armies, would sue his doctors for malpractice, and would go travelling with his (non-existent) girlfriend. He became increasingly euphoric, irritable, and aggressive, and required less sleep than usual. He had auditory hallucina tions of voices that guided his actions. The patient's mother and two sisters suffered from Huntington's disease, and there was anecdotal evidence suggesting that they had also had delusional beliefs. The patient was manic, angry, and uncooperative when formal mental status testing was attempted. Indirect observations revealed that he was disorientated as to year and location, but he learned the layout of the hospital ward and recognised hospital personnel. His neurological examina tion was characterised by severe dysarthria and prominent

abnormal range. Patients who showed complex, intricately structured delusions, had less cognitive
dilapidation and obtained higher scores on the MMSE. This inverse relationship suggests that cognitive integrity is a prerequisite for elaboration of complex delusional beliefs. The mean age of the study patients at the time of onset of delusions was 63.7 years, i.e. considerably older than expected for idiopathic psychoses of either the schizophrenic or manic-depressive type. Older age at onset may help to distinguish idiopathic from organic delusional

disorders.
This study sought to determine whether correla tions existed between the anatomical site of CNS involvement and characteristics of the associated delusions: certain preliminary conclusions appear to be justified. Dementia of the Alzheimer type affecting neocortical association areas and the hippocampus, and multi-infarct dementia with multi-focal hemisphere lesions produced the great est intellectual impairment, resulting in simple delusions that responded moderately well to treat ment with neuroleptics. Complex delusions oc curred in patients with extrapyramidal disorders or with traumatic, neoplastic or cerebrovascular le sions involving subcortical nuclei (basal ganglia, thalamus, rostral brainstem) or the limbic system. These complicated delusions tended to be more chronic, were associated with less intellectual impairment and were more resistant to treatment. Among limbic lesions, laterality effects were evi dent, in that left-sided temporal lobe lesions were more likely to be associated with chronic schizo phrenia-like disorders (Hillbom, 1960, Trimble, 1981), while right parieto-temporal lesions were
associated with more short-lived hallucinatory

chorea; CT revealed profound atrophy of the caudate

nuclei, with moderate dilatation of the ventricular system and widening of cerebral sulci. The patient left hospital before adequate treatment of the manic psychosis could

beattempted.
Case 19: Cerebral blindness with anosognosia.

This patient was a 69 year-old, right-handed man, who was discovered to be blind three years prior to admission, when he was struck by a car. He had never complained of visual problems and the exact onset of his disability could not be determined. He had a history of diabetes,

hypertension, and heart disease. On examination, the

patient had limited attention and concentration, was disorientated, and had severely impaired recent and remote memory. He could do only simple mathematical problems and was unable to abstract; he had a score of 7 on the Hachinski Ischaemia Scale (consistent with multi infarct dementia) and 7/30 on the MMSE. The patient was unable to perceive light but he denied blindness, and readily confabulated answers to questions involving visual information. Neurological examination revealed in creased tone in all extremities, with poor coordination, loss of associated movements, and shuffling gait. CT

ORGANIC DELUSIONS: PHENOMENOLOGY, ANATOMICAL CORRELATIONS, AND REVIEW

193

delusional syndromes (Levine & Finklestein 1982; Peroutka et a!, 1982). There was also an association

capacities delusional personality

to produce clinically distinguishable syndromes. Predisposing factors includ

of right hemisphere
Alexander

disturbances

with Capgras
(Ben

ing genetic constitution,

characteristics,

early life experiences,

exact location and ex

syndrome and with reduplicative

paramnesia

son et a!, 1976; Hayman

& Abrams,

1977;

et a!, 1979; Quinn, 1981; Fisher, 1982).

The anatomical observations concerning simple and complex persecutory delusions suggest a tenta tive pathophysilogicalformulation. CNS functions that are relevant to delusion formation include

tent of the lesions, age at onset, and rate of functional disruption might further contribute to the development and elaboration of delusions,
determine the idiosyncratic content unique to each patient, and explain why delusions are not a

uniform

feature

of

otherwise

similar

CNS

linguistic and verbally-mediated conceptual abili

ties processed by the left hemisphere, and visuospatial, perceptual and affective functions

disorders. This pathophysiological

formulation

would not

account for denial of illness or grandiose delusions

in mania. The former is usually one manifestation

mediated by the right hemisphere (Ross, 1981;

Bear, 1983). These functions interact with the limbic system in the assessment of the emotional significance of ongoing experience (MacLean, 1949). The limbic system, in turn, has dense projections to the basal ganglia, creating an inte grated limbic-subcortical system that mediates mood, motivation, and motion (Nauta & Domesick, 1978; Nauta, 1982). In disease states, limbic or basal ganglia dysfunction would predis

of a neglect syndrome. The latter occurs with

lesions in the region of the diencephalon and with

metabolic disturbances

and may be associated with

impairment of hypothalmic function or with disrup

tion of ascending monoamine transmitter projec tions. The preponderance of right-sided lesions among lateralised disorders producing mania sug gests that the right hemisphere plays an important role in mood regulation and the disruption of these functions may contribute to manic behaviour.

pose to abnormal emotional experiences that can be

fully elaborated by the intact hemispheric cortex and lead to complex, intricately structured delu sions. These subcortical and limbic lesions are also anatomically located so as to disrupt ascending dopaminergic pathways, thus affecting transmitter systems which are implicated in idiopathic schizo phrenia and possibly accounting for the similarity between the delusions of schizophrenia and those of

This study confirmed the importance of detecting and managing delusions in patients with organic
psychosyndromes. Persecutory beliefs were fre quently acted on: several patients installed addi tional door locks and adopted other unnecessary security measures, some refused to take medication or even to eat, because they believed they were being poisoned; beliefs in marital infidelity caused domestic discord and occasionally threatened vio lence; in one case, several suicide attempts were

limbic and subcortical disorders (Trimble & Cum

mings, 1981; Cummings et a!, 1983). In lesions affecting the cortex, right temporo-parietal lesions result in abnormal perceptual input to the limbic

motivated by delusional misjudgements. Rabins et

a!(1982) found that 47% of demented patients were

system and in the development of hallucinations

and delusions; on the other hand, focal left temporal disturbances disrupt limbic connections for verbally-mediated functions, and account for

deluded and that 83% of the families of affected

patients considered the delusions a major manage ment problem. In this series, delusions were treated by managing the underlying condition (i.e., hepatic encephalo pathy), or by administration of neuroleptics. In some cases, the delusions responded well to therapy whereas in others the delusions persisted despite treatment. Complex, rigidly held delusions were

the paranoid delusional syndromes occurring in

some patients with left hemisphere lesions (Ben son, 1973; Trimble, 1981). In dementias of the Alzheimer or multi-infarct type, simple delusions

result from disruption of limbic input and from

impaired ability to elaborate the delusional con tent. This model closely fits clinical observations: delusions arise from lesions in a variety of locations, each lesion disrupts limbic-cortical associations in a different manner, and the abnormal emotional assessment interacts with remaining intellectual

the most resistant to treatment.

Acknowledgements
This research was supported by the Veterans Administration. The author is indebted to D. Frank Benson, M.D. for many helpful ideas that aided in initiating and formulating this study. The manuscript was prepared by Norene Hiekel.

References
ABD EL NARY. S. & IIA5sANEIN. M. (1965) Neuropsychiatric manifestations of chronic manganese poisoning. Journal of Neurology,

Neurosurgery.

and Psychiatry, 28, 282288.

194

JEFFREY CUMMINGS L.

ADLER, A. E. . SNDJA.L. & WILETS. G. (1980) Cimetidine toxicity manifested as paranoia and hallucinations. American Journal of Psychiatry, 137,11121113.
ALEXANDER, M. , STUSS, D. T. & BENSON, D. F. (1979) Capgras syndrome: AMES. F. (1958) A clinical and metabolic study of acute intoxication Manic a reduplicative phenomenon. Neurology, 29, 334339. Journal Journal of of

ALPERS.B. J. (1937) Relation of the hypothalamus to disorders of personality. Archives ofNeuro!ogy and Psychiatry, 38, 291303.
with cannabis following sativa and its role in the model rapid withdrawal from baclofen. psychoses. American

Menta! Science, 104, 972999.

ARNOLD. E. S. . RUDD. S. M. & KIRSHNER, H. (1980) psychosis

Psychiatry.
AsicEvoLD.

137, 1466-1467.
F. (1959) The occurrence of paranoid incidents and abstinence delirium in abusers of amphetamines. Acta Psychiatrica et

ASHER,R. t1949) Myxoedematous madness. British Medicalfourna!, 2, 555562.

Neurologica Scandinavia, 34, 145164.
consumption. Journa!ofMentalScience, Acta Psychiatrica 106, 337343. at Neurologica Scandinavia,

BEAMISH, P. & KILOH, L. G. (1960) Psychoses due to amphetamine BEARD. A . W. (1959) The association of hepatolenticular degeneration

BEAR,D. M. (1983) Hemispheric specialization and the neurology of emotion. Archives ofNeurology, 40, 195-202.
with schizophrenia.

34,411428.

BENSOND. F. (1973) Psychiatric aspects of aphasia. British Journal ofPsychiatry, 123, 555566. .
GARDNER, H. & MEADOWS, J. C. (1976) Reduplicative BERGMAN, P. 5. (1957) Cerebral blindness. Archives paramnesia. Neuro!ogy, 26, 147151. 78, 568584. ofNeurology and Psychiatry.

Bsrrs, T. A. , SMITH. . T. & KELLY, . E. (1968) Adult metachromatic leukodystrophy (sulphatide lipidosis) simulating schizophrenia. W R
Neurology, 18,1140-1142.
BLOCKER, W. W. JR.. KA5IL. A. J. JR. & DAROFF, R. B. (1968)The psychiatric manifestations Annales ofcerebral malaria. American Journal of

Psychiatry. 125,192196.
BoURGEoIS, M. & CAMPAGNE, A. (1967) Maniaco-depressive et syndrome de Garcin. de Medico-Psychologique, 125, 451460.

BOUTON.S. M. JR. (1940) Pick's disease: clinicopathologic

BOWMAN, K. M. (1935) Psychoses with pernicious anaemia. BROMBERG. W. (1930) Mental states in chronic encephalitis.

case reports. JournalofNervous

and Mental Disease, 91, 930.

AmericanJournalofPsychiatry, 92, 371392. Psychiatric Quarterly, 4, 537566.

BRook, N. M. & COOKSON, B. (1978) Bromocriptine-induced mania? British MedicalJournal, 1, 790. I.

BURKS,J. S. , HUDDLESTONE,J. , ALFREY,A. C. , NORENBERG, . D. & LEwIN, E. (1976) A fatal encephalopathy M in chronic haemodialysis
128, 133134. syndrome. Psychiatrica Journal Journal of the

patients. Lancet, 1, 764768.

BURNELL, 0. M. & FOSTER, T. A. (1972) Psychosis with low sodium syndrome. AmericanJournalofPsychiatry, BURSTEN, N. (1961) Psychoses associated with thyrotoxicosis. Archives ofGeneral Psychiatry, 4, 267273. CAMERON, 0. G. & LANDAU, S. G. (1980) Lithium carbonate treatment of mania associated with Klinefelter's

American
CHAWLA.

Medical Association,

243, 1712.
Capgras phenomenon in a case of temporal Progressive lobe epilepsy. Fo!ia ci Neuro!ogica of Neurology,

H. M. & VERMANE. V. (1977) S. , BRUETMAN, M. E.,

Japanica. 31, 615617.

CItOKROvERTY, BERGER, V. & REYES, M. G. (1976) dialytic encephalopathy.

Neurosurgery, and Psychiatry. 39, 411419. CHRESTODOULOU, N. (1976) Delusional hyper-identification G. of the Fregoli type. Acta Psychiatrica Scandinavia, 54, 305314. CLEGHORN R. A. (1951) Adrenal cortical insufficiency: psychological and neurological observations. Canadian Medical Association , Journal, 65, 449454. COHEN, M. R. & NISKA, R. W. (1980) Localized right cerebral hemisphere dysfunction and recurrent mania. American Journal of Psychiatry, 137,847848.

& DITMAN, . S. (1963)Prolongedadversereactionsto lysergicaciddiethylamide. Archives ofGeneral Psychiatry,8, 475480. K COHN,C. K. , WRIGHT, R. III & DE VAUL,R. A. (1977) Post head trauma syndrome in an adolescent treated with lithium carbonate J. case report. Disease ofihe Nervous System, 38, 630631. COlD,J. & STRANG. (1982) Mania secondary to procyclidine (kemadrin') buse. British JournalofPsychiatry, 141, 8184. J. a
COOPER. A. T. (1967) Hypomanic psychosis precipitated by hemodialysis. Comprehensive Psychiatry, 8, 168172. CHRISTODOULOU, 0. N. (1978) Syndrome of subjective doubles. American JournalofPsychiatry, 135,249-251. CROW, T. J. . JOHNSTONE, E. C. & MCCLELLAND, H. A. (1976) The coincidence ofschizophrenia and parkinsonism: some neurochemical

implications. Psychological Medicine, 6, 227233. CUMMINGS,J. L. & BENSON, D. F. (1983) Dementia: A ClinicalApproach.
GOSENFELD, L. F.. HOULIHAN, J. P. & McCAFFREY, T. (1983)

Boston: Butterworths
disturbances

Publishers.
associated with idiopathic calcification

Neuropsychiatric

ofthebasal ganglia.iological B Psychiatry', 18,591601. CU1TING, J. (1978a) The relationship between Korsakov's syndrome

and alcoholicementia.' d

British Journal of Psychiatry,

132, 240

251. (1978b) Study of anosognosia. Journal of Neurology, Neurosurgery, and Psychiatry, 41,548555.
DAMASMORA. J. M. R., JENNER, F. A. & EACOH, S. E. (1980) On heutoscopy or the phenomenon of the double: case presentation and review of the literature. British Journal of Medical Psychology, 53, 7583. DAVISON, K. & BAGLEY,C. R. (1969) Schizophrenia-like psychoses associated with organic disorders of the central nervous system: a

review of the literature. British Journal of Psychiatry, (Spec. Issue No. 4), 113184.
DE FINE OLIvAIUU5, B. & BODER, E. (1970) Reversible
DEWHURST, K. L. (1969) The neurosyphilitic

psychosis and dementia

in myxedema.

Acta Psychiatrica
115, 3138.

Scandinavia,

46, 112. 31,

psychoses today. British Journal of Psychiatry,

OLIVER, J.,TRIcK, K. L. K. & MCKNIGHT, A. L. (1969) Neuropsychiatric

aspects of Huntington's

disease. Confinia Neurologica, Psychiatric Association.

93, 201254.

258268.
Diagnostic and Statistical Manual of Mental Disorders (third edition)
FAIRWEATHER, D. 5. (1947) Psychiatric aspects FISHER. C. M. (1982) Disorientation for place. of the postencephalitic Archives of Neurology.

1980. Washington
syndrome. Journal 39, 3336.

DC: American
of Mental

Science,

FITz. T. E. & HALLMAN. L. (1952) Mental changes associated with hyperparathyroidism. Archives of Internal Medicine, 89, 547551. B.

ORGANIC DELUSIONS:

PHENOMENOLOGY,
P. R. (1975)

ANATOMICAL CORRELATIONS,
10,363-395.
state. JournalofPsychiatric

AND REVIEW
12, 189198.

195

FLOR-HENRY,P. (1969) Psychosis and temporallobe

FOLSTEIN, M. F.. FOLSTEIN, S. E. & MCHUGH.

epilepsy. Epilepsia.
Mini-mental

Research,

Foussi, D. V. (1982) Bipolar illness after right hemispherectomy. Archives ofGenera!Psychiatry, 39, 817819. FRANCIs, A. F. & FREEMAN,H. L. (1984) Psychiatric abnormality and brain calcification over four generations. Journal ofNervous MentalDisease, 172, 166-170. FREEMAN,A. M., III. (1980) Delusions, depersonalization and unusual psychopathological symptoms. In Psychiatric Presentations Medicallllness. (ed R. C. W. Hall)New York: SP Medical and Scientific Books. GAL, P. (1958) Mental symptoms in cases of tumor of temporal lobe. American JournalofPsychiatry. 115, 157160.
GEOCARIS, K. (1957) Psychotic episodes heralding secondary the diagnosis to vitamin of multiple B12 deficiency. sclerosis. American Menninger Journal Clinical ofPsychiatry, Bulletin, 21, 107116. GOGGAN5, F. C. (1983) A case of mania 141, 300-301.

& of

GOLDHAMMER. . , Burns. J. , SAROVA-PINHAS,I. & BRAHAM,J. (1972) Subacute Y GOODMAN. L. (1953) Alzheimer's disease. A clinico-pathologic

spongiform

encephalopathy

and its relation to Jakob Journal of

Creutzfeld disease: reportof sixcases. JournalofNeurology. eurosurgery. N andPsychiatry, 35,110.

analysis of twenty-three cases with a theory of causation.

Nervous and Mental Disease, 117,97130.

GOODWIN, F. K. (1971) Behavioural effects of L-dopa in man. Seminars in Psychiatry, 3, 477492. GORMAN, W. F. & Woims, S. B. (1947) Psychosis in Addison's disease. Diseases ofthe Nervous System, 8, 267271.
GRANT, H. C. & MCMENEMEY, W. H. (1966) Giant cell encephalitis in a dement. Neuropathologica Polaska, (Suppl 4). 735740.

GREENE, J. A. & SWANSON, L. W. (1941) Psychosis

in hypoparathyroidism;

with a report

of five cases. Annals

ofinternal

Medicine,

14,

12331236.
GRUNFELD,0. & HINOSTR0zA, G. (1964) Thallium poisoning. Archives ofinternalMedicine, 114, 132138. GY5IN, W. M. & COOKE. E. T. (1950) Unusual mental symptoms in a case of hepatolenticular degeneration. System, 28,305-309.
HACHINSIU, V. C., lUFF, L. D., Ziuuc@, E., etal(1975) Cerebral blood flow in dementia. Archives ofNeurology,

Diseases ofihe Nervous

32, 632637.

HAMILToN, M. (1976) Fish's Schizophrenia,

2nd ed. Bristol, England: John Wright and Sons.

chorea. JournalofiheAmerican MedicalAssociation, 79, 804-807. presenting with organic psychosis. Journal ofNeurology, Neurosurgery,

HAMMES, E. M. (1922) Psychoses associated with Syndenham's HANNA, S. M. (1970) Hypopituitarism (Sheehan's syndrome)

andPsychiatry, 33, 192193. HAUSNER,R. S. (1980) Amantadine-associated recurrence of psychosis. American Journal ofPsychiatry, 137, 240-242. HAY, G. G., JOLLEY,D. J. & JoNsa, R. G. (1974) A case ofthe Capgras syndrome in association with pseudohypoparathyroidism. Psychiatrica Scandinavia, 50, 7377. HAYMAN,M. A. & ABw,is, R. (1977) Cagras' syndrome and cerebral dysfunction. British JournalofPsychiatry, 130, 6871.
HILLBOM, E. (1960)
& KMi_@, M.

Acta

After-effects
(1951) Psychoses

of brain
after

injuries.
brain

Acta

Psychiatrica
Acta Psychiatrica

et Neurologica
ci Neurologica

Scandinavia,
Scandinavia,

(Suppl

142),
(Suppl

1135.
60), 3047.

trauma.

HOTSON, J. R. & LANGSTON, J. W. (1976)

JACK, R. A. , RIVERS-BULKELEY, N. T.

Disulfiram-induced
P. L. (1983)

encephalopathy.
Secondary mania

Archives

ofNeurology,

33, 141-142.

HUBAIN, P. P. , S0B05KI, J. & MENDLEWICZ,J. (1982) Cimetidine-induced

& RABIN,

mania. Neuropsychobiology,
as a presentation

8, 223224.
dialysis encephalopathy.

of progressive

Journal ofNervous

and Mental Disease, 171, 193195.

Manicpsychosis in a patient with multiple metastatic brain tumors. Journal of Clinical Psychiatry,

JAMIESON, R. C. & WELLS, C. E. (1979)

40, 280282.
JAMPALA,V. C. & ABRAM5,R. (1983) Mania secondary toleft and right hemisphere damage. AmericanJournalofPsychiatry,
1963 by J. Hoenig

140, 1197
pp 95-

1199.
JASPERS, K. (1946) Generalpsychopathology. Ailgemeine Pathologis. Berlin. Translated & M. W. Hamilton,

108, Chicago: University of Chicago Press.

JEFFERSON,J. W. & MARSHALL, J. R. (1981) Neuropsychiatric Features of Medical Disorders.
associated British Journal with Kleine-Levin-Critchley

New York: Plenum:

syndrome.

Medical Book
Psychiatric

Company.
JEFFRIES, J. J. & LEFEBVRE, A. (1973) Depression following and mania mumps. Canadian

Association

Journal, 18, 439444.

Toxic psychosis of Psychiatry, 35, 13331339.

KEDDIE, K. M. G. (1965)

(1969) Hereditary ataxia, presumed to be of the Menzel type, complicated of Neurology, Neurosurgery, and Psychiatry, 32,82-87. the Nervous System, 38, 210-211.

by paranoid psychosis, in a mother and two sons. Journal

Kasip, K., LION,J. R. & MAGRAM, (1977) Lithium in the treatment of a manic patient with multiple sclerosis: a case report. Diseases of G.
KRAUTHAMMER, C. & KLERMAN, G. L. (1978) Secondary mania. Archives of General LANGWORTHY, 0. R., Kout, L. C. & ANDROP, S. (1941) Disturbances of behaviour Psychiatry, in patients 35, 13331339. with disseminated sclerosis. American

Journal of Psychiatry, 98,243-249.

LARSON,T., SJOGREN, & JACOBSON, (1963) Senile dementia. Acta Psychiatrica Scandinavia, (Suppl 167), 1259. T. G. LEHMANN,J. (1966) Mental disturbances followed by stupor in a patient with carcinoidosis. Acta Psychiatrica Scandinavia,
LEVINE, D. N. & FINKLESTEIN, 5. (1982) Delayed psychosis after right temporoparietal stroke or trauma: relation to epilepsy.

42, 153161.
Neurology,

32, 267273.
UN, J. T-Y, & ZIEGLER, D. (1976) Psychiatric symptoms with initiation of carbidopa-levodopa treatment. Neurology, 26,679-700. L0VEI-r DoUsr, J. W. & CHRISTIE, H. (1978) The pathology of love: some clinical variants of de Clerambault's syndrome. Social Science

and Medicine, 12,99106.

MACCALLUM, W. A. G. (1973) Capgras symptoms with an organic basis. British Journal MACCLEAN, P. D. (1949) Psychosomatic disease and the visceral rain. Psychosomatic b MACNEILL, A., GRENNAN, D. M., WARD, D. & DICK, W. C. (1976) Psychiatric problems of Psychiatry, 123,639652. Medicine, 11,338-353. in systemic lupus erythematosus. American Journal

British

Journal

of Psychiatry, 128,442445.
MADAKUSIRA, S. & HALL, T. B., III (1981) Capgras syndrome in a patient with myxedema. of Psychiatry, 138, 1506

1508

196
MALAMUD, N. (1967)
& BOYD, D. A.,

JEFFREY CUMMINGS L.
Psychiatric
J. (1940)

disorders
Pick's disease

with intracranial
with atrophy

tumors
ofthe

of the limbic

system.
Archives

Archives
ofNeurology

ofNeurology,
and

17, 113123.
Psychiatry, 43, 210-222.

temporallobes.

MALLIARAS. D. E. . KOSSOUVITSA, Y. T. & CHRIST0o0uL0U,

G. N. (1978)

Organic

contributors

to the intermetamorphosis

syndrome.

American JournalofPsychiatry, 135,985-987. MAPELLI. G. & BELLELLI,T. (1982) Secondary mania. Archives ofGeneralPsychiatry, 39, 743. McEvoY, J. P. (1981) Organic brain syndromes. Annals oflnternalMedicine, 95, 212220.
MCHUGH, P. R. & FOLSTEIN, M. F. (1975) Psychiatric syndromes in Huntington's chorea. In Psychiatric Aspects ofNeurologic Disease.

(eds. D. F. Benson & D. Blumer). New York: Grune and Stratton.

MENNINGER. K. A. (1926) Influenza and schizophrenia. American Journal ofPsychiatry, 82,469-529. MINDHAM. R. H. S. (1970) Psychiatric symptoms in Parkinsonism. JournalofNeurology, Neurosurgery, and Psychiatry, MISRA, P. C. & HAY, 0. 0. (1971) Encephalitis presenting as acute schizophrenia. British MedicalJournal, 1, 532533. MOONEY, H. B. (1965) Pathologic jealousy and psychochemotherapy. British Journal ofPsychiatry, I 1 1, 10231042. MoSkovrrz, MULLER. D., NASH,J. C. , MOSE, H. & KLAWANS, H. U. (1978) Studies Levodopa-induced psychosis: a kindling phenomenon. Part 1. Clinical, 33, 188-191.

American

Journal

of and

Psychiatry, 135,669675.
PILZ, H. & TER MEULEN, V. (1969) on adult metachromatic leukodystrophy. morphological

histochemical

observations

in two cases. JournalofNeurological

InSignsandSymptomsin Psychiatry.

Science, 9, 567584.
eds. J. 0. CavenarJr. illness & H. K. H. Brodie). head injury. Philadelphia: Lippincott. 22, 359361. following Psychosomatics,

L. (1983)Delusions.

NASRALLAH, H. A., FOWLER, R. C. & JUDD, L. L. (1981)

Schizophrenia-like

NAUTA,W. J . H. (1982) Limbic innervation York: Raven Press.

& DOMESICK, V. B . (1978) Crossroads

of the striatum.
oflimbic and

In Gilles dela Tourette Syndrome.

circuitry: hypothalamo-nigralconnections.

(eds. A. J. Friedhoff & T. N. Chase). New

In Limbic Mechanisms. (eds.

striatal

K. E. Livingstone & 0. Hornykiewicz). New York: Plenum Press.

NEUMANN , M. A. (1949) Pick's disease. JournalofNeuropathology and Experimental Neurology, 8,255-282. OPPLER. W. (1950) Manic psychosis in a case of parasagittal meningioma. Archives ofNeurology and Psychiatry. 64, 417430. OYEWUMI, L. K. & LAPIERRE, Y. D. (1981) Efficacy of lithium in treating mood disorders occurring after brain stem injury. American

JournalofPsychiatry,

138, 110-112.
Dopamine fr hydroxylase in a patient drugs other with Wilson'sdisease than reserpine. Journal and of

PANDEY. R. S.. SREENIVAS, K. N., PATIH, N. M. & SWAMY, H. S. (1981)

mania. American JournalofPsychiatry,

138, 16281629.
Psychiatric side effects ofantihypertensive

PAYKEL, E. S., FLEMINGER, R. & WATSON, J. P. (1982)

Clinical Psychopharmacology, 2, 1439. PERKINS.H. A. (1950) Bromide intoxication. Archives oflnternal

Medicine, 85, 783794.

and delusions following a right

PEROUTKA. S. J. , SOHMER. B. H., KUMER, A. J. , FOLSTEIN, M. & RoBINSoN. R. G. (1982) Hallucinations

temporoparieto-occipital infarction. JohnsHopkins MedicalJournal. 151,181185.

PIES. R. (1982) Capgras phenomenon,
POPE. F. M. (1970) Parasitophobia

delirium,

and transient
symptom

hepatic dysfunction.
in vitamin

Hospitaland

Community

Psychiatry,
Archives

33, 382383.
32,

as the presenting

B12 deficiency.

Practitioner,

204, 421422. ofNeurology. Journal

POWELL. H. . TINDALL. R. . SCHULTZ. P. , PAA, D. , O'BRIEN. J. & LAMPERT, P. (1975).

Adrenoleukodystrophy. pressure

250-260.
PRICE, T. R. P. & TUCKER. G. J . (1964) Psychiatric and behavioural manifestations of normal hydrocephalus. of Nervous

and Mental Disease. 164, 5155.

QUINN . D. (1981 ) The Capgras syndrome: two case reports and a review. RABINS. P. V.. MASE. N. L. & LUCAS M. J. (1982) The impact ofdementia Canadian Journal ofPsychiatry. 26, 126129. on the family. JournalofiheAmerican MedicalAssociation,

248, 333335. RAYMOND.R. W. & WILLIAMS,R. L. (1948) Infectious mononucleosis

READ. A. E.. SHERLOCK, S.. LAIDLAW, J. & WALKER, J. 0. REDLICH. F. C. & DORSEY. J. F. (1945) Denial of blindness (1967)The by patients

with psychosis. New EnglandJournalofMedicine,

neuropsychiatric with cerebral of toxic syndromes disease. associated with chronic

239,542544.
liver disease 53,

and extensive portal-systemic collateral circulation. Quarterly Journal of Medicine, 36, 135150.
Archives ofNeurology propranolol and Psychiatry, therapy.

407417.
REMICK. R. A., O'KANE. J. & SPARLING, T. G. (1981) A case report psychosis with low-dose American

Journal ofPsychiatry. 138,850851. RENNICK. P. M.. NOLAN. D. C.. BAUER. R. B. & LERNER. A. M. (1973) Neuropsychological

and neurologic

follow-up

after herpes

hominis encephalitis. Neurology. 23, 4247.

REVELEY.A. M. & REVEREY.M. A. (1983) Aqueduct stenosis and schizophrenia. Journal of Neurology. Neurosurgery, and Psychiatry, 46, 1822. RICE. E. & GENDELMAN.S. (1973) Psychiatric aspects of normal pressure hydrocephalus. Journal of the American Medical Association,

223, 409-412.
ROSEN. A. (1979) Case report: Symptomatic ofNeurology. 7,486-488.
ROSENBAUM. A. H. & Barry. M. J.. Jr. (1975) Positive therapeutic response to lithium in hypomania secondary to organic brain

mania and phencyclidine

Pathological

abuse. American Journal of Psychiatry,

of ischemicscore

136, 118119.
dementias. Annals

ROSEN. W. G.. TERRY. R. D.. FULD. P. A.. etal(l980).

verification

in differentiationof

syndrome. American Journal of Psychiatry. 132, 10721073. Ross. E. D. (1981) The aprosodias. Archives of Neurology. 38, 561569. RorH. N. (1945) The ncuropsychiatric aspects of porphyria. Psychosomatic Medicine. 7, 291301. Roi HERMICH.N. 0. & VON HAAM. E. (1941) Pancreatic encephalopathy. Journal of Clinical Endocrinology. 1, 872881. RUDNICK. D. F. (1982) The paranoid-erotic syndromes. In Extraordinary Disorders of Human Behaviour. (eds. C. T. H. Friedman

& R.

A. Fagnot). New York: Plenum Press.

RYBACK. R. S. & SCHWAB. R. S. (1971) Manic response to levodopa therapy. New England Journal of Medicine, 285, 788-789.

SANDERS.V. (1962) Ncurologic

manifestations

of myxedema.

New England Journal of Medicine. 266, 547552.599603.

ORGANICDELUSIONS: PHENOMENOLOGY, ANATOMICALCORRELATIONS,AND REVIEW

SCHENK, V. W. D. & STOLK, P. J. (1967) Psychosis following arsenic (possibly thallium) poisoning. Psychiatrica. Neurologica

197
et

Neurochirugia,

70, 3137.
changes in the uremic Mental disturbancesduring clinical and social aspects syndrome. MedicalAnnals ofDistrict ofColumbia, 28,316-323. bromo-criptine orlergotrile treatment in Parkinson's disease. of a psychiatric symptom. Journal ofMental Science, 107, 687 109,95-

SCHREINER, G. E. (1959) Mental and personality SERBY, M. , ANGRIST, B. , LIEBERMAN, A. (1978)

American Journal ofPsychiatry,

SHEPHERD, M. (1961) Morbid

135, 12221229.
some

jealousy:

753.
SLATER, E. , BEARD, A. W. & GLITHERO, E. (1963) The schizophrenia-like psychoses of epilepsy. 2, 18401845. British Journal ofPsychiatry,

150.
SMITH, A. D. M. (1960) Megaloblastic madness. Pellagra: British MedicalJournal, of 18 patients

SPILLANE.J. D. (1951) Nervous and mental disorders in Cushing's syndrome.

SPIVAK, J. U. & JACKSON, D. U. (1977) an analysis

Brain, 74, 7294.

of the literature. Influenza Johns infection Hopkins causing Medical manic Journal, psychosis.

and a review

140, 295309.
STEINBERG, D. , HIRSCH. S. R. , M,@ESToN, S. D. , REYNOLDS, K. & SUtTON, R. N. P. (1972)

BritishJournalofPsychiatry,

120, 531535.
98,716-719. 3, 205212.

STERN, K. & DANCEY, T. E. (1942) Glioma ofthe diencephalon in a manic patient. American JournalofPsychiatry, STERN, M. & ROBBINS, E. S. (1960) Psychoses in systemic lupus erythematosis. Archives ofGeneral Psychiatry. STILL, R. M. U. (1958) Psychosis following Asian influenza in Barbados. Lancet, 3, 20-21.

STRACHAN, . W. & HENDERSON,J. 0. (1967) Dementia R

SURAWICZ, F. G. & BANTA, R. (1975) Lycanthropy SYDENSTRICKER. V. P. (1943) Psychic manifestations

and folate deficiency. QuaterlyJournalofMedicine,

36, 189204.
36, 169

revisited. Canadian PsychiatricAssociation of nicotinic acid deficiency. Proceedings

Journal. 20, 537542. oft/ic Royal Society of Medicine, 80, 415455. & M. R. Trimble).

171.
SYMONDS, C. & MACKENZIE, I. (1957) Bilateral loss ofvision from cerebral infarction. Brain, TOONE, B. (1981) Psychoses in epilepsy. In Epilepsy and psychiatry. (eds. E. H. Reynolds Livingston. TRIMBLE, M. R. (1981)
& CUMMINGS, J.

New York:

Churchill

Neuropsychiatry.
U. (1981)

New York: in a woman

John

Wiley

and Sons.
following brainstem lesions. British JournalofPsychiatry, 138, 5659.

Neuropsychiatric

disturbances

VAILLANT, G. (19)5)

Schizophrenia

with temporal

lobe arteriovenous

malformation.

British Journal

of Psychiatry,

111,307

308.

L/

VILLANI, S. & WEITZEL, W. D. (1979) Secondary mania. Archives of General Psychiatry, 36, 1031. VLISSIDES, D., GILL, D. & CASTELOW, J. (1978). Bromocriptine-induced mania? British Medical Journal, 1, 510. VROOM, F. 0. & GREER, M. (1972) Mercury vapour intoxication. Brain, 95, 305318. WATERS, B. G. H. & LAPIERRE, Y. D. (1981) Secondary mania associated with sympathomimetic drug use.

American

Journal

of

Psychiatry.

138, 837838.

WEINSTEIN, E. N., KAHN, R. U., MALITZ, S. & ROZANSKI, J. (1954) Delusional reduplication of parts of the body. Brain, 77,4560. WEISERT, K. N. & HENDRIE, H. C. (1977) Secondary mania? A case report. American Journal of Psychiatry, 134,929930. WEIZMAN, A., ELDAR. M., SHOENFELD, Y., HIRSCHORN, M., WIJSENBECK, H. & PINKHAS, J. (1979). Hypercalcamiainduced psychopathology in malignant diseases. British Journal of Psychiatry. 135,363366. WESTON, M. J. & WHITLocK, F. A. (1971) The Capgras syndrome following head injury. British Journal of Psychiatry, 119,2531. Wutm, J. C. & COBB, S. (1955) Psychological changes associated with giant pituitary neoplasms. Archives of Neurology and Psychiatry,

74,383396.
WIJSENBEEK, H., KRIEGEL, Y. & LANDAU, B. (1964) A paranoid state in a patient suffering from Sheehan syndrome. American Journal of

Psychiatry, 120, 11201122.

Wu.soN, J. W. (1952) Delusions of parasitosis (acraphobia). Archives ZUCKER, D. K. LIVINGSTON, R. U. NAKRA, R. & CLAYTON, P. J. (1981) review. Biological Psychiatry, 16, 197205. of Dermatology. 66, 577585. B1, deficiency and psychiatric disorders: case report and literature

Jeffrey L. Cummings, MD.Director, Neurobehaviour Unit, 256b (691/Bill),

Administration Medical Center California 90073, United States (Brentwood Division), 11301 Wilshire

West Los Angeles Veterans

Boulevard, Los Angeles,

(Received29

July1983;

revised 14 February 1984).