Pmg. Neum-Psychophormocol. B Bml. Psychiat. 1985. Vol. 9. pp. 481-484 Printed in Great Britain. All rights reserved

027&5846/85 $0.00 + .50 Copyright 0 1985 Pergamon Press Ltd

1. 2. 3. 4. 5. 6. 7. a. 9.

PSEUDODEMENTIA

MICHAEL FISMAN

London Psychiatric Hospital London, Ontario, Canada

(Final Form, July 1985)

Contents

Abstract 481 Introduction 481 Diagnosis 481 Management 483 Diagnosis of Early Dementia 483 Stress and Pseudodementia 483 Nonprogressive Deficits and Diagnosis of Dementia 483 Mixed Depression and Dementia 484 Depression as Precursor of Dementia 484 Conclusions 484 References 484

Abstract

Fisman, Michael: Pseudodementia. Prog. Neuro-Psychopharmacol. & Biol. Psychiat. 1985, 2 (S/6): 481-484. 1. The term pseudodementia is applied to the range of functional psychiatric conditions such

as depression, schizophrenia and hysteria that may mimic organic dementia, but are essen- tially reversible on treatment. Depression is the commonest cause of pseudodementia in the elderly and is also the commonest treatable condition misdiagnosed as dementia.

2. Diagnosis and management of depressive pseudodementia are discussed, and the systematic and thorough treatment of the depression is emphasized.

3. Issues such as the diagnosis of early dementia, mental stress in the elderly resulting in confusion, patients with nonprogressive intellectual or neurological deficits, patients with a diagnosis of mixed depression and dementia, and depression as a precursor of dementia are all briefly considered.

Keywords: dementia, depression, diagnosis, management, pseudodementia

1. Introduction

The term pseudodementia refers to psychiatric conditions not associated with a true dement- ing process, that mimic an organic dementing illness. These conditions may be neurotic (Kiloh 1961), schizophrenic (Fisman 1982) or depressive. Depressive states comprise the commonest treatable condition misdiagnosed as dementia (Marsden 1972). Failure to recognize this condition may have disastrous psychosocial consequences for the patient and result in needless suffering for the family.

2. Diagnosis

The diagnosis of a major depressive episode depends upon eliciting and recognizing the key symptoms and signs: dysphoric mood, poor appetite, significant weight loss, insomnia or hypersomnia, psychomotor agitation or retardation, anhedonia, loss of energy and fatigue, feelings of worthlessness, suicidal ideation, suicide attempt, etc.

481

482 M. Fisman

In the elderly, in addition to the symptoms described above, we find that depression may also be characterized by what has been called the ABC of depression in the psychogeriatric

patient, namely: (a) anxiety or apathy; (b) bizarreness characterizing delusions or halluci-

nations; (c) confusion; and (d) dementia (pseudodementia). These characteristics of depres-

sion in the elderly lead to misdiagnosis. There are, however, clinical findings that can be very helpful in making the distinction between dementia and depression (Table 1).

Table 1

Major Clinical Features Differentiating

Pseudodementia From Dementia

Clinical Features Dementia Pseudodementia (Depression)

Onset of Illness

Progression

History

Complaints

Responses

Affect

Social Skills

Attention and Concentration

Memory Loss

Orientation

Diurnal

insidious onset acute onset

slow development progressive over

rapid progression with plateauing

years

uncommon to have prior depression

history of - previous history of affective disorder is common may have occurred many years ago, especially at age vulnerable to depression e.g. puerperium, involution

disabilities overlooked or

concealed - exaggerates cognitive loss

patients attempt tasks "near miss" answers response and performance in - keeping with level of cognitive impairment may have "catastrophic response" if unable to manage task

minimal effort to respond "don't know" answers inconsistent and variable responses and performance that reveal the presence of better cognitive function than predicted

shallow and labile affect

often retains "cocktail party skills" in early stages

usually impaired

recent memory loss severe and exceeds remote loss, in keeping with level of cognitive impairment

impaired, in keeping with level of cognitive loss

sundowner effect, increased confusion at night

- profound hopelessness and distress

- early decline

- often intact

- equal loss of recent and remote events - patchy and variable

- unimpaired, may appear patchy and variable

- worse in the morning, patient may appear improved in the afternoon

Pseudodementia 483

In addition, laboratory investigations including computerized tomography of the brain,

electroencephalogram, psychometry and dexamethasone suppression test may all be useful adjuncts to what remains essentially a clinical diagnosis because of the overlap between findings in depressive and demented populations. Thus, Jacoby and Levy (1980) suggest that the main use of computerized tomography of the brain is in the exclusion of potentially treatable conditions, as they found considerable overlap in the measurements in demented and depressed patients. Similarly, the dexamethasone suppression test may be impaired both in demented and depressed patients; dementia being one of the recognized causes of failure to suppress on this test (Balldin et al 1983). In early Alzheimer's Disease, the electroenceph- alogram 'may be normal (Pedley and Miller 1983), which suggests that the electroencephalogram may not be that useful in distinguishing dementia from depression especially when the normal variants on the electroencephalogram that are found with aging are taken into account. Similar limitations apply to psychometric testing, which may be more valuable in affirming

normal functioning than in the diagnosis of dementia (Zarit and Zarit 1983).

3. Management

Doubt about the diagnosis may persist despite thorough clinical history and investigation. In these cases, either long-term follow-up or clinical trial of treatment may be indicated. Patients with dementia will show evidence of progressive deterioration and provided a reli- able rating scale is used, the progressive deterioration should become apparent. The alter- native approach is one of therapeutic trial. The therapeutic trial should be adequate in the light of current knowledge of the management of depression. The physician should ensure that there has been a systematic and thorough approach to the management of the depression which would include the use of bilateral electroconvulsive therapy. At the same time the clinician must be aware that these same agents may contribute to an exacerbation of the picture of pseudodementia.

4. Diagnosis of Early Dementia

A discussion of the distinction between depression and dementia would not be complete with- out touching on the issue of the diagnosis of early dementia. Nott and Fleminger (1975) and Ron et al (1979) have shown that the error rate in the diagnosis of early dementia may be as high as 30 to 50%. Early diagnosis may be justified for research purposes but in the usual clinical situation a firm diagnosis of early Alzheimer's Disease should be made with caution.

5. Stress and Pseudodementia

Stress in the elderly i.e. demands and requirements which exceed the physical, emotional or intellectual capacity of the elderly, may lead to a catastrophic reaction of anxiety, anger, depression or confusion. The grief reaction, which is an example of this type of response, may result in a clinical picture mimicking an organic confusional state or dementia.

6. Nonprogressive Deficits and Diagnosis of Dementia

Patients with nonprogressive intellectual/neurological deficits - patients from socio- economically and culturally deprived backgrounds may appear impaired on standard mental status assessment. The same applies to patients who are mentally retarded. In both cases, patients may cope in a limited way in society, but when routines and support systems are disrupted - as occurs in the course of aging - the response involving a mixture of anxiety, depression and confusion may mimic a dementing illness. It is therefore important that educational attainment and level of functioning prior to onset of the illness be taken into consideration before deciding on a diagnosis of dementia.

Similarly, nonprogressive neurological lesions, such as strokes associated with aphasia, agnosiafapraxia may suggest a diagnosis of dementia, but the associated clinical and labora- tory findings should allow the correct diagnosis to be made.

484 M. Fisman

7. Mixed Depression and Dementia

Patients with dementia may become depressed in the course of the dementing illness. These depressions may respond to the usual somatic treatments, although these treatments do not af- fect the level or cause of the dementing illness. Adequate treatment of depression in these cases is important as Blessed (1984) has showen in his follow-up studies on patients with dementia that of 17 cases with diagnoses of mixed depression and dementia, 6 were found to have morphologically normal brains at autopsy.

8. Depression as Precursor of Dementia

The relationship of depression in the elderly and dementia, if any, remains controversial. Post (1972), on the basis of follow-up of 173 cases of depression in the elderly, found that the incidence of dementia arising in this subpopulation was similar to the incidence in the general population. Kral (1983) has claimed that of 22 cases of pseudodementia that he fol- lowed up, 20 cases had become permanently demented. A shortcoming of this study is that the diagnosis of dementia (Alzheimer's Disease) was confirmed in only three eases at autopsy. Folstein and McHugh (1978) on the other hand have suggested that pseudodementia should rather be regarded as the "dementia syndrome of depression related to the fall off of norandrenergie and cortical neurons in the elderly." Thus, what would present in a younger patient as straightforward depression, presents with symptoms of dementia in the elderly because of neuronal fallout.

9. Conclusions

In conclusion, the clinical significance and diagnostic issues relating to pseudodementia have been reviewed. It is evident that there is still much to be learned about the develop- ment, course and complications of this condition. Systematic prospective clinical follow-up studies collaboratively with neuropathology and neurochemistry are needed to define this condition more precisely.

References

BALDIN, J., GOTTFRIES, C., KARLSSON, I., LINDSTEDT, G., LANGSTROM, G. and WALINDER, J. (1983) Dexamethasone suppression test and serum prolactin in dementia disorders. Brit. J. Psychiat. 143: 277-281.

BLESSED, G. (1984) Clinical features and neuropathological correlations of Alzheimer type disease. In: Handbook of Studies on Psychiatry and Old AGe, D.W.K. Kay and G.D. Burrows (eds), pp 133-143. Elsevier, Amsterdam.

FISMAN, M. (1982) Pseudodementia and schizophrenia. Am. J. Psychiatry 139: 846. FOLSTEIN, M.F. and MCHUGH, P.R. (1978) Dementia syndrome of depression.-%: Alzheimer's Disease: Senile Dementia and Related Disorders, R. Katzman, R.D. Terry and K.L. Bick (eds), pp 87-96. Raven Press, New York.

JACOBY, R.J. and LEVY; R. (1980) Computed tomography in the elderly 2. Senile Dementia: diagnosis and functional impairment. Brit. J. Psychiat. 136: 256-269.

KILOH, L.G. (1961) Pseudodementia. Acta Psychiatr. Scand.3 336-351. KRAL, V.A. (1983) The relationship between senile dementia and depression. Can. J. Psychiatry 28: 304-306.

MARSDEN, C.D.%d HARRISON, M.J.G. (1972) Outcome of investigation of patients with presenile dementia. Brit. Med. J. 21: 249-252.

NOTT, P.M. and FLEMINGER, J.J. (1975) Presenile dementia: the difficulties of early diagnosis. Acta Psychiatr. Stand. 51: 210-217.

PEDLEY, T.A. and MILLER, J.A. (1983) ainical neurophysiology of aging and dementia. In: The Dementias, R. Mayeux and W.G. Rosen (eds), pp 31-49. Raven Press, New York.

POST, F. (1972) The management and nature of depressive illnesses in late life: a follow through study. Brit. J. Psychiat. 212: 393-404.

RON, M.A., TOONE, B.K., GARRALDO, M.Exnd LISHMAN, W.A. (1979) Diagnostic accuracy in presenile dementia. Brit. J. Psychiat. 134: 161-168.

RARIT, S.H. and ZARIT, J.M. (1983) Cognit% impairment. In: Clinical Neuropsychology, P.M. Lewinsohn and L. Teri feds) pp 38-80. Pergamon Press, New York.

Inquiries and reprint requests should be addressed to: Dr. Michael Fisman, London Psychia- tric Hospital, P-0, Box 2532 Terminal A, London, Ontario, CANADA, N6A 4Hl.