254 Journal ofNeurology, Neurosurgery, and Psychiatry 1990;53:254-259 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.3.254 on 1 March 1990. Downloaded from Pseudodementia twelve years on

Perminder S Sachdev, J Sydney Smith, Heather Angus-Lepan, Paul Rodriguez

Abstract deficits of . Another recent develop- This paper reports a longitudinal study ment is the challenge to the assumption that of 19 patients diagnosed as having is always a cortical phenomenon with pseudodementia more than a decade the suggestion that a "subcortical" dementia earlier. In only one patient was the earlier may exist'o 21; many of the features of diagnosis changed to definite dementia "pseudodementia" resemble those of subcor- and, in this patient, there were strong tical dementia.67922 indicators that such a diagnosis should Other authors, while not criticising the con- have been made initially. In a second cept, have argued that the diagnosis of patient, dementia could not be excluded. "pseudodementia" is often erroneous and the The remaining patients did not show patients have genuine organic brain disease, evidence of a dementing illness and the perhaps with a superimposed depression that courses of the illnesses resembled the leads to the error.2'2' In other words, the primary psychiatric disorders respon- "pseudodementia" is in fact a "pseudo- sible for the pseudodementia. The results pseudodementia".4 Some of these authors2326 validate the clinical utility of the term demonstrated that even when the depression of "pseudodementia". depressive pseudodementia had been adequately treated, the dementia did not automatically recede. That depression is com- The term "pseudodementia" has been used to mon and an underrecognised part of the describe a syndrome in which features suggest- dementia syndrome has been emphasised by ing dementia are associated with non-organic many.242728 The functional disturbance in so- psychiatric illness.' 2 The term has no diagnos- called pseudodementia, according to these tic specificity'3 as it includes a heterogeneous authors, is greater than that expected from the collection of disorders4 although depressive severity of the psychiatric illness alone,23 and disorders are most likely to be represented.2 Yet the course of the cognitive change and the its descriptive value is recognised widely by severity of the psychiatric disorder have not clinicians'" who use the term to mean one or always shown a consistent relationship.' One more of the following: 1) the impairment in study29 suggested that organic lesions were memory, learning, and related cognitive func- commonly present in patients of pseudo- http://jnnp.bmj.com/ tions is caused by a psychiatric illness; 2) the dementia. Thus, it is suggested by these critics impairment is likely to be non-progressive and that the diagnosis of pseudodementia is a trap is potentially reversible if the primary illness is as it often misses underlying dementia or other treated; 3) either no neuropathological process organic mental disorder. can be identified, or if such a process exists, it is Caine, in his influential review of the syn- minor and insufficient to explain the severity of drome,3 suggested that a longitudinal natural the cognitive deficits.6 history study of pseudodementia would Opposition to the term has been extensive enhance the understanding of the relationship on September 26, 2021 by guest. Protected copyright. and has taken various forms. The most com- of behavioural and intellectual abnormalities mon criticism is a conceptual one. Critics6 and indicate the prognostic significance of the recognise that cognitive deficits do occur as a diagnosis. If pseudodementia is a condition result of depression and some other psychiatric promoted by an organic diathesis that has disorders,7" but argue that they represent, in escaped detection, long term follow up might fact, a "true" dementia secondary to the patho- delineate such factors. If pseudodementia is Neuropsychiatric physiology causing the psychiatric disorders.' mistaken dementia, this would show up at least Institute, The Prince A number of researchers have provided direct in the medium term. Alternatively, Henry Hospital, if it is Sydney, Australia or indirect evidence to support the argument merely one manifestation of a "functional" P S Sachdev that is an intrinsic aspect of psychiatric illness with no organic basis, this J S Smith depression""' and '4 and not would again be borne out by the follow up data. H Angus-Lepan P Rodriguez merely a reflection of poor motivation." These In this paper, we report a longitudinal study critics also argue that the term "pseudo- of 19 patients diagnosed as having pseudo- Correspondence to: Dr P S Sachdev, dementia" originated at a time when dementia dementia more than a decade earlier. The Neuropsychiatric Institute, was described as a progressive, irreversible and definition of The Prince Henry Hospital, pseudodementia used in this study PO Box 233, Matraville, untreatable condition.'6 Many early studies of is detailed below, but it essentially refers to a NSW 2036, Australia. dementia used this definition.'71' Contem- picture of dementia produced by a non organic Received 9 June 1989 and in porary definitions"1 of dementia, however, psychiatric disorder. The term revised form 4 September "dementia" in 1989. accept the notion of reversibility, thus opening this paper refers to a DSM-IIIR dementia Accepted 18 September 1989 the way for its application to the cognitive which incorporates definitive or strongly Pseudodementia twelve years on 255

presumptive evidence of organic aetiology but on restrospective analysis, have significant J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.3.254 on 1 March 1990. Downloaded from does not include irreversibility. memory or intellectual dysfunction (criteria 1 and 2) to justify the diagnosis of pseudo- dementia. One was diagnosed as having a Subjects and method , currently depressed and the Between May 1973 and December 1977, the other as having paraphrenia. These patients are Neuropsychiatric Institute, Sydney, conduc- excluded from the follow up study. ted a multidisciplinary study of patients who presented with a provisional diagnosis of Initial patient characteristics dementia. The patients were referred, in the The mean age of the patients was 53 (range 26- main, by psychiatrists and neurologists and 64) years with 17 (89-50/%) in the age range 45- were assessed as inpatients. Their clinical 64 years. Fifteen (80%/) were female. Eleven details were recorded in a standardised patients (58% ) received a diagnosis of depres- interview and a number of laboratory inves- sion, three being in the depressive phase of a tigations were carried out as previously bipolar disorder. Five (26%) patients had a detailed.30 The Wechsler Adult Intelligence schizophrenic illness, two (10-5%) had a manic Scale, the Wechsler Memory Scale Form 1, the episode, and one (5-3%) had a schizophreni- Graham Kendall Memory for Designs Test, form disorder. The details of the disorders are the Benton Visual Retention Test, and a for- presented in the table. malised test of parietal lobe functioning were Sixteen patients had a long history of psy- administered. Of the 200 patients assessed in chiatric illness, the remaining three having this study, 21 (10-5%) were diagnosed as presented in their first episodes. Two patients having pseudodementia, that is, they had sig- (cases 5 and 6) had a history of possible nificant cognitive deficits which were con- pseudodementia in a previous episode of the sidered secondary to a non-organic psychiatric illness documented in their records. The index illness, usually depression or psychosis. The admission at which the diagnosis of pseudo- earlier paper30 reported 20 patients, but recent dementia was made had a mean duration of six re-examination revealed 21 patients. The diag- months. Only one patient (case 11) had sig- nosis was suspected by Smith and Kiloh' ifthe nificant brain disease in the form of a previous patients had one or more of the following: 1) cerebrovascular accident and residual left depression or psychosis was a prominent hemiparesis. Two patients had hypothyroid- feature of the presentation, and/or 2) there was ism (cases 2, 4) but were adequately treated at a history of previous psychiatric illness of the time of presentation. In terms of family comparable form followed by complete history, one patient's (case 14) father had recovery, and/or 3) the illness was of acute developed a dementing illness in the fourth onset and short duration; and there was an decade, although this history was not available absence of abnormality on electroence- until one year later. One patient's (case 1) phalogram (EEG), air encephalogram (AEG) mother had Parkinson's disease without a his- (before the availability of CT) or CT scan or tory of dementia. Five patients had histories of the abnormality, if present, was minor and affective illness in a first-degree relative. Eight judged to be not aetiologically significant. (42%/0) had an abnormal EEG, generally in the The diagnosis of pseudodementia was con- form ofintermittent non-specific slowing with- http://jnnp.bmj.com/ firmed retrospectively for the purposes of this out diagnostic significance, except for case 11 follow up if these patients fulfilled all of the (with past CVA) and case 19 (significance following criteria: 1) evidence of clinically unknown). significant disturbance in short-term and long- All patients were judged to be cognitively term memory; 2) evidence of clinically sig- impaired on neuropsychological evaluation so nificant intellectual impairment in the form of that an organic process could not be ruled out poor abstraction, poor judgment, impaired on the basis ofthe results. The patients demon- on September 26, 2021 by guest. Protected copyright. reasoning or logical processes, disturbance in strated impairment in memory and general other higher cortical functions or significant intellectual functioning. Three patients (cases personality change; 3) occurrence of the 9, 10 and 14) had features that suggested memory and intellectual impairment in clear aphasia, apraxia or agnosia. Case 9 had dressing consciousness; 4) a relatively recent onset, a few apraxia, dyscalculia, finger agnosia and dis- months to a year previously. If the history was orientation in space. Case 10 made a few longer, there had been a recent exacerbation mistakes on finger recognition and naming leading to the index presentation; 5) strong tasks and her copying of geometric figures was cross-sectional and/or historical evidence of a poor. Case 14 had minor expressive dysphasia "functional" psychiatric illness, such as an and constructional apraxia. Two other patients affective or schizophrenic disorder, that could (cases 5 and 7) had difficulty copying geometric possibly account for the current problem; 6) figures. the absence of evidence from the history, physical examination, or laboratory tests of a Follow up procedure specific organic factor (or factors) of severity An attempt was made to trace all patients in judged to be sufficient to cause the disturbance; 1987 by contacting the recorded addresses, the and 7) demonstrated or strongly presumed respective family doctors and the referring reversibility of the memory and intellectual hospitals. For the eight (420o ) subjects who deficits with appropriate treatment of the psy- had died in this interval, information was chiatric illness. obtained from medical records, death certific- Two of the 21 patients in the study did not, tes, reports ofnecropsy examination if conduc- 256 Sachdev, Smith, Angus-Lepan, Rodriguez

Table Clinicalfeatures ofpseudodementia patients and their status atfollow up J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.3.254 on 1 March 1990. Downloaded from Total Duration duration of Duration ofpsych index Family Abnormal offollow Status Case illness episode history investigations up in Final Course of No Age Sex Diagnosis (years) (months) (1' relative) (neurological) (years) 1987 diagnosis illness 1 45 F Bipolar 1 1 12 Parkinson's disease - 12 Alive Bipolar disorder, Multiple episodes depressed no dementia with full remission 2 49 F Bipolar 29 6 - EEG 12 Alive Bipolar disorder Multiple episodes depressed with full remission 3 63 F Bipolar 30 6 Affective illness - 12 Alive* Bipolar disorder, Multiple episodes depressed no dementia with one further admission (1986) 4 56 F Bipolar 26 4 Affective illness AEG 12 Alive Bipolar disorder, Multiple episodes manic no dementia with good recovery 5 50 M Bipolar 30 12 - - 11 Dead (1984) Bipolar disorder, Further manic manic no dementia episodes. Died of lithium toxicity. NE = no cerebral atrophy 6 57 F Major 10 6 2 Dead (1978) Major depression, Committed suicide; depression no dementia NE = no cerebral degeneration 7 61 F Major 10 4 EEG 6 Dead (1980) Major depression, Depressive depression no dementia episodes. Aspirated during ECT and died. No NE 8 54 F Major Affective illness 6 Dead (1980) Major depression, Intraoperative depression no dementia death. NE = No cerebral degeneration 9 63 M Major 25 5 EEG 2 Dead (1978) Major depression, One further depression possible dementia depressive episode. Possible underlying dementia (? aerteriosclerotic). Died ofpneumonia 10 62 F Major 36 12 Affective illness EEG 11 Dead (1985) Major depression, Died of Ca breast depression** alcoholism no dementia with metastases 11 63 F Major 15 15 - EEG 12 Dead (1987) Bipolar disorder, Three more depression no dementia episodes. Died following second stroke 12 57 F Major 31 10 AEG 12 Alive* Major depression, One further depression no dementia episode of depression. Currently no treatment 13 45 F Major 1 12 - 12 Alive Major depression, Variably but depression no dementia constantly depressed till 1983 and then improved 14 26 M Schiz, 4 5 Dementia EEG 6 Dead (1981) Huntington's Progressive chronic; chorea deterioration; acute exac*** diagnosis became clear at one year 15 58 F Schizo- 27 7 - EEG 12 Alive Schizophrenia, Performance poor phrenia, with residual, no but no depression dementia deterioration http://jnnp.bmj.com/ 16 50 F Schizo, 31 5 _ AEG 12 Alive Schizophrenia Cognitive chronic, chronic, no impairmnent acute exac*** dementia persistent but non- progressive 17 64 F Schizo, 27 1*5 - X-ray skull 14 Alive Schizophrenia Mild to moderate chronic, residual, no impairment, non- acute exac*** dementia progressive 18 57 M Schizophren- 0-1 Affective illness 14 Alive Schizophrenia Mild cognitive iform chronic, no deficit, non- disorder dementia progressive

19 59 F Schizo- 12 1*5 - EEG 13 Alive Schizophrenia Improved and on September 26, 2021 by guest. Protected copyright. phrenia with residual, no remained relatively depression dementia well

*Refused detailed assessment; **Possible underlying dementia; ***Chronic with acute exacerbation; NE = Necropsy examination. ted (3 cases) and interviews with relatives. Nine with the investigators, and, for these subjects, (470) subjects still alive were admitted for two information was obtained from their doctors days for a full medical and psychiatric examina- and close informants and the discharge sum- tion, investigations for dementia including maries from hospitals they had been admitted EEG and CT scan of the head, and a detailed to since the index admission. A life chart for the neuropsychological assessment which included course of illness was constructed for each subtests of the Wechsler Adult Intelligence patient and a consensus reached on the final Scale, Wechsler Memory Scale Form I and diagnosis between the investigators and the tests for frontal lobe functioning, memory and patient's primary physicians. visuo-spatial abilities. The clinical psycholo- gist was blind to the patient's medical and psychiatric history. Information was also Results obtained from a close relative and the patient's These are presented in the table. The mortality family doctor or psychiatrist about the patient's rate of our patients was 42",,. Of those alive at functioning since the index admission and follow up, six (54.50() were living at home. current status. The remaining two (105",,) Excluding case 14, all patients diagnosed as patients still alive refused personal interview having schizophrenia were alive at follow up. Pseudodementia twelve years on 257

Of the 13 patients with affective illness, six little evidence of cognitive impairment and J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.3.254 on 1 March 1990. Downloaded from (4600) were alive after 12 years, the others were all independent in activities of daily having died after a mean 7 1 years at an average living. Four lived at home (two alone and two age of 65 7 years. with family) and two in nursing homes. For the patients with affective illness who had sub- Deceased patients sequent episodes of illness, the available Eight (4200) patients died from the following documents and accounts did not suggest that causes: suicide (1), possible lithium intoxica- cognitive impairment recurred in these tion (1), Huntington's chorea (1), anaesthetic episodes. complications (2), cerebrovascular accident (1), pneumonia (1) and breast cancer (1). Review of Combinedgroup medical histories, discharge summaries from All patients with a diagnosis of affective illness hospitals and death certificates upheld the showed stability of that diagnosis. One patient primary psychiatric diagnoses in six cases. (case 11) developed a hypomanic episode for These showed cognitive recovery with treat- the first time in the follow up period. In two ment of the primary illness and no evidence of patients (cases 9 and 10), an underlying demen- cognitive decline before death. Necropsy ting process was suspected at initial assessment examination was conducted in three cases and and the depressive illness may have led to an did not show evidence ofcerebral atrophy. One exacerbation of the cognitive deficit. In one of patient (case 14), who earlier received a diag- these (case 9), dementia could not be ruled out nosis of schizophrenia was rediagnosed a year when he died two years later but an 11 year later as having Huntington's disease as his follow up of the other did not suggest a cognition deteriorated and choreiform move- progressive decline. ments became more prominent. In the eighth The patients with a diagnosis of schizo- patient (case 9), who died two years after the phrenia (cases 14-19) also showed stability of initial assessment, dementia could not be ruled diagnosis except for case 14 mentioned above out. His depression improved with treatment who was finally diagnosed as having Hunting- with electroconvulsive therapy (ECT) but mild ton's disease. A review of this patient's records memory and intellectual impairment persisted suggested that his presentation was indeed and he had apraxia and agnosia. He had a atypical. He was by far the youngest (26 years), recurrence of depressive illness two years later had evidence of marked neuropsychological and died from pneumonia, but a necropsy impairment (in particular aphasia, apraxia and examination was not conducted. He had clin- agnosia), showed transient choreiform move- ical evidence of atherosclerosis and a history ments and his father had developed dementia in of myocardial infarction, and it is possible the fourth decade, this history was unavailable that his recurrent depressive illness overlay a at the time of first assessment. Diagnosis was mild dementia resulting in the initial presenta- initially difficult because of the presence of a tion being considered pseudodementia. Both marked disorder of thought form and patients 14 and 9 had shown focal cortical signs delusions. (apraxia, aphasia or agnosia) at the time of the initial assessment. However, case 10, who had

also had such signs, did not show historical Discussion http://jnnp.bmj.com/ evidence of dementia when she died 11 years The two major indicators of outcome in our later although a formal examination of cortical patients are the mortality rate and the cognitive functions was not conducted on her. Cases 5 status of the survivors. The mortality rate and 7, who had demonstrated constructional should be considered in the light of reported apraxia at the time ofthe initial assessment, also mortality rates for patients with affective ill- did not develop dementia. ness, schizophrenia and dementia. Roth," in his study of all mental disorders in the elderly Llvlng patients (aged more than 60 years), reported that 14 8o/o on September 26, 2021 by guest. Protected copyright. None of the 11 patients alive 12-14 years after were dead in six months. Hastings,32 in a much the index admission showed evidence at follow younger (mean aged 39-6 years) group of up of a dementing illness on clinical or neuro- manic-depressives, reported a mortality of psychological assessment and their investiga- 22-40o in a six to 12 year follow up. Huston and tions such as EEG and CT (excluding the two Locher33 reported a mortality rate of 360o in a patients who refused admission) were within 6 5 year follow up of93 depressives with a mean normal limits. age of 52 years in the pre-drug era. In two Four patients (cases 15 to 18) showed cog- recent long-term prospective studies ofdepres- nitive impairment on neuropsychological sive illness,3435 23°o and 29 O were dead 18 and assessment but this was of a lesser degree than 16 years after initial contact respectively, but that recorded at the initial assessment. These these were younger than our patients. The four patients had a final diagnosis of chronic most appropriate comparison to our data is schizophrenia, with three living in nursing with that of the Huston and Locher" cohort, homes and the fourth alone at home with and the mortality trend in that study tended to intensive community support. The fifth patient approach our own. One (8%) of our patients (case 19) with schizophrenia who refused with affective illness died of suicide which is interview lived at home alone and, according to similar to rates reported in the literature.34" the report of her family physician, functioned Outcome in primary degenerative dementia is independently. poor, with most patients dying within five to The patients with affective illness showed seven years of diagnosis4 although longer 258 Sachdev, Smith, Angus-Lepan, Rodriguez J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.53.3.254 on 1 March 1990. Downloaded from survivals have been shown.6 Roth"' found that atric illness. The presence offocal cortical signs 600% were dead after six months and 80% such as apraxia, aphasia or agnosia had some within two years. In a study by Heston et al'6 predictive value for dementia. Abnormalities dementia patients under 49 survived for a mean on EEG, AEG or CT scan were minor and did of seven years and those aged 55 to 74 for 8-5 not contribute to the diagnosis in our patients years. Considering these reported studies, our except to possibly rule out identifiable causes patients had a mortality pattern more like that of dementia. Those who have previously of depressives than those with dementia. Our examined the ability of these investi- schizophrenic patients were all alive at follow gations2 182942 to differentiate between depres- up with the exception of one whose diagnosis sion and dementia have commented on the was changed to Huntington's disease. These considerable overlap of abnormalities so that findings suggest that the initial diagnosis confident separation of the two syndromes was of "pseudodementia" was correct in most often not possible. Neuroendocrinological instances. studies in recent years, particularly the dex- The absence of dementia in the survivors amethasone suppression test, have also not again validated the initial assessment. Al- been able to distinguish between the two with though cognitive impairment persisted in four any certainty.4344 patients with schizophrenia, they did not fulfil In summary, this study shows that the diag- the DSM-IIIR criteria for dementia. Such nosis of pseudodementia predicts a course of deficits are not unusual in chronic schizo- illness which seems to reflect the primary phrenia,37-39 and do not warrant a diagnosis of psychiatric illness responsible for the picture of dementia. The cognitive impairment of our cognitive impairment. The suggestion that schizophrenic patients was not progressive such patients usually have an underlying and, in fact, reversed to some degree. From dementia with a superimposed non-organic clinical experience, these patients are not psychiatric illness is not sustained. The study usually referred for assessment for possible also indicates that the presence of focal cortical dementia unless there has been a recent change signs increases the possibility of a true demen- in their condition, as was the case in our tia but does not affirm it. Constructional dif- patients. The reason for the recent deteriora- ficulties observed in our patients did not seem tion was judged to be an acute exacerbation of to have diagnostic significance. In the final the schizophrenic illness in three cases and a analysis, a diagnosis of a non-organic psy- superimposed depression in two. chiatric illness, supported if possible by past Heaton et al,3' in their review of the neuro- history and the rigorous exclusion of organic psychological studies of schizophrenia from factors, allows a process of "pseudodementia" 1965 to 1978, concluded that whereas nonpsy- to be affirmed which has predictive validity. chotic mentally ill patients could be reliably differentiated from those with known organic We thank Professors L G Kiloh and G B Parker disease, chronic schizophrenics were dis- for their comments on earlier drafts, Dianne criminated from controls with brain damage at Eva for help in data collection, Teresa Lee for an essentially chance rate of 54 per cent. The assisting in analysis and Robyn Lee for cognitive deficit in our schizophrenic patients secretarial help. Eli Lilly (Australia) and the

persisted without much improvement or de- Prince Henry Hospital Centenary Fund http://jnnp.bmj.com/ terioration over the follow up period. The provided financial assistance. patients, however, maintained independence in their activities of daily living and did not show 1 Kiloh LG. Pseudodementia. Acta Psychiatr Scand 1961; progressive loss of functioning. If this cog- 37:336-51. nitive 2 Wells CE. Pseudodementia. Am J Psychiatry 1979;136: deficit is called schizophrenic demen- 895-900. tia,39 it is a dementia which is not generally 3 Caine ED. Pseudodementia: Current concepts and future progressive. Reported studies of the course of directions. Arch Gen Psychiatry 1981;38:1359-64. 4 Lishman WA. Organic Psychiatry: the psychological con- on September 26, 2021 by guest. Protected copyright. cognitive deficit in schizophrenia40 41 support sequences of cerebral disorder. London: Blackwell Scien- the finding that general intellectual decline tific, 1987. 5 Cummings JL, Benson DF. Dementia: a clinical approach. does not occur in these patients although some Boston: Butterworths, 1983. do show 6 Mahendra B. Depression and dementia: the multifaceted patients deterioration in certain relationship. Psychol Med 1985;15:227-36. specific tasks.39 As schizophrenia is still gen- 7 McAllister TW. Overview: Pseudodementia. Am J Psy- erally regarded as a non-organic chiatry 1983;140:528-33. psychiatric 8 Weingartner H, Cohen RM, Murphy DL, et al. Cognitive disorder, cognitive impairment caused by this processes in depression. Arch Gen Psychiatry 1981;38: illness cannot arguably be considered 42-7. true 9 Sach4ev PS. Pseudodementia in schizophrenia and mania dementia and this is the position we take. (letter). Austr N Z J Psychiatry 1988;22:238-9. Re-examination of the clinical picture at 10 Hemsi LK, Whitehead A, Post F. Cognitive functioning and cerebral arousal in elderly depressives and dements. J initial presentation is revealing. The features Psychosom Res 1968;12:145-56. most important for the diagnosis were a history II Cawley RH, Post F, Whitehead A. Barbiturate tolerance and psychological functioning in elderly depressed patients. of psychiatric disorder of some standing and Psychol Med 1973;3:39-52. the presence of significant psychopathology 12 Henry GM, Weingartner H, Murphy GL. Influence of affective states and psychoactive drugs on verbal leaming cross-sectionally. The same observation has and memory. Am J Psychiatry 1973;130:966-71. been made previously.23 In all patients, 13 Davies G, Hamilton S, Hendrickson DE, et al. Psychological test performance and sedation thresholds of elderly neuropsychological assessments showed sig- dements, depressives and depressives with incipient brain nificant deficits so that organic deterioration change. Psychol Med 1978;8:103-9. 14 Taylor MA, Abrams R. Cognitive impairment in schizo- was considered a strong possibility. In no case phrenia. Am J Psychiatry 1984;141:196. could the clinical psychologist state convin- 15 Jorm AF. Cognitive deficit in the depressed elderly: A review of some basic unresolved issues. Aust N Z J cingly that the deficit was due solely to psychi- Psychiatry 1986;20:11-22. Pseudodementia twelve years on 259

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