Raymond Levy and paranoid states of late life

INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY. VOL. 11: 355-361 (1996)

RAYMOND LEVY AND PARANOID STATES OF LATE LIFE

ROBERT HOWARD Senior Lecturer, Section of Old Age Psychiatry, Institute of Psychiatry, London, U K

EARLY CLINICAL STUDIES

It is sometimes said that if you can remember the 1960s you were probably not there, and while many of those of us who have worked with Raymond do not remember the decade clearly because we were only just there, we can appreciate that this was a boom time for late paraphrenia research. Kay and Roth (1961) in their seminal paper provided excellent clinical descriptions of late paraphrenic patients together with established risk factors for the condition (female sex, deafness, abnormal premorbid personality and social isolation). Believing late paraphrenia to be the expression of schizophrenia in old age they nevertheless recognized heterogeneity within patients which they postulated reflected the differing aetiological contributions of personality, social isolation, sensory impairment and genetic factors.

While Kay and Roth believed that organic cerebral disease was present in only a small minority of patients with the late paraphrenia syndrome and observed that fewer than 12% of patients had developed dementia after 10-year follow-up, Felix Post (1966) regarded such organic cerebral change as aetiologically important. Post believed that patients with late paraphrenia represented a heterogeneous mixture of diagnoses and preferred to avoid diagnostic controversy by terming such cases ‘persistent persecutory states’. Within this broad category, he recognized three clinical syndromes: true schizophrenia, a schizo- phreniform syndrome and a paranoid hallucinosis group. Proven organic factors were present in 16 of Post’s 93 patients and he believed that in such cases, disturbed memory and concentration could clearly have been seen to precede the first emergence of persecutory delusions.

Address for correspondence: Dr R. Howard, Section of Old Age Psychiatry, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK.

CCC 0885 -6230/96/040355 -07 0 1996 by John Wiley & Sons, Ltd.

COMPUTED TOMOGRAPHY

Throughout the 1970s and 1980s, as the spotlight of old age psychiatry research effort was focused very much on the dementias, the engine of late paraphrenia research idled and then died. The credit for jump-starting stalled research activity in the mid- 1980s must go to Raymond, whose interest in the application of CT scanning to old age psychiatry, together with the presence of Mohsen Naguib, who had chosen to study late paraphrenia for his PhD thesis, produced the first systematic neuropsychological and imaging study of patients (Naguib and Levy, 1987). Forty-three late paraphrenics (defined using broad diagnostic criteria very much as suggested by Kay and Roth) underwent CT scanning at the Maudsley Hospital together with a battery of neuropsychological tests which included the digit copying test (Kendrick, 1965) and the digit symbol substitution subtest of the WAIS (Wechsler, 1955). When compared with data from 40 normal elderly controls, Naguib‘s late paraphrenics had significantly greater ventricular-brain ratios (mean 13.09) than the controls (9.75) and also performed at a significantly lower level on both the digit copying and digit symbol substitution tests. Naguib concluded that since there was no association between degree of measured ventricular enlargement and length of illness, subcortical pathology may have preceded the onset of psychotic symptoms and could have served as a non-specific risk factor for the development of the disorder.

Alistair Burns and colleagues reexamined the CT scans of this series of patients and control subjects. They assessed cortical atrophy through ratings of sulcal, interhemispheric and Sylvian fissure widths (Burns et al., 1989) and found no differences between patients and controls. In a very green spirit that has characterized many of the Section’s activities under Raymond’s leadership, this series of scans was recycled once again by Hans Forstl and myself (Forstl et al., 1991; Howard et al., 1992b) in an attempt to demonstrate correlations

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between clinical symptoms and the appearance of the brain on CT. We found that those of Naguib’s patients who had not had first-rank schizophrenic symptoms had greater cortical atrophy scores, particularly in the left frontal lobe.

CLINICAL AND COGNITIVE FOLLOW-UP

Naguib’s cohort of patients and controls were reassessed by Nigel Hymas, on average 3.7 years after their initial investigation (Hymas et al., 1989). Cognitive function in the surviving late paraphrenics, which had been mildly impaired at initial recruitment, had shown some further deterioration but only two late paraphrenics were considered by the authors to have cognitively deteriorated in a global fashion that would satisfy criteria for a dementia. Hymas also examined patients for abnormal involuntary movements which were present in 70% and were associated with the amount of medication received but not with age or ventricular-brain ratio. In terms of the clinical course of psychotic symptoms, only 35% of patients had suffered a relapse that required readmission during this follow-up period. Although a mean of 3.7 years may sound like only a very short follow-up period, Hymas’ revisiting of Naguib’s cohort of patients from whom cases of dementia had been carefully excluded at the outset represented an important first effort to chart the cognitive progress of patients with late paraphrenia that has not really been bettered to date.

LATE PARAPHRENIA AND ICD- 10

Although the diagnostic category of late paraphrenia had never been internationally accepted, because of its clinical appropriateness for a group of patients seen by old age psychiatrists who could not fit such patients into the schizophrenias (particularly if an advanced age of onset excluded the diagnosis), ICD-9 (WHO, 1978) had included the diagnoses paraphrenia, late paraphrenia and involutional paranoid states. As part of a field study of the then latest draft of ICD-10, Marie Quintal and Diana Day-Cody rated the case notes of 36 ICD-9 late paraphrenics using the newly proposed ICD- 10 diagnostic guideline (Quintal et at., 1991). Although the two raters achieved complete diagnostic agreement, they were uneasy about the low threshold for the diagnosis of

schizophrenia which had resulted in the majority of late paraphrenic cases receiving this diagnosis. When the raters were freed from the need to give primacy to schizophrenia, they preferred a wider range of diagnoses for the patients which included a number of subcategories of delusional disorder. It would seem that the staff at the World Health Organisation only read to this point in the paper, and the final published version of ICD-10 (WHO, 1992) suggested that ‘other persistent delusional disorders’ should be the diagnosis to include cases previously diagnosed as late paraphrenia. What Quintal and co-authors actually suggested (and anyone who heard Raymond speak on the subject at the IPA meeting in Sydney last year knows that he is somewhat aggrieved that their advice was not followed) was that ICD-10 should either retain a separate category for late onset schizophrenia or late paraphrenia or should at least provide some form of code for age at onset in such cases,

NEUROPSYCHOLOGY

Osvaldo Almeida joined the Section at the end of 1990 as a PhD student and I arrived soon after. When we first met it was with a degree of dis- concertion to discover that Raymond had (and we both took this as a sign of the strength of his determination to ensure that the project was completed) encouraged us both to carry out identical detailed neuropsychological and imaging studies of late paraphrenia to build on Naguib’s earlier findings. Happily the project split very neatly down the middle: Osvaldo was more interested in neuropsychological testing than myself and I had a grant from the Mental Health Foundation to pay for MR scans in late paraphrenics. Osvaldo developed a mobile battery of computerized and pencil-and-paper neuropsychological tests which he could take into the homes of late paraphrenics who might have been unwilling to travel to the Maudsley. The sight of Osvaldo loading and unloading his computer from the back of his Volkswagen Polo outside the Section became very familiar as he returned, often in triumph, after a testing session with another suspicious and impatient subject. For general cognitive assessment, the NART (Nelson and Willison, 1991), picture arrangement subtests of the WAIS (Wechs- ler, 1981) and the CAMCOG (Roth et al., 1988) were administered. To examine short-term memory function, Osvaldo used the digit span

RAYMOND LEVY A N D PARANOID STATES OF LATE LIFE 357

(Weinberg et a/., 1982), computerised spatial span (Milner, 1981) and computerised delayed matching-to-sample (Sahakian, 1990) tests. Long-term memory was investigated using the recognition memory test for words and faces (Warrington, 1984) and working memory with the computerised spatial working memory task (Owen et al., 1990). Because of the evidence suggesting that younger schizophrenic patients may have abnormalities in frontal and temporal lobe function (Frith, 1992), tests of executive function thought to be sensitive to frontal lobe lesions were also used. These included a verbal fluency test (Milner, 1964), the computerised test of extra-intra dimensional attention-shift ability (ED-ID) (Owen et al., 1990) and the computerised Tower of London task (Robbins et al., 1991) to assess executive functions.

Forty-seven late paraphrenics and 33 control subjects completed the general cognitive assessment and seven patients refused to complete the computerized tests. On tests of general functions (the CAMCOG and WAIS-R) patients’ performance was significantly poorer than that of control subjects, although there was no obvious impairment of learning in patients as measured by the digit and spatial recurring span tasks, nor of simultaneous matching-to-sample ability (Almeida et al., 1995a). However, the patients did score less well on delayed matching-to-sample and on the recognition memory test for faces (but not for words). Performance of patients on the tests of executive function outlined above was consistently worse than that of controls. Osvaldo concluded that psychotic states arising in late life in general are predominantly associated with a decline on measures of general cognitive ability and executive function and went on to look for putative cognitive subtypes (Almeida et al., 1995b). Using centroid cluster analysis, the late paraphrenics were divided into two roughly equally sized groups. ‘Type A’ patients had a wide range of psychotic (particularly schizophrenic) symptoms and cognitive deficits which were restricted to executive functions, while ‘type B’ late paraphrenics had more restricted psychotic symptomatology, an increase in neuro- logical hard and soft signs and generalized cognitive impairment.

MAGNETIC RESONANCE IMAGING

My own work involved the recruitment of 50 patients and 35 healthy aged controls to have

structural MRI scans. At the time we did not have our own scanner at the Maudsley and the nearest available machine was the 1.5 Tesla Philips Gyroscanner in the Department of Radiological Sciences at Guy’s. I was allocated 2 hours of scanning time every fortnight and since the chosen scan sequences took about 45 minutes, four subjects could be scanned each month. The numbers involved seemed daunting at the outset of the project and some of the most paranoid patients took a lot of persuading to have scans. I can remember my euphoria as I drove the first two successfully scanned subjects back to their homes from Guy’s and how this was quickly replaced by other emotions when I realized that I would have to repeat the trip at least another 40 times. Once I had persuaded patients to at least come and look at the scanner, I found that they would become so intrigued by the appearance of the machinery, the kindness of the radiographers and the journey to and from Guy’s in the back of my Morris Minor that they would often volunteer to have further investigations and would certainly be happy to see Osvaldo when he turned up at their homes with his computerized testing battery. As I ferried patients to and from Guy’s, it was often fascinating to listen to conversations in the back of the car held between two late paraphrenics who had never before met anyone who could share in and therefore absolutely believe their extraordinary stories of persecution. One patient with vivid visual hallucinations had to be collected from the Bethlem, and as I drove along Crystal Palace Parade she exclaimed from the back of the car with some alarm, ‘Doctor, we’ve just been overtaken by a speedboat’. Once in the scanner, patients tolerated the scan sequence very well and images that were of sufficient quality to permit computerized quantitative analysis were acquired from 47 of 50 patients and 33 of 35 controls. We had two main lines of enquiry with relation to the volumetric measurements and a question about the areas of signal hyperintensity or ‘white matter lesions’ seen on T2- weighted images. Firstly, would any of the brain regions that had been suggested to have reduced volume in younger schizophrenics (for example, temporal lobe, superior temporal gyrus, hippocampus, parahippocampal gyrus or basal ganglia structures) be selectively affected in late paraphrenia? Secondly, the mean MMSE scores of those late paraphrenics who satisfied ICD- 10 diagnostic criteria for schizophrenia had been significantly higher than in those with delusional disorder

358 R. HOWARD

among the group of 101 late paraphrenics that I had approached and asked to undergo MR scanning (Howard et al., 1994a). We were thus particularly interested to see if measures of ventricular enlargement, cortical atrophy or reduced volumes of particular brain regions were associated with any of these diagnostic subgroups of patients. Finally, in the light of several reports from the United States of a high prevalence of white matter signal hyperintensities in the brains of patients with late onset psychosis, suggesting that vascular lesions may have been aetiologically important, was this the case in patients with late paraphrenia from whom those with dementia or with a history or signs of stroke had been carefully excluded?

When measurements of total cerebral size, lateral and third ventricular volumes and the volume of sulcal cerebrospinal fluid from the late paraphrenic patients as a whole were compared with those of control subjects, third and lateral ventricle volumes were significantly greater among the patients (Howard et al., 1994b). The absolute differences in volumes were similar to those suggested by VBR measures from the CT studies (for example left lateral ventricle volume in late paraphrenics was 17.13 cm3 and in controls 12.25 cm3). When the late paraphrenics were divided into patients with schizophrenia (31 subjects) and delusional disorder (16 subjects), it became apparent that most of the enlargement of lateral and third ventricle volumes among patients was accounted for by the subjects with delusional disorder. Indeed, in comparison with control subject values, ventricular volumes were only slightly and non-significantly enlarged in the schizophrenic patients, but in the patients with delusional disorder they were almost double those of controls. For example, left lateral ventricle volume in the delusional disorder patients was 23.70 cm3, compared with 13.73 cm3 in schizophrenics.

When the measurements of frontal and temporal lobe, superior temporal gyrus, hippocampal and basal ganglia volumes were analysed, they indi- cated that any regional cerebral structural differences between late paraphrenic patients and the normal elderly are subtle (Howard et al., 199%). Although left temporal lobe volume was reduced in delusional disorder patients (63.64 cm3) compared to schizophrenics (68.10 cm3) and controls (69.09 cm3), this difference was not significant after the effects of multiple statistical comparisons had been considered. In fact, the volumes of none of the

other brain regions measured in patients proved significantly different from those values derived from control subjects. Since with increasing age variation in the appearance of the brains of normal individuals also increases, demonstration of minor structural abnormalities in the brains of elderly psychiatric patients compared with age-matched healthy controls is difficult. Presumably, therefore, any differences between the brains of late paraphrenic patients and the control subjects in our study would have had to have been more marked than those reported in young schizophrenics in order to emerge as statistically significant.

Finally, assessments of areas of signal hyperintensity, or ‘white matter lesions’, were made by visual inspection of T2-weighted axial images of the whole brain. Separate ratings were made of periventricular deep white matter and subcortical grey matter hyperintensities on a four-point scale by Tim Cox from the Maudsley Department of Radiology (Howard et al., 1995a). Although the most severe grades of periventricular and deep white matter hyperintensities were more common in the late paraphrenics (47.4% and 39.5% respectively) than among the controls (35.4% and 19.4%), these differences did not reach accepted levels of statistical significance. We concluded that while minor degrees of cerebrovascular disease, demonstrated by the presence of these hyperintensities on MR, may be important in the development of psychosis in later life, such an association is not as strong as that reported for late life depression or cases of more organic ‘late life psychosis’ (eg Miller et al., 1991).

GENETIC MARKERS

Mohsen Naguib (Naguib et al., 1987) investigated human leucocytic antigen (HLA) typing in his sample of late paraphrenic patients, and demonstrated that the A9 antigen, which had been linked to paranoid schizophrenia by earlier workers, was not associated with late paraphrenia. Naguib found an association with the B37 antigen and concluded that late paraphrenia was therefore genetically distinct from schizophrenia. Apolipoprotein E studies seem to have become to psychiatrists of the 1990s what HLA association studies were in the 1980s. Anxious that late paraphrenia should not be left out of this exciting area, and with a genuine scientific curiosity about any association of the disorder with established risk factors for neuro-

359 RAYMOND LEVY AND PARANOID STATES O F LATE LIFE

degenerative diseases, we genotyped 23 late paraphrenics for ApoE (Howard et nl., 1995b). The frequency of the ~4 allele was comparable with that found in groups of centenarians, but lower than that reported from populations of normal controls and patients with Alzheimer’s disease.

were the frequently encountered belief that people or materials could both see and move through walls or doors and the fantastic scenic visual hallucinations that patients would describe. Ray- mond would listen with interest to my accounts of the experiences of new patients I had recruited for the study, but rather annoyingly, had a stock of stories about past cases whose delusions and hallucinations were always more exotic. It gave FUNCTIONAL IMAGING

Raymond was one of the main supporters of imaging at the Institute and had played an important part in the acquisition of the IoP’s SPET machine which was housed across the road in the Department of Nuclear Medicine at King’s. John O’Brien, elsewhere in this volume, details some of the Alzheimer’s disease bloodflow studies that he and Sarah Eagger carried out on the scanner. In the light of PET studies from young schizophrenic patients, we carried out a small SPET study of striatal dopaminergic DZreceptors in six drug-naive late paraphrenics using the ligand 1231 iodobenzamide (Howard et al., 1993). We were unable to demonstrate any elevation or significant laterality of D2-binding in the patients compared with a group of healthy aged controls.

TREATMENT RESPONSE

Surprisingly little has been written about the treatment of late paraphrenia and no controlled and blinded studies have been reported. In a retrospective examination of treatment and response, we reviewed 64 patients all of whom had been prescribed neuroleptics for at least 3 months in the previous year. At the time of assessment, 42% of the patients showed no response, 3 1.3% a partial response and 26.6% a full response to treatment (Howard and Levy, 1992). Compliance with medication, receiving depot rather than oral treatment and use of a community psychiatric nurse if the patient was an outpatient all had a positive effect on treatment outcome. Despite their better response rate, patients prescribed depot received on average a lower daily dose in chlorpromazine equivalents than those prescribed oral medication.

PARTITION DELUSIONS AND ‘CHARLES BONNET PLUS’

Of all the phenomenological features of late paraphrenia, those which struck me as most memorable

me great satisfaction to discover that, despi‘ie a rather obscure literature on the subject, he had not heard of the expression ‘partition delusion’ to describe the characteristic experience of late paraphrenic patients that they are observed or their homes are entered through what would normally be considered to constitute an impermeable barrier. Rather than being little more than a piece of esoterica, we found partition delusions to be present in 68% of our late paraphrenics (Howard et a[., 1992a) and hopefully have put them on the map for a wider audience of old age psychiatrists.

Patients who are said to have the Charles Bonnet syndrome, but are seen in psychiatric practice, almost invariably have some cognitive impairment, incomplete insight or affective response to their hallucinations which disqualifies them from the eponymous syndrome as described. Of our 101 late paraphrenics, 18 reported complex, prolonged and repetitive visual hallucinations that resembled the characteristic experiences of individuals with the Charles Bonnet syndrome (Howard and Levy, 1994). Half of these patients had accompanying auditory hallucinations, 42% were visually impaired and only one had insight into the hallu- cinatory nature of her experiences. We suggested that such patients be referred to as ‘Charles Bonnet syndrome plus’, since this acknowledges the similarities between the experiences and the syndrome without incorrectly including such patients within it.

FUTURE DIRECTIONS

If Raymond were guiding a potential late paraphrenia researcher, now or in the immediate future, he would certainly identify clinicopathological studies as a priority. I am also sure (although Raymond is far too loyal to his juniors to express such doubts) that he attributed my own failure to secure the brains of late paraphrenics as evidence of a defeatist attitude rather than any difficulties with the patients. Although, at the time of writing,

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Raymond’s plans for emeritus appointments in Paris are still fluid, one can confidently anticipate that some young Parisian psychiatrist will be inspired to remedy my omission.

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Raymond Levy and paranoid states of late life