J.H.K.C. Psych. (1994) 4, SP2, 33-38

ORIGINAL PAPER

BENZODIAZEPINE TREATMENT OF CATATONIA IN THE ELDERLY

G.S.Ungavari, C.M. Leung, Alfred H.T. Pang, Erica White

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INTRODUCTION

Over the past two decades descriptive psychopathology has readdressed the concept of catatonia. In contemporary interpretation catatonia is a syndrome associated with a host of medical, neurological and psychiatric conditions (Gelenberg, 1976). Recent studies using newly constructed rating scales reported the frequency of catatonic symptoms among acute psychotic patients, Caucasians as well as Orientals, to be within the range of 8-10 % (Rosebush et al, 1990; Ungvari et al, 1994). Irrespective of past or recent psychotropic medication, chronic psychotic patients invariably display some form of motor mannerisms (Rogers, 1985). Reflecting the growing importance of catatonia in modem psychiatry, a number of extensive reviews have been published over the past few years (e.g. Lohr & Wisniewski, 1987; Taylor, 1990; Rogers, 1992).

It has long been known that electroconvulsive therapy (ECT) and intravenously administered barbiturates can suspend acute catatonic syndromes. However, difficulties in obtaining consent from a non-communicative patient and the narrow margin of safety of intravenous barbiturates have limited their applicability, although ECT is still regarded as the best option in life-threatening catatonic states (Mann et , 1986). The introduction of benzodiazepines proved to be a breakthrough in the treatment of catatonic syndrome. Since 1983 three prospective studies (Rosebush et al, 1990; Yassa et al, 1990; Ungvari et al, 1994) and at least 50 case reports (for reviews see F1icchione, 1989; Menza & Harris, 1989) covering 136 patients attested to the efficacy of BZDs in acutely emerging catatonia. There is anecdotal evidence that long-term BZD treatment is effective in chronic cases of catatonia as well (Gaind et al., 1994).

The aim of this report is to call attention to the fact that small doses of benzodiazepines (BZD), given orally or parenterally, can temporarily reverse catatonic symptoms. This treatment option has yet to become part of clinical lore. We chose four case vignettes of patients (three Chinese and a Caucasian) over the age of 60 for presentation because, to date, catatonia and its treatment in the elderly has received scant attention.

CASE VIGNETTES

Case 1

Mr A was a 61-year old uneducated labourer with a history of early parental loss, poverty and a disappointing marriage. Since the age of 57, the otherwise physically fit man had 3 hospitalizations for typical melancholic type depressive episodes which responded well to tricyclic antidepressants and ECT. He did not accept maintenance medication. A month prior to his current admisssion another bout of depression started with sadness, hopelessness, anhedonia, fatigue, psychomotor retardation and standard neurovegetative features. The morning before admission, he cut his wrist and became immobile and mute. Apart from mild dehydration, he was physically fit. Although motionless and uncommunicative, he was seemingly alert staring at different directions. Placebo (1 ml saline imi) coupled with suggestion was unsuccessful. However, he did not resist taking Z mg lorazepam with a few drops of water. One hour later he was ambulatory, started eating and d1inking and gave a good history of his depressive cognition. During the stupor he was fully aware of his surroundings but had no energy nor motivation to move or speak. ECT started the next morning brought about complete remission of the depressive episode.

Case 2

Mr B was a 64-year old single man living in social isolation in a compassionate housing flat receiving public allowance. He had a 25-year history of heroin abuse until 1982 when he was hospitalized for withdrawal symptoms. Since then he has been on a variety of maintenance medication, most recently tioridazine 100 mg and trihexyphenidyl 2 mg daily. His medical 11istory was unremarkable.

At te time of admission Mr B had been stuporous for a few hours, "curled in a ball", and mute. Except for slight rigidity in te limbs and bilateral eye-ball deviation in leftsuperior direction, 11is physical condition was satisfactory. CT scan showed mild cortical atrophy. Attempts to perform lumbar puncture or EEG were unsuccessful. ECG, chest Xray and extended laboratory investigations including VDRL, serum electrolytes, folate, B12 and coeruloplasmin were all non-contributory.

After admission his regular medication was stopped and only intravenous dextrose was given. Mr B's condition remained unchanged until Day 3 when he was persuaded to take a tablet of 2 mg lorazepam. 1 hour after the ingestion of lorazepam he started talking freely. He was mildly confused and reported vague suicidal intent. In the subsequent week, while on lorazepam 2 mg three times a day, 11is spontaneity and food intake improved and the above-mentioned neurological abnormalities disappeared. Repeated interviews confirmed low mood, hopelessness and suicidal ideation wit impairment of past and recent memory. He eventually agreed to ECT which resolved 11is depressive episode.

Case 3

Mr C, a 65-year old married cleaner, has always been an anxious, sensitive and dependent person. He had exaggerated responses to stressful events and was briefly hospitalized for anxiety neurosis at the age of 55. He never attended follow-up. There was no oter psyciatric or medical 11istory.

Following the unexpected loss of his job, Mr C was admitted in an anxious-agitated state. A few hours later he was found motionless, mute, uncommunicative and resisting our attempts to open his eyes (active negativism). Physical examination revealed no abnormality. Suspecting a dissociative stupor, a placebo injection ( 1 ml saline im.) was tried first accompanied by suggestive persuasion. With no response after 40 minutes, 10 mg of diazepam was given intramuscularly. Half an hour later he gradually started speaking coherently relating his recent stressful situation. He could clearly recollect events during stupor but offered only facile explanation for being immobile, mute and negativistic. Apart from being anxious, his mental state was 1101mal. Following supportive psychotherapy and decreasing doses of lorazepam over a few days, he was discharged fully recovered.

Case 4

After a successful career in accountancy, Ms D, a 78-year old Caucasian spinster, moved to an old age home because of worsening physical health. Some months prior to her first psychiatric admission she had become increasingly suspicious and developed changing delusional ideas concerning plots and conspiracies in the old age home where she was living. There was no family or past history of psyciatric illness or substance abuse. She had cildhood poliomyelitis witresidual lower limb weakness and suffered from hypertension.

On admission the only significant physical finding was a blood pressure of 230/120 mmHg which stabilized at 170/90 mmHg witin a few days without medication. Ms D was talking incessantly in a sing-song tone, interrupted only by eating during day-time and a few hours' sleep at night. Her speech was incoherent and asyntactic, consisting of a seemingly random selection of words and phrases repeated several times. Words and half-sentences from overheard conversation were echoed and incorporated in the endless flow of verbigeration. She did not answer questions, but would repeat them over and over again. Nevertheless she cooperated with nursing care. Apart from the continuous speech and echolalia she showed no other signs or symptoms of catatonia. She was not excited or inibited and her facial expression did not reflect anxiety, sadness or elation; it was neutral, as if carrying out a mechanical task. Grasping and sucking reflexes were absent. She was not available for detailed mental state examination or cognitive testing.

Full-scale laboratory investigations were non-contributory. EEG showed frequent bitemporal theta-delta activity against a slow, disorganized background. C:T scan revealed small bilaterally scattered lacunar infarcts. A diagnosis of organic delusional disorder with catatonic speech disturbances was made.

Despite introducing haloperidol (5 mg/day) and carbamazepine (400 mg/day) the incessant talk continued for 10 days witout a break. ECT was considered but met with objections from her relatives. On Day 10 1 mg lorazepam b.d. was added with dramatic results. Within an hour the flow of speech stopped and Ms D was able to converse freely. She appeared perplexed and related vague persecutory ideas. She was unable to explain why she had been talking in such a fashion although she vaguely remembered having done so. 1 mg b.d. lorazepam was enough to suppress the abnormal speech production for the next 6 days but on Day 17, twelve hours after the omission of one dose, she again started verbigerating and echoing senselessly.

On Day 22 a further attempt to withdraw lorazepam resulted in the return of the same speech pattern. Finally by Day 28 lorazepam was successfully withdrawn without the return of speech symptoms. The psychosis needed a further 2 weeks of antipsychotic treatment before full symptomatic recovery.

DISCUSSION

The discussion will center on three issues: (1) comments on the cases being reported; (2) the relationship between BZD treatment response and the phenomenology of catatonia, and (3) manifestations of catatonia in the elderly and its treatment with BZDs. They will be examined, although briefly, in a historical perspective.

COMMENTS ON OUR CASES

At present, conceptual and terminological confusion permeates catatonia research (Lohr & Wisniewski, 1987). There is no consensus what makes a motor symptom "catatonic". As a consequence, drawing the line between catatonic and other types of movement disorders (e.g. druginduced) is arbitrary (Rogers, 1985). Based on the currently prevailing syndromal concept (Gelenberg, 1976), recently published diagnostic criteria for catatonia (Lohr & Wisniewski, 1987; Rosebush et al, 1990) extended its boundaries far beyond Kahlbaum's original description (Kahlbaum, 1874/1973). For instance, modem literature regards any kind of stuporous state as catatonic (e.g. Gelenberg, 1976; Jensen, 1984; Salam & Kilzieh, 1988; Rosebush et al, 1990) altough conceptually this view is disputable (Berrios, 1981). Nevertheless, recent classifications such as ICD-10 and DSM-N, have adopted tis broad, syndromal view of catatonia.

For the sake of conformity, in this article we follow te example of current literature by using the terms "catatonia", "catatonic syndrome" and "stupor" interchangeably. However, te reader must bear in mind tat tis is a simplification of classical psychopathology made for practical purposes. Clinical and biological research of movement disorders in psychiatry is in a state of flux ( for a detailed review see Rogers, 1992). TI1ere are promising signs indicating that a unequivocal and comprehensive description of motor disorders will soon emerge {McKenna et al, 1991).

All four patients presenting wit catatonic features responded promptly to BZD challenge irrespective of their nosological diagnosis. In Case 1 a recurrent, melancholic type depressive illness culminated in a depressive stupor. By reversing the stuporous state, lorazepam revealed te patient's depressive cognition. Essentially similar results were obtained in Case 2, where a depressive episode was superimposed on an organic personality disorder owing to longstanding substance abuse. Case 3 had a stress-related dissociative stupor ("conversion catatonia"- Jensen, 1984) where diazepam brought immediate relief from anxiety and allowed ventilation of the patient's difficulties, i.e. producing an abreaction. All three patients (Cases 1-3) presented wit a virtually identical clinical picture of stupor. Without a detailed psychiatric 11istory obtained by BZD administration, it would have not been possible to reach a diagnosis and implement early treatment.

Case 4 had a catatonic speech syndrome consisting of loquacity, verbigeration and echolalia as part of an acute paranoid psychosis with possible organic origin. Loquacity, i.e. "a prodigious flow of talk [..] which does not correspond to a need for expression, but usually unburdens itself without any reference to the surroundings" (Kraepelin, 1919, p. 56) and verbigeration, i.e. "monotonous, mostly rhythmical repeat of single words or a few words" (Wen1icke, 1900, p. 6-7) have traditionally been conceptualized as speech manifestations of catatonic excitement since Kahlbaum's 01iginal 1874 description (Kahlbaum, 1973, p. 39). Echolalia can be observed in excitement as well as in psychomotor retardation {Ford, 1989). Loquacity and verbigeration have been neglected by modem descriptive psychopatology (Lohr & Wisniewski, 1987) although their frequency among drug-naive acute psychotic patients was found to be 62 and 14 % respectively (Bonner & Kent, 1936).

Among the BZDs, small doses of lorazepam (e.g. Yassa et al, 1990), diazepam (e.g. McEvoy & Lohr, 1983) and midazolam (e.g. DeLisle, 1991) are equally effective. Those with short half-life, like lorazepam and midazolam, are recommended especially in the elderly (Sheikh, 1993). In agreement wit the literature we observed no adverse effects. Cases 2 and 4 needed continuous lorazepam treatment to suppress stupor and speech disorder respectively until te underlying psychiatric disorder sufficiently improved. However, BZD treatment of catatonia rarely lasts longer than a few weeks {Gaind et al 1994), so the danger of addiction is negligable.

The practical implications of BZD treatment in catatonia are evident. Firstly, it alleys fear and anxiety frequently accompanying catatonic phenomena. During the few hour relief, diagnostic interview could be carried out, fluid and electolyte balance restored, nursing care implemented and consent for ECT sought. BZDs complement ECT in the treatment of acute catatonia {Pataki et al., 1992).

The ineffectiveness of saline in Cases 1 and 3 suggests that BZDs did not act as a placebo. To establish the specificity of BZDs, double-blind, controlled trials against placebo and active compounds like barbiturates, anticholinergic and antipsychotic drugs need to be conducted.

RESPONSE TO BENZODIAZEPINES AND THE PHENOMENOLOGY OF CATATONIA

The issue of treatment response to BZDs will be considered mainly in its relation to the psychopathology of catatonia. The prompt and full; albeit transient, reversal of catatonic symptoms by BZDs is one of the few dramatic therapeutic interventions in psychiatry. We found 50 publications ( list is available on request) reporting on BZD treatment in catatonia in 136 patients. Only three groups (Rosebush et al, 1990; Yassa et al, 1990; Ungvari et al, 1994) conducted prospective evaluation on a series of patients, the rest are brief case reports witlittle discussion on psychopathology. Therefore a meaningful and comprehensive meta-analysis would be difficult particularly when treatment failures have only been occasionally reported (e.g. Pataki et al., 1992). Although firm conclusions cannot be drawn, an interesting tendency have emerged regarding the psychopathology. In almost all instances symptoms of catatonic retardation predominate: mutism and stupor/immobility occured in over 90 % of cases. Catatonic excitement was only mentioned in 17 % and then only punctuated the clinical picture of retarded catatonia. Once symptoms of retardation resolved, the rare accompanying phenomena of excitation also disappeared. In other words BZDs act on the whole range of motor symptoms restoring the motor equilibrium.

While the current literature emphasizes the good treatment response of retarded catatonic syndrome (Rosebush et al, 1990), one of our cases (Case 4), with classical symptoms of catatonic excitement (loquacity and verbigeration) and no signs of motor retardation, showed an excellent response to lorazepam. This is in accord with earlier literature. Bleckwenn (1930) reported that amobarbital not only alleviated catatonic stupor but produced "some extremely interesting and rather striking responses" in catatonic excitement, similar to BZDs. Although Bleckwenn' s findings were endorsed by his contemporaries, this hypothetically specific action of amobarbital on catatonic excitement has not been investigated further.

Having been relieved of motor retardation, symptoms of the underlying psychiatric disorders usually reveal themselves. This happened in three of our cases, where depression (Cases 1, 2) and psychosis (Case 4) became apparent and continued unabated, i.e. not affected by BZDs. There is a remarkable consensus in the literature that, similarly to barbiturates, BZDs dissociate motor symptoms from the underlying psychiatric condition without exerting significant influence on the latter. This phenomenon has been observed and emphasized by many authors (e.g. Cremona-Barbaro, 1983; McEvoy & Lohr, 1983; Greenfield et al, 1987; Ripley & Millson, 1988; Salam & Kilzieh, 1988; Rosebush et al, 1990; Snyder et al, 1992).

The BZD treatment response appears to be independent of the patients' nosological diagnosis. Catatonic syndromes with various underlying brain pathology such as mental retardation (Gaind et al, 1994), neuroleptic malignant syndrome (Lew & Tollefson, 1983), pituitary microadenoma (Sheline & Miller, 1986), AIDS-related dementia (Snyder et al, 1992) have similar response to those associated with schizophrenia (e.g. McEvoy & Lohr, 1983), affective disorders (e.g. Rosebush et al. 1990) or reactive psychosis (Salam & Kilzieh, 1988). Age, sex, past psychiatric history, somatic condition and concommittant psychotropic medication do not seem to play a significant role in determining treatment response. Caucasian (e.g. McEvoy & Lohr, 1983), Oriental (Greenfeld et al, 1987; CremonaBarbaro, 1983) and black (Snyder et al, 1992; Jensen, 1984) patients have been equally responsive. The association between the duration of catatonia and treatment response is uncertain. The majority of papers dealt with acute catatonic states, but there is at least two convincing case reports (Ripley & Millson, 1988; Gaind et al, 1994) on chronic catatonic patients whose many year-long muteness and withdrawal were dramatically ended by lorazepam. Lorazepam was employed in most of the cases but diaze- pam (McEvoy & Lohr, 1983), clonazepam (Martenyi et al, 1989) and midazolam (Delisle, 1991) have also proven to be effective in alleviating catatonic symptoms. However, no study comparing the efficacy of various BZDs has been published.

Neurochemical hypotheses concerning the mode of action of BZD in catatonia focus on the modulation of dopamine turnover in the CNS via the GABA-ergic (Fricchione, 1985) or cholinergic (Menza & Harris, 1989) systems. While these hypotheses are logically built and consistent with experimental and human neuropharmacological data, they are not in accord with simple clinical observations, namely that symptoms of excitement also respond promptly to BZDs. Only Wetzel et al (1987) noticed that " we have no sufficient theoretical explanation so far as to why benzodiazepines show beneficial effects in "opposite" psychomotor symptoms. In keeping with the diversity of clinical presentation, it has recently been suggested that catatonia is a neurochemically heterogenous syndrome (Menza & Harris, 1990).

It may be that not only are the neurochemical hypotheses too simplistic but the traditional retarded versus excited dichotomy of catatonia is arbitrary and does not reflect clinical reality. In fact it has been observed since Kahlbaum's first description that pure retarded or excited syndromes are rare after an adequate period of observation (Kahlbaum, 1973; Bleuler, 1950; Kraepelin, 1919; Jaspers, 1963). It is likely that te relationship between various motor symptoms are far more intricate than descriptive psychopathology has postulated (Morrison, 1973). Seeking correlations between the BZD treatment response and different catatonic symptoms or syndromes in a large cohort of systematically evaluated patients may offer clues to the pathophysiology of catatonia. Such a research strategy may also contribute to a more accurate description of the psychopathology of catatonic phenomena.

CATATONIA IN THE ELDERLY

Six of the 25 patients described in Kahlbaum's original study of catatonia in 1874 (Kahlbaum, 1973) had an age of onset above 40 with the oldest being 45. Nearly four decades later in 1913, in the 8th edition of his textbook, Kraepelin mentioned two putative subtypes of dementia praecox (schizophrenia), late catatonia and tardive dementia first delineated by his contemporaries, Sommer and Stransky, respectively (Kraepelin, 1919). Both clinical syndromes were characterized by onset in old age or during involution. Late catatonia denoted a syndrome with rapidly deteriorating course beginning with affective disturbances and ending with the picture of the well-known catatonic defect state, i.e. perfectly fitting Kahlbaum's original description of catatonia as a disease entity. Tardive dementia was essentially a late-onset dementia praecox with paranoid and catatonic features. Contrary to Kraepelin's expectations both subforms soon faded into oblivion together with the whole concept of late-life catatonia. While endorsing the concept based on his clinical experience, Bleuler in 1911 did not elaborate on late catatonia any further (Bleuler, 1950, p. 242). Even Leonhard, who devised a meticulously detailed system of catatonic subtypes, made only casual remarks on the existence of late-onset catatonia, particularly in a periodic form (e.g. Leonhard, 1979, p. 419).

Careful reading of modem literature reveals that the frequency of catatonic syndrome in the elderly is probably not declining. In addition to several case reports (e.g. Greden et al., 1979; Pennatti et al., 1991; Lewis et al, 1993), 8-33 % of catatonic patients were over 60 years in unselected series published in the past decade (e.g. Johnson, 1984; Altschuler et al, 1986; Barnes et al, 1986; Fein & McGrath,1990; McCall, 1992). 3 % of lethal catatonia cases are also aged 60 or over (Mann et al, 1986).

Catatonic syndromes in the elderly are mostly associated with depression or organic brain syndromes (Shah & Cope, 1991). Twenty-two (16%) of the reported 136 catatonic patients given BZD were in the 60+ age group. Transient recovery to BZD challenge was as successful and risk-free as in young adults.

While classical and modem papers suggest that catatonia is not a rarity in the elderly, present-day psychogeriatric literature has glossed over the whole topic. Modem psychogeriatric textbooks (e.g. Busse & Blazer, 1989; Jacoby & Oppenheimer, 1991; Sadovay et al. 1991) do not even mention the term "catatonia" or "stupor". To our knowledge, the frequency of catatonic symptoms among the elderly, either demented or psychotic or suffeiing from affective disorder, has not been systematically investigated. It is likely that with the growing awareness of the safe and efficient BZD treatment, the re-examination of catatonia in geriatric psychiatry will soon follow.

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Gabor S. Ungvali PhD, FRANZCP Visiting Scholar, Department of Psychiatry, Chinese University of Hong
M. Leung MRCPsych Consultant Psychiatrist, Department of Psychiatry, Chinese University of Hong Kong.
Alfred H. T. Pang MRCPsych Lecturer, Department of Psychiatry, Chinese University of Hong Kong.
Erica White MBBS Department of Psychiatry, Geelong Hospital, Geelong, Victoria, Australia.

Correspondence : Dr Gabor S. Ungvali, Department of Psychiatry, 11/F, Plince of Wales Hospital, Shatin, T., Hong Kong