A Case of Dissociative Catatonia treated with risperidone
|Jutta Richter||Correspondence to:
By Dr. Jutta Richter, 60 Pentire Avenue, Newquay, Cornwall, TR7 1PE, United Kingdom.
W. N., a 22 year old man with mild learning disability, was admitted to an acute psychiatric ward following a deterioration in his mental health over the previous ten days. He showed depressive features, withdrawal, suicidal ideation, poor dietary intake and on one occasion, urinary incontinence . Relatives and his carer reported a marked change from usually being self-caring and being capable to manage his affairs to a state of perplexity and confusion. Having previously been cheerful and communicative he had developed poor verbal drive and lack of spontaneity. He had repeatedly expressed feelings of guilt about possible unlawful behaviour in that he had been persuaded by a new resident in his sheltered accommodation to try an illicit drug.
"Cerebral palsy" was diagnosed in early childhood, after a chicken pox infection aged two and a half years, resulting in mild learning disability. In adolescence, a diagnosis of Crohns Disease was made, not requiring any maintenance therapy.
W. came from an intact family with a very close relationship to his mother and sister. His father died 8 years ago. For some time he had been living in sheltered accommodation. He was described as having been outgoing and cheerful, setting high moral standards for himself. In the handling of his financial affairs he displayed particular conscientiousness. He had not in the past, misused illicit drugs, nor had he smoked tobacco or consumed alcohol. There was no evidence of mental illness in his family.
The mental state examination showed W. in great distress. He was not ambulant. He presented with marked perplexity and anxiety. His answers to questions were vague and monosyllabic but he also tended to perseverate about about a recent misspending, saying it had caused severe financial damage to his family. He appeared depressed and was unable to co-operate with a detailed mental state examination.
Physically he was in a good nutritional state but mildly dehydrated. Body temperature was normal and the examination of the cardiovascular, respiratory and gastrointestinal system was unremarkable. His pupils were dilated, with prompt reaction to light. There was bilaterally and equally reduced muscular power but normal tone and reflexes. He showed diminished reaction to mildly painful stimuli.
W. was admitted. An initial differential diagnosis included an acute reaction to stress with conversion disorder, acute paranoid reaction to some stressful experience or some form of drug-induced psychosis. A urine drug screen was negative. Initial routine blood samples were indicative of dehydration and showed a mild unspecific alteration of the liver function, i.e. a borderline raised ALT and total bilirubin. MSU was negative.
At first he became more alert, walking around and talking in brief sentences. Yet he remained preoccupied with beliefs of mis-conduct and guilt and admitted to feeling depressed. There was no evidence of florid psychosis. He was almost unresponsive to all our attempts to establish a trustful relationship. For the purpose of effective assessment he was kept free from psychotropic medication. Very poor dietary intake, lack of volition, increasing immobility and withdrawal were suggestive of severe depressive reaction. He episodically brightened up during his relatives very regular visits, becoming more responsive and talkative, even breaking into a laughter at times. W. was commenced on Sertraline but subsequently refused the intake. Some five days after admission he was stuporous, presenting with marked negativism, immobility, mutism and waxy flexilility. Repeated physical examinations, routine and a broad spectrum of additional blood samples as well as a brain CT scan did not reveal gross abnormalities. An EEG showed replacement of normal alpha-rhythm by fast activity. This finding apparently corresponded with our observation of episodic vivid mental processes concomittant with signs of high emotional arousal, although he remained mute, with physiological correlates of extremely widened, unreactive pupils, tachycardia and unresponsiveness to mildly painful stimuli.
He accepted medication with 2mg Lorazepam up to twice a day. The response was striking initially with a return to relaxation, eating and drinking and talkativeness within 20 minutes but followed by re-development of stupor after a couple of hours, thereby making a dissociative state more likely. Then his response became markedly weaker or altered to excitation. Lorazepam had to be stopped.
About four weeks after admission he seemed to emerge from the stupor, showing a tendency to communicate, improving dietary intake and more spontaneous behaviour although he was still unable to sustain a conversation. His movements were extremely slow but he appeared to be more aware of his environment. During this phase he began to posture his arms in a bizarre manner as if saluting. From his state of vague improvement he suddenly deteriorated and within hours developed into an excitatory form of catatonia. Placed in an arm-chair he would drop to the floor, rolling himself across the room, and to avoid serious injuries a single room was prepared for him. Here he was persistently twisting and turning, bringing himself into bizarre positions. He presented again with extremely widened pupils, mutism, very poor food and fluid intake and a loss of control over bladder and bowel functions. Negativism and waxy flexibility re-developed, more markedly than during his stuporous state and even the symptom "mitgehen" was present. It was now felt that this symptom-complex might be indicative of catatonic schizophrenia. He was placed on a Section 2 of the UK Mental Health Act (MHA - 1983) and treatment with Haloperidol 5mg bd. started. Medical causes had been excluded and he did not appear to develop side-effects during the early stages of the treatment. Blood results showed a WBC of 17.8, a raised CPK of 720 IU/L, a CRP of 25 mg/L and an extremely low TSH of 0.14 in a normal Free T4 with a spontaneous tendency to normalize; a normal Cortisol level and a raised Prolactin of 626 mIU/L were also found.
Even increased doses of 10mg Haloperidol B.D. did not influence his catatonic excitation sufficiently. He suffered a further weight loss, was dehydrated and deeply exhausted. The Section 2 was converted into Section 3 MHA. Electro-convulsive therapy was considered and a second opinion obtained. The same day Haloperidol was changed into a combination of gradually increased doses of Risperidone and 1mg Lorazepam B.D. per os.
Only after the first application of this combination our patient made a complete recovery and had reached a stable condition after 24 hours. With a smile he spoke about "something underlying he could not talk about" and freely admitted to having felt strong regrets when his sister became married. With his recovery from catatonia W. had completely left behind any depression and possibly underlying feelings of guilt as he was back to his cheerful self. There was complete amnesia for the whole episode of catatonia. During repeated attempts to elicit some more facts about any possible frightful experiences he denied still ongoing causes of concern. A diagnosis of dissociative catatonia appeared to be most likely. Following a four weeks period during which he remained stable, after repeated home leaves and gradual reduction of the Lorazepam he was discharged from the Section 3 MHA and from the hospital to stay with his mother. Prior to his discharge a dexamethasone suppression test was positive. An additional 24-hours EEG did not give evidence of epilepsy.
Catatonia is now regarded to be a non-specific syndrome characterized by psychomotor disturbances and changes in behaviour with stupor, followed by periods of marked excitation, mutism, negativism and waxy flexibility due to frontal lobe dysfunction. It might be related to a variety of psychiatric and medical illnesses and is considered to be a separate nosological entity. The literature reports dramatic responses to treatment with ECT and Lorazepam, the GABA potentiator, either as monotherapy or in combination. Several other drugs have been used successfully including lithium in periodic catatonia.
Risperidone in the treatment of catatonia has recently been described. Cook et al. reported a catatonic patient who failed to respond to any treatment but recovered on Risperidone, and Ceskova and Svestka described significant reduction of productive catatonic symptoms on moderate doses.
Hysterical dissociation is regarded to be a rare cause of catatonia. Despite W.s presentation with hysterical features on admission, the diagnosis of dissociative catatonia was made retrospectively as we could not exclude underlying schizophrenic psychosis during the course. Manfred Bleuler described many of his catatonic although schizophrenic patients as hallucinating vividly during stupor, and we ourselves observed the patient obviously experiencing vivid mental images during stupor though he had complete amnesia for the time of the catatonia.
The patients responses to Lorazepam and Haloperidol resp. as monotherapies were not convincing, corresponding with the findings of some authors . Early intervention with ECT would possibly have been the treatment of choice according to his steady deterioration.
Risperidone was finally chosen as a potent atypical neuroleptic with a low profile of side-effects, in combination with Lorazepam, which led to a prompt recovery. There was no evidence from the literature that this combination had been tried before. We assumed that the strong anxiolytic effect of Lorazepam was synergistic with a marked anxiolytic property of Risperidone, as indicated by the manufacturing firm, so that we primarily treated severe anxiety precipitating and maintaining this catatonia. Rosebush et al. reported that all responders to Lorazepam (10/12) had re-collected intense anxiety during the catatonia.
This case presentation records our remarkable experience with Risperidone in the treatment of full-blown catatonia.
COOK E.H., OLSON K., PLISKIN N. (1996) Response of Organic Catatonia to Risperidone. Arch gen Psychiatry, 53: 82-83DABHOLKAR P. O. (1988) Use of ECT in Hysterical Catatonia. British Journal of Psychiatry, 153, 246-247
FINK M. (1990) Is Catatonia a Primary Indication for ECT? Convulsive Therapy, 6(1): 1-4 (ed. by Raven Press, Ltd., New York)KAHLBAUM K. L. (1874) Die Katatonie oder das Spannungsirresein, Berlin. Translated (1972) as Catatonia. Y. Levi & T. Pirdon. Baltimore: John Hopkins University Press.
LOOPER K.J., MILROY T.M. (1997) Catatonia 20 Years Later. Am J Psychiatry, 153: 6PETRIDES G., DIVADEENAM K.M., BUSH G., FRANCIS A. (1997) Synergism of Lorazepam and Electroconvulsive Therapy in the Treatment of Catatonia. Biological Psychiatry, 42/5, 375-381
ROSEBUSH P.I., HILDEBRAND A.M., FURLONG B.G., MAZUREK M.F. (1990) Catatonic Syndrome in a General Psychiatric Inpatient Population: Frequency, Clinical Presentation, and Response to Lorazepam. J Clin Psychiatry, 51: 357-362
TAYLOR M. A. (1990) CATATONIA.A Review of a Behavioral Neurologic Syndrome. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, Vol. 3, No. 1, pp. 48-72 ( ed. by raven press, New York)
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