Journal of the Royal Society of Medicine Volume 84 February 1991 89 A psychiatric presentation of abulia - three cases of left frontal lobe ischaemia and atrophy H Forst! MD Central Institute of Mental Health, Mannheim, FRG B Sahakian PhD Age Psychiatry, Institute of Psychiatry, De Crespigny Park, London SE58AF Section of Old Keywords: stroke; major depression; laterality Extensive cerebrovascular disease may cause global psychiatric disturbances affecting mood, cognition and personality'. Comparatively minor infarcts can produce more subtle and specific neuropsychological deficits, which initiate behavioural disturbances--'. The cases of three women are described, who were admitted with a diagnosis of major depression". However, their histories, clinical features and radiological findings exhibited striking similarities, which may indicate a specific psychiatric presentation of left frontal lobe pathology quite distinct from other frontal lobe disturbances like mutism, perseveration, or disinhibition 1. It is suggested that this specific syndrome represents a psychiatric presentation of abulia, literally 'lack of will', which deserves particular diagnostic and therapeutic attention to obviate potentially fatal consequences. Case reports Case 1 In August 1987 a 57-year-Qld right-handed woman experienced an ischaemic stroke with right-sided hemiparesis. The cranial computed tomogram (CT)disclosed small infarcts of the left callosomarginal and left medial striate arteries. A short period of depressive mood was noticed. After 3 months of intensive rehabilitation, however, she appeared much improved: she was able to walk with a stick and to take up most of her usual activities. She retained a mild paresis of her right hand and a moderate paresis of her right leg. Figure 1. Cranial CT ofpatient 1: left frontal periventricular infarction (broad arrow), and left fronto-temporal cortical atrophy (slim arrow) Table 1. Test scores of patients 1 and 2 Patient 1 Patient 2 'Mini Mental-State' score 12 (maximum=30) CAMCOG score'? (maximum=107) 29 (n) 29 (n) 100 (n) 102 (n) 515 (n) 50 (n) Aphasia battery" (maximum=530) 498 (n) Token test" (maximum=50) 48 (n) Word fluency < 12 (ab) < 12 (ab) Wisconsin card sorting test (128 cards)" categories achieved 2 (ab) perseverative errors 52 (ab) 3 (ab) 47 (ab) (n) normal; (ab) abnormal In November 1988 she was admitted to a psychiatric ward with suspected major depression. She had been apathetic for 2 months, had lost her appetite and weight. She felt unable to work and spent most of her time in bed. She recovered quickly and volunteered to take part in any available activities. After one month of successful antidepressant treatment she returned home. Following her complete recovery, she relapsed into lethargy in January 1989 and was readmitted to hospital in February. She could not be motivated to get out of her bed at all. She seemed desperate about her inability to overcome her lack of initiative. This time she recovered slowly after several weeks. Her clinical and CT findings were unchanged (Figure 1). A single photon emission tomography (SPET) showed left frontal hypoperfusion. The electroencephalogram (EEG) showed focal left anterior slowing. Her neuropsychological test scores are summarized in Table 1. Case 2 A 71-year-old right-handed woman had been admitted to different medical hospitals four times during the last 12 months. She had a 6-year history of hypertension. She recalled a brief episode of transient mild right-sided hemiparesis in 1987. During the first days in the medical department she was described as depressed with a motor retardation, and a loss of appetite and interest. She always recovered completely without any recognized sign of organic mental disorder. Shortly after her discharges she regularly fell back into apathy and left her bed for only a few minutes a day to drink a sip of water. At the time of admission to our ward she was mute and rigid. After 3 days she took part in various physical and occupational therapies. Every sign of suspected parkinsonism subsided. One week later she appeared lively and sociable. The tetracyclic antidepressants we used could hardly account for this fast improvement. She seemed to look for an explanation, but was unable to understand what had been 0141-0768/91/ 020089-03/$02.00/0 © 1991 The Royal Society of Medicine 90 Journal of the Royal Society of Medicine Volume 84 February 1991 Figure 2. Cranial CT ofpatient 2: left frontal periventricular hypodensity (broad arrow), and left fronto-temporal cortical atrophy (slim arrow) going on with her during the previous months. She felt worried and sceptical about her future. Her cranial CT showed a mild left-sided cortical atrophy, two small hypodense areas, one in the left frontal cortex, the second at the rim of the left anterior horn (Figure 2). Her SPET revealed left frontal hypoperfusion. The EEG showed a slow alpha-activity. The ECG yielded signs ofleft ventricular hypertrophy. Normal flow signals were detected by extracranial Doppler sonography. Blood tests were normal. Her neuropsychological test performance is summarized in Table 1. Case 3 A woman of 72 years had been admitted to hospital 3 times during the last year. Initially a loss of appetite and weight led to a thorough gastroenterological examination including duodenoscopy, however, no somatic disease was detected. She received antidepressant treatment for suspected major masked depression and returned home. Soon thereafter she was readmitted after attempted suicide with an overdose of tricyclic antidepressants. Again she Figure 3. Cranial CT of patient 3: left frontal white matter infarction (broad arrow), left fronto-temporal cortical atrophy (slim arrow), and cerebellar cortical atrophy recovered quickly and urgently wished to return home. Two days before her planned discharge she tried to jump out of a second floor window. She was transferred to a psychiatric hospital. The symptoms of depression resolved. The next admission to hospital was necessary because of dehydration. She had refused to drink for several days. Each time she returned home she wanted to improve and go back to work, but inevitably she fell back into lethargy after a couple of days. She did not leave her bed, resisted eating or drinking, and was obviously severely upset about her condition. She was admitted to our psychiatric department after a weight loss of 30 kg within 3 months. Her history did not yield any evidence of ischaemic stroke or any other relevant organic impairment. The neurological examination was normal. Standard laboratory tests, chest X-ray, Doppler sonography of the extracranial arteries, electrocardiogram and EEG were normal. Cranial CT revealed a small left sided infarct of the anterior internal capsule and the head of the caudate, and mild left fronto-temporal cortical atrophy (Figure 3). She appeared highly motivated in carrying out the occupational therapy activities. She gained weight and said she felt very well. After 3 weeks during a visit to her family for the weekend, she went to bed and would not get up again. She was brought back to our department by ambulance. She appeared equally discouraged and agitated. Antidepressants, neuroleptics and tranquilizers did not exert any beneficial effects during the following weeks. Her condition worsened severely. She was desperate and uncooperative. It was difficult to get her out of bed, and impossible to perform any neuropsychological assessment. Finally her husband insisted on taking her home where she spends most of her time in bed. Discussion In summary these three patients had three or more hospital admissions during a 12-month period. They presented with severe psychomotor retardation, weight-loss, exhaustion and self-reproach. Their histories and symptoms suggested a diagnosis of major depression", The symptoms of major depression can be closely mimicked by post-stroke depression as a secondary affective disorder, which may provide insights into the relevant brain areas or mechanisms of affective disorders in general 2,3,5. Cranial CTs '. Conversely, several intriguing hypotheses were offered to explain the laterality of emotions after ischaemic strokes. Left hemisphere stroke induces a stronger decrease of cortical serotoninreceptors than right hemisphere stroke. Therefore a failure of serotonin-regulation after left-sided stroke was considered as a potential cause for post-stroke depression-s. In the cases presented here the underlying deficits elicited strikingly similar reactive disturbances. Domestic difficulties were uniformly admitted by the patients and their families. Immediately after discharge the patients experienced a painful lack of initiative and energy in the presence of the more permissive and less structured familiar setting. This disappointment after a seemingly perfect recovery proved increasingly distressing to the patients and their families. The patients reacted with guilt and self-reproach, while their families' attitudes changed from those of support and challenge, to pity and anger. The fact that these disturbances resolved quickly in the structured hospital environment indicates the relevance of these reactive behavioural disturbances. Each admission added to the patients' fear of a repeated relapse. In view of this potentially threatening development, it has to be concluded that patients with this disturbance deserve particular and timely therapeutic attention, which should not end with their discharge. In addition to the treatment with antidepressants they need continued professional treatment provided by day centres because sufficiently structured therapy can not be provided by their own families. Family counselling may also be beneficial in helping the families adjust to the changes in behaviour of a family member. Despite the complexity of the clinical features and underlying pathology our patients showed compelling similarities. 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