590 ing the red nucleus, within the mesencephalic tegmentum, the left inferior colliculus and the mammillary bodies." These findings were compatible with Wernicke's encephalopathy. Wallis et al,6 described a case of Wernicke's encephalopathy with hypothermia being "akinetic and mute," only slightly reacting to nociceptive stimulation, forty hours after the start of thiamine therapy their patient was eating by himself and answering simple questions. The anatomical lesions of Wernicke's encephalopathy involve the mammillary bodies symmetrically, and in various degrees the paraventricular regions of the thalamus and the hypothalamus, the periaqueductal region of the midbrain, the reticular formation of the midbrain, the inferior colliculi, the floor of the fourth ventricle and the superior vermis. The type and topography of these lesions may correspond well to the "tiny lesions of the posterior diencephalon and adjacent midbrain" held responsible for akinetic mutism."4 MW MANN JD DEGOS Department of Neurology, CHU H. Mondor, F-94010 Creteil, France References I Cairns H, Oldfield RC, Pennybacker JB, Whitteridge D. Akinetic mutism with an epidermoid cyst of the 3rd ventricle. Brain 1941 ;64:273-90. 2 Fischbeck KH, Simon RP. Neurological manifestations of accidental hypothermia. Ann Neurol 1981;10:384-7. 3 Nielsen JM. Wernicke's encephalopathy. Correlation of sites of lesions with symptomatology. J Nerv Ment Dis 1953;118:429-34. 4 Plum F, Posner J. Diagnosis of Stupor and Coma. 3rd Ed. Philadelphia: FA Davis Company, 1982. 5 Victor M, Adams RD, Collins GH. The Wernicke-Korsakoff-Syndrome. Oxford: Blackwell Scientific Publications, 1971. 6 Wallis WE, Willoughby E, Baker P. Coma in the Wernicke-Korsakoff-syndrome. Lancet 1978;ii:400-1. 7 Wernicke C. Lehrbuch der Gehirnkrankheiten fuer Aerzte und Studierende. Berlin: Theodor-Fischer-Verlag, 1881:2:220-42. Accepted 2 November 1987 Hemichorea and its denial in a case of caudate infarction diagnosed by magnetic resonance imaging Letters Computed tomography (CT) performed erable attention,' but few case reports of cognitive deficits due to lesions localised to on 6 October 1986 (on the 17th day from the basal ganglia have appeared in the litera- onset) showed a small low density area in ture. We report a case of denial of hemi- the head of the left caudate nucleus (approxchorea in a patient with a discrete lesion in imately 4cm rostral to the orbito-meatal the head of the left caudate nucleus, which line). The low density area did not extend to was diagnosed by magnetic resonance imag- the posterior portion of the internal capsule or to the globus pallidus, and no other ing (MRI). A 51 year old right-handed man was abnormalities were seen. Enhancement after admitted to Kawasaki Seitetsu Chiba Hos- contrast infusion in the region of the left pital (Chiba, Japan) on 22 September 1986, caudate nucleus indicated recent infarction. because of the sudden onset of right-sided Magnetic resonance imaging (Picker Interinvoluntary movements 2 days previously. national Ltd., VISTR-MR) was performed According to family members, the move- with a 0-5 Tesla superconducting magnet ments were not seen when the patient was using the inversion recovery technique (on 20 December, the 92nd day from onset). The asleep. On admission, the patient was fully con- width of the slice was 10mm and the scious and oriented, garrulous and seem- patient's head was positioned supine. Horiingly happy. His wife said he had a forth- zontal (fig a) and left lateral sagittal (fig b) right personality. Visual acuity and the images showed a small low intensity area in visual fields on confrontation were normal; the head of the left caudate nucleus. There the pupils were equal and reacted normally were no other abnormalities. The course of the disease has been favourto light. Extraocular movements were also normal. Other cranial nerve functions, limb able. The patient was treated with halomuscle power, and muscle stretch reflexes peridol (0-75 mg, thrice daily) for three days, were intact. There was some decrease of the starting on 1 October, the 12th day from tone of right-sided muscles and the plantar onset. The severity of the involuntary moveresponses were flexor. Nearly continual dis- ments decreased and the haloperidol thertal choreic movements of the right arm and apy was then stopped. The hemichorea leg were observed without proximal ballistic gradually improved and had disappeared movements. There was a slight decrease in within six months. In contrast, the patient's pinprick sensation and vibration on the denial of the hemichorea continued for three right leg but position and light touch sensa- weeks from onset, but disappeared during tion were normal. These sensory abnormal- the period when hemichorea was still ities disappeared rapidly within 3 days. observed. The patient was found to be totally The present case showed sudden onset of unconcerned about the chorea. Although right-sided chorea and some decrease of the involuntary movements made the play- muscular tone, but na symptoms of the pyring of games, such as chess, impossible, he amidal tract, such as motor paresis. Mild invited other patients to play and tried to sensory abnormalities were observed in the undertake activities which were manifestly right leg but rapidly disappeared and the impossible. Moreover, when asked about his patient was diagnosed as acute hemichorea. right limbs, he responded that they were fine MRI clearly revealed a lesion localised to or had recovered, despite the fact that vio- the head of the caudate nucleus conlent involuntary movements were ongoing. tralateral to the involuntary movements. In this respect, he showed clear signs of Particularly noteworthy about this case denial of the hemichorea. was the denial of the hemichorea during the Neither hemineglect (as determined by early stages of the disease. This finding is horizontal line bisection, copying pictures analogous to the denial of hemiplegia and Albert's line-crossing test) nor construc- (anosognosia) first reported by Babinski2 tional apraxia (copying figures such as a dia- and indicates that anosognosia can also be mond shape, a Greek cross and a cube) were found in cases of involuntary movements. found. There was no exinction on double Weinstein3 has previously described a case simultaneous tactile and visual stimulation. with diffuse brain tumour in which there was Facial recognition, identification of over- denial of involuntary movements, and Goldlapping figures (Poppelreuter), colour nam- blatt et al4 have also reported the denial of ing, limb and facial praxis to command, left- chorea in the acute stage in a case of hemiright discrimination, finger naming and chorea in which infarcts were confined to simple verbal calculations were intact. His two locations in the caudate nucleus and the Wechsler Adult Intelligence Scale was at a putamen. normal level (Verbal IQ 103, PerAnosognosia is normally considered to be formance IQ 92 and Full Scale IQ = a deficit of higher cortical functions, and 110). thought to be a right parietal sign.5 How= Sir: The possible cognitive functions of the basal ganglia have recently received consid- = Letters Fig MRI (92 days after symptom onset) (inversion recovery technique). (a) Horizontal view [time of repetition (TR) 2080 ms, time of inversion (TI) 500 ms], (b) Left lateral sagittal view (10 mm from midline) (TR 2080 ms, TI500 ms), showing a small low intensity area at the head of the left caudate nucleus (arrows). ever, on the basis of experimental results in the cat, in which sensory neglect was brought about by lesions of the ventral half of the frontal lobe (including a portion of the caudate nucleus and putamen),6 Goldblatt et al4 have previously suggested that denial might be caused by damage to the basal ganglia. Among conditions conducive to the emergence of denial symptoms, the patient's personality prior to the disease has been emphasised,7 and great care must be taken in considering the denial as indicative of a localised lesion. Nevertheless, recent 591 research on the cognitive functions of both hands. It was exacerbated by anxiety patients with Parkinson's disease have indi- but not relieved by alcohol. His elder cated that the basal ganglia may have an brother also had a tremor. He had no other important role in cognition' and, from this complaints. There was no relevant past hisperspective as well, the present case is of tory. He was a smoker. On examination at considerable interest. that time, the only abnormality to be found MITSURU KAWAMURA was a postural tremor of the outstretched NOBUYOSHI TAKAHASHI hands. There were no features of ParkinKEIZO HIRAYAMA sonism. Idiopathic essential tremor was Department of Neurology, diagnosed, and he responded well to proBrain Research Institute, pranolol. School of Medicine, Six months later he presented again, with Chiba University, right sided weakness of acute onset. He was 1-8-1 Inohana, found to have a mild right hemiparesis with Chiba 280, brisk tendon reflexes and upgoing plantar Japan response. A CT scan showed a small infarct in the posterior limb of the internal capsule References on the left, as it passed between the thalI Marsden CD. Function of the basal ganglia as amus and the putamen (Fig). At review 6 revealed by cognitive and motor disorders in months later the weakness had resolved Parkinson's disease. Can J Neurol Sci completely. While the tremor persisted on 1984;11:129-35. the left, it had completely resolved on the 2 Babinski J. Contribution a l'etude des troubles right. Again, no features of Parkinsonism mentaux dans l'hemiplegie organique cere- were found. brale (anosognosie). Rev Neurol (Paris) Using Marsden's classification,' 4 this 1914;22:845-8. 3 Weinstein EA, Kahn RL. Denial of Illness, 1st patient's tremor is likely to be Type II, or ed. Springfield, Charles C Thomas, 1955: 10 benign pathologic essential tremor. This is postural, affects mainly the arms, and has a and 131. 4 Goldblatt D, Markesbery W, Reeves AG. frequency range of 5-7 Hz. There is often a Recurrent hemichorea following striatal family history, and the pathogenesis is lesions. Arch Neurol 1974;31:51-4. thought to involve a central oscillator. The 5 Hecaen H, Albert ML. Human Neuro- site of the oscillator is unknown, but is likely psychology, 1st ed. New York: J Wiley and to be associated with the cerebello-rubroSons, 1978:303-7. 6 Reeves AG, Hagamen WD. Behabioral and thalamo-cortical pathways.' Surgical treatEEG asymmetry following unilateral lesions ment presumably either destroys the oscilof the forebrain and midbrain in cats. lator or interrupts the circuit elsewhere. In the present case, the lesion occurred Electroencephalogr Clin Neurophysiol 197 1;30:83-6. 7 Weinstein EA, Kahn RL. Denial of Illness, 1 st ed. Springfield, Charles C Thomas, 1955:71-84. ivilm .I- Accepted 2 November 1987 F Essential tremor cured by infarction adjacent to the thalamus Sir: The thalamic neucleus ventralis is thought to be important in the pathophysiology of essential tremor,' and stereo(ventralis Vim tactic intermedius) thalamotomy2 and chemothalamectomy3 have been used with some success in the treatment of essential tremor. We have seen a case in which tremor ceased unilaterally following an infarct of the internal capsule in close relation to the thalamus. The patient presented at the age of 59 years with a one year history of tremor of A k lips Fig CT scan showing infarction (arrowed) in the left internal capsule adjacent to the thalamus