842 In: Kertesz A, ed. Localization in neuropsychology. New York: Academic Press, 1983: 323-56. 4 Damasio AR, Damasio H. The anatomic basis of pure alexia. Neurology 1983;33:1573-83. 5 Greenblatt SH. Subangular alexia without agraphia or hemianopia. Brain Lang 1976;3: 229-45. 6 Assal G, Hadj-Djilani M. Une nouvelle observation d'alexie pure sans hemianopsie. Cortex 1976;12:169-84. 7 Pirozzolo FJ, Kerr KL, Obrzut JE, et al. Neurolinguistic analysis of the language abilities of a patient with a "double disconnection syndrome": A case of subangular alexia in the presence of mixed transcortical aphasia. J Neurol Neurosurg Psychiatry 1981;44:152-5. 8 Friedman RB, Albert ML. Alexia. In: Heilman KM, Valenstein E, eds. Clinical neuropsychology. New York: Oxford University Press, 1985:49-73. 9 Kinkel PR, Kinkel WR, Jacobs L. Nuclear magnetic resonance imaging in patients with stroke. Semin Neurol 1986;6:43-52. Minor hemisphere syndrome following left hemispheric lesion in a right handed patient Some degree of unawareness of hemiplegia occurs in about one third of cases of right hemisphere patients with left hemiplegia.' Anosognosia for hemiplegia may be associated with left hemiasomatognosia. Such patients behave as if the left half of their body was no longer part of themselves.3 In contrast to the relative frequency of such phenomena following damage to the right hemisphere, anosognosia and hemiasomatognosia have rarely been reported following left hemisphere lesions. None of the reported cases has concerned authentic right-handed patients and the degree of language impairment has often been unknown. We describe a case of a strongly right handed patient with asomatognosia and anosognosia for right hemiplegia. She exhibited other deficits relating to the socalled minor hemisphere syndrome, and had no language disorders. On the thirteenth day after aortic valve replacement for aortic regurgitation, the patient, a 68 year old right handed woman, developed an acute hemiplegia. On the fourth day following onset, neurological examination showed massive right motor deficit affecting the face, the arm and the leg. Right plantar reflex was extensor, there was severe hypesthesia and tactile extinction on the right side of the body, and right homonymous hemianopia on confrontation. Language and praxis were normal on bedside evaluation. The patient had motor impersistence and strongly tended to keep her head and eyes turned to the left, even on verbal stimulation from the right. CT scan at 10 days post onset revealed a left hemispheric infarct involving the territory of the middle cerebral artery, both deep and superficial, and the territory of the anterior choroidal artery. The following observations were gathered during the first three weeks following the stroke, during which period the neurological condition of the patient remained essentially unchanged. Right sided visual neglect was seen on the dot cancellation test: she failed to cancel 7/9 dots in the right half of the test sheet, although she did not miss any of the eight dots in the left half. The patient was Letters to the Editor presented with a list of 40 pairs of items (10 pairs of digit names, 20 pairs of object names, 10 pairs of sentence fragments). She showed clearcut right auditory neglect: she correctly reported all of the 40 items presented to her left ear, but none of those presented to her right ear. certainly dominant for language. If the left hemisphere was dominant for language, or if language was bilaterally represented, the extensive left hemispheric softening would have caused aphasic symptoms, which was not the case. Second, her left hemisphere was strongly dominant for manuality, spatial attention, and -body schema. Few cases of right asomatognosia or anosognosia for right hemiplegia have been reported. Dronkers and Knight8 have described a left handed patient with clear-cut anosognosia for right hemiplegia, right spatial neglect and aprosodia, following left hemispheric infarct. Cambier et al9 have reported a similar case, but their patient seems to be ambidextrous. Such is also the case of the patient reported by Hermann and Potzl." Among their patients with lefthemispheric lesions, Hecaen and Sauguet" mention right hemiasomatognosia in two out of 47 left-handed patients, but in none of 293 that were right-handed. Gross and Kaltenback' have described two patients with such a denial of right hemiplegia, including one case with hemiasomatognosia. These patients were both aphasic, but there is no mention of their manual dominance. Cutting2 has reported three instances of denial of hemiplegia out of 22 testable right hemiplegic patients. Their manual dominance and degree of language impairment, however, are not reported. She was largely unaware of her hemiplegia. When asked if she could move her right hand, sew, or knit, she answered that she could. When asked if she could move her right leg, she answered positively and moved her left leg as a proof. Sometimes, the patient admitted that she needed some help with walking or running. Once, when asked if she could cut her meat and eat all by herself, she affirmed that she could, if only helped to sit in her bed. She occasionally showed some abstract knowledge ofher deficit. She said that doctors had told her she had hemiplegia, but that she did not believe it, since she was not paralysed and could walk. The patient also showed a variable degree of right asomatognosia. In several instances, when shown her right hand, she would answer that it was the hand of a corpse that had been introduced into her bed. However, she sometimes correctly identified the hand as her own. Touching it with her left hand apparently facilitated the identification. When asked to designate her right hand she was initially unable to find it in the bed. Twelve days after onset, she could correctly designate The dominant hemisphere for body her right arm, leg, eye and cheek. schema is usually the right hemisphere. Her spontaneous speech was considerably However, as we have just seen, considerable aprosodic and she was initially unable to sing evidence exists of reversed dominance, as at all, although she previously used to parrevealed by right asomatognosia and anosoticipate in an amateur choir. Two weeks after gnosia for right hemiplegia. The left hemithe stroke, her few attempts at singing were sphere is usually dominant for manuality and very much out of tune. Moreover, her perceplanguage, although reversed dominance in tion of melodies was also impaired. Five days this domain is also well known. But are all the post-onset, she could not identify common different patterns of co-dominance concerntunes that were hummed to her, but recoging language, manuality and body-schema nised them readily as soon as the lyrics were biologically possible? Or are some of these added. Three weeks later, she could identify functions necessarily supported by the same five out of 10 popular tunes whose melodies hemisphere (or by opposite hemispheres)? were sung to her. We shall consider each pair of functions in The patient described herselfas completely turn. First, the left hemisphere is usually right handed, and denied having been forced dominant for both language and manuality. to use her right hand as a child. There was no Our patient falls into the 4% of those that are record of any significant cerebral trauma in right handed with right hemispheric dominbirth or early childhood. She was submitted ance for language, according to Rasmussen to a 24 item questionnaire about her preferred and Milner's figures'2 (for discussion, see hand or foot in various everyday-life Geschwind and Galaburda'3). Second, manactivities. She always unambiguously chose uality and body schema are usually disthe right side. Her parents, grand-parents, sociated since in most right handed subjects, and two children were all reported to be right the right hemisphere is dominant for body handed. schema. The patient reported by Dronkers Language evaluation was normal in all and Knight8 shows exactly the opposite patrespects. Spontaneous speech, repetition, tern of dominance. However, Hecaen and object and picture naming, designation, Sauguet" mention several left handed fluency in controlled association, comprehenpatients with left asomatognosia, suggesting sion, and reading were flawless. She was too that the right hemisphere can occasionally awkward with her left hand to allow evaluasupport both functions. The pattern of tion of writing. There was no left hand impairment in our patient demonstrates that apraxia. Visual identification of objects, that can also occur for the left hemisphere. colours and faces was normal. Third, language and body-schema are usually The patient was a right handed woman, dissociated, but one hemisphere can with no family history of left handedness. occasionally be dominant for both functions, After a left parieto-temporal infarction, she as illustrated by the patients of Gross and showed several symptoms that usually follow Kaltenback,' who have at the same time right hemispheric lesions, that is, symptoms aphasia and anosognosia for hemiplegia folencompassed in the so-called minor hemi- lowing left hemispheric lesion. Our patient's sphere syndrome. She had right hemispatial dominance pattern is the exact opposite ofthe neglect,' right hemiasomatognosia, anoso- pattern which prevails in most of those that gnosia for right hemiplegia, motor aprosodia6 are right handed, since her left hemisphere is and a severe impairment in identifying and dominant for body schema, and her right producing musical tunes7 but no aphasia. hemisphere for language. Two main conclusions can be drawn conThe case favours the idea that there is no cerning the patient's pattern of cerebral obligatory link between any two of the three dominance. First, her right hemisphere was cerebral functions we have considered, and Letters to the Editor that each can be supported by one hemisphere or the other. LAURENT COHEN PHILIPPE RtMY ANNE LEROY CHRISTIAN GtNY JEAN-DENIS DEGOS Clinique des Maladies du Systeme Nerveux, *H6pital de la Salpetriere, Paris, Service de Neurologie, H6pital Henri Mondor, Creteil, France Correspondence to: L Cohen, Clinique des Maladies du Systeme Nerveux, Hopital de la Salpetriere, 47 Bd de l'H6pital, 75651 Paris Cedex 13, France. 1 Gross H, Kaltenback E. Die Anosognosie. Wiener Zeitschrift fur Nervenheilkunde Pure sensory stroke due to midbrain haemorrhage After reading the interesting case reported by Azouvi et al,' we would like to report a similar case, but in our patient the underlying disease was a cavernous angioma. A 42 year old woman was admitted to our hospital because of a mild occipital pain, and dysaesthesia in the left part of her body. Neurological examination showed a fully oriented patient, loss of touch and pain sensations then involved the entire left side of her body, including the face. Vibration and position sensations were normal as were motor and cerebellar functions. Tendon jerks were symmetrical and plantar responses were flexor. Laboratory examinations, ECG and chest radiographs were normal. A CT showed a haematoma in the right dorsal and lateral aspect of the pons. An arteriographic study of both vertebral arteries showed no abnormalities. The neurological disorder resolved within three months. An MRI performed three months later revealed a hypodensity, of 0 8 x 1 8 cm diameter, in the right dorsal and lateral aspect of the pons, suggesting a cavernous angioma (fig). Since the first description in 1977,2 only eight cases of haemorrhagic pure sensory stroke (PSS) have been described. All of them were secondary to small haematomas in the 843 1955;11:374-418. 2 Cutting J. Study of anosognosia. J Neurol, Neurosurg Psychiatry 1978;41:548-55. 3 Bisiach E, Vallar G, Perani D, Papagno C, Berti A. Unawareness ofdisease following lesions of the right hemisphere: anosognosia for hemiplegia and anosognosia for hemianopia. Neuropsychologia 1986;24:471-82. 4 Hecaen H. Introduction a la neuropsychologie. Larousse: Paris, 1972. 5 Heilman KM, Watson RT, Valenstein E. Neglect and related disorders. In: Heilman KM, Valenstein E, eds. Clinical neuropsychology. New York: Oxford University Press, 1985. 6 Ross ED. The aprosodias: Functional-anatomic organisation of the affective components of language in the right hemisphere. Arch Neurol 1951 ;38:561-9. 7 Zatorre RJ. Musical perception and cerebral function. a critical review. Music Perception 184;2:196-22 1. 8 Dronkers NF, Knight RT. Right-sided neglect in a left-hander: Evidence for reversed hemispheric specialisation of attention capacity. Neuropsychologia 1988;27:729-35. 9 Cambier J, Masson M, Guillot M, Robine B. Negligence droite avec hemiasomatognosie, confusion mentale, apraxie et agraphie sans aphasie. Revue Neurologique 1985;141:802-6. 10 Hermann G, Potzl 0. UberAgraphie und ihre lokaldiagnostischen Beziehungen. S Karger: Berlin, 1926. 11 Hecaen H, Sauguet J. Cerebral dominance in left-handed subjects. Cortex 1971;7:19-48. 12 Rasmussen T, Milner B. Clinical and surgical studies ofthe cerebral speech areas in man. In: Zulch KJ, Creutzfeldt 0, Galbraith GC, eds. Otfried Foerster symposium on cerebral lateralisation. Heidelberg: Springer, 1975. 13 Geschwind N, Galaburda AM. Cerebral lateralisation. Biological mechanisms, associations, and pathology: 1. A hypothesis and a program for research. Arch Neurol 1985;42:428-59. thalamus, internal capsule or pons.' As far as we know, this is the first case of haemorrhagic PSS secondary to cavernous angioma located in the pons. In our patient, as in the one reported by Azouvi et al,' the damage was restricted to the right dorsal spinothalamic tract without involving the medial lemniscus. We agree with the authors that small haematomas located on the sensory pathways, before they reach the thalamus, can produce partial PSS. MRI is useful in detecting vascular malformations, even when, as in our case, angiographic studies are normal. Parkinsonism and defects of praxis following methanol poisoning J ALVAREZ-SABIN J MONTALBAN M TINTORE A CODINA Department of Neurology, Hospital General Vall d'Hebron, Barcelona, Spain Correspondence to: Dr Alvarez-Sabin, Rda San Antonio, 5 Ppal, 08011 Barcelona, Spain. 1 Azouvi Ph, Tougeron A, Hussonois C, Schouman-Claeys E, Bussel B, Helkd JP. Pure sensory stroke due to midbrain haemorrhage limited to the spinothalamic pathway. J Neurol Neurosurg Psychiatry 1989;52:1427-8. 2 Groothuis DR, Duncan GW, Fisher CM. The human thalamocortical sensory path in the internal capsule: evidence from a small capsular haemorrhage causing a pure sensory stroke. Ann Neurol 1977;2:328-31. The neurological sequelae of methanol intoxication shows marked individual variation, but Parkinsonism, optic atrophy and focal cranial nerve deficits have been described.'3 We report a patient who presented with Parkinsonism and dyspraxia and who recovered from acute severe methanol poisoning. The MRI scan showed damage of the deep grey nuclei. A 28 year old woman with a history of depression and recurrent alcohol abuse experienced nausea, vomiting, ataxia and blurred vision for 24 hours before she was admitted stuperose, with dilated pupils that did not react to light. The optic fundi were normal, and there were no localising neurological signs. The liver was enlarged. She had a leucocytosis of 12900/mm3 and a severe metabolic acidosis (pH 715; bicarbonate 2-8 m Eq/l; P02 129 mm Hg; pCO2 8 mm Hg). With the possibility of methanol poisoning in mind, she was given intravenous infusions of sodium bicarbonate and ethanol, and haemodialysis. The level of methanol in the blood was 2-85 g/l. After three hours, the acidosis was controlled. When the patient's level of consciousness improved, she admitted drinking some 200 ml of methanol in the past 48 hours. She left the hospital after four days without apparent neurological or ocular abnormalities. She was examined two years later, complaining of motor slowness and loss of memory. She had been working at the same factory at which she was employed before taking the methanol. The work required sequential and repetitive movements of both hands and feet. The employers stated that her productivity was reduced by 50%. Neurological examination showed a mild dysarthia, a Parkinsonian-like syndrome, with an expressionless face, limb bradykinesia, and abnormal postural reflexes. Rapid alternating finger movements were poorly performed. The glabella tap sign was positive and palmar-mental and peri-oral reflexes were present; her gait was characterised by poverty Figure Axial and sagittal T, MRI showing a cavernous angioma in the right dorsal part of the pons. of associated movements, with reduced armswinging and body turning. The optic fundi displayed bitemporal pallor. Visual acuity was normal. Chest radiographs, ECG and EEG were normal. An unenhanced CT scan showed bilateral areas of decreased density, especially in the putamen. An MRI scan (fig) showed bilateral lesions involving the claus-