Journal of Neurology J Neurol (1985) 232 : 381-382 © Springer-Verlag 1985 Pure motor hemiparesis due to non-hypertensive putaminal haemorrhage S. Jain 1, N. K. Mishra e, and M. C. Maheshwari I Departments of 1Neurology and ~Neuroradiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi-110029, India Summary. The syndrome of pure motor hemiplegia (PMH) has been traditionally regarded to be due to lacunar infarcts at various places in the brain. Recently, attention has been drawn towards various other aetiological factors which have been responsible for this clinical presentation. PMH as a result of hypertensive putaminal haemorrhage is extremely uncommon. A case of P M H as a result of non-hypertensive putaminal haemorrhage is described. Key words: PMH - non-hypertensive - putaminal haemorrhage Introduction Pure motor hemiplegia (PMH) is a well-established but uncommon syndrome defined as a complete or incomplete paralysis of the face, arm and leg on one side, not accompanied by sensory signs, visual defect, dysphasia or apractognosia [3]. The commonest cause of PMH has been lacunar infarcts located either in the internal capsule or in the pons [3]. Isolated cases of PMH resulting from infarcts in the cortex [15], pyramid [1, 3, 12] and midbrain [6] have also been reported. Occasionally, other aetiological factors leading on to PMH have also been described. These include abscess [14], metastasis [1, 15], multiple sclerosis [15], postcraniotomy haemorrhage [7], pontine haemorrhage [4] and capsular haematoma [t0, 11, 15]. PMH as a result of hypertensive putaminal haemorrhage (HPH) is considered to be extremely rare and only two such dear-cut cases have been described recently [8, 13]. We report one case presenting as PMH due to a nonhypertensive intracerebral putaminal haemorrhage. To the best of our knowledge, such a case has not been reported in the literature as yet. Case report While trying to lift a heavy bag, a 48-year-old right-handed male complained of weakness of right upper and lower limbs at 8 p.m. on 29 April 1985. He had no headache, vomiting or altered sensorium. Next morning he was admitted to the neurology services of the All India Indstitute of Medical Sciences, New Delhi. When examined about 14 h after the onset, his blood pressure was 150/90 mmHg. He was fully conscious and alert. He had minimal slurring of speech but no dysphasia. Fundus examination was normal with no hypertensive vascular changes. The visual fields, pupils and eye movements were normal. He had a right supranuclear facial paresis. The Offprint requests to: Dr. S. Jain (address see above) facial sensations and palatal and tongue movements were normal. He had minimal right hemiparesis. Right upper and lower limb power was grade IV/V MRC [9]. The tendon reflexes were brisk on the right side with an upgoing plantar reflex. Left plantar reflex was flexor. There was no inco-ordination or dyspraxia. Sensory examination was normal. There were no parietal lobe signs. He was known to have had noninsulin-dependent diabetes mellitus for the last 6 years. His diabetic status was under control with dietary regulation and a small dose of oral hypoglycaemic agent. He was not a known hypertensive. Routine blood chemistry revealed evidence of mild diabetes mellitus. Other biochemical parameters were normal. E C G was normal. A 2-D echocardiogram was normal. A n unenhanced CT scan done 2 days after admission showed a welldefined area of high attenuation (mean value: 71 Hounsfield units) at the level of right middle and posterior putamen, suggestive of fresh haemorrhage. It was surrounded by a thin zone of perifocal low attenuation. There was no compression of the body of the right lateral ventricle. The volume of this haematoma was estimated to be 1.37 ml (Fig. l a and b). A left internal carotid angiogram done via the percutaneous transfemoral route revealed no evidence of any aneurysm or arteriovenous malformation. During hospital stay his blood pressure varied between 130/80 and 140/90 m m H g without any drugs. The right hemiparesis gradually improved, with the lower limb recovering earlier than the upper limb. When he was discharged on 10 May 1985, there was no hemiparesis. Power in the limbs was V/V MRC. His speech was absolutely clear. He had a residual minimal right supranuclear facial weakness. The tendon reflexes were normal and plantar reflexes were bilaterally flexor. A t follow-up 6 weeks after the onset, he had no neurological deficit. The right facial weakness had completely improved. His only complaint was a feeling of stiffness in the right half of the tongue while speaking. He had no dysphasia. His blood pressure was 130/90 mmHg. His diabetic status was under control with only dietary regulation. Discussion The syndrome of PMH has traditionally been associated with lacunar infarcts located at various sites [1, 3, 6, 12, 15]. Besides other uncommon causes, a haemorrhagic origin of PMH has been reported to be rare. Fisher and Curry [3] did not find any case of intracerebral haemorrhage in their series, but did not exclude the existence of haemorrhage as a causative factor of PMH. In two large series of 63 cases with PMH, CT scan re- 382 P M H is another point which supports this hypothesis. In the first such case, the only residual deficit was a moderate right facial palsy 15 days after the onset, while the power in the limbs had already returned to normal by the 4th day [13]. In the only other reported case, the patient was asymptomatic and back to her normal work within three weeks [8]. It is probable that, as the h a e m a t o m a resolves, the pressure effects wear off and the patient improves. In the present case also, the patient was asymptomatic except for a minimal facial weakness 11 days after the onset. He had recovered fully within 6 weeks. It must be emphasized that it is extremely rare for H P H to present as PMH. This is borne out by the fact that only two clear cut cases have been reported till now [8, 13]. In the patient reported here, the situation is different and more interesting. He was not a known hypertensive. The angiogram did not reveal any possible aetiological cause for his haematoma. The possibility of a very small aneurysm or a cryptic arteriovenous malformation cannot be ruled out. However, P M H as a result of haemorrhage in the putaminal area carries a good prognosis, as has been seen in all these three cases. After an extensive review of the literature, we could not find another case report of a non-hypertensive putaminal haemorrhage presenting as PMH. Acknowledgement. The authors thank Mr. Raghuvansh Sharma for his secretarial help. References Fig. la, h. CT scan (unenhanced) showing a well-defined haematoma at the level of the right middle and posterior putamen vealed the presence of a capsular haemorrhage in only 5 cases [11, 15]. Being part of large series, these reports lack the detailed description of the clinical features of these 5 cases. Only two cases of P M H as a result of H P H have been reported where the detailed neurological evaluation has been described [8, 131. HPH, being a c o m m o n clinical entity, is known to present with a wide spectrum of neurological deficits [2, 5]. CT scan has made it possible for us to correlate the clinical syndrome of P M H with haemorrhage in the basis pontis [4], internal capsule [10, 11, 15] or H P H [8, 13]. Although a clinical rarity, such cases must have existed earlier also. In H P H , the size and location of the haematoma have been thought to be very important. It has been suggested that the posterior and lateral location of the haemorrhage may be causing P M H only by pressure effects rather than the actual destruction of the fibres in the internal capsule [8, 13]. The very early recovery of the major neurological deficit in these cases of H P H presenting as 1. Chokroverty S, Rubino FA (1975) 'Pure' motor hemiplegia. J Neurol Neurosurg Psychiatry 38 : 896-899 2. Fisher CM (1961) Clinical syndromes in cerebral hemorrhage. In: Fields WS (ed) Pathogenesis and treatment of cerebrovascular disease. Thomas, Springfield, IL, pp 318--342 3. Fisher CM, Curry HB (1965) Pure motor hemiplegia of vascular origin. Arch Neurol 13 : 30-44 4. Gobernado JM, Fernandez de Molina AR, Gimeno A (1980) Pure motor hemiplegia due to haemorrhage in the lower pons. Arch Neurol 37 : 393 5. Hier DB, Davis KR, Richardson EP, Mohr JP (1977) Hypertensive putaminal hemorrhage. Ann Neurol 1 : 152-159 6. Ho KL (1982) Pure motor hemiplegia due to infarction of the cerebral peduncle. Arch Neurol 39 : 524-526 7. Igapashi S, Mori K, Ishijimi Y (1972) Pure motor hemiplegia after recraniotomy for post-operative bleeding. Arch Jpn Chir 41 : 32-37 8. Jain S, Maheshwari MC, Dhamija RM, Mishra NK (1985) Pure motor hemiparesis due to hypertensive putaminal haemorrhage. Eur Neurol 24 : 205-207 9. M.R.C. (1976) Motor testing. In: Aids to the examination of the peripheral nervous system. Medical Research Council, London, Memorandum no. 45 10. Obeso JA, Marti-Masso JF, Carrera N, Austudillo W (1980) Pure motor quadriplegia secondary to bilateral capsular hematomas. Arch Neurol 37: 248 11. Rascol A, Clanet M, Manelfe C, Guiraud B, Bonafe A (1982) Pure motor hemiplegia: CT study of 30 cases. Stroke 13 : 11-17 12. Ropper AM, Fisher CM, Kleinman GM (1979) Pyramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face. Neurology (NY) 29:91-95 13. Tapia JF, Kase CS, Sawyer RH, Mohr JP (1983) Hypertensive putaminal hemorrhage presenting as pure motor hemiparesis. Stroke 14 : 505-506 14. Weintraub MI, Glasser GH (1970) Nocardial brain abscess and pure motor hemiplegia. N ¥ State J Med 70:2717-2721 15. Weisberg LA (1979) Computed tomography and pure motor hemiparesis. Neurology (NY) 29 : 490-495 Received June 14, 1985 / Accepted July 25, 1985