© 1985 S. Karger AG, Basel 0014-3022/8 5/0243-0205S2.75/0 Eur. Neurol. 24: 205-207 (1985) Pure Motor Hemiparesis due to Hypertensive Putaminal Haemorrhage .S'. Jain3. M.C. Maheshwaria. R.M. Dhamijaa, N.K. Mishrab Departments of “Neurology and bNeuroradiology. All India Institute of Medical Sciences. New Delhi, India Key Words. Pure motor hemiparesis Hypertensive putaminal haemorrhage • CT scan Abstract. A hypertensive woman presenting as pure motor hemiparesis with rapid and complete recovery from the neurological deficit is described. The probable aetiology was pri­ mary hypertensive putaminal haemorrhage, as revealed by C'T scan. This rare presentation has been described only once earlier and emphasizes the value of CT scanning as a tool for diagnosis of such cases. Pure motor hemiplegia (PMH) is a welldefined syndrome usually caused by isch­ aemic lesions of lacunar type located either in the internal capsule or in the pons [I], Subse­ quently, several isolated cases were published revealing the other possible sites of ischaemic lesions: infarcts of cortical [2], pyramidal [I. 3. 4] or midbrain location [5]. In addition, other aetiologies of PMH have been de­ scribed and include: post-craniotomy haem­ orrhage [6], haemorrhages in the basis pontis [7] or internal capsule [2, 8. 9], multiple scle­ rosis [2], metastasis [2, 3] and abscess [ 10]. A haemorrhagic origin of PMH is considered classically to be rare. Only I clear-cut case of PMH in the setting of primary hypertensive putaminal haemorrhage (HPH) has been de­ scribed [11]. We report one such case pre­ senting as PMH due to putaminal haemor­ rhage with subsequent total recovery. Case Report A 4 1-year-old right-handed hypertensive female noticed heaviness and weakness of the left upper limb on January 17. 1984. About half an hour later she noticed weakness of the left leg and was unable to stand unaided. She complained of headache and vom­ ited once while she was still in the office. When exam­ ined 4 h after the onset, she was conscious, oriented and described her illness accurately. Her speech was slightly dysarthric but she had no dysphasia. Cranial nerve testing revealed a left supranuclear facial paresis. The visual fields, extraocular move­ ments and pupils were normal. There was no nystag- Downloaded by: MacQuarie University 137.111.162.20 - 2/14/2019 11:17:20 AM Introduction Jain/Mahcshwari/Dhamija/Mishra 206 simultaneous tactile stimulation. Stcreognosis. barognosis and trace figure identification were normal and symmetric. Routine blood chemistry was normal. ECG re­ vealed evidence of left ventricular hypertrophy. CT scan on admission showed a well-defined area of high attenuation (Mean 66 Hounsficld units) at the level of right midposterior putamen, consistent with fresh haemorrhage (fig. la, b). There was a thin zone of peri­ focal low attenuation with slight compression of the body of the right lateral ventricle. The volume of this hacmaioma was estimated to be 8.72 ml. The left hemiparesis progressively improved over the next 4 days following admission. At the time of discharge (7 days from the onset) power in the left arm and leg was IV/V. Left facial weakness had recovered completely. When seen on follow-up 3 weeks from onset, the motor strength of the left limbs had returned to normal and she was back to her office work. Fig. I. a, b CT scan (uncnhanced) showing a welldefined hacmaioma at the level of the right midposter­ ior putamen. mus. The facial sensations and palatal and tongue movements were intact. Motor examination showed a moderate paresis of left upper limb, power grade I/V MRC [12] and mild weakness of the left lower extrem­ ity (Ill/V). The deep tendon reflexes were diminished in the left arm and leg and plantar reflexes were bilat­ erally flexor. Coordination was intact. There was no dyspraxia. Sensory examination for touch and pin prick was normal. Joint position and vibration sense was intact. There was no sensory extinction on double PMH constitutes a neurological syndrome usually associated with ischaemic lesions of lacunar type located at various sites [1-5]. Only 6 CT-documented cases of PMH due to haemorrhage into the internal capsule have been described [2, 8, 9]. 5 of these cases, being part of two large scries of PMH patients [2, 8], lack the detail description of their clin­ ical features. Only 1 clear-cut case of PMH with detailed neurological evaluation has been described [11], In this case the aetiology was a primary HPH. HPH has been described to present with a wide variety of neurological deficits. The clinical spectrum of HPH includes combina­ tions of motor, sensory, oculomotor, visual, language and behavioural deficits [13, 14], It has only recently been emphasized that PMH may also be a rare manifestation of HPH [11], Visualization of such rare things has been made possible by the advent ofCT scan in the last few years. Downloaded by: MacQuarie University 137.111.162.20 - 2/14/2019 11:17:20 AM Discussion 207 Pure Motor Hcmiparcsis due to Putaminal Haemorrhage References 1 Fisher, C.M.; Curry, H.B.: Pure motor hemiplegia of vascular origin. Archs Neurol. 13: 30-44 (1965). 2 Weisberg, L.A.: Computed tomography and pure motor hemiparesis. Neurology. N.Y. 29: 490-495 (1979). 3 Chokroverty, S.; Rubino, F.A.: 'Pure' motor hemi­ plegia. J. Neurol. Neurosurg. Psychiat. 38: 896899 (1975). 4 Roppcr, A.H.; Fisher, C.M.; Kleinman. G.M.: Py­ ramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face. Neurology, N.Y. 29: 91-95 (1979). 5 Ho, K.L.: Pure motor hemiplegia due to infarction of the cerebral peduncle. Archs. Neurol. 39: 524526 (1982). 6 Igapashi, S.: Mori. K.; Ishijimi, Y.: Pure motor hemiplegia after recraniotomy for post-operative bleeding. Arch. jap. Chir. 41: 32-37 (1972). 7 Gobemado, J.M.; Fernandez dc Molina, A.R.; Gimeno. A.: Pure motor hemiplegia due to haemor­ rhage in the lower pons. Archs Neurol. 37: 393 (1980). 8 Rascol, A.; Clanet, M.; Manelfe, C ; Guiraud, B.; Bonafc, A.: Pure motor hemiplegia: CT study of 30 cases. Stroke 13: 11-17 (1982). 9 Obeso, J.A.; Marti-Masso. J.F.; Carrera, N.; Austudillo, W.: Pure motor quadriplcgia secondary to bilateral capsular hematomas. Archs Neurol. 37: 248 (1980). 10 Weintraub. M.I.; Glasscr. G.H.: Neocardial brain abscess and pure motor hemiplegia. N.Y. St. J. Med. 70: 2717-2721 (1970). 11 Tapia, J.F.; Kase, C.S.; Sawyer, R.H.; Mohr, J.P.: Hypertensive putaminal hemorrhage presenting as pure motor hemiparesis. Stroke 14: 505-506 (1983). 12 M RC: Motor testing; in Aids to the examination of the peripheral nervous system. Memorandum No. 45 (Medical Research Council, London 1976). 13 Fisher, C.M.: Clinical syndromes in cerebral hem­ orrhage; in Fields. Pathogenesis and treatment of cerebrovascular disease, pp. 318-342 (Thomas, Springfield 1961). 14 Hier, D.B.; Davis, K.R.; Richardson. E.P.; Mohr, J.P.: Hypertensive putaminal hemorrhage. Ann. Neurol. 1: 152-159 (1977). Received: February 29, 1984 Accepted: August 1, 1984 M.C. Maheshwari, MD, Department of Neurology. AI1MS. New Delhi - 110029 (India) Downloaded by: MacQuarie University 137.111.162.20 - 2/14/2019 11:17:20 AM The size of HPH and its location are also important. In the only case of HPH present­ ing as PMH reported earlier [ 11 ], it measured 8.5 mm3 and was located along the mid and posterior aspects of the putamen. In our pa­ tient, the volume of this hacmatoma was esti­ mated to be 8.72 ml and it was located at almost a similar site. It has been presumed that the posterior and lateral location of the haematoma is responsible for pressure ef­ fects, rather than acutal destruction of the adjacent internal capsule [II], Similar ana­ tomical features in our case can account for the clinical presentation (PMH) and com­ plete recovery within 3 weeks of the onset. However, HPH presenting as pure motor hemiparesis with complete recovery remains a distinctly uncommon clinical situation. PMH with good prognosis may rarely be included into the wide variety of clinical pre­ sentations as a result of primary HPH.