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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-

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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.

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Discussion

207

Pure Motor Hcmiparcsis due to Putaminal Haemorrhage

References
1 Fisher, C.M.; Curry, H.B.: Pure motor hemiplegia
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(1965).
2 Weisberg, L.A.: Computed tomography and pure
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3 Chokroverty, S.; Rubino, F.A.: 'Pure' motor hemi­
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4 Roppcr, A.H.; Fisher, C.M.; Kleinman. G.M.: Py­
ramidal infarction in the medulla: a cause of pure
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5 Ho, K.L.: Pure motor hemiplegia due to infarction
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Received: February 29, 1984
Accepted: August 1, 1984
M.C. Maheshwari, MD,
Department of Neurology.
AI1MS. New Delhi - 110029 (India)

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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.