Acta Neurol Belg
DOI 10.1007/s13760-016-0699-x

LETTER TO THE EDITOR

Pure motor hemiparesis due to occlusion of the internal
carotid artery
Adrià Arboix1 • Elisenda Grivé2 • Marı́a-José Sánchez3

Received: 8 September 2016 / Accepted: 19 September 2016
Ó Belgian Neurological Society 2016

To the Editor-in-Chief,
Pure motor hemiparesis (PMH), also known as pure motor
stroke, is one of the classical lacunar syndromes, along
with pure sensory stroke, sensorimotor stroke, ataxic
hemiparesis, and dysarthria-clumsy hand. It is considered
as the most common lacunar syndrome in clinical practice,
accounting for one-half to two-thirds of cases. The clinical
criteria for diagnosis of PMH include the presence of
unilateral partial or complete paresis involving at least two
of three body areas (face, upper limb, or lower limb) and no
evidence of aphasia, apraxia, and agnosia, or visual field
defect, eye movement disturbance, ataxia, sensory loss or
evidence of bilateral weakness [1]. This lacunar syndrome
is commonly due to lacunar infarct resulting from small
vessel disease. We present a rare case of PMH not due to a
lacunar infarct, following an occlusion of the contralateral
internal carotid artery.
An 83-year-old man with a previous history of arterial
hypertension, heavy smoking ([20 cigarettes/day), obesity
and dyslipidemia presented to our department with motor
disturbance affecting his right brachio-crural distribution,
lasting 24 h. Symptoms developed suddenly, and there

& Adrià Arboix
aarboix@hscor.com
1

Cerebrovascular Division, Department of Neurology,
Hospital Universitari del Sagrat Cor, Universitat de
Barcelona, Viladomat 288, 08029 Barcelona, Catalonia,
Spain

2

Department of Neuroradiology, Hospital Universitari Sagrat
Cor, Barcelona, Catalonia, Spain

3

Medical Library, Hospital Universitari Sagrat Cor,
Barcelona, Catalonia, Spain

were no headache, nausea, vomiting, or speech disturbances. Sensory disturbances in upper or lower extremities
or in ipsilateral thoraco-abdominal anatomy were absent.
He had neither nuchal rigidity nor semiology of meningeal
syndrome. The patient had a proportional right arm and leg
weakness with movement against gravity, and Babinski
sign, compatible with pure motor hemiparesis (modified
Rankin Scale = 2, NIHSS = 5).
The following investigations were normal or unremarkable: chest roentgenography, 12-lead electrocardiography, brain CT scan, two-dimensional echocardiography,
complete hematological screening, routine biochemical
profile, urinalysis, serology for syphilis (VDRL),
immunological blood test (including ANA, ENA, lupus
anticoagulant, IgG and IgM anticardiolipin antibodies, and
rheumatoid factor), and basic hemostasis study.
Cerebral magnetic resonance imaging (MRI) at day 3
post-stroke showed increased signal on FLAIR and T2weighted sequences, and diffusion-weighted imaging
revealed restriction involving, partially, the left frontoparietal cortex compatible with an acute infarct in the
primary motor cortex (Fig. 1). Echo-Doppler of the
supra-aortic trunks and angio-MRI showed thrombotic
occlusion at the origin of the left internal carotid artery,
with mild right carotid artery stenosis (\30 %) clinically
silent.
Antithrombotic therapy with bemiparine (7500 UI/
24 h sc) was prescribed for secondary stroke prevention
together with strict control of cardiovascular risk factors,
and intensive physiotherapy. The clinical course was
favorable. A gradual regression of symptomatology was
observed, and 21 days after the onset of stroke, focal
neurological deficit was partially recovered.
PMH has been reported from autopsied cases as a focal
small (\20 mm in diameter), deep infarction, involving the

123

Acta Neurol Belg
Fig. 1 Left cortical
frontoparietal infarct revealed
on the MRI performed 3 days
post-stroke: increased signal on
FLAIR (a), and T2-weighted
sequences (b), restriction on
diffusion-weighted imaging (c),
and left extracranial internal
carotid artery occlusion on MRI
angiography (d)

Table 1 Pure motor hemiparesis not due to lacunar infarcts
Non-lacunar ischemic stroke

a

Cardioembolic infarct
Atherothrombotic infarct
Internal carotid artery occlusion in the neck
Ventromedial pontine infarction due to a propagating
thrombosis of the basilar branch
Complex aortic atheroma plaques
Ischemic stroke of unusual etiology
Ischemia-edema after craniotomy for postoperative bleeding
Intracerebral hemorrhage
Subdural hematoma
Brain abscess of the motor cortex
Cerebral metastasis
Demyelinating disease
a

Cerebral cortical surface infarction or large deep infarction ([20
mm diameter)

internal capsule, corona radiate, pons, and medullary
pyramid [1]. Other topographies are centrum semiovale,
basal ganglia, and mesencephalon. Rare causes of PMS

123

[2, 3] are shown in Table 1. Among these unusual causes,
we highlight the internal carotid artery occlusion in the
neck, as the clinical case we describe. These unusual
causes can, nowadays, be easily detected by imaging
techniques.
In a previous clinical study [4] of 222 patients with
PMH, we found 189 (85 %) lacunar infarcts, whereas
ischemic lacunar syndromes not due to lacunar infarcts
occurred in 23 (10.4 %) (atherothrombotic stroke in 12,
cardioembolic stroke in 7, infarction of undetermined origin in 3 and infarction of unusual etiology in 1), and
hemorrhagic lacunar syndromes in 10 (4.5 %). However, in
that study, no pure motor hemiparesis was due to occlusion
of the carotid artery.
Aleksic and George [5] presented two similar case
reports of pure motor hemiplegia with occlusion of the
extracranial internal carotid artery and suggested that
hemodynamic cerebral ischemia was likely to be an
important manifestation of this process.
In conclusion, our case shows that extracranial internal
carotid artery occlusion is a rare etiology of PMH, and may

Acta Neurol Belg

play a role in the pathogenesis of the clinical lacunar
syndrome of pure motor hemiparesis.
Acknowledgments We thank Drs J. Massons, M. Oliveres, and E.
Comes for their assistance in this study.
Compliance with ethical standards
Conflict of interest None declared.
Ethical approval All procedures performed in this study were in
accordance with the ethical standards of the institutional research
committe and with the Helsinki declaration; no formal ethical review
was required.
Informed consent Informed consent was obtained from the individual participant included in the study.

References
1. Del Bene A, Palumbo V, Lamassa M, Sala V, Piccardi B, Inzitari D
(2012) Progressive lacunar stroke: review of mechanisms, prognostic features, and putative treatments. Int J Stroke 7:321–329
2. Arboix A, Bechich S, Oliveres M, Garcia-Eroles L, Massons J,
Targa C (2001) Ischemic stroke of unusual cause: clinical features,
etiology and outcome. Eur J Neurol 8:133–139
3. Arboix A, Massons J, Garcı́a-Eroles L, Targa C, Comes E, Parra O
(2010) Clinical predictors of lacunar syndrome not due to lacunar
infarcts. BMC Neurol 10:31
4. Arboix A, Padilla I, Garcı́a-Eroles L, Massons J, Comes E, Targa
C (2001) Pure motor hemiparesis: a clinical study of 222 patients.
J Neurol Neurosurg Psychiatry 71:239–242
5. Aleksic SN, George AE (1973) Pure motor hemiplegia with
occlusion of the extracranial carotid artery. J Neurol Sci
19:331–339

123