Pure motor hemiplegia including the face induced by an infarct of the medullary pyramid

doi:10.1016/0303-8467(95)00082-8

Clinical Neurology and Neurosurgery

Volume 98, Issue 1, February 1996, Pages 21-23

https://doi.org/10.1016/0303-8467(95)00082-8 Get rights and content

Abstract

Four autopsy cases of pure motor hemiparesis due to medullary pyramid infarcts have been previously reported. The deficits that were described included overt limb weakness and “slight facial weakness”. According to current neurological teaching, the lesion responsible for an upper motor neuron facial palsy affects the corticobulbar tract at the level of the midpons or more rostrally.

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Cited by (19)

Modified hypoglossal-facial nerve anastomosis for peripheral-type facial palsy caused by pontine infarction: A case report and literature review
2023, Heliyon
Peripheral-type facial palsy could be caused by a lesion in the tegmentum of the pons, such as infarction, with a rare occurrence. We herein described a case of unilateral peripheral-type facial palsy induced by dorsolateral pontine infarction and treated this patient using modified hypoglossal-facial nerve anastomosis.
A 60-year-old female presented with dizziness, hearing drop, diplopia, and peripheral-type facial palsy. Brain Magnetic Resonance Imaging showed a dorsolateral pontine infarction on the right side which exactly refers to the location of the ipsilateral facial nucleus or facial nerve fascicles at the pons. Subsequent electrophysiological examinations confirmed poor facial nerve function of this patient and modified hypoglossal-facial nerve anastomosis was then performed.
This case reminded medical practitioners not to ignore the possibility of involvement of a central cause in peripheral-type facial palsy patients. In addition, modified hypoglossal-facial nerve anastomosis served as a useful skill improvement that may help reduce hemiglossal dysfunction while restoring facial muscle function.
Clinical Study of 27 Patients with Medial Medullary Infarction
2017, Journal of Stroke and Cerebrovascular Diseases
Citation Excerpt :
MMI involved the descending corticobulbar tract, and thus caused contralateral facial wekness.17 Our result was consistent with the previous report.17 Ipsilateral lingual palsy in MMI is caused by involvement of the hypoglossal nerve nucleus or its infranuclear fibers in the medulla.5
Medial medullary infarction (MMI) is a rare ischemic stroke. Frequency of each neurological finding in MMI was different in each study.
We retrospectively evaluated the medical records of patients with cerebral infarction who were admitted between March 1998 and October 2015. Patients in our study were diagnosed as having MMI by magnetic resonance image examination.
Of 2727 patients with ischemic stroke, 27 patients (20 males and 7 females) had MMI. The MMI was complicated by infarcts located in the pons (n = 6), cerebellum (n = 2), and lateral medulla (n = 1). One patient had bilateral MMI. Large-artery atherosclerosis was the most common etiology. Motor weakness of the extremities was the most common neurological finding. Diminished contralateral superficial sensation was more common than diminished contralateral vibratory sensation, and these 2 types of sensory disturbance were often complicated. The patients with large MMI significantly more often accompanied diminished touch (P = .003), pain (P = .017), and vibratory (P = .019) sensation. Facial weakness was shown more common contralateral to the infarcts than ipsilateral (n = 8 contralateral, n = 1 ipsilateral). Lingual palsy was also more common contralateral to the lesions (n = 3 contralateral, n = 1 ipsilateral). One patient alone fulfilled the classical Dejerine triad.
In MMI, motor weakness of extremities was commonly shown, and complication of diminished sensations indicated the large infarcts. As for facial weakness and lingual palsy, the supranuclear type was more prominent than the infranuclear type.
Pure ipsilateral central facial palsy and contralateral hemiparesis secondary to ventro-medial medullary stroke
2013, Journal of the Neurological Sciences
Citation Excerpt :
As opposed to our case, the infarct extended beyond the pyramids and the patient had additional signs suggestive of medial lemniscus injury [8]. Pure hemiparesis affecting the lower facial muscles is a rare manifestation of medullary infarcts restricted to the pyramids [3,9,10]. However in all previous reports, central type facial palsy was contralateral to the lesion [3,9,10].
Medullary infarcts are occasionally associated with facial palsy of the central type (C-FP). This finding can be explained by the course of the facial corticobulbar (F-CB) fibers. It is believed that fibers that project to the upper facial muscles decussate at the level of the facial nucleus, whereas those destined to the lower facial muscles decussate more caudally, at the level of the mid or upper medulla. It has been proposed that the lower F-CB fibers descend ventromedially near the corticospinal tract to the upper medulla where they cross midline and ascend dorsolaterally. Accordingly, ventromedial medullary infarcts are expected to result in contralateral facial and limb weakness. We report a patient with a medial medullary infarct restricted to the right pyramid and associated with ipsilateral C-FP and contralateral hemiparesis. The neurological findings are discussed in light of the hypothetical course of the F-CB fibers in the medulla.
Peripheral Type Facial Palsy in a Patient with Dorsolateral Medullary Infarction with Infranuclear Involvement of the Caudal Pons
2008, Journal of Stroke and Cerebrovascular Diseases
Citation Excerpt :
It has been firstly hypothesized that facial CBT fibers leave the pyramidal tract at the pontomedullary junction and descend caudally to at least the middle medullary levels before most of them cross to the opposite facial nucleus.7 Cavazos et al8 have described some fibers of the facial CBT as descending ipsilaterally, making a loop as caudally as the upper medulla before decussating and ascending to the contralateral facial nucleus. A more recent study reported that C-FP occurred more often in patients with a lesion extending from the lower pons to the upper medulla than in those with a lesion in the middle to lower medulla, regardless of whether the lesion was located ventromedially or dorsolaterally.4
The corticobulbar tract fibers descend near the corticospinal tract, mostly to the upper medulla, where they decussate and ascend in the dorsolateral medulla to connect with the contralateral facial nucleus. Therefore, central type facial palsy can be present in patients with ipsilateral dorsolateral upper medullar lesion. We describe a 71-year-old man with lateral medullary infarction who showed ipsilateral peripheral type facial palsy. Brain diffusion-weighted image showed hyperintensities on the left dorsolateral portion of upper medulla and adjacent inferomedial tegmentum of the lower pons. Transfemoral cerebral angiography depicted prominence of ipsilateral posterior inferior cerebellar artery with focal stenosis. Left posterior inferior cerebellar artery might supply the inferolateral tegmentum of the lower pons, which is usually supplied from anterior inferior cerebellar artery. The peripheral type facial palsy in our patient may have resulted from facial infranuclear involvement of the caudal pons extended from dorsolateral upper medullary lesion in ascending pathway of corticobulbar tract fibers.
Brachial monoparesis as an isolated manifestation of a paramedian pontine ischemic lesion
2007, Clinical Neurology and Neurosurgery
Pure monoparesis is a rare condition characterized by weakness limited to one limb without any other neurologic deficits. We herein report an extremely infrequent case of pure motor monoparesis not due to cortical infarctions but due to a paramedian pontine infarction. A 41-year-old woman was admitted with a sudden onset of weakness in her right upper extremity. On neurological examination, there were no abnormalities except for monoparesis (motor grade IV/V) in the right upper extremity. A magnetic resonance imaging of the brain showed an acute small ischemic lesion in the left paramedian pontine area.
Intramedullary hemorrhage caused by arteriovenous malformation: A case of mixed lateral and medial medullary syndrome
2001, Journal of Stroke and Cerebrovascular Diseases
Citation Excerpt :
Transiently, a left supranuclear facial palsy was observed. Cavazos et al.14 have hypothesized that some of the facial corticobulbar fibers descend ipsilaterally as far as the upper medulla, forming a loop before decussating and ascending to the contralateral facial nucleus. Ipsilateral central facial weakness in this case may have resulted from injury to these ascending fibers.
A 48-year-old man with no known risk factor for cerebrovascular disease, other than cigarette smoking, experienced the sudden onset of a mixed lateral and medial medullary syndrome. Computed tomography scan failed to show any definite abnormality. Magnetic resonance imaging scans revealed hemorrhage restricted to the left dorsolateral medulla. Angiography showed abnormal arteries originating from the left vertebral artery with small niduses located on the surface of the medulla and contralateral cerebellum. Small brain-stem hemorrhages are a contraindication to thrombolytic or anticoagulant therapy, and therefore must be recognized in the acute stage. Copyright © 2001 by National Stroke Association

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Original articlePure motor hemiplegia including the face induced by an infarct of the medullary pyramid

Abstract

Pure motor hemiplegia of vascular origin

Arch Neurol

Pontine versus capsular pure motor hemiparesis

Neurology

Pure motor hemiplegia due to pyramidal infarction

Arch Neurol

Pure motor hemiplegia, medullary pyramid lesion, and olivary hypertrophy

J Neurol Neurosurg Psychiatry

Pyramidal infarction in the medulla: A cause of pure motor hemiplegia sparing the face

Neurology

Original article
Pure motor hemiplegia including the face induced by an infarct of the medullary pyramid