Printer Friendly

Midbrain infarction presenting with Weber's syndrome and central facial palsy: a case report/Orta beyin infarktina bagli gelisen Weber sendromu ve santral fasyal parezi: olgu sunumu.


A 68-year-old woman was admitted to the Dumlupinar University Hospital because of central type facial palsy on right side, right hemiparesis, and paresthesia with deep sensory disturbance of right upper and lower extremities (Figure 1A). She had ptosis, midriasis and lateral-inferior deviation of the left eye due to oculomotor nerve palsy (Figure 1 B).

Our patient noticed weakness of the right arm and leg and diplopia on waking in the morning. She had been diabetic and hypertensive for the past 20 years. Her medications included gliclazide, metformin and insulin. On admission she was alert and had a blood pressure of 155/75 mm/Hg with no arrhythmia. Neurological examination revealed a conscious individual with normal higher cortical functions.

Cranial examination revealed complete left 3rd nerve palsy and normal ocular fundi. The strength of the frontalis and orbicularis oculi muscles was well preserved, but she had a right lower facial weakness with mild flattening of the right nasolabial fold and paralytic dysarthria. Motor system showed right-sided spastic weakness with grade 4/5 power. Deep tendon reflexes were brisk on the right side with upgoing plantar response. Initial computerized tomography (CT) scan was normal. Cranial magnetic resonance imaging (MRI) performed 10 days after the onset showed an infarction in the left ventromedial part of the upper mesencephalon and old multiple chronic lacunar infarctions in the deep white matter of the cerebral hemispheres (Figure 1C)

Over the next week her hemiparesis resolved completely and her diplopia was getting better. Two weeks later, she was discharged with normal neurological findings.




Weber's syndrome was described by the German physician Hermann Weber in 1863 111 The clinical findings of classic Weber's syndrome include an ipsilateral oculomotor nerve palsy and a contralateral limb weakness due to a lesion in the midbrain (crus cerebri).

Most of the muscles of the eye innervates by the oculomotor nerve. The motor nucleus of this nerve is located at the upper mesencephalic level of brainstem. Nerve nascicles run forward and laterally through the red nuclei and get closer at the inter-peduncular fossa. So nuclei and fascicles of the oculomotor nerve are expanding a relatively wide area within midbrain. Therefore midbrain lesions generally lead to partial third nerve palsy. It enters the orbit through the superior orbital fissure after come out from the midbrain and branching into upper and lower fibers. While the levator palpebrae superioris and superior rectus muscles were innervated by the upper branch, the medial rectus, the inferior rectus, and the inferior oblique muscles were innervated by the lower branch (2-4).


The preganglionic parasympathetic fibers of the 3rd nerve which are transported by the nerve to the inferior oblique muscle arrive to the ciliary ganglion and from here the post-ganglionic parasympathetic fibers emerge. The ciliary muscle and the muscles of the iris are innervatod by these post-ganglionic parasympathetic fibers. The nerve fibers to levator palpebrae muscle and the pupil loconstrictor fibers for the muscles of the iris are located in a superficial and dorsal position on the nerve relaying in the ciliary ganglion. Before external ophthalmoplegia develops, a fixed dilated pupil is often the first sign of 3rd nerve (oculomotor) compression, and ptosis the second, upon this anatomical characteristic (5).

The clinical manifestation of the patients with isolated mesencephalic infarct was shown up nuclear or fascicular oculomotor nerve palsy and contralateral motor deficits (6,7).

In patients with isolated mesencephalic infarct, the clinical picture was dominated by nuclear or fascicularthird-nerve palsy and contralateral motor deficits (6,8).

On the other hand the corticobulbar tract (CBT) is commonly used to describe the pathway taken by motor fibers innervatiog the cranial nerve nuclei, especially trigeminal, facial, hypoglossal motor nuclei, nucleus ambiguus, and spinal accessory nucleus. The oculomotor, trochlear and abducens nuclei receive no input from the CBT. The cell bodies of primary motor neurons are located in primary motor cortex (9).

The motor nucleus of the facial nerve, which supplies the muscles of the facial expression, is located at the lower pontine level, dorsolaterally in the caudal pons 141. The CBT fibers that connect the motor cortex with the facial nucleus provide strongly unilateral innervation to the contralateral lower facial muscles and bilateral innervation to the upper facial muscles. The facial CBT fibers descend at the ventromedial region of the crus cerebri, near the corticospinal tract (10).

The clinical manifestations of midbrain infarcts mostly show the location of the lesion directly, but these features could not always match with classical syndromes which described previously in the literature, just like our case that we present in this report (11).

Posterior cerebral artery branch disease may be caused by occlusion of the arterial branch with atherothrombotic plaque (4). In these cases, hypertension is a major risk factor, as seen in our patient (10).

Kumral et al. presented the topographic and clinical distribution of the acute posterior circulation infarcts involving mesencephalon. They described four patients with Weber's syndrome and central facial palsy due to isolated midbrain infarct around ventromedial crural region within 41 patients with mesencephalic infarction. These were the only cases in the literature identical to our patient (6).

Some minor infarctions at the midbrain which resulted in localized paralysis like weakness of a single extra ocular muscle (121, isolated contralateral superior rectus palsy (13) have been demonstrated previously. Some interesting cases, such as presence of left oculomotor nerve palsy with normal pupil and right hemiparesis, were described. An ischemic lesion of the lower midbrain, which corresponds to the motor nucleus of the oculomotor nerve, was demonstrated in this case (3).

Terao et al. reported two patients with contralateral central facial paralysis and hemiparesis of the limbs, resulted from unilateral ventromedial medullary infarction (141. According to these cases, they described the course of the facial corticobulbar tract as consisting of looping fibers that descend at least to the medullary level and then decussate. In another study with larger group (70 patients), they attempted to further clarify the course and the distribution of the facial corticobulbar tract (101. But the authors could not coincide with third nerve palsy or Weber's syndrome within these central facial palsy patients.

Finally, this report demonstrates an extremely rare case of crossed hemiplegia with oculomotor and facial nerve palsy due to an infarct in the upper part of the midbrain as documented by the MRI scan. The other interesting feature to note in our report is that the patient completely recovered six month later. This indicates that some of these patients may have a good prognosis.

Received/Gelis tarihi: 20.05.2009 Accepted/Kabul tarihi: 22.09.2009


(1.) Silverman IE, Liu GT, Volpe NJ et al. The Crossed Paralyses. The Original Brain-Stem Syndromes of Millard-Gubler, Foville, Weber and Raymond-Cestan. Arch Neurol 1995; 52:635-8. (Abstract) / (PDF)

(2.) Liu CT, Cremer CW, Logigian EL et al. Midbrain syndrome of Benedict, Claude, Nothnagel-setting record straight. Neurology 1992;42:1820-2.

(3.) Umasankar U, Huwez FU. A patient with reversible pupil-sparing Weber's syndrome . Neurol India 2003; 51:388-9. (Abstract) / (Full Text) / (PDF)

(4.) Hendelman WJ. Atlas of Functional Neuroanatomy. 2nd edition CRC Pres Taylor & Francis Group. 2006; pp. 126.

(5.) Sunderland S. Neurovascular relations and anomalies at the base of the brain. J Neurol Neurosurg Psychiatry 1948;11:243. (Full Text) / (PDF)

(6.) Kumral E, Bayulkem G, Akyol A, et al. Mesencephalic and associated posterior circulation infarcts. Stroke. 2002; 33:2224-31. (Abstract) / (Full Text) / (PDF)

(7.) Cormier PJ, Long ER, Russell EJ. MR imaging of posterior fossa infarctions: vascular territories and clinical correlates. Radiographics 1992;12:1079-96. (Abstract) / (PDF)

(8.) Johnson MH, Christman CW. Posterior circulation infarction: anatomy, pathophysiology, and clinical correlation. Semin Ultrasound CT MR. 1995;16:237-52. (Abstract)

(9.) Nolte J. The Human Brain: An Introduction to its Functional Anatomy, Edition 5th, Elsevier Health Science; pp. 461.

(10.) Terao S, Miura N, Takeda A et al. Course and distribution of facial corticobulbar tract fibres in the lower brain stem. J Neurol Neurosurg Psychiatry 2000; 69:262-5. (Abstract) / (PDF)

(11.) Kim JS, Kang JK, Lee SA et al. Isolated or predominant ocular motor nevre palsy as a manifestation of brain stem stroke. Stroke. 1993; 24:581-6. (Abstract) / (Full Text) / (PDF)

(12.) Kwon JH, Kwon SU, Ahn HS et al. Isolated Superior Rectus Palsy Due to Contralateral Midbrain Infarction. Arch Neurol 2003;60:1633-5. (Abstract) / (Full Text) / (PDF)

(13.) Terao S, Takatsu S, Izumi M et al. Central facial weakness due to medial medullary infarction: the course of facial corticobulbar fibres. J Neurol Neurosurg Psychiatry 1997; 63:391-3. (Abstract) / (Full Text) / (PDF)

Demet ILHAN ALGIN, Figen TASER *, Sayime AYDIN **, Elif AKSAKALLI ***

Dumlupinar University Faculty of Medicine, Department of Neurology, Kutahya

* Dumlupinar University Faculty of Medicine, Department of Anatomy, Kutahya

** Dumlupinar University Faculty of Medicine, Department of Ophthalmology, Kutahya

*** Dumlupinar University Faculty of Medicine, Department of Physical therapy and Rehabilitation, Kutahya, Turkey

Address for Correspondence/Yazisma Adresi: Dr. Demet Ilhan Algin, Dumlupinar University Faculty of Medicine, Department of Neurology, Kutahya, Turkey E-mail:
COPYRIGHT 2009 Galenos Yayinevi Tic. Ltd.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2009 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Case Report/Olgu Sunumu
Author:Algin, Demet Ilhan; Taser, Figen; Aydin, Sayime; Aksakalli, Elif
Publication:Archives of Neuropsychiatry
Article Type:Case study
Geographic Code:7TURK
Date:Dec 1, 2009
Previous Article:Posterior (bilateral parieto-occipital) cortical atrophy: a case study/Posterior (bilateral parietooksipital) kortikal atrofi: bir olgu sunumu.
Next Article:A nonconvulsive status epilepticus case presenting with diffuse delta wave frequency activity/ Diffuz delta dalga frekansli elektriksel aktivite...

Terms of use | Privacy policy | Copyright © 2020 Farlex, Inc. | Feedback | For webmasters