Raymond syndrome is a pontine syndrome consisting of ipsilateral abducens nerve palsy, contralateral facial paralysis, and contralateral hemiparesis. However, subsequent clinical observations argued on the presentation of facial involvement. The only differentiating point between the facial including called classic type and the facial sparing Raymond syndrome is the location of the lesion. The classic type involves abducens nerve, corticofacial, and corticospinal tracts; while in the facial sparing type, corticofacial tracts, and peripheral facial nerves are spared. We experienced a 78-year-old man presented with sudden onset dizziness, binocular horizontal diplopia, and right-sided motor weakness. Neurological examination showed he had left abducens nerve palsy and right hemiparesis without facial involvement. Brain magnetic resonance imaging showed acute ischemic infarction in the left ponto-medullary junction. Regardless of the presence or absence of facial palsy, the combination of abducence nerve palsy and contralateral hemiparesis should direct the clinician’s attention towards the medial ventral caudal ponto-medullary junction.
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For differential diagnosis between vestibular neuritis and lateral medullary
infarction with similar clinical features, bedside examination of nystagmus is
important. We report a 45-year-old male who presented with acute vertigo for
two days. He showed spontaneous right-beating nystagmus. However, left-beating
nystagmus was evoked during bilateral horizontal gaze and by horizontal head
oscillation. Brain MRI revealed an acute infarction in the left lateral medulla.
Sudden hearing loss and vertigo are the typical presentation of anterior inferior cerebellar artery infarction, but may rarely occur in posterior inferior cerebellar artery (PICA) infarction. Here we describe a 65-year-old man who presented with sudden hearing loss in his left ear and severe vertigo. The diffusion-weighted magnetic resonance imaging revealed acute infarction in the territory of PICA and cerebral angiography showed non-visualization of left vertebral artery. Sudden hearing loss and vertigo may be a presentation of PICA infarction.
Body lateropulsion is a common manifestation of lateral medullary infarction (LMI), and usually associated with vertigo, limb ataxia, sensory disturbance, and Horner’s syndrome. However, isolated body lateropulsion as a presenting symptom of LMI is rare, and the responsible lesion for lateropulsion remains uncertain. We report a 71-year-old woman who showed isolated body lateropulsion as a presenting symptom of LMI. Ipsilateral body lateropulsion in our patient may be ascribed to the involvement of the ascending dorsal spinocerebellar tract rather than the descending lateral vestibulospinal tract, which runs more ventromedially.
We report a rare case of primary dorsal medullary hemorrhage showing lateral medullary syndrome with ipsilesional nystagmus. A 41-year woman, presented with the first degree horizontal vestibular nystagmus and ocular tilt reaction to the left in lateral medullary hemorrhagic lesion. Primary medullary hemorrhage is rare and details of the abnormal eye movement in the lesion have never been described well. While most of the reported vestibular nystagmus in the lateral medullary infarction was contralesional., the nystagmus in this case was ipsilesional. This ipsilesional beating of the nystagmus might be explained that either destruction of the rostral part of vestibular nuclei or irritative effect of blood to vestibular nuclei is responsible. In addition, ocular tilt reaction (OTR) can be more important in deciding the side of the lesion in medullary hemorrhage.
Key Words: Lateral medullary syndrome; Medulla oblongata, Hemorrhage; Nystagmus, Pathologic
Background and Objectives: Central role of the vestibular system on control of blood pressure and interrelationships between the vestibular nucleus and solitary nucleus during acute hypotension were investigated in bilateral labyrinthectomized (BLX) or sinoaortic denervated (SAD) rats. Changes of electrical activity in the medial vestibular nucleus (MVN), solitary tract nucleus (STN), and rostral ventrolateral medullary nucleus (RVLM) were investigated in rats in while acute hypotension was induced by sodium nitroprusside (SNP).
Results Evoked potential in MVN neuron caused by electrical stimulation of the peripheral vestibular system was composed of 3 waves with latencies of 0.48±0.10 ms, 1.04±0.09 ms and 1.98±0.19 ms. Electrical stimulation to MVN or RVLM increased blood pressure. MVN at the induction of acute hypotension showed excitation in 61% of type I neurons and inhibition in 68% of type II neurons. In STN, acute hypotension produced excitation in 62.1% of neurons recorded in intact abyrinthine animals, inhibition in 72.3% of neurons recorded in BL animals, and excitation in 60% of recorded neurons in SAD animals. In RVLM, acute hypotension produced excitation in 66.7% of neurons recorded in intact labyrinthine animals and inhibition in 64.9% of neurons recorded in BL animals. In spatial distribution of STN neurons responded to acute hypotension, excitatory responses were mainly recorded in rostral and ventral portion, and inhibitory responses were mainly recorded in caudal and lateral portion. In RVLM, excitatory responses were mainly recorded in rostral and dorsomedial portion, and inhibitory responses were mainly recorded in caudal and ventrolateral portion.
Conclusion These results suggest that afferent signals from the peripheral vestibular receptors are transmitted to STN through the vestibular nuclei and assist to the baroreceptors for controlling blood pressure following acute hypotension.
Department of Otolaryngology, Head and Neck Surgery1, and Neurology2, Seoul National University Bundang Hospital,
Seoul National University College of Medicine, Seongnam, Korea
Background and Objectives : Central positional nystagmus is induced by positional changes from brainstem or
cerebellar lesions. Differentiation central from peripheral positional nystagmus is important in clinical practice. To
delineate characteristics of the positional nystagmus observed in central lesions, we analyzed the parameters of
positional nystagmus from focal brain lesions.
Materials and Methods : Ten patients with central positional nystagmus were recruited from the dizziness clinic
of Seoul National University Bundang Hospital. All the patients had focal brainstem or cerebellar lesions documented
by magnetic resonance imaging. The nystagmus was observed with and without fixation by using Frenzel glasses or
Video Goggles. The nystagmus was videotaped or recorded with video-oculography. Provoking positional maneuvers,
direction, latency, duration, phase reversal, and fatigue phenomenon of the nystagmus were analyzed.
Results : Of the 10 patients, seven had infarctions in the lateral medulla or inferior cerebellum while two
experienced cerebellar hemorrhage and remaining one showed a compression of the ventrolateral medulla by cavernous
malformation of the vertebral artery. The directions of the positional nystagmus were variable depending on the lesions
and provoking maneuvers. Most patients exhibited direction-changing nystagmus without latency, direction-reversal and
fatigue phenomenon. However, some of the patients also showed patterns of nystagmus characteristic of peripheral
positional nystagmus. In two of the four patients with infarction in the territory of medial posterior inferior cerebellar
artery, the positional nystagmus was the only abnormal findings.
Conclusions : Central positional nystagmus may share many characteristics with peripheral type of positional
nystagmus. In individual cases, the patterns of nystagmus should be interpreted with caution in differentiating central
from peripheral positional nystagmus. Considering the isolated positional nystagmus in some patients with caudal
cerebellar lesions, systematic positional maneuvers should be applied to all the patients with vertigo
Key Words : Positional nystagmus, Medulla, Cerebellum