Wallenberg's Lateral Medullary Syndrome Research Articles

Wallenberg's lateral medullary syndrome with facial palsy caused by anterior inferior cerebellar artery infarct

Wallenberg's lateral medullary syndrome with facial palsy caused by anterior inferior cerebellar artery infarct

Spontaneous Unilateral Brainstem Infarction in Swiss Mice

Spontaneous vestibular syndrome in mice, characterized clinically by head tilt, circling or rolling, can be caused by otitis media, arteritis or central nervous system lesions. Postmortem examination of eleven non-inbred Swiss mice submitted for necropsy due to acute onset of vestibular signs revealed lesions consistent with brainstem infarction. The lesions were characterized by unilateral, well-demarcated areas of necrosis, malacia, and gliosis, with variable amounts of hemorrhage, in the lateral aspect of the medulla and caudal pons. The affected area included the medial, lateral and superior vestibular nuclei, the facial nucleus and the spinal trigeminal nucleus. While vestibular disease secondary to otitis media, periarteritis, and central nervous system neoplasia has been reported in many mouse strains, these unilateral brainstem infarctions were only seen in Swiss mice. These lesions share features with Wallenberg's Lateral Medullary Syndrome, the most common type of brainstem infarct in humans.

Bilateral brainstem activation by thermal stimulation of the face in healthy volunteers

Contralateral sensory deficits in Wallenberg's lateral medullary syndrome suggest bilateral processing of trigeminal afferent input in the human brainstem. On the basis of experiments in rodents and clinical data, the present study addresses the hypothesis of bilateral projection of facial nociceptive input onto the spinal trigeminal nucleus (STN) in healthy humans. Nociceptive processing in the brainstem was investigated by functional magnetic resonance imaging (fMRI) in 18 healthy volunteers. Heat stimuli (39, 43, 46 degrees C) were applied by a Peltier type thermode to the left forehead (V1) and the left mental region (V3). Analyses of fMRI data were performed with SPM2 and BrainVoyager software. A region-of-interest approach analyzed local activation in the STN. Heat evoked significant bilateral activation in the STN (P < 0.01, T > 2.8). Contralateral activation was more frequent during stimulation of the V1 than of the V3 region. Whereas activation by V1 stimulation was located in caudal STN, V3 stimulation induced activity in more rostral parts of the STN. Functional MRI data in humans suggest bilateral brainstem activation when heat is applied to the face. Contralateral brainstem activity is more pronounced by stimulation of V1 as compared to V3. The results indicate similar nociceptive processing in humans and rodents and may explain clinical findings.

Wallenberg's lateral medullary syndrome: diffusion‐weighted imaging findings

To investigate the efficacy of diffusion-weighted imaging in patients with Wallenberg's lateral medullary syndrome. Thirteen patients with Wallenberg's lateral medullary syndrome were examined with conventional and echoplanar diffusion-weighted magnetic resonance (MR) imaging in a 1.5 T magnetic resonance unit. MR examinations were obtained in the acute or subacute stage of clinical syndrome, and diffusion-weighted imaging (DWI) was considered to be positive for infarction when an increase in signal was seen on b = 1000 s/mm2 images in the posterolateral medullary localization. DWIs were positive in 12 patients in the acute or subacute stages of this clinical syndrome. A false-negative result was obtained in only one patient examined within the first day, 10 h after onset of the symptoms. In the visual evaluation of the DWI, the contrast between normal and infarcted brainstem area was better in the high b-value images than in the apparent diffusion coefficient map images. DWI is a valuable technique for examining patients presenting with the signs and symptoms of Wallenberg's syndrome and high b-value images can provide complementary data to T2-weighted images. However, because most of our case group were in either the acute or subacute stage, true sensitivity of the method in the hyperacute stage of the syndrome remains unclear.

Afferent input to the medullary dorsal horn from the contralateral face in rat

Sensory deficits on the contralateral face in Wallenberg's lateral medullary syndrome (WS) may be due to an involvement of the crossing contralateral trigeminothalamic tract. Alternatively, neurons within the medullary dorsal horn (MDH) get input from the contralateral face. MDH neurons supplying the supraorbital nerve area in rat were recorded by electrophysiological techniques. In this first study on contralateral projections, about 60% of the neurons received excitatory afferent input from the contralateral face as well as the ipsilateral supraorbital area. Thus, contralateral sensory deficits in WS may be due to an involvement of these neurons.

Saccadic gain adaptivity in the two eyes in Wallenberg's lateral medullary syndrome

Saccadic movements and their adaptive gain control in the two eyes were explored in six patients with an ischemic infarction in the lateral medulla oblongata (Wallenberg's syndrome). Eye movements were recorded binocularly with the search coil method to examine their conjugacy. Gain adaptivity of experimentally induced hypermetric saccades was tested with the double target step paradigm.All patients had persistent saccadic dysmetria as compared to control subjects. The dysmetria was direction-specific and not equal in the two eyes. Ipsiversive saccades were on average by 20.5% larger than contraversive saccades. The amplitude of ipsiversive saccades was on average by 1.6% and that of contraversive saccades by 3.9% larger in the ab- than in the adducting eye, compared to 0.75% in normal subjects. There is strong evidence that gain adaptivity of horizontal saccades was diminished. The reduced capability to readjust saccadic gain to altered visual feedback was, however, equal in the two eyes. The author spec...

Wallenberg's lateral medullary syndrome. Clinical-magnetic resonance imaging correlations.

To correlate clinical and radiologic findings in patients with lateral medullary infarction. Case series with "blinded" evaluation of brain imaging. Hospitalized and ambulatory patients at the Neurological Institute of New York (NY). Thirty-three consecutive patients with lateral medullary syndrome were evaluated by the Stroke Center between 1983 and 1989. Ataxia (70%), numbness either of the ipsilateral face or of the contralateral body (64%), vertigo (51%), and dysphagia (51%) were the most frequent symptoms at onset. Eleven patients had ocular symptoms (diplopia or blurred vision). Horner's syndrome was found in 91%, ipsilateral ataxia in 85%, and contralateral hypalgesia in 85%. Nystagmus (61%) and facial weakness (42%) were less frequent. Head computed tomography was abnormal only when a cerebellar infarction was present (three cases). Magnetic resonance imaging, obtained in 22 cases, was normal in two; a lateral medullary infarction alone was present in 12, and a lesion extending beyond the lateral medulla was found in eight. No correlation was noted between facial weakness or ocular symptoms and infarction extending beyond the lateral medullary region. Vertebral artery disease was confirmed by vascular imaging or insonation studies in 73% of patients. The triad of Horner's syndrome, ipsilateral ataxia, and contralateral hypalgesia will clinically identify patients with lateral medullary infarction. Facial weakness and ocular symptoms are frequent and do not necessarily imply that the infarction extends beyond the lateral medulla. Cerebellar infarcts only infrequently accompany lateral medullary syndrome, suggesting that most of the posterior inferior cerebellar artery territory is spared, despite the high frequency of vertebral artery occlusion.

ENDURING DYSMETRIA AND IMPAIRED GAIN ADAPTIVITY OF SACCADIC EYE MOVEMENTS IN WALLENBERG'S LATERAL MEDULLARY SYNDROME

Saccadic eye movements and the adaptive control of their amplitudes were examined in patients with Wallenberg's lateral medullary syndrome. Half of the patients had permanent saccadic dysmetria. Their primary saccades had asymmetric amplitudes: those made in response to an ipsilateral target step (i.e. to the lesion side) tended to be hypermetric and saccades made in response to a contralateral target step were strongly hypometric. Multiple correction saccades were needed for target fixation. The adjustment of the amplitude of artificially induced hypermetric saccades, called gain adaptivity, was examined experimentally by using double target steps. The first target step elicited the primary saccade which triggered a further target displacement. This second, intra-saccadic target displacement was opposite to the first target step and caused the primary saccade to overshoot the final target position. In this way a post-saccadic target position error was generated which had to be corrected for foveal fixation. With repetition of this stimulus sequence the saccadic control system of normal subjects made an adjustment in amplitude of the main saccade such that the overshooting gradually diminished. After a few hundred trials primary saccades became orthometric with respect to the final target position; in respect to the first target step they were, however, strongly hypometric. The experimental data show that patients with Wallenberg's syndrome had a reduced capability to readjust saccadic amplitude. This observation together with the enduring saccadic dysmetria suggest that adaptive gain control of saccades is impaired in patients with lesions restricted to the dorsolateral medulla. It is speculated that these lesions most likely disrupt olivo-cerebellar pathways which are believed to be of paramount importance in visuo-motor adaptation of the cerebellum.

Oculomotor Control and Cognitive Processes: Normal and Pathological Aspects

Neural networks applied to the oculomotor system (D.A. Robinson). Eye movements in neurological diagnosis: Huntington's disease and congenital nystagmus (D.S. Zee). Neurophysiology of Eye Movements. Localization of targets in humans: the role of ocular muscle proprioception (D. Nommay et al). Effects of severance of the vestibular commissural pathway on the neural integrator of the oculomotor system in cat (E. Godaux, G. Cheron). Representation of three-dimensional eye movements in the cerebellar flocculus of the rabbit (J. van der Steen et al). Effects of floccular injections of noradrenergic agonists and antagonists on adaptive changes in the VOR gain (J. van Neerven et al). The Control of Eye Movements. Human vestibuloocular reflex (VOR) and vestibular velocity storage as influenced by optokinetic stimuli (E. Koenig et al). Vertical gaze stability in cat: otolithic contribution (V.E. Pettorossi et al). Post-rotational nystagmus suppression by the presentation of a single visual target in cat and man (G. Magenes et al). Adaptive mechanisms in the monkey saccadic system (P. Inchingolo et al). Human express saccades: catch trails influence the probability of their occurrence (M. Juttner, W. Wolf). Eye-Head Coordination. Adaptation of eye and head movements to reduced peripheral vision (G.M. Gauthier et al). Coupled and dissociated modes of eye-head coordination in humans to flashed visual target (S. Ron, A. Berthoz). Superior colliculus and feedback control of gaze shift in the head-free cat (D. Pelisson et al). Strategies of eye-head coordination (R. Schmid, D. Zambarbieri). Eye Movements in Pathology. Sensory and motor aspects of congenital nystagmus (R.V. Abadi et al). Head-shaking nystagmus - A clinical tool to detect peripheral and central vestibular asymmetries (M. Fetter et al). Saccadic and smooth pursuit eye movements in olivo-ponto-cerebellar atrophies (M. Spanio et al). Slow eye movement abnormalities in Wallenberg's lateral medullary syndrome (W. Waespe). Eye tracking dysfunctions in schizophrenic patients - Why is there no neuroleptic side-effect? (N. Hock et al). Eye Movements and Cognitive Processes. A mathematical analysis of the convenient viewing position hypothesis and its components (M. Brysbaert, G. d'Ydewalle). Is there an optimal landing position in words during reading of texts? (F. Vitu, J.K. O'Regan). Processing of prepositions as reflected by gaze durations (A. Wilbertz et al). The latency of saccadic eye movements to texture-defined stimuli (H. Deubel, H. Frank). Does thinking aloud influence the structure of cognitive processes? (U. Lass et al). Eye movements in visual search: a test of the limited cognitive effort hypothesis and an analysis of the search operating characteristic (A.M. Jacobs). Applied Research. Colour, effective contrast and search performance (J.L. Barbur et al). Video-oculography - An alternative method for measurement of three-dimensional eye movements (A.H. Clarke et al).

OCULOMOTOR DISTURBANCES DURING VISUAL-VESTIBULAR INTERACTION IN WALLENBERG'S LATERAL MEDULLARY SYNDROME

Transient and lasting oculomotor disturbances during visual-vestibular interaction are described in 9 patients with Wallenberg's lateral medullary syndrome. In all patients magnetic resonance imaging (MRI) demonstrated a single focal area of pathological signal intensity in the (dorso)-lateral medulla suggesting infarction. In 2 of these 9 patients and in 3 further patients with no medullary signs, the infarction involved the cerebellar territory of the posterior inferior cerebellar artery (PICA). Acutely, all patients with Wallenberg's syndrome (except 1) had saccadic lateropulsion and spontaneous nystagmus in light with the horizontal fast component beating to the contralateral normal side. The velocity of the slow drift to the side of the lesion was dependent on eye position and induced a characteristic asymmetry of the visually and vestibularly elicited slow eye movements. In most patients smooth pursuit, optokinetic nystagmus and visual suppression of the vestibulo-ocular reflex were still impaired when this spontaneous drift was minimal or absent. The oculomotor disturbances in patients with and without cerebellar infarction are compared. The following conclusions are made. (1) The spontaneous drift that is dependent on eye position is mostly created by 'ocular lateropulsion', that is, a tonic bias within the oculomotor system which may have several sources. (2) The abnormalities and asymmetries of oculomotor responses during visual-vestibular stimulation cannot solely be explained by this spontaneous drift and its interaction with otherwise normal eye movements. Instead, structures and pathways are damaged in Wallenberg's syndrome which mediate visual and/or motor signals important for the cerebellar control of visually-guided slow eye movements. (3) Damage to these pathways occurs in the lateral medulla, as the MRI findings show that in most patients the cerebellum is rarely involved, but no definite conclusion can be made as to which of the fibres travelling in the inferior peduncle to the cerebellum may be interrupted.

Pain and neuroma formation in Wallenberg's lateral medullary syndrome

We report a patient with a Wallenberg's lateral medullary syndrome in which pain was a prominent feature. This led to substitution of the original and correct diagnosis by that of a thalamic syndrome for which a prefrontal leucotomy was performed. The patient died some years later from a myocardial infarction and autopsy was performed. In the dorsolateral part of the medulla oblongata a cavity was found in which aberrant nerve fibres with neuroma-like formations could be seen. These fibres coursed along blood vessels, and penetrated from the surface of the medulla oblongata. On the base of the clinico-pathological correlations, it is conjectured that destruction of the lateral reticular formation cannot be the sole cause of the severe pain.

Pain in wallenberg's lateral medullary syndrome

Pain in wallenberg's lateral medullary syndrome

Effects of brain-stem and thalamic lesions on the corneal reflex: an electrophysiological and anatomical study.

In 9 patients with Wallenberg's lateral medullary syndrome, one patient with a midbrain lesion involving the right side of the tegmentum, and 2 patients with a thalamic lesion, corneal reflexes were investigated by a new electromyographic technique. The electrophysical results were compared with the results obtained by clinical observation. In the lateral medullary lesions the electrophysiologically obtained reflex responses showed four types of abnormality. Type A consisted of a bilateral delay and type B a bilateral absence of the corneal reflex response to stimulation on the affected side in combination with a normal reflex response on both sides when the cornea on the normal side was stimulated. Type C, which was present in one case, and type D which was seen in 3 cases, consisted of a bilateral absence of the corneal reflex upon stimulation on the affected side; stimulation on the unaffected side produced a normal reflex response on the intact side in combination with, respectively, a delay or absence of the corneal reflex response on the affected side. Comparison of the clinical observations with the electrophysiological findings revealed minor discrepancies in type A and B abnormalities. However, the electrophysiological type C and D abnormalities were not detected by clinical observation. These findings demonstrate that electrophysiological recording of the corneal reflex may reveal clinically undetectable abnormalities. From the electrophysiological findings it is concluded that the corneal reflex is conducted along medullary pathways running both ipsilaterally and contralaterally from the stimulated side before connecting, respectively, with the ipsilateral and contralateral facial nucleus. From the anatomical findings it is suggested that the ascending pathways from the spinal fifth nerve complex to the facial nuclei are located in the lateral reticular formation of the lower brain-stem. The normal corneal reflex responses in the presence of thalamic and midbrain lesions involving nociceptive fibres in the trigeminothalamic tract do not support a previously postulated long-loop reflex arc passing through this tract. The suprabulbar influence upon the corneal reflex is discussed.

Angiographic Findings in Wallenberg's Lateral Medullary Syndrome

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Angiographic findings in Wallenberg's lateral medullary syndrome.

T HIS report concerns 7 cases of Wallenberg's lateral medullary syndrome studied by vertebral angiography. Krayenbiihl 4 and Krayenbtthl and Ya~argil s in two reports mentioned that they have studied 12 cases but actually 5 cases were reported, 3 in their first publication and ~ in the second (several were not clinically lateral medullary syndromes). They found partial or complete occlusion of the vertebral ar tery at the arch of the atlas as the characteristic angiographic picture for this clinical syndrome. There are other scattered reports of angiographic studies done in cases of the lateral medullary syndrome usually as part of a large series of vertebral angiograms but, as far as we know, KrayenbUhl and Ya~argil's is the largest series reported previously. An excellent demonstration of the pathologic findings in this syndrome has been given by Fisher et al. 3 Those authors found occlusion of the vertebral ar tery in 7 of 16 pathologically proven cases, occlusion of the vertebral and the posterior inferior cerebellar arteries in 5, occlusion of the posterior inferior cerebellar ar tery alone in r and in ~ cases no vascular occlusion was found. In those cases in which just occlusion of the vertebral ar tery was present, small branches of tha t ar tery had supplied the infarcted lateral medullary area and the posterior inferior cerebellar ar tery was absent or not involved in the

Some comments on Wallenberg's lateral medullary syndrome.

Some comments on Wallenberg's lateral medullary syndrome.