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Results for “Lateral Medullary Syndrome”

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At least 19 recordsLinked to original sources
PubMed1991

[Pathogenesis of ipsilateral hemiparesis in patients with lateral medullary syndrome].

Lateral medullary syndrome is known to cause hemiparesis ipsilateral to the medullary lesion. However, it's clinical significance has not been fully evaluated. In this study, we made clinical and angiographic studies in patients with syndrome to elucidate the pathogenesis of ipsilateral hemiparesis. Thirty-four patients with cerebral infarction presenting with this syndrome were studied. Their mean age was 51 years and all the patients were examined within 6 months of their first attack. Diagnosis of ipsilateral hemiparesis was made if subjective feeling of weakness in the upper and lower extremities was associated with increased deep tendon reflexes. Ipsilateral hemiparesis was observed in 38% of all the patients. Cerebral angiography was performed in 26 patients and divided into two groups; group A with ipsilateral hemiparesis (n = 9) and group B without ipsilateral hemiparesis (n = 7). In 56% of patients in group A, angiography showed non-visualization of ipsilateral vertebral artery (VA) and posterior inferior cerebellar artery (PICA). Non-visualization of these two arteries never occurred in the patients of group B. On the other hand, non-visualization of VA alone was observed in 35% of the patients in group B, but it was none in the patients of group A. However, there were no differences in concerning the frequency of non-visualization of PICA alone or non-occlusion at all between both groups. Therefore, the focal ischemia in the region below the pyramidal decussation due to the occlusion of both VA and PICA, regardless of thrombotic or embolic episode, was considered to be responsible for ipsilateral hemiparesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The lateral medullary syndrome.

The lateral medullary syndrome is a rare syndrome resulting from a cerebrovascular accident involving part of the medulla oblongata with consequent loss of pain and temperature sensation in the orofacial region, loss of taste, and palatal palsy and loss of gag reflex, together with Horner's syndrome and ataxia. A case is presented and the literature reviewed.

Humans↗
PubMed1997

[A case of vertebral artery dissection with lateral inferior pontine syndrome and lateral medullary syndrome].

A 55-years-old woman had left neck pain and headache, dizziness, left Horner's sign, left abducens palsy, diplopia, left peripheral facial palsy, left loss of hearing, left tinnitus, left paralysis of vocal cord and soft palate, dysphagia, left limb ataxia, truncal ataxia, disturbance of temperature and pain sensation over Th10 on the right involving the right face. Left vertebral angiography revealed tapering occlusion of the left vertebral artery. Right vertebral angiography showed normal angiogram of the basilar artery and bilateral anterior inferior cerebellar arteries. MRI disclosed infarcts in the left lateral inferior pons, left lateral medulla, and cerebellum of territories in the anterior inferior cerebellar artery and posterior inferior cerebellar artery. T2 weighted image showed septum (intimal flap) in the left vertebral artery. This is the very rare case of lateral inferior pontine syndrome and lateral medullary syndrome due to the vertebral artery dissection.

Aortic Dissection↗
PubMed2000

Loss of ability to sneeze in lateral medullary syndrome.

Four consecutive patients with lateral medullary syndrome reported reversible inability to complete a reflex sneeze, despite retaining the urge to do so and the ability to mimic the motor act. This previously undescribed feature of a relatively common syndrome is in keeping with the known location of a "sneeze center" in the lateral medulla of cat. In man, unilateral brainstem lesion is sufficient to abolish the sneeze reflex temporarily.

Adult↗
PubMed1990

[A case of fibromuscular dysplasia presenting lateral medullary syndrome].

We reported a case of fibromuscular dysplasia (FMD) presenting lateral medullary syndrome accompanied with left truncal ataxia, left Horner's syndrome and superficial sensory deficit in the right extremities. He was 46-year-old man and had no remarkable risk factors for the cerebrovascular disease such as hypertension, diabetes mellitus and valvular heart disease. Cerebral angiography was performed and there was the string-of-beads-like shadow in the left vertebral artery, revealing a localized FMD. Wedge-shaped area of low signal intensity in the left lower medulla was recognized in magnetic resonance imaging (spin echo Tr/Te 600/30). It was suggested that the lesion of the lower medulla caused the patient's several symptoms. In Japan, there have been a few case reports of cervical or intracranial FMD, but we cannot find any report of FMD localizing in the unilateral vertebral artery. In general, it has been said that the etiology of lateral medullary syndrome under fifty years old differs from those of geriatric patients. The authors pointed out the significance of FMD as one of those risk factors causing lateral medullary syndrome and also discussed the mechanism of the sensory disturbance sparing face.

Arterial Occlusive Diseases↗
PubMed2005

Vestibular assessment in a patient with confirmed lateral medullary syndrome.

The results of vestibular investigations in a patient with confirmed lateral medullary syndrome are presented. This patient showed a unilateral weakness on caloric testing which has not been reported previously in a patient with lateral medullary syndrome. The case for the possibility of a 'central' canal paresis on caloric testing is presented.

Electronystagmography↗
PubMed1986

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.

Brain Neoplasms↗
PubMed2000

Restricted dissociated sensory loss in a patient with a lateral medullary syndrome: A clinical-MRI study.

BACKGROUND: Various sensory syndromes in lateral medullary infarctions are described. A small variation in the location of a lesion may lead to very different clinical features, owing to the complex anatomy of the medulla oblongata. MRI may identify the location and extent of the ischemic lesions, allowing a clear clinical-anatomical correlation. CASE DESCRIPTION: We describe a man with an ischemic lesion in the right portion of the lower medulla that presented a contralateral impairment of spinothalamic sensory modalities and an ipsilateral impairment of lemniscal modalities with a restricted distribution (left forearm and hand, right hand and fingers, respectively). The restricted and dissociated sensory abnormalities represent the only permanent neurological consequence of that lesion. CONCLUSIONS: The atypical sensory syndrome may be explained by the involvement of the medial portion of spinothalamic tract and the lateral portion of archiform fibers at the level of the lemniscal decussation.

Arm↗
PubMedDate not supplied

Magnetic resonance imaging in Wallenberg's lateral medullary syndrome.

Four patients with a clinical diagnosis of Wallenberg's lateral medullary syndrome were studied with both Magnetic Resonance Imaging (MRI) and cranial Computed Tomography (CT). Using transverse images and both T1 and T2--weighted sequences, MRI demonstrated a medullary infarction not seen on CT in all four cases. MRI also demonstrated a coexisting cerebellar infarction in three cases which was unsuspected clinically and undetected by CT.

Adult↗
PubMed2004

Wallenberg's lateral medullary syndrome: diffusion-weighted imaging findings.

PURPOSE: To investigate the efficacy of diffusion-weighted imaging in patients with Wallenberg's lateral medullary syndrome. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Adult↗
PubMed1992

Ocular motor abnormalities in Wallenberg's lateral medullary syndrome.

The ocular motor abnormalities that commonly occur in Wallenberg's lateral medullary syndrome are often unappreciated. These abnormalities include signs of dysfunction of ocular alignment (skew deviation, ocular tilt reaction, and environmental tilt), various types of nystagmus, smooth pursuit and gaze-holding abnormalities (eye deviation, ipsipulsion or lateropulsion, and impaired contralateral pursuit), and saccadic abnormalities (ipsipulsion and torsipulsion). These impairments of ocular motor control and their proposed mechanisms are discussed.

Humans↗
PubMedDate not supplied

Hiccups associated with lateral medullary syndrome. A case report.

We present a case of persistent hiccups (singultus) after a lateral medullary cerebrovascular accident. The patient presented with a two-day history of nausea and vomiting. Clinically, the patient had a loss of pain and temperature on the left side of the face, a loss of pain and temperature on the right side of the trunk, a mild left hemiparesis, and a left-sided ataxia. Nystagmus, diplopia, and hiccups were also evident. A left lateral medullary syndrome in the vascular distribution of the posterior inferior cerebellar artery was diagnosed. Work-up included a magnetic resonance imaging angiogram, which revealed an occlusion v high-grade stenosis of the basilar artery. The patient reported that the most distressing symptom was the chronic hiccups (25/min), which interfered with nutrition, sleep, and activity. While in the acute care hospital, the patient was treated with prochlorperazine, promethazine, and chlorpromazine. Each of these medications was unsuccessful in stopping the hiccups. After a search of the European literature revealed that baclofen was recommended as the drug of choice for stopping persistent hiccups, the patient was given 5 mg of baclofen by mouth three times per day, and the hiccups abated within 48 hours. The baclofen was discontinued after one week of therapy, and the hiccups did not return. We recommend consideration of baclofen for the treatment of persistent hiccups after lateral medullary syndrome because of its desirable side effects and reported success rate compared with other drugs used to treat chronic hiccups.

Aged↗
PubMed1988

Torsional nystagmus in the lateral medullary syndrome.

Torsional nystagmus was recorded in 3 patients with the lateral medullary syndrome. Magnetic search coil oculography demonstrated slow phases of nystagmus of increasing, decreasing, and constant velocity. Neural integration of torsional eye velocity commands to position commands is impaired by lateral medullary infarction. Torsional pulsion of saccades, consisting of torsional fast eye movements induced during saccades downward or away from the side of infarction, was recorded in 2 patients. All patients had skew deviation with hypotropia on the side of brainstem damage. The torsional nystagmus beat away from the side of infarction in each patient, but in one it alternated direction as the eyes drifted about a neutral position of torsion. We attribute the torsional nystagmus to an imbalance of central projections from the anterior and posterior semicircular canals and the otolith receptors that mediate ocular counterroll.

Aged↗
PubMed1993

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

OBJECTIVE: To correlate clinical and radiologic findings in patients with lateral medullary infarction. DESIGN: Case series with "blinded" evaluation of brain imaging. SETTING: Hospitalized and ambulatory patients at the Neurological Institute of New York (NY). PATIENTS: Thirty-three consecutive patients with lateral medullary syndrome were evaluated by the Stroke Center between 1983 and 1989. RESULTS: 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. CONCLUSIONS: 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.

Adult↗
PubMed2003

Relapsing polychondritis with involvement of posterior inferior cerebellar artery causing acute lateral medullary syndrome.

We present a patient with relapsing polychondritis who presented with findings of lateral medullary syndrome, known as the syndrome of Wallenberg, produced by infarction of a wedge of lateral medulla lying posterior to the inferior olivary nucleus. Angiographic examination showed complete occlusion of the right posterior inferior cerebellar artery and segmental narrowings in the basilar artery. We believe that the angiographic findings were based on an underlying vasculitis because of his relapsing polychondritis. This is the first case of relapsing polychondritis with angiographically demonstrated posterior inferior cerebellar artery involvement. Although this syndrome is usually a result of atherosclerosis, our case suggests that vasculitis must also be considered because it may respond to treatment with corticosteroids.

Journal Article↗
PubMed1989

[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration].

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2004

Fibromuscular dysplasia of the vertebral artery presenting with lateral medullary syndrome: a case report.

We have recently encountered a rare case of fibromuscular dysplasia (FMD) of the vertebral artery (VA) presenting as lateral medullary syndrome. A 39-year-old male was admitted to our hospital due to vertigo, dysarthria and numbness of the left face and the right limbs. A magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of brain revealed lateral medullary infarction in the territory of the left posterior inferior cerebellar artery (PICA). The angiography of the VA revealed tubular stenosis of the left extracranial VA and a focal vascular kinking as well as web in the right extracranial VA, confirming the diagnosis of FMD. We present this rare case to emphasize that FMD could be one of the risk factors causing lateral medullary syndrome in young people.

Adult↗
PubMed2002

Lateral medullary syndrome after prone position for general surgery.

IMPLICATIONS: We describe postoperative lateral medullary syndrome with myoclonic spasm. Improper head rotation during positioning in the anesthetized patient might obstruct the flow of the vertebral artery at the neck and result in diminished perfusion of the associated regions in patients with a history of cervical spinal trauma.

Adult↗