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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

we report a patient with Wallenberg's syndrome caused by glioma of the lateral medulla oblongata, and review the literature for Wallenberg's syndrome associated with neoplastic disease. A 46-year-old man was admitted because of progressive dysphagia and vertigo. Neurological examination revealed atypical symptoms and signs of Wallenberg's syndrome on the right side, hypalgesia on the second and third divisions of the left trigeminal nerve, paresis of the right palate and uvula, and ataxia of the right extremities. Although CT showed no abnormality in the posterior fossa, MRI demonstrated a mass with abnormal signal intensities in the right dorsolateral portion of the medulla. Biopsy specimens showed astrocytoma (grade III). Based on the present case and a review of 10 previously reported cases of Wallenberg's syndrome caused by neoplastic disease, the clinical features of this syndrome are characterized by gradual development and steady progression of symptoms, non-classical or atypical symptomatology, numerous additional symptoms and signs depending on the site and size of tumors, and poor prognosis.
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PMID:[Wallenberg's syndrome caused by a brain tumor--a case report and literature review]. 216 89

Eleven cases presenting a syndrome of the medulla oblongata are discussed with reference to the findings of clinical and angiographic investigation. The diagnosis of Wallenberg's syndrome is justified when the classic symptoms are apparent (Horner's syndrome, nystagmus, dysphonia and dysphagia, ataxia, ipsilateral sensory impairment of the face and contralateral elsewhere, and accompanying vegetative disturbances). If additional symptoms such as a facial or extra-ocular muscle paresis, especially hemiparesis, exist, another, more lateral or medial, syndrome of the oblongata should be considered. Angiographic findings vary considerably, ranging from a normal vertebral artery or posterior inferior cerebellar artery (PICA) to an occlusion of these arteries (in three and two of the 11 cases respectively). Modification are often seen in the anterior inferior cerebellar artery (AICA). A kind of complementary supply in the PICA-AICA region must occasionally exist. Localised processes affecting these vessels rather than diffuse multifocal vascular processes would lead to Wallenberg's syndrome. It is difficult to conclude from the clinical picture where a possible responsible vascular narrowing or obliteration may lie, even if pareses of the limb were present.
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PMID:[Clinical and angiographic findings in vascular medullary syndromes (author's transl)]. 731 26

A patient with a dissecting aneurysm of a posterior inferior cerebellar artery who presented with Wallenberg's syndrome is reported. A 31-year-old man suddenly experienced an occipital headache, vertigo, and vomiting, followed by dysphagia. A neurological examination revealed partial Wallenberg's syndrome. Vertebral angiography revealed aneurysmal dilatation at the origin of the left posterior inferior cerebellar artery, with distal luminal narrowing. T1-weighted magnetic resonance imaging demonstrated an area of high-signal intensity, indicating an intramural hemorrhage in the arterial wall of the narrowed lumen. The dissecting aneurysm with a typical intramural hematoma of the posterior inferior cerebellar artery was entrapped with clips after an anastomosis of the left occipital artery to the distal posterior inferior cerebellar artery. The diagnosis and the treatment of dissecting aneurysms of the posterior inferior cerebellar artery are discussed.
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PMID:Dissecting aneurysm of the posterior inferior cerebellar artery: case report. 823 17

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.
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PMID:[Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients]. 904 27

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.
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PMID:[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction]. 1042 53

A 65-year old man was admitted with severe dysphagia, ataxia and aspiration pneumonia. Dysphagia and ataxia were caused by lateral medullary infarction (Wallenberg's syndrome). The swallowing abnormality was assessed by videofluorography and we attempted the balloon dilatation method for cricopharyngeal dysphagia. Three months after initiation of swallowing training, videofluorography (VF) showed that the magnitude of aspiration to the trachea had decreased and the patient began taking food by mouth. The balloon dilatation method is successful for chronic stage cricopharyngeal dysphagia and the VF test is useful for quantitative assessment of dysphagia and for deciding when to start oral intake in elderly patients.
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PMID:[Swallowing rehabilitation using balloon catheter treatment evaluated by videofluorography in an elderly patient with Wallenberg's syndrome]. 1099 32

A 68-year-old man presented with Wallenberg's syndrome consisting of ataxia, dysphagia, hypesthesia on the left side of the body, and Horner's syndrome on the right. Magnetic resonance (MR) imaging revealed a right lateral medullary infarction and small multiple lacunae scattered in the upper medulla. Neurological symptoms improved in a week and the patient was discharged with mild residual hypesthesia on the left side. However, 31 days later, he was emergently admitted after suddenly becoming apneic and losing consciousness. MR imaging detected no new lesion. The patient was placed under ventilation support for 48 hours before regaining normal respiratory function. Medullary infarction sometimes causes catastrophic respiratory failure, but Wallenberg's syndrome caused by lateral medullary infarction is rarely associated with central respiratory dysfunction, and delayed onset of central respiratory dysfunction is extremely unusual. Delayed onset of central respiratory failure is a life-threatening complication of the medullary infarction causing Wallenberg's syndrome, which in general is not recognized.
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PMID:Delayed central respiratory dysfunction after Wallenberg's syndrome--case report. 1176 Mar 86

We report here a case of atypical Wallenberg's syndrome due to spontaneous vertebral artery (VA) dissection. A 52-year-old woman was admitted to our department because of a sudden onset of left orbital pain. Emergency CT scan disclosed no evidence of intracranial hemorrhage. Neurological examination at the time of the current admission, showed dysphagia, left soft palate palsy, hoarseness, left Horner syndrome, hypalgesia with thermohypesthesia on the right side of her face, however, hypalgesia with thermohypesthesia on the right side of her body. The diagnosis of atypical Wallenberg's syndrome was based on the above findings. MR images disclosed the infarcted lesion at the left lateral medulla depicted as high-intensity on T2-weighted & FLAIR images. We carried out conservative treatment with antiplatelet & hemodilution therapies and the blood pressure control. Left vertebral angiograms obtained 18 days after the onset, showed the segmental severe stenosis of the VA between the ramification of the posterior inferior cerebellar artery (PICA) and the union of the VAs. In the venous phase, retention of contrast medium in the VA and the PICA was observed. The flow rate of the parent artery was decreased. We strongly suspected that her initial symptom of left orbital pain was due to dissection of the VA itself. Three-dimensional CT angiograms obtained 30 days after the onset, demonstrated the defect of the left VA between the ramification of the left PICA and the union of the VAs. Left vertebral angiograms obtained 36 days after the onset, showed the occlusion of the VA between the ramification of the PICA and the union of the VAs. The neurological findings gradually improved and the patient was discharged. Follow up left vertebral angiograms obtained 4 months & 16 months after the onset, revealed almost no changes of left VA occlusion.
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PMID:[Atypical Wallenberg's syndrome due to spontaneous vertebral arterial dissection: case report]. 1532 42

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.
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PMID:[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]. 1551 11

Wallenberg's syndrome is one of the most common clinically recognized conditions due to brain stem infarct, which can nowadays be identified by modern neuro-imaging techniques. We describe a patient complaining of miosis, dysphonia, and dysphagia followed by ataxia. An MRI evaluation was performed including diffusion-weighted imaging, apparent diffusion coefficient, T2-weighted images, fluid attenuated inversion recovery (FLAIR) and perfusion. A brief discussion of imaging findings is presented as well as a clinical correlation of the symptoms with the anatomic location of the lesion. This case report emphasizes the importance of imaging findings and their clinical correlation with neurological examination.
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PMID:[Wallenberg syndrome: magnetic imaging findings and clinical correlation]. 1824 38


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