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

The clinical and pathological findings of a 41-year-old male patient with atypical Charcot-Marie-Tooth disease were reported. There were 3 cases of subarachnoid haemorrhage, 2 nerve deafness and 2 hereditary motor and sensory neuropathy (HMSN) in his family. He had suffered from progressive nerve deafness since 5 years old and gait disturbance since 37 years old. He had been admitted to the psychiatric hospital 3 times because of hallucinatory-delusional state and behavior abnormalities. Neurological examinations at 39 years old revealed that he had mental deterioration (IQ 66), nerve deafness, diffuse muscle atrophy, most marked distally, sensory disturbance, areflexia, positive Romberg's sign, orthostatic hypotension, dysphagia and slurred speech. MCV of median nerve was 27.8 m/sec, and SCV was not evoked. EEG revealed nonspecific dysfunction of the brain. He died of ileus-like condition at 41 years old. General autopsy showed haemorrhagic infarction of the jejunum and ileum due to compression of the superior mesenteric artery and vein by an adhesion band of connective tissue formed after previous appendectomy. Neuropathological examinations revealed axonal degeneration and loss of myelinated fibers with schwannosis of anterior and posterior spinal nerve roots as well as peripheral nerves. The posterior roots were more severely affected than the anterior ones. Ganglion cells of the posterior root ganglia showed remarkable degeneration and loss. There was severe degeneration of the posterior columns, especially in the gracilis, of the spinal cord. Nerve cells in the anterior horns and Clarke's columns also displayed conspicuous atrophy or central chromatolysis followed by gliosis. There was slight degeneration of the posterior spinocerebellar tracts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of neuronal type Charcot-Marie-Tooth disease (HMSN type II) with nerve deafness and psychiatric symptoms]. 138 65

A case of the anterior inferior cerebellar artery aneurysm with a sudden onset of caudal cranial nerve symptoms was reported. A 20-year-old female suffered from sudden onset of dysphagia and throat pain. Three days later, she was admitted to our hospital, suffering from sudden onset of headache, nausea, vomiting and consciousness disturbance. On admission, consciousness disturbance, bilateral abducent nerve palsy, and left caudal cranial nerve palsy was observed. CT scan revealed a subarachnoid hemorrhage in the basal cisterns with the densest area in the left ambient cistern. Left vertebral angiogram revealed an aneurysm at the left anterior inferior cerebellar artery (AICA). On the third day after admission, operation was performed. The aneurysm was found near the jugular foramen, surrounded by thick clots. The dome was attached to the caudal cranial nerves, and the neck was located at the bending portion of AICA without branches. Neck ligation and clipping was performed. On the fortieth day after the operation, the patient was discharged from our hospital without neurological deficits. To our knowledge, aneurysm at the AICA is rare and only 33 cases have been reported. However, a case with a sudden onset of caudal cranial nerve symptoms, before evident symptoms due to subarachnoid hemorrhage, has never been reported previously.
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PMID:[Anterior inferior cerebellar artery aneurysm with a sudden onset of caudal cranial nerve symptoms]. 277 Sep 75

We reviewed 24 patients with intracranial vertebral artery dissections treated during the last 12 years. Sixteen patients were admitted with subarachnoid hemorrhage (SAH) and 8 did not have SAH. The mean age at the time of onset was 50.0 years. Male preponderance was noted. Among 21 patients with acute onset, 6 (29%) experienced prodromal neck pain and 3 (60%) of 5 SAH patients showed nuchal stiffness when examined within 6 hours of onset. The preoperative angiographical findings were uniform in SAH cases in contrast to the varied angiographical findings seen in non-SAH cases. So-called pearl and string sign was observed in most SAH cases, but the "string" was often so short and wide that the term "constriction" appeared more suitable. From intraoperative observations, the angiographical point of constriction seemed to represent the proximal or distal end of dissection. As for treatment, 19 patients underwent 20 surgeries. Trapping was performed in eight surgeries, base clipping was performed in five, and proximal clipping was performed in seven. Both trapping and base clipping prevented further bleeding, but trapping was associated with a high rate of postoperative lower cranial nerve palsy. Postoperative neurological complications were less frequent after proximal clipping, but subsequent postoperative bleeding occurred in one patient treated by this technique. The overall long-term outcome in the surgically treated cases in our series was favorable, but most patients suffered from various degrees of uncomfortable dysphagia or hoarseness for some period after surgery. It was also noted that, in half of the disabled cases, the major disability was attributable to lower cranial nerve palsy and respiratory troubles that developed postoperatively.
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PMID:Intracranial vertebral artery dissections: clinical, radiological features, and surgical considerations. 800 58

Three weeks after an automobile accident, a 35-year-old man experienced left throat and neck pain, numbness of the left face and tongue, dysphagia, left arm pain and weakness, and left miosis. At age 27, he had suffered an aneurysmal subarachnoid hemorrhage. Angiography at that time had also demonstrated a fenestration of the left intracranial vertebral artery. At the time of the second presentation, angiography showed that one of the limbs of the fenestration had become occluded. Although the vast majority of intracranial arterial fenestrations are asymptomatic, occlusion of one of the limbs of a fenestration may be the cause of stroke.
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PMID:Traumatic occlusion of one limb of an intracranial arterial fenestration: an uncommon cause of stroke. 871 96

Functional outcome of primary subarachnoid haemorrhage survivors was examined following rehabilitation in Singapore. Thirty-nine inpatients admitted over a 4-year period were studied retrospectively. There were 21 (53.8%) males and 18 (46.2%) females, mean age 50.9 (SD 12.7) years, at 37.3 days (SD 16.8) post-injury. Seven (17.9%) had dysphagia and 12 (30.8%) had dysphasia; 17 (43.6%) nondysphasics had cognitive impairment; 26 patients (66.7%) had Medical Research Council motor power under grade 4. Modified Barthel Index on Admission (MBIA) and Discharge (MBID) were 45.7 (SD 22.3) and 78.3 (SD 18.9), respectively (p = 0.001). Correlation between MBIA and MBID was statistically significant (r = 0.529, p = 0.001). Mean length of stay in rehabilitation was 42.3 days (SD 27.6). Thirty-four patients (87.2%) were discharged home. Nine out of 24 previously employed patients (37.5%) returned to gainful employment. Despite multiple deficits, the patients made significant functional improvement.
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PMID:Rehabilitation outcome after primary subarachnoid haemorrhage. 1211 84

Subarachnoid hemorrhage and cerebral hemorrhage are the most frequent causes of sudden death due to stroke. Brainstem hemorrhage, which is the cause of respiratory and vasomotor centers dysfunction, is frequently the direct cause of sudden death caused by stroke, and not only cerebral edema, but also secondary lethal arrhythmia, myocardial infarction, pulmonary embolism, or asphyxiation by dysphagia may be indirect causes of death associated with stroke. To prevent sudden death due to stroke, management of respiratory and circulatory systems as well as treatment corresponding to the type or severity of the disease are required. In this issue, we discuss the cause, management, and prevention of sudden death due to stroke.
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PMID:[Sudden death due to stroke and its management]. 1600 84

Elevated muscular tone associated with spastic syndromes can cause excessive contractility at the upper esophageal sphincter and impede swallowing. A 47-year-old male patient with spasticity predominantly of the lower extremities after a subarachnoid hemorrhage suffered from severe dysphagia and chronic salivary aspiration. He was dependent on a cuffed tracheostomy tube and a percutaneous enterogastric feeding tube. Barium swallow and esophageal manometry revealed cricopharyngeal spasm, while laryngeal elevation and pharyngeal contractility were well preserved. We endoscopically injected 180 MU botulinum toxin A into the cricopharyngeus muscle. Two days post injection, swallowing function had improved and oral nutrition was possible. This improvement lasted for six weeks. After another injection 8 weeks later, an undesired diffusion into the hypopharynx occurred and manometry showed diminished contractility without amelioration of dysphagia. Botulinum toxin therapy of cricopharyngeal spasm improves swallowing function in a subgroup of patients with spastic syndromes. The therapeutic effect is of limited duration. Toxin diffusion into the pharynx should be avoided. Manometry is useful in planning and monitoring the therapy.
Dysphagia 2008 Dec
PMID:Botulinum toxin a treatment of cricopharyngeal dysphagia after subarachnoid hemorrhage. 1843 65

Subarachnoid blood has been reported as a cause of chronic spinal arachnoiditis. Although syringomyelia has been thought to be caused by spinal arachnoiditis, reports of syringomyelia following aneurysmal subarachnoid hemorrhage (SAH) are very rare. We describe two patients with syringomyelia associated with chronic spinal arachnoiditis following SAH. From January 2001 to December 2010, 198 patients with aneurysmal SAH were treated at Kinki University School of Medicine. Two of the 198 patients had syringomyelia following aneurysmal SAH; thus the rate of syringomyelia associated with aneurysmal SAH was 1.0%. Patient 1 was a 54-year-old woman who presented with back pain, back numbness and gait disturbance 20 months after SAH. Her MRI revealed syringomyelia of the spinal cord from C2 to T10. She underwent shunting of the syrinx to the subarachnoid space. Patient 2 was a 49-year-old man, who was admitted to the hospital with headache, diplopia, hoarseness, dysphagia and ataxia five months after SAH. MRI revealed syringomyelia from the medulla oblongata to C6, and an enlargement of the lateral and fourth ventricles. After foramen magnum decompression and C1 laminectomy, a fourth ventricle-subarachnoid shunt was placed by insertion of a catheter. Spinal arachnoiditis and spinal syringomyelia are rare but important chronic complications after SAH.
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PMID:Spinal syringomyelia following subarachnoid hemorrhage. 2228 78

We report an unusual case of lateral medullary infarction after successful embolization of the vertebral artery dissecting aneurysm (VADA). A 49-year-old man who had no noteworthy previous medical history was admitted to our hospital with a severe headache. Computed tomography (CT) revealed a subarachnoid hemorrhage, located in the basal cistern and posterior fossa. Cerebral angiography showed a VADA, that did not involve the origin of the posterior inferior cerebellar artery (PICA). We treated this aneurysm via endovascular trapping of the vertebral artery distal to the PICA. After operation, CT revealed post-hemorrhagic hydrocephalus, which we resolved with a permanent ventriculoperitoneal shunt procedure. Postoperatively, the patient experienced transient mild hoarsness and dysphagia. Magnetic resonance image (MRI) showed a small infarction in the right side of the medulla. The patient recovered well, though he still had some residual symptom of dysphagia at discharge. Such an event is uncommon but can be a major clinical concern. Further investigation to reveal risk factors and/or causative mechanisms for the medullary infarction after successful endovascular trapping of the VADA are sorely needed, to minimize such a complication.
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PMID:A case of lateral medullary infarction after endovascular trapping of the vertebral artery dissecting aneurysm. 2263 14

The craniocervical junction (CCJ) functions within a complicated regional anatomy necessary to protect and support vital neurovascular structures. In select instances, vascular pathology can be attributed to this complicated interplay of motion and structure found within this narrow space. The authors report 3 cases of complex vascular pathology related to motion at the CCJ and detail the management of these cases. Two cases involved posterior circulation vascular compression syndromes, and one case involved a vascular anomaly and its relation to aneurysm formation and rupture. The patient in Case 1 was a 66-year-old man with a history of syncopal episodes resulting from the bilateral vertebral artery becoming occluded when he rotated his head. Successful microsurgical decompression at the skull base resulted in patent bilateral vertebral artery V3 segments upon head movement in all directions. The patient in Case 2 was a 53-year-old woman who underwent elective resection of a right temporal meningioma and who experienced postoperative drowsiness, dysphagia, and mild right-arm ataxia. Subsequent MRI demonstrated bilateral posterior inferior cerebel-lar artery (PICA) strokes. Cerebral angiography showed a single PICA, of extradural origin, supplying both cerebellar hemispheres. The PICA exhibited dynamic extradural compression when the patient rotated her head; the bilateral PICA strokes were due to head rotation during surgical positioning. In Case 3, a 37-year-old woman found unconscious in her home had diffuse subarachnoid hemorrhage and evidence of a right PICA aneurysm. A right far-lateral craniectomy was performed for aneurysm clipping, and she was found to have a dissecting aneurysm with an associated PICA originating extradurally. There was a shearing phenomenon of the extradural PICA along the dura of the foramen magnum, and this microtraumatic stress imposed on the vessel resulted in a dissecting aneurysm. This series of complex and unusual cases highlights the authors' understanding of vascular pathology of the CCJ and its management.
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PMID:Motion-related vascular abnormalities at the craniocervical junction: illustrative case series and literature review. 2582


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