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

Two siblings with diabetes mellitus and optic atrophy (Wolfram syndrome) are described. As often noted, they also had atonic urinary bladders. Only one of the siblings had some impairment of hearing. Other findings not previously reported that appeared in each subject were esophageal dysphagia and vertigo. An autopsy in one revealed brain stem hypoplasia and thinning and flattening of the optic nerves with atrophy of the lateral geniculate bodies.
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PMID:Diabetes mellitus and optic atrophy in two siblings: a report on a new association and a review of the literature. 683 24

Aneurysms of the carotid arteries are relatively rare and can present difficult diagnostic problems. They may occur anywhere along the course of the carotid artery in its cervical route, petrous portion, or intracranial extension. The associated clinical findings may range from a simple neck mass to a variety of neurologic deficits. Symptoms of headache, facial pain, tinnitus, vertigo, epistaxis, hoarseness, and dysphagia may require otolaryngologic evaluation. The high morbidity and mortality associated with the natural history of carotid aneurysms makes their early detection essential. Although these lesions have been a subject of great interest in the neurological and neurosurgical literature, surprisingly little has been written to bring them to the attention of otolaryngologists. A review of the literature and an assessment of 10 cases of extracranial carotid aneurysms treated at the University of Pennsylvania in the past 10 years form the basis of this report. Patients with aneurysms involving various portions of the carotid system are presented to illustrate the numerous head and neck manifestations these lesions produce. Differential diagnosis, etiology, natural history, and current management of carotid aneurysms are discussed.
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PMID:Carotid artery aneurysms: an otolaryngologic perspective. 738 5

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

A 59-year-old female was admitted with complaints of vertigo, dysarthria and dysphagia. On neurological examination, right-sided cranial nerve signs included ptosis, Bruns's nystagmus, decreased corneal sensation, diminished facial pain and temperature sensation, decreased palatal excursion and loss of gag reflex. There was no evident motor weakness, but deep tendon reflexes were slightly exaggerated on the left extremities. Coordination testing showed right cerebellar signs. Sensory examination of the remaining parts of the body was quite normal. X-ray CT scan showed multiple high density areas in the right medulla, right pons, right temporal and frontal lobes. T2 weighted MRI demonstrated these lesions as mixed signal intensity areas with marked low signal intensity rim. There were multiple black dots in the bilateral frontal and temporal lobes, cerebellar hemispheres on T2-weighted images. Carotid and vertebral angiograms showed no abnormality. This is the first report of the cavernous malformation presenting as lateral medullary syndrome.
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PMID:[Lateral medullary syndrome due to cavernous malformation in the brain stem]. 840 82

We describe here a 50-year-old patient who had multiple cranial nerve palsies (lt.VIII,IX,X,XI and rt.VII, IX,X) with varicella-zoster virus (VZV). He developed hoarseness, dysphagia on 30th, November, 1994. On the 8th day after the onset, he suffered from left tinnitus and left facial nerve palsy. Neurological examination on the 10th day revealed left peripheral facial nerve palsy, lt. vocal cord palsy, mild dysphagia and loss of bilateral taste. He did not show signs of meningeal irritation. On the 11th day, he felt vertigo and had horizontal nystagmus on the right lateral gaze. The cerebrospinal fluid findings revealed increased protein content but not pleocytosis. The antibody titer for varicella zoster virus elevated both in cerebrospinal fluid and in serum. Cranial magnetic resonance imaging (MRI) revealed gadlinium enhancement on the left geniculate ganglion and left superior or inferior ganglion of IX and X nerves, indicating that multiple cranial nerve palsies associated with VZV infection originate in the cranial ganglia. Focal brainstem encephalitis does not seem to be the main cause of multiple cranial neuropathy in this case.
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PMID:[A case of multiple cranial neuropathy due to varicella-zoster virus infection: detection of involvement of cranial ganglia with MRI]. 877 11

Syringobulbia is an uncommon lesion of the central nervous system. It is defined as a pathological cavitation of the brain stem. The most common symptoms are headache, vertigo, dysphonia or dysarthria, trigeminal paraesthesia, dysphagia, diplopia, tinnitus, palatal palsy. Syringobulbia occurs with atlantoaxial congenital abnormalities (Chiari malformation), infection, tumours, and other causes. The idiopathic syringobulbia is however a rare finding. Early surgical treatment is the treatment of choice. We report on a 58-year old female patient with idiopathic syringobulbia. She complained of occipital headaches and vertigo. On examination she had horizontal nystagmus and diplopia. Occipital headaches and vertigo were improved after operation. We review the literature on syringobulbia, and discuss the clinical features of this uncommon condition.
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PMID:[Isolated idiopathic syringobulbia: case report and summary of the literature]. 877 68

A 24-year-old pregnant woman started to have hyperemesis gravidarum 6 weeks before admission. Four weeks later she had vertigo, diplopia, staggering gait, mild dyspnea, dysphagia, and incontinence of urine. On admission she presented with ophthalmoplegia, ptosis, ataxia, decreased tendon reflex, and memory disturbance. Brain magnetic resonance imaging revealed abnormal intensities in medial thalamic-hypothalamic regions and the periaqueductal area, and she was diagnosed with Wernicke's encephalopathy. Urodynamic studies revealed decreased bladder volume and detrusor hyperreflexia. Six weeks after the administration of 100 mg/day of thiamine, urge incontinence gradually recovered, together with neurological signs. Lesions of the medial thalamic-hypothalamic area and the periaqueductal gray matter seemed to be mainly responsible for micturitional disturbance in our patient with Wernicke's encephalopathy.
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PMID:Micturitional disturbance in Wernicke's encephalopathy. 904 73

A 37-year-old woman underwent microvascular decompression of the superior vestibular nerve for disabling positional vertigo. Immediately following the operation, she noted severe and spontaneous gagging and dysphagia. Multiple magnetic resonance images were obtained but failed to demonstrate a brainstem lesion and attempts at medical management failed. Two years later she underwent exploration of the posterior fossa. At the second operation, the vertebral artery as well as the posterior inferior cerebellar artery were noted to be compressing the vagus nerve. The vessels were mobilized and held away from the nerve with Teflon felt. The patient's symptoms resolved immediately after the second operation and she has remained symptom free. The authors hypothesize that at least one artery was shifted at the time of her first operation, or immediately thereafter, which resulted in vascular compression of the vagus nerve. To the authors' knowledge, this is the first reported case of a hyperactive gagging response treated with microvascular decompression. The case also illustrates the occurrence of a possibly iatrogenic neurovascular compression syndrome.
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PMID:Hyperactive rhizopathy of the vagus nerve and microvascular decompression. Case report. 1006 35

In Alzheimer's disease (AD), an association was found between autonomic dysfunction and frontal hypoperfusion in brain during orthostatic testing. To ascertain whether frontal hypoperfusion is dependent on longitudinal effects of hemodynamic disturbances, or contributes to them, we studied the relationship between the presence of orthostatic hypotension (OH) and resting cerebral blood flow (CBF) in late stages of AD. Twelve women with senile dementia of Alzheimer type (SDAT), and 15 non-demented women (mean age 82.6 years, SD 3.8 vs 81.8 years, SD 3.5) were examined with the orthostatic test. Four of 12 patients with SDAT, and 9 controls had OH (defined as systolic blood pressure fall > or = 20 mmHg). CBF was determined under resting conditions using 600 Mbq 99mTc HMPAO single photon emission computerized tomography (SPECT), and quantified in cortical areas in relation to cerebellum. In patients with SDAT and OH, CBF was lower in frontal and parieto-frontal cortical areas than in SDAT patients without OH. The former group was younger and had a shorter dementia duration. No significant differences in CBF were observed between controls with vs without OH. No differences in SDAT patients with or without OH were observed in the Berger dementia scale or Katz' ADL index. No difference in incidence of symptoms related to autonomic disturbances (diarrhea, obstipation, dysphagia, vertigo) was observed in either the SDAT or control group with regard to OH presence. We conclude that during the course of AD, OH can contribute to frontal brain changes and may exacerbate the disease. The further involvement of frontal dysfunction in aggravating blood pressure dysregulation in the elderly is discussed.
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PMID:Orthostatic hypotension in Alzheimer's disease: result or cause of brain dysfunction? 1047 10

The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus.
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PMID:Course and distribution of facial corticobulbar tract fibres in the lower brain stem. 1089 7


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