Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old woman presented with an isolated axial lateropulsion as a sole manifestation of lateral medullary infarction. She had no vertigo, nystagmus, dysphagia, hiccup, facial/hemisensory loss, Horner syndrome, and limb ataxia. Brain MRI showed a small infarct selectively involving the most dorsolateral portion of the rostral medulla. This patient illustrates that lateral medullary infarction may present as an isolated lateropulsion. The possible mechanism of an isolated lateropulsion is described.
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PMID:Axial lateropulsion as a sole manifestation of lateral medullary infarction: a clinical variant related to rostral-dorsolateral lesion. 1250 Jun 99

Opsoclonus-myoclonus-ataxia syndrome (OMA) in children is most commonly associated with occult neuroblastoma (NB). Although children with OMA and NB have decreased mortality, they suffer from increased neurologic morbidity. The pathogenesis of OMA in NB is not well understood, but current research and treatments support an immune-mediated process. The authors describe an unusual presentation of OMA occurring following 6 months of chemotherapy in a child with stage 4S NB who presented with partial Horner syndrome. Histopathologic examination of his primary cervical tumor showed NB maturation, which may have played a role in precipitating OMA syndrome. Further study of unusual cases of OMA in NB may provide better understanding of the syndrome and additional treatment options for these children.
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PMID:Late presentation of opsoclonus-myoclonus-ataxia syndrome in a child with stage 4S neuroblastoma. 1595 91

We describe here the first documented case in Austria of the cattle ear mite Raillietia auris in a four-year-old dairy cow. The cow was mildly depressed, and keratoconjunctivitis was diagnosed in both eyes with Horner's syndrome in the left eye. The animal showed a mild head tilt to the left and a generalized ataxia with a tendency to move to the right side, which became exacerbated if the animal was blind-folded. Head pressing to the right side, dysphagia and a dropped jaw were also observed. Numerous rather mobile ear mites were observed at necropsy in the basal part of the left ear canal. The clinical significance of the cattle ear mite is uncertain and the clinical signs could have been caused by listerial encephalitis, which was also confirmed histologically in this case.
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PMID:Occurrence of the ear-mite Raillietia auris in cattle in Austria. 1642 97

Multiple system atrophy (MSA) is characterized pathologically by a systemic degeneration of the olivopontocerebellar (OPC), striatonigral (SN) and autonomic systems. Massive glial cytoplasmic inclusions (GCIs) are specific for this disease. Massive lipid-laden macrophage infiltration in the degenerating tracts has not been described up to now. We here report a case of MSA with this rare event in the ponto-cerebellar (cerebellopetal) fibers. The patient, 54-year-old housewife, developed ataxia. At the age of 55 years, she was diagnosed as having MSA by cerebellar ataxia, extrapyramidal signs, autonomic failure and Horner syndrome. She died from asphyxia at the age of 57. The autopsy revealed OPC and SN system atrophy, degeneration and numerous GCIs, compatible with MSA. Numerous lipid-laden macrophages were seen in the pontine nuclei and its transverse fibers including the white matter of the cerebellum, which has not been reported up to now. There was no macrophage infiltration in the other areas. Transient ischemia, infarction and wallerian degeneration do not account for this rare event. The ponto-cerebellar (cerebellopetal) tract pathology, as observed by postmortem neuropathological study, may occur in the context of MSA.
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PMID:Multiple system atrophy (MSA) with massive macrophage infiltration in the ponto-cerebellar afferent system. 1789 92

We report a 67-year-old man who presented sudden loss of temperature sensation associated with hyperalgesia in the left trunk and extremities. No abnormal lesions were found on routine magnetic resonance image (MRI) in the brain and spinal cord. He did not show common manifestations of the lateral medullary syndrome including vertigo, nystagmus, ataxia, Horner's syndrome and ipsilateral facial sensory loss. We however suspected this syndrome, because he complained of characteristic, severe pain and electrical sensations in one side of his body. Reexamined, thinly sliced T2-weighted MRI showed a very small high intensity spot in the right medulla, corresponding to the location of lateral spinothalamic tract. Oral carbamazepine was partially effective to ameliorate the intractable central poststroke pain.
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PMID:[Hyperalgesia with loss of temperature sensation in one side of the body due to pinpoint infarction of contralateral spinothalamic tract]. 1959 3

A 64-year-old man presented with sudden onset of right-sided hemiparesis, headache, gait disturbance, and recurrent vomiting. A physical examination revealed right-sided hemiparesis, right Horner syndrome, ataxia of the right limbs, and diminished sensation on the left side of his body. Diffusion-weighted MRI revealed an acute right lateral medullary infarction extending from the rostral medulla to the upper cervical cord, and an acute cerebellar infarction in the territory of the medial branch of the posterior inferior cerebellar artery. Magnetic resonance angiography revealed suspicious severe stenosis or near occlusion of the proximal and distal parts of the right vertebral artery, and hypoplasia of the left vertebral artery. We diagnosed ipsilateral hemiparesis with lateral medullary infarction (Opalski's syndrome) and concomitant cerebellar infarction.
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PMID:Opalski's Syndrome with Cerebellar Infarction. 2039 33

A 68-year-old man was referred to our hospital for a dysphagia evolving for 10 days. Clinical examination had found neurological signs as contralateral Horner's syndrome, ipsilateral palatal paresis, gait ataxia and hoarseness. Video-fluoroscopy showed a lack of passage of contrast medium to the distal esophagus. Esogastroduodenoscopy was normal. The cranial MRI had shown an acute ischemic stroke in the left lateral medullar region and the diagnosis of Wallenberg syndrome (WS) was established. WS remains an unknown cause of dysphagia in the clinical practice of the gastroenterologist.
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PMID:Dysphagia caused by a lateral medullary infarction syndrome (Wallenberg's syndrome). 2307 13

The patient, a 32-year-old man, presented with sudden onset of occipital headache, vertigo, dysarthria, gait ataxia, right Horner syndrome, numbness of the right hand, and mild right hemiparesis. On magnetic resonance imaging, an acute small infarction was located on the right side of the caudal medulla extending dorsomedially. Magnetic resonance angiography showed severe right vertebral artery stenosis. Lateral medullary infarction associated with ipsilateral sensorimotor deficits in the limb is very rare, and the lesion probably involved the ipsilateral dorsal column or decussating lemniscal fibers and corticospinal fibers caudal to the pyramidal decussation or compression of the decussation.
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PMID:Ipsilateral sensorimotor deficits in lateral medullary infarction: a case report. 2321 98

Spontaneous dissection of a vertebral artery is uncommon, but potentially harmful and initially easily misdiagnosed as ordinary headache, neck pain or dizziness. The condition may progress with infarctions in the brainstem and cerebellar areas and ataxia, nystagmus, Horner syndrome, dysarthria, cranial nerve palsy or hemiparesis. We report an initially misdiagnosed case and remind about the clinical clues which lead to a correct diagnosis: young age, no risk factors for thromboembolism, the typical clinical findings and the presence of neck pain.
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PMID:[Dissection in the vertebral arteries is uncommon and may be misdiagnosed]. 2549 59

The study aimed to evaluate the correlations between the clinical and paraclinical data in the lateral bulbar infarction, benefiting from the access to the semiologic characteristics of a group studied and the MRI angiography, without a contrast agent, through the 3D TOF technique combined with MIP, as an imaging technique for the evaluation of the arterial lesion. The study group included 20 patients with lateral bulbar infarction, 14 men, and 6 women aged between 21 and 80 years, the mean age being 56, 9 years, who were enrolled in the study in the period 2012 and 2014, following the admission in the National Institute of Neurology and Neurovascular Diseases. All the patients enrolled in this stage study, performed brain MRI - in the Medinst laboratory, which included the following sequences T1, T2, Flair, DWI, MRI angiography without contrast agent (3D TOF combined with MIP). The study was retrospective. Following the analysis of the 3D TOF sequences combined with MIP, it was found that in the group studied, 8 patients had damage at the level of the vertebral artery, 2 at the level of the posterior inferior cerebellar artery and 10 patients presented mixed lesions of both the vertebral artery and of the PICA artery. In terms of the mechanism involved, most of the lateral bulbar infarctions were generated by arterial dissection (9 cases) and 6 cases had atheroma as etiology. Regarding the risk factors, dyslipidemia and smoking predominated in the studied group and the most common signs and symptoms were gait abnormalities, the ataxia of the limbs, dysphonia, and Horner syndrome. Abbreviations: 3D TOF = 3D time of flight angiography, MIP = maximum intensity projection, MRI = magnetic resonance imaging, CT = computed tomography, FLAIR = fluid attenuated inversion recovery, DWI = diffusion weighted imaging, HTA = hypertension, DZ II = diabetes mellitus, VA = vertebral artery, PICA = posterior inferior cerebellar artery, VG = vertigo, NT = nystagmus, N/ E = nausea/ emesis, DP = dysphagia, PVP = pharyngeal/ vocal cord paresis, HS = Horner syndrome, PTH = pain/ temperature hypesthesia, LA = ipsilateral limb ataxia, GA = Gait ataxia, C-R-F = Cardiovascular risk factors, L = left, R = right.
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PMID:Correlations between the semiologic changes and the imaging aspects in the lateral bulbar infarction. 2797 32


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