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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Topiramate is a highly effective drug in migraine prophylaxis and is considered a first-line treatment. The evidence for the efficacy of topiramate is based upon the results of several large, randomized, double-blind, placebo-controlled trials. Adverse events (AEs) are common and require discontinuation of the treatment in about 20-25% of patients, but they are rarely severe. There are reviews regarding topiramate-related AEs representing a large number of patients treated in controlled trials. The most common AEs are weight loss, dizziness, somnolence, abnormal thinking, fatigue, ataxia, confusion, paresthesias, impaired concentration, nervousness, amnesia, and language difficulties. The development of cough has never been reported as an AE during topiramate prophylaxis for migraine. We present 3 cases in which the prophylactic treatment for migraine with topiramate was discontinued due to the onset of primary intractable coughing.
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PMID:Topiramate-induced intractable cough during migraine prophylaxis. 1975 66

Aflatoxins are a group of mycotoxins principally produced by Aspergillus flavus and A. parasiticus, which are both natural contaminants of food and feedstuff. Aflatoxin B(1) is the most prevalent member of this group that is normally detected and is the most powerful hepatocarcinogen known. Few naturally occurring episodes of aflatoxicosis in horses have been reported in the literature. Indeed, the published information about aflatoxin exposure, metabolism and the effects on horses is limited and controversial, possibly indicating a lack of awareness rather than the rarity of the occurrence. The target organ in horses, as in other animal species, is the liver and horses suffering from aflatoxicosis show signs of inappetence, depression, fever, tremor, ataxia and cough. Necropsy findings include a yellow-brown liver with centrilobular necrosis, icterus, haemorrhage, tracheal exudates and brown urine. A possible link between aflatoxin exposure and chronic obstructive pulmonary disease has been hypothesised.
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PMID:Toxicological effects of aflatoxins in horses. 2061 6

Acute autonomic and sensory neuropathy is a rare disorder that has been only anecdotally reported. We characterized the clinical, electrophysiological, pathological and prognostic features of 21 patients with acute autonomic and sensory neuropathy. An antecedent event, mostly an upper respiratory tract or gastrointestinal tract infection, was reported in two-thirds of patients. Profound autonomic failure with various degrees of sensory impairment characterized the neuropathic features in all patients. The initial symptoms were those related to autonomic disturbance or superficial sensory impairment in all patients, while deep sensory impairment accompanied by sensory ataxia subsequently appeared in 12 patients. The severity of sensory ataxia tended to become worse as the duration from the onset to the peak phase of neuropathy became longer (P<0.001). The distribution of sensory manifestations included the proximal regions of the limbs, face, scalp and trunk in most patients. It tended to be asymmetrical and segmental, rather than presenting as a symmetric polyneuropathy. Pain of the involved region was a common and serious symptom. In addition to autonomic and sensory symptoms, coughing episodes, psychiatric symptoms, sleep apnoea and aspiration, pneumonia made it difficult to manage the clinical condition. Nerve conduction studies revealed the reduction of sensory nerve action potentials in patients with sensory ataxia, while it was relatively preserved in patients without sensory ataxia. Magnetic resonance imaging of the spinal cord revealed a high-intensity area in the posterior column on T(2)*-weighted gradient echo image in patients with sensory ataxia but not in those without it. Sural nerve biopsy revealed small-fibre predominant axonal loss without evidence of nerve regeneration. In an autopsy case with impairment of both superficial and deep sensations, we observed severe neuronal cell loss in the thoracic sympathetic and dorsal root ganglia, and Auerbach's plexus with well preserved anterior hone cells. Myelinated fibres in the anterior spinal root were preserved, while those in the posterior spinal root and the posterior column of the spinal cord were depleted. Although recovery of sensory impairment was poor, autonomic dysfunction was ameliorated to some degree within several months in most patients. In conclusion, an immune-mediated mechanism may be associated with acute autonomic and sensory neuropathy. Small neuronal cells in the autonomic and sensory ganglia may be affected in the initial phase, and subsequently, large neuronal cells in the sensory ganglia are damaged.
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PMID:Clinicopathological features of acute autonomic and sensory neuropathy. 2073 88

A 17-month-old previously healthy child presented with a 2-day history of inability to fully open his eyes and slight gait ataxia. In the month preceding admission, he had had low grade, intermittent fevers, followed by a nonproductive cough and sneezing. During hospital admission he lost deep tendon reflexes and was unable to walk. Lumbar puncture revealed abnormally high protein, and a nasopharyngeal specimen was positive for influenza A (pH1N1). He received intravenous immunoglobulin and oseltamivir with clinical improvement. Although it is difficult to ascertain whether pH1N1 or another microorganism was responsible for this toddler's neurologic syndrome, this is the first reported case of Miller Fisher syndrome associated with pH1N1. During pandemics, one may expect to see an increased incidence of uncommon neurologic complications of influenza.
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PMID:Miller Fisher syndrome in a toddler with influenza A (pH1N1) infection. 2111 46

Altitude illness affects 25 to 85 percent of travelers to high altitudes, depending on their rate of ascent, home altitude, individual susceptibility, and other risk factors. Acute mountain sickness is the most common presentation of altitude illness and typically causes headache and malaise within six to 12 hours of gaining altitude. It may progress to high-altitude cerebral edema in some persons. Onset is heralded by worsening symptoms of acute mountain sickness, progressing to ataxia and eventually to coma and death if not treated. High-altitude pulmonary edema is uncommon, but is the leading cause of altitude illness-related death. It may appear in otherwise healthy persons and may progress rapidly with cough, dyspnea, and frothy sputum. Slow ascent is the most important measure to prevent the onset of altitude illness. If this is not possible, or if symptoms occur despite slow ascent, acetazolamide or dexamethasone may be used for prophylaxis or treatment of acute mountain sickness. Descent is mandatory for all persons with high-altitude cerebral or pulmonary edema. Patients with stable coronary and pulmonary disease may travel to high altitudes but are at risk of exacerbation of these illnesses. Medical management is prudent in these patients.
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PMID:Altitude illness: risk factors, prevention, presentation, and treatment. 2112 56

Legionnaires' disease is primarily a pneumonic process caused by Legionella pneumophilia, a gram-negative aerobic bacillus but also has multiple system involvement. The most common manifestation is encephalopathy suggesting a generalized brain dysfunction but focal neurological manifestations have been reported. We report a patient with Legionella pneumonia associated with cerebellar dysfunction and unilateral facial nerve weakness. 51-year-old previously healthy male presented with shortness of breath, cough, slurred speech, and unsteadiness on feet associated with malaise, fevers and myalgias. Patient's family reported facial asymmetry for 2 days. Patient had no significant medical history and was not on any medication. He denied smoking, alcohol or illicit drug use. Chest X-ray showed bilateral lower lobe infiltrates. Urinary antigen assay for Legionella pneumophilia serogroup 1 was positive. Patient was started on intravenous moxifloxacin. On day 5 the patient was discharged home and continued oral moxifloxacin for two weeks. After the two weeks, his respiratory symptoms, gait ataxia and dysarthria resolved. We report the first case of Legionnaires' disease with cerebellar dysfunction and seventh nerve palsy. Legionnaires' disease should be considered in patients with any neurological symptoms in the setting of pneumonia. Failure to recognize and treat the infection may lead to poor outcomes.
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PMID:Legionnaires' disease with facial nerve palsy. 2146 Oct 48

Four dogs with acute neurological signs caused by haemorrhages in the central nervous system were diagnosed with Angiostrongylus vasorum infection as the underlying aetiology. Two dogs presented with brain lesions, one dog with spinal cord lesions and one with lesions in both the brain and spinal cord. Only one dog presented with concurrent signs of classical pulmonary angiostrongylosis (respiratory distress, cough), and only two dogs displayed overt clinical signs of haemorrhages. Results of coagulation assays were inconsistent. Neurological signs reflected the site of pathology and included seizures, various cranial nerve deficits, vestibular signs, proprioceptive deficits, ataxia and paraplegia. One dog died and three were euthanised due to lack of improvement despite medical treatment. This emphasises canine angiostrongylosis as a potential cause of fatal lesions of the central nervous system and the importance of including A. vasorum as a differential diagnosis in young dogs with acute neurological signs in Denmark.
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PMID:Acute neurological signs as the predominant clinical manifestation in four dogs with Angiostrongylus vasorum infections in Denmark. 2171 38

Milliary Tuberculosis (TB) occurs through lymphohaematogenous dissemination of M. tuberculosis and paradoxical response (PR) is a recognized feature. Respiratory failure, choroid tubercles and brain tuberculomas are some of the complications. Brain tuberculomas mainly occur in the cerebrum, cerebellum, where as involvement of the brainstem is rare. A 31 years old female presented with history of ill health, easy fatigability, excessive sweating and fever of one month duration, dry cough for one week and shortness of breath for 3 days. Provisional diagnosis was disseminated TB complicated by hypoxemic respiratory failure and bilateral choroid tubercles. She was started on anti-TB treatment with adjuvant steroids. The initial response to treatment was remarkable but after about 3 weeks of anti-TB therapy, she suddenly deteriorated developing spastic ataxia. After exclusion of other possible causes she was successfully treated under the impression of having PR.
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PMID:Milliary tuberculosis with unusual paradoxical response at 3 weeks of antituberculous treatment. 2223 90

We report a case of a 5-year-old boy with acute disseminated encephalomyelitis as the initial presentation of neuroborreliosis. Parents report an upper-airway infection a few days before the development of acute encephalopathy, mild facial palsy, and seizures. The patient needed mechanical ventilation for 10 days, and after extubation, he presented hypotonia, ataxia, dysarthria, as well as weak gag and cough reflexes. Brain magnetic resonance imaging showed hyperintense lesions on T2- and fluid-attenuated inversion recovery sequences on the right subcortical occipital and parietal region, left posterior arm of the internal capsule, and in the medulla oblongata. Borrelia burgdorferi was identified in the plasma and cerebrospinal fluid by polymerase chain reaction and in the plasma by Western blotting. He was treated with ceftriaxone, methylprednisolone, and human immunoglobulin. Recovery was partial.
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PMID:Neuroborreliosis presenting as acute disseminated encephalomyelitis. 2322 6

Hereditary ataxias are a heterogeneous group of neurological diseases characterized by progressive cerebellar syndrome and numerous other features, which result in great diversity of ataxia subtypes. Despite the characterization of a number of both autosomal dominant and autosomal recessive ataxias, it is thought that a large group of these conditions remains to be identified. In this study, we report the characterization of five patients (three Mexicans and two Italians) who exhibit a peculiar form of recessive ataxia associated with coughing. The main clinical and neurophysiological features of these patients include cerebellar ataxia, paroxysmal cough, restless legs syndrome (RLS), choreic movements, atrophy of distal muscles, and oculomotor disorders. Brain magnetic resonance imaging (MRI) revealed cerebellar atrophy, while video polysomnography (VPSG) studies showed a severe pattern of breathing-related sleep disorder, including sleep apnea, snoring, and significant oxygen saturation in the absence of risk factors. All patients share clinical features in the peripheral nervous system, including reduction of amplitude and prolonged latency of sensory potentials in median and sural nerves. Altogether, clinical criteria as well as molecular genetic testing that was negative for different autosomal dominant and autosomal recessive ataxias suggest the presence of a new form of recessive ataxia. This ataxia, in which cerebellar signs are preceded by paroxysmal cough, affects not only the cerebellum and its fiber connections, but also the sensory peripheral nervous system and extracerebellar central pathways.
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PMID:Recessive spinocerebellar ataxia with paroxysmal cough attacks: a report of five cases. 2409 5


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