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)

In early clinical trials, oxaliplatin has demonstrated significant activity against colorectal cancer in combination with 5-fluorouracil (5-FU) and folinic acid (FA), both in metastatic as in radically resected disease. The drug differs from the other two most important platinum compounds (cisplatin and carboplatin) for the absence of nephrotoxicity or for the reduced drug-induced ototoxicity. During its administration, two different types of neurological symptoms can be experienced: the first one occurs during or immediately after the end of the infusion and it appears as a transient peripheral sensory neuropathy manifesting as paresthesias and dysesthesia in the extremities sometimes accompanied by muscular contractions of the extremities or the jaw (triggered or enhanced by exposure to cold). The second one occurs after long-term administration of oxaliplatin presenting with deep sensory loss, sensory ataxia and functional impairment (similar to those observed with cisplatin). This type of neurotoxicity is usually late-onset and correlated with the cumulative-dose of oxaliplatin. The aim of this review is to analyse the mechanism underlying induction of neurotoxicity and the possible treatments to prevent and to treat it.
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PMID:Oxaliplatin-related neurotoxicity: how and why? 1680 62

Topiramate (Topamax), an effective seizure disorder treatment, received additional FDA approval for prevention of migraine headaches in August 2004 and has gained attention for its off-label uses, including psychiatric and eating disorders, neuropathic pain, and alcohol and drug dependency. Side effects of sedation, dizziness, ataxia, speech difficulty, nystagmus, paresthesia, and metabolic acidosis are described. The manufacturer reports that tolerance to the antiseizure properties does not develop. With its established efficacy for epilepsy treatment and its increased use for other disorders, topiramate-positive findings are more common in death-investigation and human-performance casework. To evaluate the role of topiramate, we reviewed all topiramate-positive cases from our laboratory between 1998 and 2004, which constituted 132 cases (63 death investigations, 68 suspected impaired drivers, and 1 sexual assault case). The subjects were predominantly female (69%) with a mean and median age of 42. Blood topiramate concentrations ranged from 1 to 180 mg/L (median 6.4 mg/L, mean 8.4 mg/L), and 94% were positive for at least one additional drug. There was evidence of psychomotor impairment in some drivers with blood concentrations within the normal therapeutic range, and deaths attributed to topiramate alone occurred at concentrations as low as 50 mg/L.
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PMID:Topiramate-positive death-investigation and impaired-driving cases in Washington State. 1713 58

Bortezomib, a proteasome inhibitor used in the treatment of multiple myeloma, is known to induce an axonal, dose-dependent neuropathy clinically characterized by pain, paresthesias, burning dysesthesias and numbness. In this study, we describe a patient treated with high-dose bortezomib whose main clinical feature was severe sensory ataxia. Electrodiagnostic studies showed, other than axonal changes, myelin involvement.
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PMID:A high-dose bortezomib neuropathy with sensory ataxia and myelin involvement. 1761 69

A case of Graves' disease with white matter abnormalities is presented here. The diagnosis as Graves' disease was made when the patient was 5 years old, and a subtotal thyroidectomy was performed when she was 10. Her neurological symptoms began at age 19 with paresthesia of her legs and lower body. Cranial magnetic resonance imaging was normal; thoracic magnetic resonance imaging revealed demyelinating lesions. Intravenous pulse steroid therapy improved her symptoms. Ten months later she described dizziness, lower body paresthesia, and ataxia. Both her cranial and thoracic magnetic resonance imagings revealed demyelinating lesions. After pulse steroid therapy, glatiramer acetate therapy was initiated with diagnosis of an autoimmune multiphasic demyelinating syndrome. Five months later, she presented with right-sided mild optic neuritis followed by rapid spontaneous remission. Antithyroglobulin antibody levels remained normal; antithyroid peroxidase antibody level was high. This presents a rare case of Graves' disease associated with multiphasic demyelinating autoimmune syndrome.
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PMID:White matter alteration in a patient with Graves' disease. 1789 Apr 14

Acute peripheral neuropathy caused by a disulfiram overdose is very rare and there is no report of it leading to vocal fold palsy. A 49-year-old woman was transferred to our department because of quadriparesis, lancinating pain, sensory loss, and paresthesia of the distal limbs. One month previously, she had taken a single high dose of disulfiram (130 tablets of ALCOHOL STOP TAB, Shin-Poong Pharm. Co., Ansan, Korea) in a suicide attempt. She was not an alcoholic. For the first few days after ingestion, she was in a confused state and had mild to moderate ataxia and giddiness. She noticed hoarseness and distally accentuated motor and sensory dysfunction after she had recovered from this state. A nerve conduction study was consistent with severe sensorimotor axonal polyneuropathy. Laryngeal electromyography (thyroarytenoid muscle) showed ample denervation potentials. Laryngoscopy revealed asymmetric vocal fold movements during phonation. Her vocal change and weakness began to improve spontaneously about 3 weeks after transfer. This was a case of acute palsy of the recurrent laryngeal nerve and superimposed severe acute sensorimotor axonal polyneuropathy caused by high-dose disulfiram intoxication.
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PMID:Acute vocal fold palsy after acute disulfiram intoxication. 1802 25

Pernicious anemia can result in significant hematologic and neurologic impairments due to a reduction in cobalamin absorption. Typically thought to be a disease of elderly whites, a growing body of literature has documented the disease in blacks and in younger age groups. We describe a case of a young black woman with gradually progressive lower extremity paresthesias, weakness, and ataxia as the primary presenting symptoms of pernicious anemia. This case is presented to make emergency physicians aware of pernicious anemia as a cause of ambulatory dysfunction in younger patients. We review the current body of literature on the diagnosis and management as well as evidence that the demographic profile of the disease is changing. Furthermore, in women of reproductive age, there is the potential for significant fetal and infant morbidity.
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PMID:Ambulatory dysfunction due to unrecognized pernicious anemia. 1806 89

A 41-year-old farmer sustained a high-voltage electrical injury resulting in confusion, electrical burns and paroxysmal atrial fibrillation which spontaneously reverted to sinus rhythm after a few hours. Two weeks later he presented with a sudden onset of headache, unsteadiness, horizontal oscillopsia and paraesthesia in the right side of his face. Examination revealed nystagmus to the right, right-sided limb ataxia and a tendency to veer toward the right when walking. An MRI of the brain demonstrated an acute infarct of the right cerebellar hemisphere in the territory of the right posterior inferior cerebellar artery. A transesophageal echocardiogram showed a ruptured mitral valve chordae. This is the first report of a cardio-embolic stroke secondary to mitral valve chordae rupture as a delayed complication of high-voltage electrical injury. Although many mechanisms of direct cerebral electrical injury have been speculated, a cardio-embolic origin should not be overlooked as a cause of stroke secondary to high-voltage electrical injury.
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PMID:Cardio-embolic cerebellar stroke secondary to mitral valve chordae rupture as a delayed complication of a high-voltage electrical injury. 1806 86

We report a case of hypertrophic olivary degeneration due to cerebellar surgery for a low-grade tumor. A 27-year-old female presented with right-sided paresthesias and intermittent leg paresis following a right cerebellar resection of a tumor 2 weeks prior. One month later, her symptoms remained stable while her neurological examination demonstrated slight right hemi-body hypoesthesia and subtle appendicular ataxia in her right upper extremity. An MRI scan revealed a hypertrophied left anterolateral medulla with increased T2 signal and no diffusion abnormality. The T2 hyperintensity and hypertrophy slowly resolved and she clinically improved without further intervention. Hypertrophic olivary degeneration may be mistaken for tumor progression, post-operative vasculopathy or granulation tissue and should be considered in patients undergoing cerebellar surgery.
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PMID:Hypertrophic olivary degeneration after resection of a cerebellar tumor. 1821 9

Neurotoxicity is the most frequent dose-limiting toxicity of oxaliplatin. Acute sensory neurotoxicity manifests as rapid onset of cold-induced distal dysesthesia and/or paresthesia, sometimes accompanied by cold-dependent muscular contractions of the extremities or the jaw. The symptoms, often occurring during or shortly after infusion, are usually transient and mild. A cumulative sensory peripheral neuropathy may also develop with prolonged treatment with oxaliplatin, eventually causing superficial and deep sensory loss, sensory ataxia, and functional impairment. Studies have shown patients with acute sensory symptoms to display little or no axonal degeneration. The similarity of acute symptoms induced by oxaliplatin to those caused by several drugs or toxins acting on neuronal or muscular ion channels suggests that these symptoms may result from a specific interaction of oxaliplatin with voltage-gated sodium (Na(+)) channels. The current recommendations for the management of the acute and cumulative neurotoxicity from oxaliplatin include education about exposure to cold, dose modification, "stop and go", and use of neuromodulatory agents, in particular, intravenous calcium and magnesium infusion. Upon the approval of oxaliplatin-based regimens both for adjuvant and metastatic treatment of colon cancer, it is crucial to compile knowledge about the recognition and management of neurotoxicity from oxaliplatin.
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PMID:Management of oxaliplatin-induced peripheral neuropathy. 1836 May 67

On October 20, 2007, a Minnesota resident died from rabies, approximately 1 month after initial symptoms of limb paresthesia, which progressed to flaccid weakness and ataxia. This was the only human rabies case reported in the United States in 2007. A presumptive diagnosis of idiopathic transverse myelitis was considered initially, because of abnormalities detected via spinal cord imaging studies and a lack of laboratory confirmation of a specific infectious etiology. The presumptive diagnosis subsequently was changed to include rabies, based on the patient's rapidly deteriorating neurologic status and elicitation of a history involving bat exposure during the month before illness onset. This report summarizes the medical and epidemiologic investigation by the Minnesota Department of Public Health and CDC and the ensuing public health response. The findings underscore the need for early inclusion of rabies in the differential diagnosis of rapidly progressive encephalitis, improved public awareness of the risks associated with animal bites, and appropriate rabies prophylaxis after exposure.
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PMID:Human rabies--Minnesota, 2007. 1845 57


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