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)

The new antiepileptic drug zonisamide was evaluated in a European multicenter parallel-group double-blind trial as add-on treatment for 139 patients with refractory partial epilepsy. During treatment with zonisamide complex partial seizures decreased by 27.7% compared to placebo (P < 0.05) and the median rate dropped from 12/month to 7.1/month with no changes in the placebo group (P < 0.007). During the 12-week double-blind phase a 50% reduction of all seizures was recorded in 29.9% of the patients treated with zonisamide vs. 9.4% during placebo. Complete remission was observed during treatment with zonisamide in 6.2%. The plasma concentrations of the concomitant antiepileptic drugs did not change markedly when zonisamide was added. Adverse events, mostly fatigue, somnolence, dizziness and ataxia, occurred in 59.2% of the patients compared to 27.9% during placebo. Zonisamide was withdrawn in two patients due to adverse events. Kidney stones were not observed nor any relevant clinical chemistry or hematological changes. Zonisamide is an effective antiepileptic drug for add-on treatment of refractory partial epilepsy.
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PMID:Zonisamide for add-on treatment of refractory partial epilepsy: a European double-blind trial. 832 80

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25

Eye movement abnormalities consisting of poor or absent smooth pursuit and vestibulo-ocular reflex suppression, gaze-paretic and rebound nystagmus, slow build-up of optokinetic nystagmus, mildly hyperactive vestibulo-ocular reflex, and a high incidence of strabismus were inherited in an autosomal dominant fashion in 10 members of a non-consanguineous English caucasian family. The onset was in early childhood, but was not congenital. In 7 cases there was no tremor, dizziness, consistent ataxia, or other cerebellar signs that are often associated with these ocular motor deficits, and apart from strabismus, patients were asymptomatic. Magnetic resonance imaging of the propositus was normal. After childhood there appears to be no progression, with the oldest affected member being 40 years. Two members had been prone to falling in childhood, and one admitted to dizziness when tired. This condition, which is probably benign, has not been previously described and may represent a very mild variant of episodic ataxia or a new vestibulocerebellar syndrome.
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PMID:Eye movements in a familial vestibulocerebellar disorder. 835 16

The results from 100 patients with 103 acoustic neurinomas who were operated on between February 1979 and April 1992 are presented. All patients were placed in the half-sitting position and operated on by the same surgeon using the suboccipital-trans-meatal approach. Postoperative facial nerve function was good in 56%, moderate in 20% and poor in 24% of our patients. Preservation of useful hearing was achieved in 21%: the smaller the tumor, the better the functional result. However, the early symptoms of acoustic neuromas (tinnitus, dizziness, feeling of unsteadiness) were only slightly improved by the operation. The result concerning tinnitus seemed to be better after sacrificing the cochlear nerve. The number of patients with ataxia increased postoperatively, although objective ataxia decreased. Dizziness improved regardless of the tumor size.
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PMID:[Results of 100 consecutively operated patients with acoustic neuroma]. 850 11

Experimental studies have shown that dextromethorphan, a noncompetitive N-methyl-D-aspartate antagonist is neuroprotective in experimental models of ischemic cerebral injury. The authors studied the safety and tolerability of oral dextromethorphan (DM) in humans, and correlated serum levels of this drug with cerebrospinal fluid (CSF) and brain levels. Neurosurgical patients undergoing intracranial surgery or endovascular procedures were given ascending doses of oral DM prior to and 24 hours after surgery. Serum, CSF, and brain levels of DM and its active metabolite, dextrorphan, were measured. One hundred eighty-one patients received a total of 212 courses of DM treatment in dose ranges of 0.8 to 9.64 mg/kg. Serum DM levels correlated highly with CSF and brain DM levels. Brain levels were 68-fold higher than serum levels, whereas CSF levels were fourfold lower than serum levels. The maximum DM levels attained were 1514 ng/ml (serum) 118 ng/ml (CSF), and 92,700 ng/g (brain). The maximum dextrorphan levels were 501 ng/ml (serum), 167 ng/ml (CSF), and 6840 ng/g (brain). In 11 patients, brain and plasma levels of DM were comparable to levels that have been shown to be neuroprotective in animal studies. Frequent side effects occurring at neuroprotective levels of DM included nystagmus (64%), nausea and vomiting (27%) distorted vision (27%), feeling "drunk" (27%), ataxia (27%), and dizziness (27%). All symptoms were reversible and no patient suffered severe adverse reactions. This study demonstrates that potentially neuroprotective doses of DM can be administered safely to neurosurgical patients. Brain and CSF levels of DM can be estimated from serum levels of the drug. Side effects, even at the highest levels, proved to be tolerable and reversible. Administration of DM to patients at risk for cerebral injury should be further explored.
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PMID:Dose escalation safety and tolerance study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients. 862 62

Fosphenytoin is a water-soluble disodium phosphate ester of phenytoin that is converted in plasma to phenytoin. Fosphenytoin is compatible with most common i.v. solutions and can be administered safely through the i.m.route. An additional safety factor is the absence of propylene glycol in the fosphenytoin formulation. Propylene glycol is used as a vehicle in the i.v. phenytoin preparation and by itself may produce serious cardiovascular complications. Studies of the pharmacokinetics, safety, and tolerance of i.v. fosphenytoin have demonstrated that fosphenytoin produces phenytoin plasma concentrations similar to those achieved with oral and i.v. phenytoin, but without significant cardiovascular effects and only minimal discomfort at the injection site. Aside from local reactions, the most common adverse events associated with fosphenytoin have been pruritus and reactions typical of phenytoin (e.g., dizziness, somnolence, and ataxia). Fosphenytoin represents a significant advance in the treatment of patients with seizures who require parenteral therapy.
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PMID:Intravenous administration of fosphenytoin: options for the management of seizures. 864 9

Phenobarbital, diazepam, lorazepam, and phenytoin are all currently used for the treatment of acute seizures, including status epilepticus. None of these drugs is considered ideal. Fosphenytoin is a new phenytoin prodrug that fulfills many of the properties of an ideal anticonvulsant drug. The safety, tolerance, and pharmacokinetics of intramuscularly administered fosphenytoin have been evaluated in three clinical trials involving patients requiring loading or maintenance doses of phenytoin. These investigations demonstrated that fosphenytoin is rapidly and completely absorbed after injection into muscle and is quickly converted to produce therapeutic phenytoin plasma concentrations within 30 min of administration. Plasma concentrations of phenytoin achieved with i.m. fosphenytoin exceeded those associated with an equimolar dose of oral phenytoin. i.m. fosphenytoin was well tolerated both locally and systemically. Only mild and transient reactions occurred at the injection site. The most common systemic adverse events reported--somnolence, nystagmus, dizziness, and ataxia--are side effects commonly seen with phenytoin and tended to be mild. Preexisting seizure disorders remained stable. Combination treatment with i.v. diazepam or lorazepam to attain rapid seizure control and i.m. fosphenytoin to maintain the anticonvulsant effect theoretically offers many advantages for control of acute seizures and should be studied.
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PMID:Intramuscular use of fosphenytoin: an overview. 864 11

Fabry's disease (FD) is a rare, sex-linked disorder resulting from alpha-galactosidase deficiency. Cerebrovascular complications have been reported in the literature but have not been systematically analyzed. We report 2 patients and review 51 previously reported cases (descriptive meta-analysis) to clarify the clinical, radiologic, and pathologic features. The average age at onset of cerebrovascular symptoms was 33.8 years for hemizygous individuals (n = 43) and 40.3 years of heterozygotes (n = 10). The most frequent symptoms and signs were as follows (in descending order of frequency): hemiparesis, vertigo/dizziness, diplopia, dysarthria, nystagmus, nausea/vomiting, head pain, hemiataxia, and ataxia of gait, in the hemizygote group; and memory loss, dizziness, ataxia, hemiparesis, loss of consciousness and hemisensory symptoms, in the heterozygote group. The vertebrobasilar circulation was symptomatic in 67% of the hemizygotes and 60% of the heterozygotes. Intracerebral hemorrhage was found in 4 patients (3 hemizygotes and 1 heterozygote). Elongated, ectatic, tortuous vertebral and basilar arteries were the most common angiographic and pathologic features. For the hemizygotes, the recurrence rate for cerebrovascular disease was 76% and the death rate was 55%; 86% of the heterozygotes had recurrent cerebrovascular event(s) and 40% died. The cerebrovascular manifestations of FD, in both hemizygotes and heterozygotes, are predominantly due to dilative arteriopathy of the vertebrobasilar circulation, frequently recur, and portend a poor prognosis.
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PMID:Cerebrovascular complications of Fabry's disease. 868 96

The clinical neurological and electroneuromyographycal examination were performed in 75 patients with chronic alcoholism including 15 patients with abstinence (withdrawal) syndrome. The abstinence period without any alcohol consumption did not last more that 6 days before observation time. The clear, specific neurological symptoms were revealed in alcohol abstinence syndrome (AAS), exactly: the general brain disturbances in the form of headache, dizziness, horizontal small-swinging nystagmus, dynamic ataxia, the increase of tendinous reflexes preferentially from upper limbs, the tremor of head, tongue and of streched out arms fingers, the sympathic adrenal type vegetative disturbances. The increase of impulse conduction rate along the median nerve as well as elevation of craniocaudal coefficient and neuromuscular conduction disturbances were also characteristic for AAS.
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PMID:[Neurological and neurophysiological aspects of the alcohol abstinence syndrome]. 878 80

Thirty-one patients, aged 12.6 +/- 5.6 years, with refractory seizures for 8 +/- 4.3 years, were treated with adjunctive vigabatrin. Twenty-four percent had a > 50% reduction in seizure frequency (95% one-sided confidence interval). Generalized myoclonic, atonic, and tonic clonic and partial, with and without secondary generalization, seizures were all reduced at a mean dose of 70 +/- 38 mg/kg/day. Comparison of vigabatrin therapy duration, for partial and generalized seizure groups, utilizing Kaplan-Meier methodology showed similar survival times. Vigabatrin therapy was ineffective in the four children with tuberous sclerosis. Transient somnolence, ataxia and dizziness were the most frequent side effects. A severe aggressive agitation occurred in three patients, and necessitated discontinuation of vigabatrin in one patient. Vigabatrin was as effective in generalized as in partial seizures in this study. Clinical utility may be limited by unacceptable behavioral side effects in some patients.
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PMID:Vigabatrin in childhood epilepsy: comparable efficacy for generalized and partial seizures. 882 92


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