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

Vestibular toxicity is known to occur from gentamicin. Over a five-year period seven patients with severe and prolonged ataxia from gentamicin vestibular toxicity were seen. Two of these patients were not in renal failure. Case reports of five of these are presented. The possible explanations for prolonged disability are discussed.
 ...
PMID:Gentamicin vestibulotoxicity. Long term disability. 31 9

Five patients developed neurological adverse effects as they were treated with amiodarone for 2 to 18 months. The daily maintenance dose did not exceed 400 mg. The neurological manifestations included tremor, ataxia, peripheral neuropathy, dyskinesia, myoclonic jerks, extrapyramidal hypertony, and altered mental status. These side effects resolved within 3 days to 3 months after amiodarone withdrawal. Advanced age, renal failure, diabetes mellitus, and alcoholism seemed to be risk factors for development of amiodarone neurotoxicity. Both peripheral and central nervous systems are involved in these amiodarone-induced complications.
 ...
PMID:[Neurological toxicity of amiodarone. 5 case reports]. 134 23

A mother and two of her daughters had deafness and cortical reflex myoclonus; the mother also had mild truncal ataxia. Muscle and skin biopsy specimens revealed abundant ragged-red fibres and abnormal mitochondria. The son of one of the daughters had sensorineural deafness. Three other grandchildren were asymptomatic. The two daughters also had diabetes mellitus, hypertension and cardiomyopathy. Another daughter died of renal failure. The mother lost her hearing in her 70s, one daughter in her 30s, and the other daughter and the grandson in their 20s. The mother has had transient episodes (24-48 hours) of temporal disorientation, severe action myoclonus, and ataxia for about eight years. This is the first reported family with inherited deafness, myoclonus, and ataxia with mitochondrial pathology.
 ...
PMID:Abnormal muscle and skin mitochondria in family with myoclonus, ataxia, and deafness (May and White syndrome). 153 18

We report here an autopsy case of chronic germanium intoxication with major pathological changes in the central and peripheral sensory nervous systems. The patient was a 4-year-old girl who had suffered from gait disturbance and generalized muscle weakness for 22 months. She had been given orally germanium compounds (containing germanium dioxide, 225-450 mg/day) for the previous 28 months. In addition to the findings of chronic renal failure and anemia, she presented characteristic neurological symptoms exemplified by diffuse muscle atrophy, tongue fasciculation, sensory impairment and truncal ataxia as well as areflexia. Median and ulnar sensory nerve conduction velocities were also reduced. On the 17th hospital day, she died of renal failure. In addition to conspicuous degeneration of renal tubular cells, pathological studies revealed marked nerve fiber loss, degeneration and gliosis in the dorsal column of the spinal cord, which were most conspicuous in the thoracic and cervical cord. Axonal degenerative changes were also conspicuous in the sural and sciatic nerves. High concentration of germanium was detected in the brain, cerebellum, spinal cord, sciatic nerve, liver and kidney. It was suggested that the neural involvement in the current case was caused by chronic toxicity of germanium.
 ...
PMID:[An autopsy case of chronic germanium intoxication presenting peripheral neuropathy, spinal ataxia, and chronic renal failure]. 164 14

Four weeks after starting tuberculostatic treatment (with isoniazid, rifampicin, streptomycin and pyrazinamide) a 21-year-old man with pulmonary tuberculosis developed symptoms of a radiculomyelopathy as well as mild renal failure. After isoniazid and streptomycin had been discontinued and ethambutol and high doses of vitamin B6 had been added all signs and symptoms improved. However, 4 weeks later tuberculous meningitis occurred which at first seemed to respond to administration of 5 antituberculosis drugs and dexamethasone. But 3 weeks later the patient sustained a partial hemiparesis. Its cause was proven to be a tuberculoma in the region of the brainstem. During further administration of tuberculostatic drugs and glucocorticoids the symptoms gradually receded over 8 months. A 54-year-old man with pulmonary tuberculosis developed cranial nerve pareses and symptoms of cerebellar involvement (trunk ataxia, intention tremor, dysdiadochokinesia) 3 weeks after starting tuberculostatic treatment. Computed tomography revealed multiple intracerebral tuberculomas which gradually shrank with continuation of the tuberculostatic treatment plus glucocorticoids. These two case reports illustrate that in tuberculosis involvement of the CNS can express itself clinically through complex symptoms, sometimes even after the start of tuberculostatic treatment.
 ...
PMID:[Involvement of the central nervous system in disseminated tuberculosis]. 193 77

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
 ...
PMID:Quinine toxicity. 354 70

A 17-year-old Japanese boy was found to have ataxia, generalized angiokeratomas, skeletal deformities, visual impairment, and macular cherry-red spots, without hepatomegaly, splenomegaly, or renal failure. Laboratory examination disclosed a deficiency of beta-galactosidase as well as of neuraminidase activity in the leukocytes and fibroblasts, while alpha-galactosidase and alpha-L-fucosidase activities were normal. On electron microscopic examination, numerous cytoplasmic vacuoles containing flocculated material were found in the vascular endothelial cells, histiocytes, perineurial cells, and Schwann's cells.
 ...
PMID:beta-Galactosidase and neuraminidase deficiency associated with angiokeratoma corporis diffusum. 643 42

The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
 ...
PMID:Encephalopathy in infants and children with chronic renal disease. 729 12

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
 ...
PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26

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)
 ...
PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25


1 2 3 4 5 Next >>