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 Kilham rat virus (KRV) is a parvovirus originally isolated from a rat sarcoma in the late 1950s. The clinical signs associated with a natural KRV infection include foetal resorption in dams, runting, ataxia, cerebellar hypoplasia and jaundice in suckling rats, and sudden death, scrotal cyanosis, abdominal swelling and dehydration in juvenile rats. The ability of this virus to produce persistent infections has resulted in a high frequency of contamination of cell cultures and transplantable-tumor system. In addition, the virus may interfere with research in other ways. The remarkable resistance to environmental conditions determines the importance of the detection and control of this agent, especially in the laboratory animal production. This study determines the seroprevalence of Kilham antibodies from sera of adult rats from conventional facilities, using the haemagglutination inhibition test. The seroprevalence varied between 27.8% and 75%. This result confirms that the virus is circulating in Argentinean conventional facilities and might be interfering with research. The recognized Kilham virus may be prevented from supply sources by implementing a health monitoring schedule including a regular serological surveillance, and by keeping the animals under barrier systems.
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PMID:Prevalence of antibodies against Kilham virus in experimental rat colonies of Argentina. 2046 Dec 90

Ten lions (Panthera leo) that were treated with a single injection of doramectin at a dose ranging between 0.2 mg/kg and 0.5 mg/kg showed clinical signs consistent with avermectin toxicity, namely ataxia, hallucinations, and mydriasis. Two subsequently died whereas the other eight lions recovered after 4-5 days with symptomatic therapy. Post-mortem examinations of the two that died showed cyanosis, severe pulmonary oedema, pleural effusion, and pericardial effusion, with histopathology not revealing any abnormalities. In both these lions, doramectin brain and liver tissue concentrations were elevated. Although doramectin is regularly used in wild felids, to date there have been no reports of avermectin toxicity in the literature. This article highlights the potential for doramectin toxicity in this species.
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PMID:Doramectin toxicity in a group of lions (Panthera leo). 2332 44

Pneumocephalus is a clinical condition caused by dysbarism, trauma, and iatrogenic causes. The most common iatrogenic causes of pneumocephalus are major interventions as a neurosurgery and cardiovascular operations, endoscopy, and minor interventions as a peripheral and central venous access. Especially during insertion of central venous line and intravenous drug and fluid infusion, the venous air embolism may occur in emergency department. In these patients, retrograde pneumocephalus occurs as a result of the air entering the right atrium to the brain. Clinical effects of the air delivery rates are known to be more specific than the total amount of air. In general, intravenous administration of 300 to 500 mL air in the speed of 100 mL/min is considered to be lethal. Large amounts of air embolism can cause hypotension and acute circulatory collapse with intracardiac obstruction. The most common symptoms of venous air embolism are anxiety, dyspnea, chest pain, cyanosis, tachycardia, tachypnea, headache, confusion, agitation, syncope, slurred speech, blurred vision, seizures, and ataxia. The mortality of pneumocephalus caused by central venous catheters in patients presented with symptoms of focal neurologic was 8%, whereas the mortality of pneumocephalus in patients presented with encephalopathy was 36%. In our report, a case of pneumocephalus secondary to disconnection of catheter cap in chronic renal failure patient who has hemodialysis via catheter has been presented.
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PMID:Retrograde cerebral air embolism. 2499 85

Pathogenic variants in SCN8A have originally been described in patients with developmental and epileptic encephalopathy (DEE). However, recent studies have shown that SCN8A variants can be associated with a broader phenotypic spectrum, including the following: (1) Patients with early onset, severe DEE, developing severe cognitive and motor regression, pyramidal/extrapyramidal signs, and cortical blindness. Severe SCN8A-DEE is characterized by intractable seizures beginning in the first months of life. The seizures are often prolonged focal hypomotor and occur in clusters, with prominent vegetative symptoms (apnea, cyanosis, mydriasis), evolving to clonic or bilateral tonic-clonic manifestations. Spasm-like episodes, cortical myoclonus, and recurrent episodes of status epilepticus are also common. Electroencephalograms (EEGs) show progressive background deterioration and multifocal abnormalities, predominant in the posterior regions. (2) Sporadic and familial patients with mild-to-moderate intellectual disability, discrete neurological signs, and treatable epilepsy. EEG is abnormal in half of the cases, showing multifocal or diffuse epileptiform abnormalities. (3) Familial cases with benign infantile seizures, sometimes associated with paroxysmal dyskinesia later in life, with no other neurological deficits, normal cognition, and usually normal interictal EEG. (4) Patients without epilepsy but with cognitive and/or behavioral disturbances, or with movement disorders. Extrapyramidal features, such as dyskinesia, ataxia, and choreoathetosis are common in all groups. Early death has been reported in about 5% of the patients, most often in the subgroup of severe DEE. Premature death occurs during early childhood and often for causes other than sudden unexpected death in epilepsy. All epilepsy subgroups exhibit better seizure control with sodium channel blockers, usually at supratherapeutic doses in the severe cases. In severe SCN8A-DEE, ketogenic diet often has a good effect, whereas levetiracetam has a negative effect, if any. The familial SCN8A-related epilepsies show an autosomal dominant pattern of inheritance, whereas the vast majority of SCN8A-DEEs occur de novo.
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PMID:Phenotypic and genetic spectrum of SCN8A-related disorders, treatment options, and outcomes. 3190 24

Ischemic stroke involving multiple artery territory with normal vessels gives a clue for an embolic stroke. Paradoxical embolization is a recognized cause of ischemic stroke. We describe a 48-year-old male who presented with acute onset giddiness, mild dysarthria, right hemiparesis, and ataxia. Clinical examinations indicated left cerebellar signs with right hemiparesis. Additionally, the patient had significant clubbing and mild cyanosis. A strong family history of epistaxis and hemoptysis was noted. His Magnetic resonance imaging of the brain showed acute left cerebellar and left frontal cortical infarct with normal vessels. The routine stroke and cardiac workup were normal. Chest X-ray showed bilateral lower zone opacities. Contrast-enhanced computerized tomogram (CT) of the chest showed bilateral pulmonary arteriovenous malformation. Paradoxical embolism due to pulmonary arteriovenous malformation resulted in ischemic stroke in our patient. He fulfilled all of the four criteria for diagnosing definite hereditary hemorrhagic telangiectasia. Our case highlights the importance of a systematic search for paradoxical embolism in a cryptogenic stroke.
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PMID:Paradoxical Embolism in a Case of Hereditary Hemorrhagic Telangiectasia: Case Report with Literature Review. 3264 84


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