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

Bajiaolian (Dysosma pleianthum), one species in the Mayapple family, has been widely used as a general remedy and for the treatment of snake bite, weakness, condyloma accuminata, lymphadenopathy and tumours in China for thousands of years. However, the textbooks of traditional Chinese medicine mention little about the toxicity of Bajiaolian. Within 1 year, the authors saw five people who manifested nausea, vomiting, diarrhoea, abdominal pain, thrombocytopenia, leucopenia, abnormal liver function tests, sensory ataxia, altered consciousness and persistant peripheral tingling or numbness after drinking infusions made with Bajiaolian. The herb was recommended by either traditional Chinese medical doctors or herbal pharmacies for postpartum recovery and treatment of a neck mass, hepatoma, lumbago and dysmenorrhoea. Podophyllotoxin is one of the main ingredients of the Bajiaolian root. The clinical manifestations observed in our patients were consistent with podophyllum intoxication. Podophyllotoxin intoxication usually results from the accidental ingestion or topical application of podophyllum resin. However, these cases of Bajiaolian intoxication were iatrogenic and results from 'therapeutic doses' of Bajiaolian cited in the textbooks of traditional Chinese medicine.
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PMID:Podophyllotoxin intoxication: toxic effect of Bajiaolian in herbal therapeutics. 136 Nov 36

The traditional treatment of African sleeping sickness (trypanosomiasis) with central nervous system involvement is an organic arsenical compound, melarsoprol, which is associated with severe and even life-threatening side effects. A polyamine biosynthesis inhibitor, eflornithine (chemical name, DL-alpha-difluoromethylornithine, supplied as monohydrochloride monohydrate), was used to treat a 3 1/2-year-old child with newly diagnosed severe trypanosomiasis that had been acquired more than two years previously in Zaire or the Congo. Treatment consisted of 300 to 400 mg/kg/d of eflornithine by continuous intravenous infusion for 25 days followed by 300 mg/kg/d of eflornithine by mouth divided in four equal doses daily for 17 days. The child's recovery was dramatic, with eradication of blood and cerebrospinal fluid parasites in the first week. Cerebrospinal fluid pleocytosis resolved completely. Her generalized adenopathy and fever gradually resolved. Severe ataxia, inability to walk or to change posture on her own, marked language regression, and lethargy all improved during and after her therapy. The drug was well tolerated; the only noted adverse effect was transient thrombocytopenia during the fourth week of therapy. Eflornithine was a safe and effective agent for treatment of trypanosomiasis with central nervous system involvement in this child.
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PMID:African sleeping sickness in the United States. Successful treatment with eflornithine. 312 3

A 4-year-old English Springer Spaniel with ataxia was examined because of progression of neurologic signs. Complete physical examination and results of CBC and serum biochemical analysis revealed no other abnormalities. The dog developed respiratory arrest and was euthanatized during recovery from general anesthesia, which had been performed to obtain a CSF sample. Results of CSF analysis were within reference limits. Necropsy revealed a single, well-circumscribed mass in the cerebellum, which was diagnosed as lymphosarcoma. The dog had no peripheral lymphadenopathy or organomegaly suggestive of the generalized form of the disease.
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PMID:Ataxia associated with lymphosarcoma in a dog. 755 25

We describe a 12-year-old black male who presented with cervical lymphadenopathy, hepatosplenomegaly of 3 months duration, and ataxia and incoordination of recent onset. Hodgkin's disease, stage IVB, was diagnosed. An MRI of the head demonstrated a nonenhancing, well-defined pontine lesion. The pontine lesion and the associated neurologic symptoms were consistent with central pontine myelinolysis. Treatment of Hodgkin's disease resulted in complete remission and complete disappearance of the pontine abnormality.
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PMID:Hodgkin's disease associated with central pontine myelinolysis. 768 85

A 4-year-old female German Shepherd Dog was examined to determine the cause of ataxia, progressive head tilt, anorexia, lethargy, and weight loss of 3 weeks' duration. A vestibular syndrome, generalized lymphadenopathy, bilateral uveitis, and chorioretinitis with complete detachment of the left retina were detected. Abnormal clinicopathologic findings were isosthenuria and hyperglobulinemia. The non-functional left eye was enucleated and fungal organisms resembling Aspergillus spp were identified on histologic examination. Microbial culture of a urine sample yielded Acremonium sp, which was initially considered a contaminant. The dog was considered to have systemic aspergillosis and was treated with itraconazole for 7 months, until it was euthanatized because of persistent vomiting and anorexia. Postmortem examination revealed multisystemic pyogranulomatous and necrotizing inflammation of the myocardium, pericardium, liver, and kidneys; and granulomatous splenitis, lymphadenitis, retinitis, endometritis, and meningoencephalitis. Fungal culture of affected organs yielded Acremonium sp. These findings indicated that Acremonium spp can be pathogenic and should not be ignored when cultured.
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PMID:Systemic mycosis caused by Acremonium sp in a dog. 825 22

Plasma cell myelomas in horses have been reported infrequently. Data from 10 cases, 9 from the literature and 1 new case, are used to characterize the disease in the horse. Hot-blooded horses (7/10), specifically Quarter Horses (4/10), were most often affected. Median age at diagnosis was 11 years (range, 3 mo-22 yr) and both male (5) and female horses (5) were represented equally. Clinical findings included weight loss (6/8), anorexia (4/8), fever (4/8), limb edema (4/8), pneumonia (3/8), rear leg paresis/ataxia (3/8), epistaxis (3/8), palpable lymphadenopathy (2/8), and bone pain (2/8). Anemia (8/8) was present routinely, and in three horses, RBCs were macrocytic. Leukopenia (2/8), thrombocytopenia (2/8), and circulating plasma cells (3/8) were variable findings. Except for abnormal protein concentrations and hyponatremia (3), abnormal results from serum biochemical analysis including hypocholesterolemia (1), hypercalcemia (1), and azotemia (1) were reported infrequently. Hyperproteinemia (8/9), hypoalbuminemia (7/9), and hyperglobulinemia (8/9) were characteristic but not invariable findings. Monoclonal proteins (7/7) were detected in the alpha 2, beta, or gamma region by serum electrophoresis. The paraprotein's heavy chain, determined in four horses, was a subclass of IgG. Three horses had decreased concentrations of normal immunoglobulins. Variable proteinuria (trace to 4+) was detected by routine urinalysis in four of six horses. Bence Jones proteinuria was detected in one of five horses (heat precipitation) and monoclonal proteins were detected in two of three electrophoresed urine samples. Three of the horses had lytic bone lesions detected radiographically. Bone marrow aspirates were diagnostic in two of five horses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma cell myeloma in the horse. A case report and literature review. 833 11

We report a patient with neurosarcoidosis, which developed 22 years after augmentation mammoplasty by the injection of silicone gel. She presented with bilateral hilar lymphadenopathy, left-sided lower cranial nerve palsies (8th, 9th, and 10th), and vestibular ataxia, which improved following the administration of prednisolone. Biopsy of the breast nodules showed granulomatous changes identical with those of sarcoidosis, while infrared spectrophotometry disclosed that the nodules contained polydimethylsiloxane, a major component of the silicone gel injection. This is the first report of neurosarcoidosis following silicone mammoplasty.
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PMID:Neurosarcoidosis following augmentation mammoplasty with silicone. 887 48

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
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PMID:[Neurologic disorders in Whipple's disease]. 910 28

A 59-year-old woman presented with acute-onset, bilateral, painless loss of vision, dysarthria, and ataxia. Ophthalmoscopy showed bilateral optic disc edema. A magnetic resonance scan of the head was normal. Chest radiography showed mediastinal adenopathy. Mediastinoscopy and biopsy identified small-cell carcinoma of the lung. An autoantibody to optic nerve and retina was demonstrated in the patient's serum. An electroretinogram was normal. The patient was diagnosed with a paraneoplastic optic neuropathy and paraneoplastic cerebellar syndrome. After treatment for her lung cancer, the patient remains stable from a visual and neurologic standpoint.
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PMID:Paraneoplastic optic neuropathy and autoantibody production in small-cell carcinoma of the lung. 2110 28

In an experiment on bovine immunodeficiency-like virus (BIV), the virological and serological aspects of which were reported in an earlier paper, three groups (A, B and C) of three calves were inoculated subcutaneously with a recently isolated strain (FL112). For group B and group C, the virus was suspended in milk, and for group C (controls) the viral suspension was subjected to pasteurization before inoculation. The calves were killed for necropsy 12 months later. Clinical assessment revealed subtle ataxia in two group A calves, which took the form of an intermittent "shifting" (from one leg to another) lameness, and palpable enlargement of the pre-scapular lymph nodes in one group B animal. At necropsy, haemal lymph nodes (0.1 to 0.5 cm in diameter), occurring singly, were observed in all animals. However, in groups A and B (but not C), enlarged haemal lymph nodes (< or = 2 cm in diameter) were also seen, occurring singly and in chains; and in one group A animal they occurred in grape-like clusters. In groups A and B (but not C), histopathological examination revealed generalized hyperplastic changes in lymph nodes, especially the haemal lymph nodes. This finding was particularly striking in the two clinically ataxic animals from group A, which also showed a non-suppurative meningo-encephalitis; the latter was possibly the cause of the subtle clinical signs. This study supports previous findings on lymphadenopathy resulting from experimental infection with BIV.
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PMID:Lymphadenopathy and non-suppurative meningo-encephalitis in calves experimentally infected with bovine immunodeficiency-like virus (FL112). 974 57


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