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

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5 micrograms/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be greater than 2.4 micrograms/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elemental mercury poisoning. 174 59

The patient, a 30 year-old man, dentist, started having an influenza-like infection which lasted five days, with malaise, muscle pain throughout the body and fever. One day before the hospital admission he presented urinary retention followed in the next day by ataxia and numbness sensation in both feet and lower third of his legs. The neurological examination disclosed a thoracic spinal cord impairment at T9-T10 level and the diagnosis of a post- infectious transverse myelitis was made. The plain Rx of the spine showed a spina bifida oculta in the T7 vertebra, which is roughly at the same level of the T9-T10 spinal cord segment. An iodinated myelography showed no abnormalities. The CSF examination showed small increase in the white cells (6.4 cells/cu.mm). The patient received dexamethasone (4. 5g /day) and two weeks later was entirely free of symptoms. The authors think that the congenital bone defect (spina bifida) might have played a role in the development of the myelitis, probably because of an ontogenetically determined "vulnerable point" ("locus minor resistentia ") at that level, either anatomical or immunological.
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PMID:[Post-infectious transverse myelitis and thoracic spina bifida: report of a case]. 637 43

Side effects play a significant role in the selection of drugs to be used in panic disorder/agoraphobia whose polyphobic symptomatology often includes a suspiciousness about taking drugs and a fear of undesired side effects which may lead to the refusal of treatment. The safety, side effects and patients' acceptance of alprazolam and imipramine versus placebo were evaluated in 1168 subjects with panic disorder/agoraphobia who had been enrolled in the second phase of the Upjohn World Wide Panic Study. Side effects that worsened over baseline to a greater extent with alprazolam than with imipramine and placebo were sedation, fatigue/weakness, memory problems, ataxia and slurred speech. In the imipramine group blurred vision, tachycardia/palpitations, insomnia, sleep disturbance, excitement/nervousness, malaise, dizziness/faintness, headache, nausea/vomiting and decrease in appetite were worse than in the other groups. In the placebo group the anxious symptoms were most prominent. The highest level of compliance was shown in the alprazolam-treated group and the lowest in the placebo-treated group. Strong predictors of side effects were not observed. If a side effect profile is known, it will be easier for a clinician to choose the right drug and the appropriate management by taking into account compliance, safety and efficacy in each patient under treatment. Further information about side effects in long-term maintenance treatment would be of great clinical pertinence in ensuring safety and enhancing patients' quality of life.
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PMID:Adverse effects associated with the short-term treatment of panic disorder with imipramine, alprazolam or placebo. 820 96

A 9-year-old, intact male llama with mild ataxia and generalized malaise of 1 month's duration was euthanized following clinical evaluation. Excessive liver copper concentrations were found in the llama and also in clinically normal herdmates. This case documents multiple animals with increased hepatic stores from standard diets and mineral supplements.
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PMID:Subclinical copper accumulation in llamas. 1036 60

After two days of malaise, headache, nausea, and vomiting, a 26-year-old man suddenly developed opsoclonus and stance and gait ataxia, without myoclonus. Having excluded a paraneoplastic etiology, we assumed that the disorder was probably related to a viral infection. Spontaneous resolution occurred in about two months. Opsoclonus became flutter dysmetria and then resolved. Saccadic eye movement recording disclosed the occurrence of hypermetria, increased velocity, and delayed latency, which also resolved. In this patient, the correspondence between clinical and ocular motor abnormality courses suggests a transient cerebellar dysfunction as the possible pathophysiologic mechanism for opsoclonus.
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PMID:Opsoclonus in a patient with cerebellar dysfunction. 1060 72

Angelman's syndrome is an association of severe mental retardation with absence of language, ataxia, convulsions and hyperactive, joyful behaviour with frequent bouts of laughing. Genetic diagnosis is possible in about 80% of cases. No cardiovascular abnormalities have been described in this syndrome to date. The authors report the cases of three children with Angelman's syndrome who presented with severe malaise due to increased vagal tone. The age of onset of symptoms was between 20 months and 8 years. One of the children had malaises triggered by bouts of laughing. The diagnosis was confirmed in all three cases by the results of Holter 24 hour ECG recording and oculo-cardiac reflex. The treatment chosen was Diphemanil (Prantal) in the two patients under 2 years of age (after failure of a trial of betablockers in one case) and Disopyramide for the oldest child with excellent results in all cases. However, one child died suddenly at the age of 6, two years after stopping diphemanil. Based on these observations, the authors suggest that all malaises in patients with Angelman's syndrome should be investigated by Holter ECG and oculo-cardiac reflex (or tilt test). In view of the potential gravity of the syncopal attacks, long-term medical treatment seems to be justified.
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PMID:[Angelman syndrome and severe vagal hypertonia. Three pediatric case reports]. 1085 53

We report a case of a 35-year-old man with nocardiosis infection involving soft tissue and the central nervous system who had received a cadaveric donor kidney. The patient was admitted with fever, malaise and right shoulder pain. Soft tissue abscess was seen on ultrasound examination. It was presumed due to gram (+) microorganisms, so 4 g day (IV) ampicillin/sulbactam was started empirically once the abscess was drained. Nocardia asteroides was found in the pus specimen. On the second day in hospital, severe headache, ataxia and signs of meningeal irritation appeared. The cranial CT showed two intracranial abscesses in the frontal lobe and cerebellum. We assumed Nocardia asteroides was the infective agent for the cerebral abscesses, so antibiotic therapy was switched to trimethoprim-sulphamethox-asole (3x160/800 mg/d). Nausea and vomiting occurred on the fifth day of therapy, improving after drainage from the frontal abscess. However, these complaints recurred five days later. CT showed cerebellar abscess had become bigger. The patient's complaints improved after the second surgical drainage. N. asteroides was again grown in the aspiration fluids of both cerebral abscesses. Complete regression of the abscesses was seen in the CT after two months. Co-trimoxazole was continued for six months then withdrawn. Graft dysfunction was not observed. Early medical and surgical interventions may be life-saving in this potentially lethal disease.
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PMID:Successful therapy combined with surgery for severe post-transplant nocardiosis. 1150 55

A 6-year-old 41.8-kg (92-lb) sexually intact male German Shepherd Dog used as an attack and pursuit dog by the local police department was examined because of general malaise and sudden onset of ataxia. Abnormal findings included a high WBC count, fever, and ongoing weight loss. Physical examination was unrevealing initially, in part because of the aggressive nature of the dog. Following treatment with antibiotics, an abdominal mass was detected during a second physical examination, and was confirmed radiographically. Subsequent ultrasound examination revealed a walled mass of mixed echogenicity, with areas of detectable fluid movement. A laparotomy was performed to remove the mass, which weighed 2.2 kg (4.5 lb). Histologic findings were consistent with botryomycosis, and Staphylococcus intermedius was isolated on bacteriologic culture. Postoperative treatment consisted of intravenous, intra-abdominal, and oral administration of antibiotics. Diagnosis of botryomycosis requires histologic examination and bacteriologic culture of the lesion. Treatment consists of surgical intervention and administration of antimicrobials. Botryomycosis is a poorly understood and rarely reported disease found in many species. A computer search of the literature failed to reveal any previous reports of intra-abdominal botryomycosis in dogs.
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PMID:Intra-abdominal botryomycosis in a dog. 1242 Jul 81

Approximately 5,000 to 80,000 of the US service personnel involved in the Persian Gulf War have complained of a variety of nonspecific symptoms since their return in 1991. These symptoms have been collectively labeled Gulf War Illness and include muscle fatigue, general malaise, myalgia, impaired cognition, ataxia, headaches, fever, joint pain, skin rash, gastrointestinal disturbances, sleep disturbances, and respiratory difficulties. Exposures of military and service personnel were diverse and included the prescribed anti-nerve gas agent pyridostigmine bromide (PYR), N.N-diethyl-m-toluamide (DEET) insect repellent, and environmental exposures to jet fuel. Thus, studies in our laboratory were undertaken to determine if concurrent exposure to these agents, singly or in combination, would contribute to significant alterations in immunological function and disease susceptibility. To assess immune status, eight-week old B6C3F1 female mice were exposed for 14 days to single compounds or tertiary mixtures of 15.5 mg/kg DEET, 2 mg/kg PYR, and 500 mg/kg JP-8 (termed low dose), or 31 mg/kg DEET, 5 mg/kg PYR, and 1,000 mg/kg JP-8 (termed high dose). Immunosuppression was assessed 24 h after the last exposure. No remarkable alterations were evident in hematological parameters, spleen and thymus organ weight and total cellularity, natural killer (NK) cell activity, cytotoxic T-cell activity, or mitogen-induced lymphocyte proliferation after exposure to either single or tertiary mixtures at low or high doses. A few changes in CD4/CD8 flow cytometric lymphocyte subpopulations were detected after exposure to the tertiary mixture at the high dose. Delayed type hypersensitivity (DTH) was decreased by 88% after exposure to the high-dose mixture, and suppression of antibody-specific IgM immune responses (plaque-forming cell, PFC) occurred after exposure to all single and tertiary mixtures at both dose levels. In the PFC response, antagonism was apparent in the mixture, while coexposure to these agents resulted in a synergistic effect in the DTH response. Susceptibility to B16F10 tumor or Listeria monocytogenes challenge was not affected after single or tertiary exposures. These data suggest that combined exposure to DEET, PYR, and JP-8 does not profoundly alter many immunological endpoints, but does selectively target functional endpoints such as the PFC and DTH response. This should be considered when assessing human health risks in the military environment.
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PMID:Evaluation of immunotoxicity induced by single or concurrent exposure to N,N-diethyl-m-toluamide (DEET), pyridostigmine bromide (PYR), and JP-8 jet fuel. 1253 64

Gulf War syndrome (GWS) is a perplexing multi-symptom condition comprising a constellation of signs and symptoms consistently described in the literature. These include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. Excessive chemical sensitivity and odour intolerance is reported. Epidemiological analysis suggests association with pyridostigmine bromide (PB) use as nerve gas prophylaxis, insect repellent, certain vaccination regimes, a variety of possible chemical exposures and physical and psychological stress. Pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) are potent vasoactive (vasodilatory) neuropeptides (VNs) having pleiotropic functions as immunomodulators, neuroregulators and hormones. VNs also have neurotrophic and anti-apoptotic roles. VNs act on G protein-coupled receptors (GPCRs) to activate adenylate cyclase, an important step in cyclic AMP metabolism. Autoimmune dysfunction of these VNs or their receptors is postulated to give rise to fatigue-related conditions such as chronic fatigue syndrome (CFS). Complex mechanisms involving heat shock proteins (hsps) and cytosine-guanine dinucleotide (CpG) DNA fragments may also be associated with autoimmunity to VNs or their GPCRs in contributing to fatigue-related conditions. Dysfunction of certain VNs may be the missing link in explaining the nebulous nexus between PB and GWS. This paper explores a possible link between exposures to PB and other chemical, physical and psychological stressors in producing a fatigue-related illness possibly related to autoimmune dysfunction of certain VNs. Treatment options involving restoration of VN function are considered in the context of analogues with other neurotransmitter fatigue-related conditions such as myasthenia gravis (MG). While evidence associating these conditions is thin, vasoactive neuropeptide neurotransmitters of the VIP/PACAP family have acetylcholine co-transmission functions via specific GPCRs. Autoimmune reactions to these receptors may have parallels with muscarinic (e.g., Sjogren's syndrome) and nicotinic (e.g., MG) acetylcholine neurotransmission. Hence theoretically, treatment options such as thymectomy, corticosteroids, plasma exchange, anti-idiotype antibodies and receptor genomic expression reactivation/suppression may be considered. Paradoxically pyridostigmine may prove to have a role in therapy although VN treatment/replacement may be associated with tachyphylaxis.
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PMID:Do vasoactive neuropeptide autoimmune disorders explain pyridostigmine's association with Gulf War syndrome? 1600 38


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