Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine according to the criteria of the International Headache Society, occurs in about 3 to 7% of all children. Despite this high incidence, and unlike the situation with adult migraine, only a very few controlled trials have investigated the acute and prophylactic treatment of migraine in children. In the acute migraine attack, ibuprofen 10 mg/kg and paracetamol (acetaminophen) 15 mg/kg have been shown to be effective, with only a few adverse effects. In severe migraine attacks, dihydroergotamine mesylate (dihydroergotamine) administered orally (20 to 40 microg/kg) or intravenously (maximum 1 mg/day) may be helpful, but there have been no large placebo-controlled trials of this treatment. Oral sumatriptan has not been effective in several double-blind and placebo-controlled trials; administered subcutaneously, this drug might be helpful but the only data for this application come from open trials. For migraine prophylaxis, only flunarizine 5 mg/day has been shown to be effective in more than 1 double-blind, placebo-controlled trial. Some evidence also exists that propranolol >60 mg/day and pizotifen 0.5 to 1.5 mg/day are effective; however, the results from different trials are contradictory. For all other drugs studied in migraine prophylaxis, the results remain vague (e.g. amitriptyline, nimodipine, trazodone) or suggest inefficacy (e.g. timolol, clonidine, tryptophan). In migraine-related disorders, pizotifen 0.5 to 0.75 mg/day for abdominal migraine and flunarizine 10 to 25 mg/day for alternating hemiplegia have been shown to be effective. Most of the drugs used in the treatment of migraine in children are well tolerated and without relevant adverse effects. In migraine prophylaxis, the most common adverse effects are drowsiness and bodyweight gain.
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PMID:Drug treatment of migraine in children: a comparative review. 1093 75

Based on previous reports suggesting a role of the neurotransmitter serotonin in the pathomechanism of alternating hemiplegia of childhood and speculation that it may be a migraine variant, we measured brain serotonin synthesis in children with alternating hemiplegia of childhood. Clinical and neurodevelopmental data, as well as standard uptake values in 25 brain regions and whole-brain serotonin synthesis capacity (unidirectional uptake rate constant or K-complex), were assessed in six patients with alternating hemiplegia of childhood (three girls and three boys; mean age = 7 6/12 years) using alpha[11C]methyl-L-tryptophan positron emission tomography (PET). The PET studies were performed interictally in three patients, during the ictal state in two patients, and postictally in one patient. The PET data were compared to those obtained interictally from six age-matched patients with focal epilepsy (two girls and four boys; mean age = 7 8/12 years) and six non-age-matched apparently normal siblings of autistic children (two girls and four boys; mean age = 9 11/12 years). Patients with alternating hemiplegia of childhood studied in the ictal or postictal state showed increased serotonin synthesis capacity in the frontoparietal cortex, lateral and medial temporal structures, striatum, and thalamus when compared to controls, and subjects with alternating hemiplegia of childhood studied interictally. The involvement of these brain regions was consistent with the semiology of the hemiplegic attacks. In patients with interictal studies and in the controls, the PET scans revealed similar and bilaterally symmetric regional patterns of serotonin synthesis capacity. Increased whole-brain serotonin synthesis capacity (reported in migraine subjects without aura) was not found in the alternating hemiplegia of childhood group. There was no correlation between the neurodevelopmental scores and regional standard uptake values; however, patients with a larger estimated lifetime attack number showed greater delay in communication (P = .005) and daily living skills (P = .042). These studies suggest increased regional serotonergic activity associated with attacks in alternating hemiplegia of childhood. Furthermore, the attack number may have an effect on neurodevelopmental delay, thus supporting the notion that alternating hemiplegia of childhood may be a progressive disorder.
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PMID:Alpha[11C] methyl-L-typtophan positron emission tomography in patients with alternating hemiplegia of childhood. 1208 79

Purple urine bag syndrome (PUBS) is a rare syndrome characterized by production of indigo (blue) and indirubin (red) pigments due to bacterial colonization in urinary catheter. The pathogenesis of PUBS is related to the combination of these two pigments produced from the metabolism of tryptophan. Tryptophan turns into indole by deamination, indole turns into indoxyl sulphate by hepatic conjugation and indoxyl sulphate is secreted into urine. Sulphatases and phosphatases enzymes produced by bacteria like Providencia stuartii and Providencia rettgeri, Klebsiella pneumoniae, Proteus mirabilis, Escherichia coli, Enterococcus spp., Morganella morganii, Pseudomonas aeruginosa, Citrobacter spp. and group B streptococci convert indoxyl sulphate to indoxyl. In the urinary tract, oxidation of indoxyl results in the production of indigo and indirubin pigments. These pigments react with polyvinyl chloride (PVC) lining of the urinary catheter bag and the reaction results purple discoloration of urine. Urine discoloration is very important clinical sign in the differential diagnosis of several pathological conditions such as hematuria, urinary system tumors and drug side effects and may be disquieting for patients, families and healthcare workers. Purple urine discoloration is rarely reported in the literature and it is generally associated with urinary tract infection. In this report, a 60 years old woman with a past medical history of significant chronic kidney disease undergoing regular hemodialysis, chronic constipation and hepatitis B was admitted to our neurology clinic because of acute intracerebral hemorrhage. She had confusion and right hemiplegia in her neurological examination and required urinary catheterization due to immobilization. Red coloration was observed in urine on the tenth hospital day. Although this coloration was thought to be hematuria, according to urine examination it was not hematuria. Then urine color turned into purple within two days. The next day, because of fever, full blood count and other blood investigations were performed and urine was sent to the laboratory for culture. Empirical piperacillin-tazobactam and teicoplanin antibiotic treatments were commenced. In the urine culture, 105 cfu/ml Enterococcus faecalis was isolated. According to the antibiotic susceptibility results the therapy was changed and meropenem was added to the treatment. For her constipation, supportive managements such as hydration, nutrition and laxative treatment were applied. After all the treatments, the patient's constipation regressed, the urine had become normal colored and the following urine cultures were not revealed any bacterial growth. As in this case, when the urine discoloration occurs, PUBS should be kept in mind which is especially seen in elderly female patients with chronic constipation, urinary catheterization, urinary tract infection and renal failure.
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PMID:[Purple Urine Bag Syndrome: A Rare Clinical Case]. 3170 43