Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methotrexate-induced neurotoxicity (MTX-Ntox) is a frequent complication of methotrexate (MTX) therapy for patients with both malignant and inflammatory diseases. MTX-Ntox can occur after intrathecal MTX or after low-, intermediate-, or high-dose systemic administration. Symptoms can present in the acute, subacute, or late setting form, and can range from affective disorders, malaise, and headaches, to somnolence, focal neurologic deficits, and seizures. While the pathogenesis of MTX-Ntox is likely multifactorial, one potential biochemical pathway leading from MTX to neurotoxicity involves the folate dependent remethylation of homocysteine (Hcy). MTX therapy is known to cause elevations of both plasma and CSF Hcy. Hcy is directly toxic to vascular endothelium and it and its metabolites are excitatory agonists of the N-methyl-D-aspartate (NMDA) receptor. Competitive or noncompetitive antagonists might afford protection from or reversal of MTX-Ntox. Using high-performance liquid chromatography (HPLC) with coulometric electrochemical detection, the authors measured CSF Hcy in sequential patients with severe subacute MTX-Ntox. CSF Hcy was higher in these patients (n = 9, median = 0.93 microM) than in asymptomatic patients (n = 11, median 0.2 microM, p < .01). Five patients with severe subacute MTX-Ntox (most with dysarthria and/or hemiplegia) were treated with 1-2 mg/kg oral dextromethorphan (DM), a noncompetitive antagonist of the N-methyl-1-aspartate (NMDA) receptor. All five had resolution of symptoms. These data provide additional clinical support for elevated CSF Hcy in the induction of MTX-Ntox through activation of the NMDA-receptor. These data provide support for a placebo-controlled clinical trial to examine the ability of DM to prevent or alleviate MTX-Ntox.
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PMID:Dextromethorphan is effective in the treatment of subacute methotrexate neurotoxicity. 1207 63

Tuberculous meningitis (TBM) presents clinically as either acute meningitis syndrome characterized by coma, raised intracranial pressures, seizures, and focal neurological deficits, or as a slowly progressive dementing illness. When the infection presents as the former, characteristic signs and symptoms are headache, malaise meningismus, papilloedema, vomiting, confusion, seizures, and cranial nerve deficits. Patients admitted with lethargy or stupor may enter coma in a matter of days, and fever may or may not be present. However, TBM more commonly presents as a slowly progressive dementing illness, with memory deficits and personality changes typical of frontal lobe-like disease. TBM is described with regard to its history, clinical presentations, complications, diagnosis, C.S.F. abnormalities, treatment, prognostic factors, and indications of steroids. Combination drug therapy involving isoniazid, rifampin, pyrazinamide, and pyridoxine is the recommended treatment strategy for adults. The patient's level of consciousness at the start of therapy is the most important prognostic factor reported in TBM cases, with the greater the change in mental status, the worse the outcome. The mortality rate of patients who are comatose before the initiation of therapy is 50-70%.
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PMID:Tuberculous meningitis. 1229 51

A first-trimester primigravid patient presented with hyperemesis and malaise. Work-up was consistent with primary hyperparathryoidism. During acute treatment, she developed generalized motor seizures considered to be secondary to hypercalcemia. Evaluation and treatment of women with primary hyperparathyroidism and hypercalcemia are reviewed, and the pathogenesis of seizures associated with hypercalcemia is discussed.
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PMID:Primary hyperparathyroidism, hypercalcemic crisis and subsequent seizures occurring during pregnancy: a case report. 1260 69

Dexamethasone-cyclophosphamide pulse (DCP) is the prefered mode of therapy in pemphigus in India because it is relatively free from the side effects seen with heavy doses of daily oral steroids. One hundred forty-six pemphigus patients treated with DCP were observed for side effects of this regimen. One hundred forty mg of dexamethasone was administered IV in 200 ml of 5% dextrose over a period of 60-90 minutes on 3 consecutive days. Five hundred mg of cyclophosphamide was added on first day of the pulse and 50 mg given orally daily in the intervening period. DCP was repeated every 4 weeks and continued for 6 months after subsidence of the disease (no new lesions). Flushing over the face was the most common event recorded during the adiministration in 78 subjects followed by palpitations in 11, hiccups in 9, and numbness of feet in 6. Fourteen patients had polyurea, and 3 developed skin rash. Shivering, shooting pains along thighs, breathlessness, seizure and unilateral limb edema were observed in one patient each. Generalized weakness/malaise was the most troublesome delayed side effect in 81 (55.4%) patients; it lasted for 8-15 days after the pulse. Thirty-six (24.6%) had inadequate sleep syndrome, 23 (15.7%) had headache, 21 (14.3%) complained of arthralgias, 19 (13%) experienced alteration in taste, and 13 (9%) had diffuse hair loss. 28 females developed menstrual disturbances, and 14 (9.5%) had blurring of vision (glaucoma in 3 and posterior subcapsular cataract in 1). Thirteen of eighteen diabetics had an increase in blood sugar requiring higher doses of insulin. Five NIDDM patients needed insulin. Four (2.7%) developed hypertension. Pulse therapy is not absolutely free from side effects. Hypertension and diabetes occur less frequently as compared to conventional steroid therapy. Generalized weakness, flushing, headache and taste alteration occur exclusively with pulse therapy.
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PMID:Immediate and delayed complications of dexamethasone cyclophosphamide pulse (DCP) therapy. 1468 52

OBJECTIVE: To describe a case of movement disorder associated with cisapride use. METHOD: Case report.RESULTS: This is the case of a male eight months old child who began to use cisapride, 0,2 mg/kg tid to treat gastroesophageal reflux disease. One month after beginning with the drug, he started to present repetitive movements of the hands characterized by opening and closing hands with flexion and extension of the wrists. According to the mother, these movements became more evident as the dose of the medication was increased, and, thereafter, started to happen also on the feet. When the child was six months old, time of the first neurological evaluation, he presented normal neurological development, except for the Parachute reflex, which was absent. After excluding metabolic, toxic and infectious diseases, the drug was withdrew. The child evolution was benign, with gradual disappearance of the movements, and he was completely normal 30 days after.CONCLUSIONS: The authors stress the need suspending the use of cisapride in any case of neurologic symptoms as seizures, somnolence, malaise or involuntary movements in previously normal patients.
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PMID:[Cisapride related movement disorders] 1468 4

Headache originating front-orbital area can be divided to (1) Which has no autonomic symptoms such as lacrimation, rhinorrea, rhinostasis. This include psychogenic headache and epileptic headache. In the case of psychogenic headache, pericranial tenderness is not observed, and headache is medium in intensity. Most often patient complains of a headache originating frontal area. There are more than five various symptoms such as general malaise, numbness, tingling sensation, vertigo, sleeplessness. However, although symptoms are multiple, patients spend a life commonly. In other words, a patient is protected by a headache against his or her stress. No medication is needed in such a case. In epileptic headache, pressing type pain is felt over the forehead for several minutes to a few hours. Tremor or convulsion sometimes follow the headache. EEG shows spike and wave activities. In the case of focal epilepsy, headache occurs contralateral to the focus. Anti-epileptic drugs such as VPA or CBZ is a choice in such case, and headache as well as seizure disappears. (2) Front-orbital headache with autonomic symptoms include various trigeminal autonomic cephalalgias. These include cluster headache, episodic paroxysmal hemicrania, hemicrania continua, among others. Precise history taking is necessary for the treatment, because no drug is 100% effective.
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PMID:[Headache originating front-orbital area]. 1565 1

A 39-years-old woman was admitted to our hospital with musculoskeletal complaints (myalgias and symmetric arthralgias in proximal interphalangeal, metacarpophalangeal joints of the hands and in knees), systemic symptoms like fever, fatigue, malaise and a six months previous history of a transient ischemic attack. The presence of antibodies to double-stranded deoxyribonucleic-acid (DNA) and antiphospholipid antibodies led to the diagnosis of systemic lupus erythematosus with secondary antiphospholipid syndrome. Cerebral infarction develops significantly more often in patients with lupus and antiphospholipid antibodies, but other clinical syndromes are associated with lupus anticoagulant: cognitive dysfunction, seizures, polyneuropathy, aseptic meningitis, myelopathy.
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PMID:[Systemic lupus erythematosus with neurologic onset and secondary antiphospholipid syndrome. A Case Study]. 1660 81

The aim of this controlled historical cohort study was to assess the validity of post-concussion syndrome in children. We identified 301 children aged 4-15 years who had sustained an isolated brain concussion, and another group of 301 children who sustained any other mild body injury excluding the head. Parents from both groups filled in standardized questionnaires containing questions about the health condition of the children: headache, neck pain, dizziness, malaise, fatigability, exercise or noise intolerance, irritability, weepiness, sadness, anxiety, nocturnal enuresis, tics, sleep disorders, memory or learning difficulties, hyperactivity, seizures, attention disorder, buzzing in the ears, subjective parental concerns about the child's health condition, and parental concerns about their child having a brain disorder. The severity of the complaints was rated on the Visual Analogue Scale. After the final exclusion, 102 pairs strictly matched by sex, age, and the date of trauma were analyzed. The differences of parental complaints about the health condition of their children between case and control groups were statistically insignificant for all symptoms, except parental concerns about their child having brain damage which were significantly higher in the case group. The likelihood of parental concerns about the possibility of their child having brain damage was 2.7 times higher in the case group. Headache, learning difficulties, and sleep disorders were significant variables predicting the concerns. These results question the validity of the post-concussion syndrome in children.
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PMID:The validity of post-concussion syndrome in children: a controlled historical cohort study. 1668 58

A 70-year-old patient treated with oxcarbazepine experienced severe hyponatremia. The patient used oxcarbazepine (600 mg twice a day) concomitantly with diuretics (torasemide 10 mg and indapamide 1.25 mg once per day), perindopril, an angiotensin-converting enzyme inhibitor, and amlodipine, a Ca(2+) channel blocker. The patient complained of a nausea, malaise, diplopia, drowsiness, apathy, decreased diuresis (creatinine clearance - 41.51 ml/min), and exacerbation of epileptic seizures. Sodium concentration in the plasma was 113 mmol/l. The patient was hospitalized. It was suggested that a decrease in plasma sodium concentration was caused by oxcarbazepine used together with diuretics for six months. Oxcarbazepine-induced hyponatremia is reported in 22.2-50% of patients, although symptoms are present only in 5.9% of patients. The most common symptoms of central nervous system injury, experienced by patients, are drowsiness, dizziness, decreased cognitive function, coordination impairment, etc. Physicians not always in time pay proper attention to undesirable antiepileptic drug-induced effects, which can be dangerous.
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PMID:[A case of severe hyponatremia in a patient suffering from epilepsy and using oxcarbazepine]. 1696 31

Kindling is a model in which an initially subconvulsive electrical stimulation of certain brain areas eventually develops a generalized seizure that produces behavioral and long term neuronal changes. In the present study we evaluated if kindling can modify conditioning taste aversion (CTA). In this paradigm animals acquire aversion to saccharin when it is presented as the conditioned stimulus (CS) followed by an injection of lithium chloride (LiCl) that induces a gastric irritation as the unconditioned stimulus (US). Male Wistar rats were implanted with bipolar electrodes aimed at the right amygdala (AMG) or at the right insular cortex (IC). The animals were stimulated daily until they reached stages 2-4 (intermediate) or until kindling was fully established (three consecutive stage 5 seizures). At least two weeks after kindling stimulation had ceased the animals were deprived of water for 24 h and given 10-min drinking sessions twice a day for 4 days. On day 5 (morning session) tap water was replaced by saccharin solution (0.1%), 20 min later the animals were injected with LiCl (7.5 ml/kg i.p., 0.2 M) to induce gastric malaise or taste aversion. After three more days of baseline consumption, water was substituted by a fresh 0.1% saccharin solution to test the aversion. AMG-kindling delayed the extinction of CTA. Animals with kindling in the IC had a higher retention than the sham kindling group; that is, they drank significantly less saccharin solution than the other groups. The results of the present experiment show that local modification of brain function induced by kindling stimulation can prolong the aversive effects of CTA.
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PMID:Kindling increases aversion to saccharin in taste aversion learning. 1714 Jul 39


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