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)

The clinical and laboratory findings from studies of patients with chronic fatigue syndrome (CFS) from northern Nevada are summarized. Physicians caring for these patients have estimated that greater than 400 patients with CFS from northern Nevada and nearby communities in California were identified between 1984 and 1988. As a result of these studies, a cluster of clinical and laboratory features associated with the illness in moderately to severely affected patients has been identified: profound fatigue of prolonged duration; cervical lymphadenopathy; recurrent sore throat and/or symptoms of influenza; loss of cognitive function manifested by loss of memory and loss of ability to concentrate; myalgia; impairment of fine motor skills; abnormal findings on magnetic resonance imaging brain scan; depressed level of antibody to Epstein-Barr virus (EBV) nuclear antigen; elevated level of antibody to EBV early antigen restricted component; elevated ratio of CD4 helper to CD8 suppressor cells; and strong evidence of association of this syndrome with infection with human herpesvirus 6. More-serious and longer-lasting neurologic impairments, including seizures, psychosis, and dementia, have also been observed in some of these patients.
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PMID:Chronic fatigue syndrome in northern Nevada. 185 May 42

During 1988, an endemic outbreak of aseptic meningitis was noted in the Kaohsiung area. Throughout the year, a total of 89 cases were identified by cerebrospinal fluid (CSF) examination at the Pediatric Department of Kaohsiung Medical College. The peak incidence was from June to October. Scattered cases still occurred during November and December. The male to female ratio was 1.7:1 and the age distribution ranged from 1 month to 15 years old. Two peaks of age distribution were observed; one in infancy and the other in the 4-7 year old age group. Most of them exhibited fever (94.4%), headache (68.9%), and vomiting (68.5%). Other associated symptoms and signs included neck stiffness, sore throat, cough, Brudzinski's sign, abdominal pain, seizure, dizziness, rhinorrhea, diarrhea, Kernig's sign, skin rash, hyperemic conjunctiva, apnea, and oral ulcers. Most of them had CSF white blood cell (WBC) counts less than 1000/mm3, normal or mild elevated protein, and normal CSF/plasma sugar ratio. Three patients were found to have a virus in their CSF without pleocytosis. Virus isolations from CSF throat swabs and/or rectal swabs were performed in 65 patients, half of them (35/65, 53.8%) had positive results including echovirus type 9 (sixteen), echovirus type 30 (eighteen), and adenovirus type 3 (one). Echovirus type 9 was predominant during July and August whereas echovirus type 30 became predominant after September. All patients recovered spontaneously without any sequelae.
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PMID:Clinical observations and virological study of aseptic meningitis in the Kaohsiung area. 198 74

In the case described, electroencephalography (EEG) proved valuable for determining the nature of spells of loss of consciousness with brief clonic jerks associated with ear and throat pain. A 70-year-old woman had a history of episodic brief attacks of pain below the right ear and deep in the neck that had started three years previously. The spells became more severe and progressed to loss of awareness associated with clonic jerks of the extremities. Because of a concern that the spells represented seizures, an EEG was performed, with electrocardiographic monitoring. Multiple spells were recorded; they began with profound bradycardia followed by generalized slow-wave activity and then by suppression of all EEG activity correlating with loss of consciousness and clonic jerking. The spells were thought to represent syncopal attacks associated with glossopharyngeal neuralgia.
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PMID:An electroencephalographic study of glossopharyngeal neuralgia with syncope. 335 4

Cerebellar and thalamic stimulation has been known for many years to improve control of epileptic seizures. In the past few years electrical vagus nerve stimulation (VNS) has been introduced and has been effective in controlling seizures in animal models. These encouraging results led to the development of a transcutaneous programmable pulse generator and electrode lead for human use. 2 pilot studies and a multicenter, prospectively-randomized, parallel, double-blind study of patients with refractory partial seizures were performed. In a 3-22 month follow-up, in about 50% of patients seizures were reduced by 30-50%. There were no significant complications of the implant. Side-effects associated with VNS included intermittent hoarseness, coughing and throat pain. Additional controlled clinical trials with many patients and long follow-up are needed. We report 2 patients, the first in Israel, who underwent VNS.
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PMID:[Vagus nerve stimulation for partial seizures]. 755 11

Vagus nerve stimulation (VNS) significantly reduces the frequency of partial seizures in refractory epilepsy patients. We examined the serious adverse events, side effects, and tolerability as they relate to the surgical implant procedure and the stimulating device. We also reviewed potential drug interactions, device output complications, and impact of the therapy on overall health status. We analyzed the first 67 patients to exist the acute phase of the EO3 VNS trial comparing high (therapeutic) VNS to low (less or noneffective) VNS. Data were collected from case report forms used at each of the four visits during the 12-week baseline and at each of the four visits during the 14-week randomized phase of the trial. No significant complications were reported as a result of the implant procedure. Serious adverse events included 1 patient who experienced direct current to the vagus nerve owing to generator malfunction resulting in left vocal cord paralysis and withdrawal of the patient from the study. No clinically significant effects on vital signs, cardiac function, or gastric function were detected. Side effects associated with VNS in the high group were hoarseness (35.5%), coughing (13.9%), and throat pain (12.9%). In the low group, only hoarseness (13.9%) and throat pain (13.9%) were associated with VNS. These effects generally wrre not considered clinically significant and occurred primarily during the stimulation pulses. No patients discontinued VNS therapy during the acute phase because of side effects associated with normal stimulation. Except for the one instance of a short circuit in the system resulting in a direct current, stimulating system complications were minor, limited to programming, unscheduled stimulation, and high lead impedance. Patients, investigators, and patient companions rated patients receiving high stimulation as more "improved" than those receiving low stimulation in regards to overall health status. Antiepileptic drug (AED) plasma concentrations were not affected by VNS. The implant procedure, stimulating system, and therapy proved safe and tolerable during the study. The high percentage (67 of 68) of patients completing the study reflects patient acceptance and tolerability of this mode of therapy.
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PMID:Vagus nerve stimulation for treatment of partial seizures: 2. Safety, side effects, and tolerability. First International Vagus Nerve Stimulation Study Group. 802 9

The herbicide pendimethalin (STOMP) shares a similar chemical structure with nitro compounds such as dinitrobenzene, which was previously demonstrated to cause methemoglobinemia in mammals. However, reports on STOMP poisoning in humans are rare. We reviewed 71 STOMP poisoning cases (42 men and 29 women of mean age 43.9 +/- 2.5 y) reported to the Poison Control Center--Taiwan from September 1986 to September 1997 and summarized their clinical manifestations. Two incidences resulted from skin and eye contact. The rest were due to oral ingestion intentionally or accidentally. The average ingestion was 106.1 +/- 13.4 ml. Among them, 20 cases had no symptoms or signs, 38 had mild effects such as nausea, vomiting and sore throat, 7 had effects such as severe retching, hematemesis and seizures. Four patients expired due to also taking other herbicides (mainly organophosphates) and because of inadequate airway management. Adequate ventilation support was the major therapy in salvaging the poisoning cases.
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PMID:Clinical experience with pendimethalin (STOMP) poisoning in Taiwan. 961 Apr 93

Acute autonomic and sensory neuropathy (AASN) is a rare neuropathy characterized by acute autonomic dysfunction and objective sensory disturbances. A 26-year-old pregnant woman with severe autonomic and sensory dysfunction is reported. This patient suddenly developed marked nausea and vomitting in about 2 days after having a sore throat. She then developed signs of autonomic dysfunction including dilated non-reactive pupils, dryness of the eyes and oral mucous membranes, generalized anhidrosis, paralytic ileus, orthostatic hypotension, and continuous tachycardia. She also had severe generalized sensory impairments of all modalities, and all deep tendon reflexes were absent. Sensation was almost totally lost for all modalities below the neck. There was marked pseudoathetosis and sensory ataxia in all extremities. Motor examination was normal. She had inability to urinate. At this time she was 38 weeks pregnant, and when she showed signs of fetal distress, a Caesarean section was performed. Albumino-cytological dissociation was seen in the CSF. Serum noradrenaline was reduced, no sensory nerve action potentials could be elicited, and reduced coefficient of variation of the R-R interval on electrocardiography was observed. Plasma exchange was performed every other day for 3 days for about 3 weeks after the onset of the illness, but no favorable effects. Seven months after the onset, her autonomic dysfunction slightly improved, but there was no recovery from the sensory disturbances. Many symptoms and signs that characterize AASN occurred in this patient, and each was severe. The patient developed SIADH, sleep apnea, personality change, and amenorrhea in the course of the disease. We suggest that AASN patients might have both peripheral and central nervous system manifestations including seizures and personality changes.
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PMID:[A severe case of acute autonomic and sensory neuropathy]. 986 13

A 21-year-old male soldier was admitted due to a sore throat, headache, generalized lymphadenopathy and persistent fever for 12 days. Despite empirical antibiotic treatment for four days at a clinic prior to admission, he continued to have persistent abdominal pain over his right upper quadrant region and progressive jaundice was followed by shock. After admission, he developed an episode of clonic seizures and became delirious and agitated. An electrocardiogram showed first degree atrioventricular (AV) block and non-specific ST-T wave changes. Hematological studies revealed thrombocytopenia, hypofibrinogenemia, abnormal partial thromboplastin time (PTT) and a positive test for D-dimer. The cerebrospinal fluid analysis showed pleocytosis with white cells of 84/mm3 with a lymphocyte predominance, protein of 97 mg/dL and glucose of 79 mg/dL. Indirect immunofluorescence assay showed a fourfold rise in antibodies to Orientia tsutsugamushi in paired serum with IgM antibody titer of 1:640. The patient had a favorable response after parenteral chloramphenicol in addition to oral tetracycline. Early ricognition of scrub typhus and early prescription of anti-rickettsial agents prevent complications of central nervous system involvement and further deterioration of cardiac and hematological function.
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PMID:Meningoencephalitis, myocarditis and disseminated intravascular coagulation in a patient with scrub typhus. 1156 71

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29

A 32-year-old black female was started on phenytoin for seizure prophylaxis following the clipping of an aneurysm. This was stopped after 3 weeks when she developed a generalized skin rash. Over the next week she developed fever, sore throat, dysphagia, and headache. She had an erythematous throat with white exudates on the right tonsil and 1 to 3 cm firm, tender lymphadenopathy in multiple regions. Blood, throat swab and cerebrospinal fluid studies were negative for bacterial or viral infections, except for elevated liver enzymes. CT scan of chest, abdomen, and pelvis showed no lymphadenopathy. Lymph node biopsy suggested necrosis but no evidence of infection, granuloma, or lymphoma. Her lymphadenopathy resolved spontaneously and liver enzymes normalized in 3 weeks. Hypersensitivity syndrome due to antiepileptics manifests as fever, rash, generalized lymphadenopathy, and probably represents a T-cell mediated drug reaction. This reaction may persist despite cessation of the drug, and it may engender expensive evaluation. Careful observation up to 3 weeks after drug cessation may be the best management.
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PMID:Necrotizing lymphadenitis associated with the phenytoin-induced hypersensitivity syndrome. 1621 91


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