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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical symptoms and treatment of acute isoniazid toxicity are presented. The use of supportive measures and chemotherapy are discussed in detail. The pharmacology and biochemistry underlying the symptons of isoniazid poisoning are aslo presented. It is concluded that diazepam in combination with pyridoxine is the treatment of choice for the management of convulsions associated with isoniazid toxicity. Pyridoxine should be administered intravenously in amounts equal to the estimated quantity of isoniazid ingested, even if seizures have not occurred.
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PMID:Treatment of acute isoniazid toxicity. 113 66

The effects of pyridoxine deficiency and the administration of supplemental vitamin B6 on audiogenic and electroconvulsive seizures were studied in two inbred strains of mice and their F1 hybrids. Pyridoxine deficient diets increased seizure risk, whereas supplemental vitamin B6 protected these animals against seizures. Penicillamine and thiosemicarbazide, at doses which lowered brain levels of pyridoxine by only 10%, increased seizure risk. Diets deficient in zinc and copper did not alter susceptibility to either audiogenic or electroconvulsive seizures. DBA/2J mice, genetically susceptible to audiogenic seizures, have the same endogenous levels of pyridoxine in the brain as do C57Bl/6J mice, which are resistant to audiogenic seizures.
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PMID:Levels of pyridoxine and susceptibility to electroconvulsive and audiogenic seizures. 117 97

Pretreatment of rats with hydrazine (100 mg/kg), a compound which raises brain gamma-aminobutyric acid (GAGA) 175 percent in 12 hr was not able to prevent the occurrence of seizures induced by monosodium L-glutamate (MSG). Pyridoxine (50 mg/kg) the cofactor essential in the conversion of glutamate to GABA, also failed to prevent convulsions induced by parenteral MSG administration. It is concluded that the mechanism of action of MSG-induced seizures is neither by decreasing brain GABA levels or interfering with the pyridoxine cofactor.
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PMID:Lack of protection by pyridoxine or hydrazine pretreatment against monosodium L-glutamate-induced seizures. 120 36

This investigation tested the hypothesis that the degree of pyridoxine depletion rather than the status of neuronal maturity determines seizure proneness in the pyridoxine-deficient rat. Dietary pyridoxine deficiency was induced in neuronally mature rats. Seizure activity was monitored using computerized EEG analysis. Dietary pyridoxine deficiency of 10 weeks' duration induced in neuronally mature rats led to spontaneous convulsive seizure activity. Even moderately pyridoxine-deficient adult rats (on the deficient diet for less than 8 weeks) exhibited seizure-like diffuse spike and wave activity and electrocortical inhibition. Picrotoxin-, pentylenetetrazol-, or domoic acid-induced seizure thresholds were significantly reduced in pyridoxine-deficient rats when compared with normal controls. Pyridoxine-deficient rats exhibited increased dominance of delta and theta activities and increased hemispherical asymmetries in response to convulsant treatment.
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PMID:Seizure activity in pyridoxine-deficient adult rats. 154 53

Isoniazid overdose is known to result in the rapid onset of seizures, metabolic acidosis, and prolonged obtundation. Pyridoxine has been reported to be effective in treating isoniazid-induced seizures. We report three cases of obtundation secondary to isoniazid overdose that was immediately reversed by intravenous pyridoxine. In two of these cases, status seizures were stopped by intravenous pyridoxine administration, but the patients remained comatose for prolonged periods. The comas were immediately reversed by the administration of additional pyridoxine. In the third case, the patient's lethargy was treated by intravenous pyridoxine on presentation and was followed by immediate awakening. Pyridoxine is effective in treating not only isoniazid-induced seizures, but also the mental status changes associated with this overdose. The dose required to induce awakening may be higher than that required to control seizures.
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PMID:Reversal of prolonged isoniazid-induced coma by pyridoxine. 129 May 58

Theophylline overdosage can cause life-threatening symptoms, that include seizures and cardiac arrhythmias, and can be fatal. Neither the onset of toxicity nor the severity of symptoms is well predicted by serum theophylline concentrations. Since depressed vitamin B6 plasma levels can occur in patients receiving theophylline, we explored a B6-theophylline interaction in a rabbit model. Administration of theophylline preparations intraperitoneally (aminophylline) or orally (sustained release anhydrous theophylline) resulted in a 47% depression of plasma pyridoxal 5'-phosphate (PLP) levels. The 87% increase in PLP with pyridoxine administration was only 18% when aminophylline was also given. The mechanism of the theophylline-B6 interaction is obscure. Ethylenediamine in some theophylline preparations binds directly to PLP, potentially increasing the less direct theophylline effect. Pyridoxine supplementation resulted in higher average PLP levels but did not prevent death in animals with profoundly low PLP levels. If these data apply to humans, B6 deficiency may contribute to chronic theophylline toxicity; however, pyridoxine administration in the dosage used may not prevent toxicity. Larger doses may prove beneficial after further investigation.
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PMID:Depression of vitamin B6 levels due to theophylline. 236 33

The authors present an account on 14 patients with markedly pharmaco-resistant age-conditioned epileptic encephalopathies (4 x West's syndrome, 5 x Lennox-Gastaut's syndrome and 5 x an intermediate stage of the two), treated with large doses of vitamin B6 (Pyridoxin Spofa). The mean age at the onset of therapy was 2.5 years (0.5-6 years). In addition to hitherto unsuccessful medication, the patients were given at first five-day treatment of vitamin B6 50-100 mg/day by the i.m. route, and then 200-300 mg/day orally. A marked clinical effect was recorded in five children, in another five it was less marked and usually only transient. Only in four patients the seizures were not affected, incl. three times in Lennox-Gastaut's syndrome. The EEG changes correlated with the clinical course. The authors recommend to attempt early administration of large doses of vitamin B6 in refractory age-conditioned epilepsies in the first three years of life.
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PMID:[Administration of high doses of B6 in age-related epileptic encephalopathies]. 271 42

Pyridoxine dependency is a rare cause of neonatal seizures. Newborns with this disorder are often hyperirritable and fail to respond to the usual anticonvulsants. The diagnosis is established by cessation of seizures after the administration of parenteral pyridoxine. Reported is a case of pyridoxine dependency that illustrates several problems in management. The amount of pyridoxine required to control seizures is variable and may exceed 100 mg per day. The electroencephalogram (EEG) may not change significantly during the initiation of therapy. During intercurrent illnesses, parenteral pyridoxine may need to be given. Additional pyridoxine may be needed even when the EEG is normal. Treatment should continue indefinitely.
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PMID:Pyridoxine dependency seizures: report of a case with unusual features. 311 62

An international questionnaire survey has been conducted to define better the natural history of homocystinuria due to cystathionine beta-synthase deficiency and permit evaluation of treatment. Data were compiled for 629 patients. Among patients not discovered by newborn screening, B6-responsive individuals on the average have significantly better mental capabilities (mean IQ, 79) than do B6-nonresponsive individuals (mean IQ, 57). Time-to-event curves are presented for the other major clinical abnormalities produced by this disease. Each occurred at significantly lower rates in untreated B6-responsive than in untreated B6-nonresponsive patients, as shown by the following examples: (1) dislocation of optic lenses (at age 10, chances of dislocation: 55% and 82%, respectively); (2) initial clinically detected thromboembolic events (at age 15, chances of having had such an event: 12% and 27%, respectively); (3) radiologic detection of spinal osteoporosis (at age 15, chances of such osteoporosis having been detected: 36% and 64%, respectively); and (4) mortality (at age 30, chances of not surviving: 4% and 23%, respectively). Methionine restriction initiated neonatally prevented mental retardation, retarded the rate of lens dislocation, and may have reduced the incidence of seizures. Pyridoxine treatment of late-detected B6-responsive patients retarded the rate of occurrence of initial thromboembolic events. Following 586 surgical procedures, 25 postoperative thromboembolic complications occurred, six of which were fatal. Reproductive histories were reported predominantly for B6-responsive patients. Living offspring of either men or women patients had few abnormalities. The evidence is inconclusive whether untreated maternal cystathionine beta-synthase deficiency leads to excessive fetal loss. Only 13% of patients detected in screening programs of newborns and classified as to B6-responsiveness were B6-responsive, compared to 47% among late-detected patients. Current screening programs that identify neonatal hypermethioninemia may be preferentially failing to detect B6-responsive patients.
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PMID:The natural history of homocystinuria due to cystathionine beta-synthase deficiency. 387 65

Pyridoxine-dependent seizures occur as a result of an increased requirement of the vitamin within the central nervous system. With early intervention, these seizures can be completely controlled by continued administration of pharmacologic doses of the vitamin. Without prompt treatment, continued seizures and irreversible neurologic damage result. This disorder should be considered in any infant with seizures that are hard to control.
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PMID:Pyridoxine-dependent seizures. 682 89


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