acidosis/crise épileptique

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Lactic acidosis and hypoglycemia: experimental evidence to show lactate prevents insulin induced seizures in rats.

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A 52-year-old man with lactic acidosis and severe hypoglycemia was fully conscious and alert with a blood sugar of 8 mgs%. We believe normal level of consciousness was maintained due to the presence of hyperlactatemia. We show experimental evidence to suggest that lactate prevents the development of

The Denver Seizure Score: anion gap metabolic acidosis predicts generalized seizure.

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OBJECTIVE Anion gap (AG) and serum bicarbonate concentration (BICARB) may help confirm a diagnosis of seizure in an unwitnessed collapse; however, little data exist to support this practice. Our objective was to assess the association between AG metabolic acidosis and generalized seizure and to

Lactic acidosis, hyperglycaemia and convulsions following nalidixic acid overdosage.

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A woman survived ingestion of 32 g nalidixic acid despite developing lactic acidosis, hyperglycaemia, convulsions and abnormal behaviour. The maximum recorded plasma concentration of nalidixic acid was 185 mg/l and the elimination half-life was 3.2 h. Carboxy-nalidixic acid was demonstrated in the

Expanding the Phenotype: Neurodevelopmental Disorder, Mitochondrial, With Abnormal Movements and Lactic Acidosis, With or Without Seizures (NEMMLAS) due to WARS2 Biallelic Variants, Encoding Mitochondrial Tryptophanyl-tRNA Synthase.

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WARS2 encodes a tryptophanyl tRNA synthetase, which is involved in mitochondrial protein synthesis. Biallelic mutations in WARS2 are rare and have been associated with a spectrum of clinical presentations, including neurodevelopmental disorder with abnormal movements, lactic acidosis

Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia.

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To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (+/- S.E.M.) venous lactate concentration was 12.7 +/- 1.0 meq per liter, the mean carbon dioxide

Benzonatate toxicity in a teenager resulting in coma, seizures, and severe metabolic acidosis.

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We report a benzonatate overdose in a teenager resulting in life-threatening toxicity to increase awareness of this overdose, and discuss recent pediatric warnings and labeling information provided by the US Food and Drug Administration (FDA). After an overdose of benzonatate, a 13-yr-old female

Seizure-induced damage to substantia nigra and globus pallidus is accompanied by pronounced intra- and extracellular acidosis.

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Status epilepticus of greater than 30-min duration in rats gives rise to a conspicuous lesion in the substantia nigra pars reticulata (SNPR) and globus pallidus (GP). The objective of the present study was to explore whether the lesion, which encompasses necrosis of both neurons and glial cells, is

[Pyridoxine for severe metabolic acidosis and seizures due to isoniazid overdose].

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A 15-year-old girl took 3 g of isoniazid (15 tablets) in a suicide attempt and was brought unconscious to the emergency room. She was in respiratory failure, with seizures that could not be stopped with diazepam. Severe metabolic acidosis with normal serum lactate developed (pH 6.85), but did not

Effect of keto-acidosis on seizure occurrence in diabetic patients.

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It has been observed anecdotally that diabetics are usually non-ketotic at the time of their seizure presentation. In order to establish some validity on this observation, we reviewed the medical records of patients with diagnoses of diabetes and seizure. Study subjects were diabetics presenting

Metabolic acidosis and generalized seizures secondary to citalopram overdose: a case report.

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Selective serotonin re-uptake inhibitors (SSRIs) are widely used in the community for treating many forms of mental illnesses. Citalopram, a newer generation SSRI, is commonly prescribed, but despite its low toxicity profile has a potential to cause seizures and dysarrythmias in overdose. Data on

Hyperchloremic acidosis during grand mal seizure lactic acidosis.

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OBJECTIVE To evaluate the prevalence and the mechanism of hyperchloremic acidosis component (HClA) during lactic acidosis secondary to grand mal seizures. METHODS Retrospective study. METHODS Medical intensive care unit in a university hospital. METHODS 35 patients admitted for grand mal seizures

Convulsions as the etiology of lactic acidosis in acute diazinon toxicity in rats.

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Diazinon, in acute doses (40 mg/kg, i.p.) in rats produced tremors and convulsions with lactic acidosis which was accompanied by depletion of glycogen and activation of glycogen phosphorylase activity in triceps and diaphragm muscles, 2 h after its administration. Prevention of convulsions with

Aplasia of the retinal vessels combined with optic nerve hypoplasia, neonatal epileptic seizures, and lactic acidosis due to mitochondrial complex I deficiency.

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A newborn male with mitochondrial complex I deficiency suffered from neonatal epileptic seizures, which later developed into infantile spasms. The infant was blind due to aplasia of the retinal vessels and hypoplasia of the optic nerve. There was congenital lactic acidosis, which persisted in later

Lactic acidosis following convulsions.

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Lactic acidosis is a common cause of metabolic acidosis and is usually connected with high mortality. However, changes in the level of lactate and pH can also be seen after generalized epileptic attacks, due to local muscle hypoxia during the seizures. Although these changes can be quite marked, the

Acute cocaine poisoning. Importance of treating seizures and acidosis.

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Cocaine poisoning has increased recently, and survival is rare because of its sudden onset and rapidly fatal course. A patient is described in whom cocaine poisoning developed. This condition was manifest by the findings of acute agitation, diaphoresis, and tachycardia, and was complicated by grand

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