sodium-bromide and Epilepsy

To evaluate clinical signs, risk factors, and outcomes associated with bromide toxicosis (bromism) in dogs with idiopathic epilepsy treated with potassium or sodium bromide.. Retrospective case-control study.. 83 clinically ill epileptic dogs with (cases; n = 31) and without (controls; 52) bromism.. Medical records were reviewed for information regarding signalment, epilepsy history, treatment, diet, clinicopathologic test results, concurrent diseases, clinical signs, and outcome. Case and control dogs were matched by the veterinary hospitals from which they were referred and by month of admission. A presumptive diagnosis of bromism was made in case dogs when treatment for primary clinical signs was limited to induction of diuresis or reduction in the dose of bromide administered, and this diagnosis was supported by serum bromide concentrations. Potential risk factors for bromism were identified via univariate and subsequent multivariate logistic regression analyses.. Common clinical signs of bromism included alterations in consciousness, ataxia, and upper and lower motor neuron tetraparesis and paraparesis. The multivariate analysis identified bromide dose at admission to the hospital as the only factor significantly associated with bromism. In all dogs with bromism, treatment via dose reduction or facilitated renal excretion of bromide resulted in rapid clinical improvement, although breakthrough seizures happened during treatment in 8 of 31 (26%) dogs.. Bromism is a clinically heterogeneous, dose-dependent neurotoxicosis that is largely reversible with treatment. Regular serial monitoring of serum bromide concentrations is recommended to optimize anticonvulsant treatment in dogs with idiopathic epilepsy.

Topics: Animals; Anticonvulsants; Bromides; Dog Diseases; Dogs; Dose-Response Relationship, Drug; Epilepsy; Potassium Compounds; Retrospective Studies; Risk Factors; Sodium Compounds

Topics: Bromides; Epilepsy; History, 19th Century; History, 20th Century; Hospitals, Special; Humans; Male; Sodium Compounds

We investigated the evolution of epilepsy, seizure types, and effective drugs in Wolf-Hirschhorn syndrome, which is a malformation syndrome often with refractory seizures and status epilepticus.. We reviewed 11 cases of Wolf-Hirschhorn syndrome (age range, 2-25 years; SD, 7.2 years) and who were treated in Osaka University or Osaka Medical Center of Research Institute for Maternal and Child Health.. In all patients, febrile or afebrile convulsions had developed. Epileptic seizures included alternative hemiconvulsions, generalized tonic-clonic seizures, focal clonic seizures, tonic seizures, and epileptic spasms. Seizures were often induced by a high fever or a hot bath. Status epilepticus occurred in all patients, including one patient who died at the first status epilepticus. In some cases, intratracheal intubation was needed because of respiratory insufficiency. The effective antiepileptic drugs for long-term use were sodium bromide (four of four), followed by clorazepate (CLP; one of two), and nitrazepam (NZP; two of four). Sodium bromide was particularly effective for preventing status epilepticus. The mean age of last status epilepticus in patients receiving sodium bromide (1 year 8 months) was significantly younger than that in those not treated with sodium bromide (3 year 4 months).. We identified that, in most patients of Wolf-Hirschhorn syndrome, the frequency of both seizures and status epilepticus decreased gradually after age 5 years. However, during infancy, status epilepticus sometimes resulted in permanent disability or even death. We propose that sodium bromide should be used as the initial treatment for the prevention of the development of status epilepticus associated with Wolf-Hirschhorn syndrome.

Topics: Abnormalities, Multiple; Adolescent; Bromides; Child; Child, Preschool; Chromosome Deletion; Chromosomes, Human, Pair 4; Electroencephalography; Epilepsy; Facies; Female; Humans; Japan; Male; Sodium Compounds; Status Epilepticus; Translocation, Genetic

Results regarding the anticonvulsant potency of bromide have been questioned, and the mechanisms of its action are unclear. Using combined rat hippocampus-entorhinal cortex slices we analyzed the effects of NaBr on four types of epileptiform discharges in two different models of epilepsy, the low-Ca2+ and the low-Mg2+ model. NaBr concentration-dependently reduced the frequency and finally blocked the low Ca2+-induced discharges. Low Mg2+-induced short recurrent discharges were also reduced in a concentration-dependent manner. In the entorhinal cortex the frequency of seizure-like events was reduced by 3 and 5 mM and the discharges were blocked by 7 mM NaBr. Also, the late recurrent discharges in the entorhinal cortex which do not respond to most clinically employed anticonvulsants were reduced by concentrations of 10 and 15 mM and completely blocked by 30 mM NaBr. Using pH-sensitive microelectrodes different effects of NaBr were seen than those of acetazolamide on extracellular pH under control conditions and after stimulation. Acetazolamide at 1 mM caused a reversible acidification of delta pH: 0.2+/-0.14 at rest whereas no change on extracellular pH was seen with 5 mM NaBr. Acetazolamide increased the transient alkalosis induced by repetitive stimulation of the stratum radiatum in area CA1 and reduced the subsequent acidosis. NaBr also increased the alkalosis but had no effect on the subsequent acidosis. A significant increase in paired-pulse inhibition was seen in a paired-pulse stimulation protocol used to monitor the efficacy of GABAergic inhibition at concentrations of 5 mM NaBr. This finding was confirmed in whole-cell patch clamp recordings from cultured hippocampal neurons showing an increase in inhibitory postsynaptic current amplitude. In summary, our results suggest a broad-spectrum anticonvulsant activity which is likely to be caused by its effects on membrane excitability, by an increase in GABAergic inhibition and is less likely caused by its effects on extracellular pH.

Topics: Acetazolamide; Algorithms; Animals; Anticonvulsants; Bromides; Calcium; Carbonic Anhydrase Inhibitors; Electric Stimulation; Electrophysiology; Epilepsy; Excitatory Postsynaptic Potentials; Extracellular Space; Female; gamma-Aminobutyric Acid; Hydrogen-Ion Concentration; In Vitro Techniques; Magnesium; Male; Membrane Potentials; Microelectrodes; Patch-Clamp Techniques; Rats; Rats, Wistar; Sodium Compounds; Time Factors