The metabolic basis for the genesis of seizures: the role of the potassium-ammonia axis.
A conceptual approach to the understanding of the pathogenesis of idiopathic seizures is presented. Hypokalemia and/or alkalosis promotes the elaboration of an alkaline urine, which increases the renal return of ammonia and exposes the brain to chronically higher concentrations of ammonia. In the brain, ammonia is preferentially detoxified to glutamine and therefore depletes the available glutamic acid, which is also a precursor of GABA, the major mediator of central inhibition. Mild chronic elevations of ammonia may also result in long-term nutritional alterations of amino-acid precursors of other brain neurotransmitters. A linkage thus exists for the metabolic basis of seizures: the role of the potassium-ammonia axis may be important in the selective depletion of GABA, the major mediator of central inhibition.
D000471:Alkalosis / Q000150:complications / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism*; D001806:Blood Urea Nitrogen; D001921:Brain / Q000378:metabolism; D006801:Humans; D007008:Hypokalemia / Q000150:complications / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D012640:Seizures / Q000209:etiology* / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005680:gamma-Aminobutyric Acid; D000641:Ammonia; D011188:Potassium