Epilepsy pathology

Because alcohol intoxication may be simulated by many pathologic conditions, including diabetic acidosis, the postconvulsive depression of epilepsy, uremia, head injuries, and poisonings by any other central nervous depressant and some stimulants (280), a diagnosis of acute alcoholism should not be made casually chemical testing of blood, urine, or expired air is always desirable. 

These approaches will be considered in respect of the different NTs although most interest has centred on the amino acids not only because of their possible involvement in the pathology, as already emphasised, but because increased neuronal activity in epilepsy must reflect, even if it is not initiated by, augmented glutamate and/or reduced GABA function. 

Ionotropic glutamate receptors mediate fast excitatory neurotransmission in practically all areas of the central nervous system (CNS). They are also critical for both the induction and expression of synaptic plasticity, and have been implicated in diverse pathological conditions, such as epilepsy, ischemic brain damage, anxiety, and addiction. There are three subtypes of ionotropic glutamate receptors that are named after their high-affinity agonists as a-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), N-1nethyl-D-aspartate (NMDA), and kainate (KA) receptors (1). 

Dinretics are widely used in medicine for very diverse pathologies, primarily for relieving edema, treating hypertension, cardiac insufficiency, hypercalcinuria, glaucoma, and a few forms of epilepsy, liver cirrhosis, and nephrosis. 

As to the phenomenology, normal dreams and the pathological dreamy states of epilepsy share the following formal features ... 

Pathological activation of glutamate receptors is a common feature and one of the primary causes of neuronal death in acute neuronal injury (such as trauma, epilepsy, and brain ischemia) and chronic neurodegenerative diseases (such as Parkinson s disease, Alzheimer diseases, amyotrophic lateral sclerosis, and AIDS dementia) (Choi, 1988 Doble, 1999 Lipton and Rosemberg, 1994). In particular, elevation of extracellular glutamate level is a key factor in the development of neuronal damage under ischemic conditions. 

Evidence for the idea that Mn deficiency may be a cause, rather than an effect, of some human pathologies has recently been provided by Carl et al. (13) who reported that the low blood Mn concentrations observed in epileptics tend to occur in the subgroup of patients characterized by epilepsy of unknown origin, rather than in the subgroup in which the epilepsy was known to be the result of head injury. This observation suggests that the low Mn concentrations are not a function of either seizure activity or medication, as these two parameters were similar in the two patient subgroups reported on. Thus, it is reasonable to suggest that Mn deficiency may be a causative factor in some epileptics. 

Jackson JH (1873) On the anatomical, physiological and pathological investigation of epilepsies. 

Fujita, T, Tanaka, T, Yonemasu, Y, Cendes, E, Cashman, N.R., and Andermann, F. 1996. Electroclinical and pathological studies after parenteral administration of domoic acid in freely moving nonanesthetized rats an animal model of excito-toxicity. J Epilepsy 9, 87-93. 

Neocortical dendritic pathology in human partial epilepsy a quantitative Golgi study. Epilepsia 35 728-36. 

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