Seizure etiology

Many aspects of KD therapy are based more on lore than on scientific fact. For example, the diet duration, formulation, need for initial fast and fluid restriction, and optimal patient selection (age, seizure type, seizure etiology) have not been subject to scientific scrutiny. Many of these factors can be addressed using animal models, but surprisingly few experimental studies on the KD have been carried out (Stafstrom,... 

Regardless of the underlying etiology, all seizures involve a sudden electrical disturbance of the cerebral cortex. A population of neurons fires rapidly and repetitively for seconds to minutes. Cortical electrical discharges become excessively rapid, rhythmic, and synchronous. This phenomenon is presumably related to an excess of excitatory neurotransmitter action, a failure of inhibitory neurotransmitter action, or a combination of the two. In the individual patient, however, it is usually impossible to identify which neurochemical factors are responsible. 

Classification of epilepsies and epilepsy syndromes is helpful in determining appropriate pharmacotherapy. This classification scheme is based on the type of seizures a patient has and an attempt to identify the etiology of the epilepsy or epilepsy syndrome. 

Idiopathic epilepsies These syndromes are thought to be due to genetic alterations, but the underlying etiology is not identified. Neurologic functions are completely normal apart from the occurrence of seizures. 

It is important to evaluate for possible etiologies of status epilepticus and treat any underlying causes in order to optimize seizure control. 

Apart from this epileptic seizure classification, an additional classification specifies epileptic syndromes, which refer to a cluster of symptoms frequently occurring together and include seizure type, etiology, age of onset and other factors [2]. The epileptic syndromes have been categorized into partial versus generalized epilepsies. The partial... 

Epilepsy is a chronic brain disease of diverse etiology it is characterized by recurrent paroxysmal episodes of uncontrolled excitation of brain neurons. Involving larger or smaller parts of the brain, the electrical discharge is evident in the electroencephalogram (EEG) as synchronized rhythmic activity and manifests itself in motor, sensory, psychic, and vegetative (visceral) phenomena Because both the affected brain region and the cause of abnormal excitability may differ, epileptic seizures can take many forms. Erom a pharmaco-therapeutic viewpoint, these may be classified as ... 

Seizure disorders Because TCAs lower the seizure threshold, use with caution in patients with a history of seizures or other predisposing factors (eg, brain damage of varying etiology, alcoholism, concomitant drugs known to lower the seizure threshold). However, seizures have occurred both in patients with and without a history of seizure disorders. Seizure was identified as the most significant risk of clomipramine use. 

Interest in the possibility of human Mn deficiency increased in 1979 with the report of Papavasiliou and co-workers (6) that some epileptics were characterized by lower than normal blood concentrations of Mn. Based on the knowledge that Mn deficiency in experimental animals could result in increased susceptibility to electroshock and drug-induced seizures (7), these authors suggested that Mn deficiency could be an etiological factor for epilepsy in some individuals. 

Despite the recent reports of neurotoxicity of star fruit in uremic patients, the first one on star fruit toxicity was described by Muir and Lam [27] in 1980. They related toxic effects of star fruit extract after its intraperitoneal administration in mice. This extract induced seizures and death. In 1993, Martin LC et al. reported the outcome of intractable hiccups in uremic patients associated to star fruit consume [3]. However, the first report of neurotoxicity in human beings was performed by Moyses-Neto M et al (4). Subsequently, many similar case reports were described, but only in 2002 an etiological agent was proposed oxalic acid would be the star fruit neurotoxin [28]. 

Because severe exposure to both cyanide and nerve agent produces seizures in patients, a table to help clinically differentiate the two etiologies is provided (Table 24.3). Additionally, children s doses of antidotes are shown in Table 24.4. 

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