Epileptic seizures stroke

Excitotoxicity is the over-activity of the glutamatergic system responsible for the large number of dead neurons observed after ischemia (stroke) or epileptic seizures. This neuronal death is due to an overexcitation of the neurons and the massive Ca2+ entry... 

As a result of the conceptual and political split between psychiatry and neurology caused first by the mind-body problem and deeply aggravated by Sigmund Freud s inadvertent dualism, it took dream science an inordinately long time to notice that cerebrovascular accidents (better known as strokes) and epileptic seizures (better known as fits) could cause decreases and increases in the formal features of dreams, respectively. 

Partial or generalized epileptic seizures occur for the first time in about 2% of those with acute strokes at around the time of onset, rising to approximately 10% at five years, more with large cortical infarcts or intracranial hemorrhage (Ch. 9) (Ferro and Pinto 2004). Seizures are more common with large strokes, especially if hemorrhagic, and with cortical as opposed to lacunar strokes. Cerebrovascular disease is the most common cause of epilepsy in the elderly, and late-onset epilepsy is a predictor of subsequent stroke (Cleary et al. 2004). Seizures may cause neurological deterioration or be mistaken for recurrent stroke. Intractable recurrent seizures are distinctly unusual. 

Many clinical responses are described in terms of events. An event might be death, a stroke, a myocardial infarction, an epileptic seizure, admission to hospital, need for supplementary treatment, and so on. The occurrence of an event or the time to an event can be modeled using a survival function. The word survival relates most obviously to a death event, but the term is commonly used in a much broader context to describe the probability that the event under study will not occur. 

Because the molecules are delivered rapidly into the bloodstream, there is a much more rapid onset of action than with any other non-i.v. delivery method. This can be particularly useful in indications where speed is important such as pain control, relief of muscle spasm, panic/anxiety attacks, hypertensive crises, cardiac arrythmias, anaphylaxis (severe allergies to food and insect bites), nausea, cardiovascular conditions (arrhythmia, strokes), Parkinson s lock-up, and epileptic seizures. 

It is not known what causes epileptic seizures, but suggestions include increased excitatory nerve transmission, decreased inhibitory transmission or some abnormality of the nerve cells themselves. Such abnormalities may be the result of head trauma, stroke or tumours, but in most cases, the cause is unknown. 

Louis Sokoloff and his colleagues at the NIH identified increased FDG accumulation at the site of origin of focal epileptic seizures (Sokoloff, 1979) when no structural abnormalities could be seen with computed tomography (CT). Regions of decreased glucose utilization in the brain were found in patients with stroke, senile dementia of the Alzheimer type (SDAT), and Huntington s disease (HD). These were often foimd before structural changes could be seen. 

Suggested Alternatives for Differential Diagnosis Meningitis, basilar artery blood clots (thrombosis), cardioembolic stroke, cavernous sinus syndromes, cerebral venous blood clots (thrombosis), confusional states and acute memory disorders, epileptic and epileptiform encephalopathies, febrile seizures, haemophilus meningitis, intracranial hemorrhage, leptomeningeal carcinomatosis, subdural pus (empyema), or bruise (hematoma). 

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