Читать книгу Emergency Medical Services - Группа авторов - Страница 383

The concept of a seizure threshold suggests that everyone has the capacity to experience seizures at some level of individual physiological stress. The precipitating events may be electrolyte abnormalities, medications, medication withdrawal, toxins, hypoxia, CNS infections, systemic infections, trauma, or even sleep deprivation. A fundamental distinction in management is to determine whether a seizure results from some identifiable cause or if it is unprovoked. When seizures are secondary to some other condition, they are symptomatic seizures or provoked seizures. Unprovoked seizures occur without an identifiable cause. Again, epilepsy is defined by episodes of unprovoked seizures.

At a cellular level, seizures are thought to originate in the cerebral cortex or thalamus. Lesions of the brainstem, deep white matter, and cerebellum are not epileptogenic. Seizures result from excitation of susceptible groups of cerebral neurons, with progressively larger groups of neurons developing synchronous discharges. Clinical signs and symptoms follow when a critical mass of neurons is reached [4]. At a biochemical level, there is a disturbance in the balance of cellular excitation and inhibition. Glutamate is the most common excitatory neurotransmitter and acts at the n‐methyl‐D‐asparate (NMDA) receptor. Current theory is that failure of inhibition mediated by the neurotransmitter gamma‐aminobutyric acid (GABA) system leads to prolongation of many seizures. The neurotransmitter receptor sites are thought to be the sites of action of the antiepileptic drugs. With frequent or persistent seizure activity, physiological changes of hypoxia, acidosis, hyperthermia, hypotension, and reduced cerebral perfusion may occur. At one time, these were thought to be the cause of neuronal injury. However, many different avenues of investigation have suggested that injury follows prolonged excessive neuronal discharges even if systemic pathophysiological factors are controlled [4]. Some experimental evidence suggests that neurotransmitter receptors may change in sensitivity or quantity with prolonged seizures; the potential effectiveness of medications might change as seizure duration persists [5, 6].