Pathophysiology and Definitions of Seizures and Status Epilepticus

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Pathophysiology

Provoked seizures can occur in anyone and do not constitute epilepsy. The terms secondary seizures or acute symptomatic seizures are sometimes used to describe seizures from a variety of identifiable causes, eg, electrolyte abnormalities, toxins, and tumors. Epilepsy is present when seizures occur without a provoking factor because of an enduring tendency to seizures. Altered brain physiology is always present in patients with epilepsy, yet seizures occur essentially at random for entirely

Seizure and epilepsy definitions

The vocabulary of seizures and epilepsy is sometimes confusing with inexact labels, jargon, and arcane terminology that hinders communication.6, 7 At times definitions differ between not only patients and clinicians but also between reference works. The correct classification of seizures is important because the diagnostic strategy and treatment of seizures may vary with the type of seizure or epileptic syndrome.

Although clinicians know what constitutes a seizure, seizure definitions are often

Seizure etiology and classification

Another component in the classification of seizures is their etiology. Provoked seizures, sometimes referred to as acute symptomatic seizures, are seizures from an identifiable cause such as electrolyte abnormalities, head injury, toxins, or infection. This is an important concept, because treatment of symptomatic seizures must take into consideration treatment not only of the seizure, but also of the underlying cause. As mentioned previously, epilepsy is defined by recurrent spontaneous

Status epilepticus definitions

SE has been generally defined as enduring seizure activity that is not likely to stop spontaneously. The traditional SE definition is 30 minutes of continuous seizure activity or 2 or more seizures without full recovery of consciousness between the seizures. There are as many types of SE as there are types of seizures. The distinction between convulsive and nonconvulsive SE depends on clinical observation and on a clear understanding of several SE types.5, 14

Generalized convulsive SE (GCSE) is

Epileptic syndromes

Epileptic syndromes are used to condense clinical seizure information into meaningful groupings. If seizures are symptoms, and epilepsy is a disease, then there are some subsets of seizure disorders that may be made following correlation of clinical information and neurodiagnostic testing. These subsets are epilepsy syndromes and the correct assignment to a syndrome may help to convey clinical information. Unlike a seizure, a syndrome cannot be observed because it requires knowledge of data

Why Do Some Seizures Fail to Stop?

Some endogenous seizure-terminating process must exist or every seizure would persist. These processes are really unknown, but a variety of mechanisms have been postulated for seizure termination. The appearance of an abnormally prolonged seizure may be a manifestation of excessive excitation, a failure of inhibition, or a combination of the two processes. In the case of excitatory toxins, eg, cholinergic drug overdose, substances act directly on receptors to overexcite glutamate receptors.

Future directions

Continued progress with basic research may affect treatment of seizures and SE in the emergency department. Current thoughts of pathophysiology of GCSE suggest that aggressive prompt termination of GCSE may positively affect patient outcomes. New formulations of existing drugs, such as intranasal administration of benzodiazepines, and new parenteral drugs to abort seizures will be available in the near future and will change treatment strategies. New neuroprotective drugs that prevent neuronal

Summary

Seizures result from recurrent excitatory connections in the cerebral cortex and a loss of synchronization between aggregates of neurons. Seizures produce a number of physiologic consequences, and if seizures are prolonged, homeostatic mechanisms deteriorate. Animal models suggest that even if systemic factors such as acidosis and hypoxia are controlled, prolonged SE results in neuronal damage from neurotoxic amino acids and calcium influx. It appears that SE alone may result in cognitive

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  • Cited by (34)

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      In the simplest terms, seizure is the dysregulated propagation of electrical activity from hyperexcitable cortical neurons, which can also be conceptualized as excessive synchrony within a cluster of neurons. By studying the voltage required for electroconvulsive therapy, we know that all humans have a seizure threshold that varies among individuals,19 modified by inherited and acquired factors, commonly lowered by genetic influences, electrolyte abnormalities, infections, toxins, or structural lesions, and raised by ASDs, ketosis, and hypothermia.20,21 Importantly, even correctable causes of seizure can lead to SE or epilepsy if severe enough.22

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      Patients presenting with convulsive SE are easily recognized because of their prominent motor manifestations. Cortical electric discharges may manifest as sustained muscle contractions (tonic activity), rhythmic jerking of muscles (clonic activity), or a combination of these movements (tonic-clonic activity) (Huff and Fountain, 2011). Catecholamine release during prolonged convulsive seizure activity leads to pupillary dilatation, incontinence, tachycardia, hyperpyrexia, hyperglycemia, and a cascade of other systemic complications (Glaser, 1983; Baumgartner et al., 2001).

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      The mechanism of each seizure type is distinct, and this may have important implications for SEGP and TASE biology. For example, ictal EEG activity stops abruptly, and without post-ictal sequelae, in absence seizures: yet neither may be the case in generalised or complex partial seizures [1]. Moreover, in another example, the mechanism which prevents the spatial cortical propagation of epilepsia partialis continuans is likely to be different from that which terminates typical seizure activity (and which subsequently initiates the onset of the refractory period).

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