Probably the most common cause of sudden death due to an intracranial lesion is epilepsy. Epileptic deaths constitute approximately 3-4% of all natural deaths coming to autopsy in a medical examiner's office. The estimated incidence of sudden unexplained death among epileptics is 2-17%.43 Very few of these individuals die in status epilepticus.
Typically, individuals dying suddenly and unexpectedly of epilepsy are young and show either subtherapeutic levels or absence of epileptic medications on toxicological analysis. Usually, but not always, such deaths are unwitnessed, with the victims often found dead in bed in the morning. If a death is witnessed, there may be no seizures or only one seizure with collapse.43,44 In individuals found dead in bed, there is usually no evidence of seizures, either in the environment (sheets and blankets undisturbed, no loss of urine) or on the body (bite marks of the tongue are absent in 75% of the cases). That individuals are commonly found dead in bed is probably because sleep predisposes to epileptic attacks and, in fact, is used as a provocative diagnostic technique. Sleep has also been found to affect cardiac vulnerability to arrhythmia in that sudden death secondary to arrhythmias often occurs in the morning, immediately before or at the time of awakening.
Diagnosis of death due to epilepsy is, for the most part, a diagnosis of exclusion. At autopsy, there are no pathonomonic findings. In approximately 25% of the cases, a bite mark of the tongue might indicate a seizure, but seizures as a terminal event can occur in other entities. To make a diagnosis of death due to epilepsy, the examiner must have a clinical diagnosis of epilepsy in the past or a well-documented history of seizures, a scene not inconsistent with such a finding, and a complete autopsy, including removal of the tongue, with no findings, grossly, microscopically, or toxicologically, to explain death.
Most epileptic deaths are natural. If, however, the epilepsy was due to trauma, documented, and uncontestable, then the manner would more properly be classified as accident. Some epileptics die of accidental means precipitated by an epileptic attack; for example, an individual may have an epileptic attack while in water and drown (Figure 3.8). No matter what the manner of death, it is very common for epileptics dying suddenly to have
subtherapeutic levels or absence of anticonvulsive medication. Careful examination of the brain in most instances does not reveal a lesion that could have caused the epilepsy. The actual incidence of finding such lesions varies considerably, depending on the authority, but, to a degree, is influenced by the type of population being handled. The only thing that one can say is that, in the vast majority of the cases, no lesion to explain the seizure disorder will be found at autopsy. If lesions are found, they may be foci of sclerosis, arteriovenous malformations, or adhesions between cortex and dura. Again, it must be realized that the finding of such lesions is uncommon. One finding, sclerosis of Ammon's horn, is most probably a secondary phenomenon related to cerebral edema during epileptic attacks, with compression of the vessels supplying blood to this region (branches of the posterior cerebral artery) against the edge of the tentorium by a herniating hippocampal gyrus.
Because the diagnosis of death due to epilepsy is on an exclusionary basis, the actual incidence of such deaths is probably underestimated. Thus, if an individual dying of a seizure disorder happens to have significant coronary atherosclerosis, the cause of death would probably be ascribed to the coronary artery disease rather than the epilepsy.
The mechanism of death in epilepsy is most probably due to a cardiac arrhythmia precipitated by an autonomic discharge.43-45 Alterations in cardiac activity and respiration have been documented in individuals dying during an epileptic attack. It is not known, however, why a seizure, apparently no different from those that the patient had previously had in the past, should prove fatal at this particular time. The autonomic nervous system, especially the sympathetic portion, is important in the regulation of cardiac and vascular physiology. Cortical loci exert a more specific autonomic control of cardiovascular changes than do the lower levels of the brain. Cortical stimulation can produce changes in heart rate, blood pressure, and cardiac extrasystoles. Stimulation of portions of the hypothalamus can also produce cardiovascular changes, for example, cardiac arrhythmias, because the hypothalamus exerts considerable control over the autonomic function. Production of extrasystoles by stimulation of the hypothalamus is due to the stimulation of the sympathetic pathways to the heart or stimulation of pathways controlling secretion of epinephrine.
The sympathetic nervous system can lower the vulnerable threshold of even electrically stable myocardium, thereby facilitating the onset of ventricular fibrillation, if the activity of the sympathetic nervous system is increased by neural or neurohumoral action. Increased sympathetic nervous activity can predispose to ventricular fibrillation by the direct action of neuroepi-nephrine on neuroeffector sites in the myocardium. The aforementioned findings indicate that sudden death during epileptic seizures is most likely due to a lethal cardiac arrhythmia induced or propagated by the disorganized neural discharges of a seizure.
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