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This noteworthy paper of Kloster and Engelskohn in this issue (pp 439–44) supports an important hypothesis in relation to the cause of sudden unexpected death in epilepsy (SUDEP)—namely, that SUDEP is largely seizure related. Their finding of a preponderance of the prone position of the body is also of interest and may have a bearing on proposed mechanisms as well as the potential for the prevention of these deaths.
But firstly, certain methodological aspects should be noted. The control group of non-SUDEP deceased epilepsy cases is not appropriate for all variables studied. Epilepsy diagnosis is an example. The non-SUDEP group would include cases dying of the underlying condition causing or associated with the epilepsy and is expected to include more symptomatic cases. The authors do not define the terms used with regard to epilepsy diagnosis, in particular idiopathic epilepsy,1which has had a different meaning in epidemiological studies to that in the International League against Epilepsy (ILAE) classification. Some caution is required in interpreting the interesting cardiac and neuropathological findings unavoidably performed in different units without a predefined protocol and presumably differing levels of expertise. The severity of epilepsy, from the point of view of safety and mortality, cannot be equated with seizure frequency, as seizure type and severity are at least equally relevant if not more so. Importantly, the authors, having selected a relatively strict definition of SUDEP, apply it rather liberally. Readers may take issue with the inclusion of a few cases (such as with severe hyponatraemia and chest pain requiring ECG before death). My intention is not to downplay other mechanisms or associated conditions important in individual cases and, more generally, likely to be particularly relevant among elderly patients. The intention is to emphasise that the category of SUDEP, a significant one in proportional mortality studies, is intended to include only those where the history and postmortem findings do not suggest alternative pathology.
Nevertheless, this is a very useful study with valid conclusions. The findings support previous evidence suggesting that most of these deaths are seizure related. This view is widely subscribed to by United Kingdom based workers, but has met with resistance elsewhere, particularly across the Atlantic. Although keeping an open mind is at times admirable, in this situation, an attachment to the mystery of the unexplained, has only served to constrain efforts at prevention. Whereas seizures may not be the only cause of SUDEP, they are the cause of most cases.
Another particularly interesting discussion in this report relates to the finding of a more commonly found prone position among SUDEP cases than would be expected by chance. Although not subscribing to the simplistic notion of attributing nocturnal epilepsy deaths to suffocation face down alone, if the various factors leading to hypoxia during generalised convulsive seizures are considered, position is yet another factor that could contribute to a fatal outcome. This is in addition to central ictal and postictal hypoventilation, pulmonary oedema, excessive secretions, and postictal coma. Central and obstructive apnoea (whether intrinsic or extrinsic) are potentially amenable to intervention by stimulating and positioning the patient. A simple answer will not prevent all cases, but aggressive treatment of the epilepsy, particularly prevention of generalised convulsions, and the presence of a person capable of giving assistance in the event of a seizure are likely to prevent some of these deaths. The first has implications to service provision, optimal medical treatment of the epilepsy, and patient education, the second to supervision with its attendant limitations. The first translates to better health care, the second to informed choice.2
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