Atonic phenomena in focal seizures: Nomenclature, clinical findings and pathophysiological concepts
Introduction from Dr Markus Reuber, editor-in-chief of Seizure
The contrast between “negative” neurological symptoms (such as weakness, reduced sensation, vision or hearing) and “positive” neurological symptoms (including excessive movement or hallucinations) is often used to help medical students distinguish between clinical presentations likely to be caused by cerebral ischaemia and those which could be caused by epileptic discharges. Even health professionals who are very experienced in the management of epileptic seizure disorders often pay more attention to the “positive” manifestations of abnormal electrical activity in the brain than to “negative” symptoms. Such negative symptoms are not limited to the postictal effects or interictal neuropsychological associations of epilepsy but also include atonic seizures.
Whilst not the most dramatic seizure type, atonic seizures causing sudden collapse without warning (and significant injury) can be the most disabling seizure type in symptomatic epilepsy syndromes. Focal atonic seizures are much less well understood (and even more often overlooked) although the concept of “epileptic interference” causing focal ictal deficits of neurological function was described over fifty years ago by Penfield and Jasper (1).
In this issue of Seizure Kovac and Diehl focus on this neglected epileptic seizure type and provide a comprehensive review of the nomenclature and clinical phenomenology of as well as the pathophysiological concepts underpinning atonic seizures (2). This Editor’s Choice review should help clinicians identify and understand atonic seizures and should inspire researchers to focus more of their attention on an important epileptological phenomenon.
(1) Penfield, Jasper. Epilepsy and the functional anatomy of human brain. Boston: Little, Brown; 1954.
(2) Kovac S, Diehl B. Atonic phenomena in focal seizures: nomenclature, clinical findings and pathophysiological concepts. Seizure 2012; 21: 561-567.