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VIEWS & REVIEWS: P. Gallmetzer, F. Leutmezer, W. Serles, E. Assem-Hilger, J. Spatt, and C. Baumgartner Postictal paresis in focal epilepsies—Incidence, duration, and causes: A video-EEG monitoring study Neurology 2004; 62: 2160-2164 [Abstract] [Full text] [PDF]

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Postictal paresis in focal epilepsies—Incidence, duration, and causes: A video-EEG monitoring study

Patrick C.A.J. Vroomen   (3 August 2004)

Reply to Vroomen

Paolo Gallmetzer, Christoph Baumgartner   (3 August 2004)

Postictal paresis in focal epilepsies—Incidence, duration, and causes: A video-EEG monitoring study 3 August 2004
Patrick C.A.J. Vroomen, M.D., Ph.D., Neurologist University Hospital Groningen, P.O. Box 30001, 9700 RB Groningen Send Correspondence to journal: Re: Postictal paresis in focal epilepsies—Incidence, duration, and causes: A video-EEG monitoring study c.a.j.vroomen{at}neuro.azg.nl Patrick C.A.J. Vroomen	Gallmetzer et al provided us with a thorough study of postictal paresis (PP) in patients with presurgical epilepsy evaluation. After an introductory quote of Todd including “limbs will remain paralytic for some hours”, they undertake a systematic analysis of PP. They show that the average duration of PP is 173 seconds with a maximum of 22 minutes. They also “found no differences regarding the incidence and the duration of PP depending on the location of the seizure onset zone” and that “a morphologic lesion does not seem to predispose to longer PP”. While the results seem to hold for the study population, both the Introduction and Discussion suggest the results may be generalized to the average patient with a Todd’s paresis. Thus, a deficit lasting much longer than 22 minutes can hardly be a Todd’s paresis and location of lesion and seizure onset is unrelated to the occurence and duration of a Todd’s paresis, This asumption, however, is not justified due to the lack of generalizability of the study results. The typical patient seen by a neurologist with a Todd’s paresis will have clonic features followed by a paresis often in relation to an indentified structural lesion such as an astrocytoma or ischemia in proximity to the motor cortex and with a duration sometimes greatly exceeding 22 minutes. The majority of these patients are unlikely to be referred to a tertriary referral center for presurgical epilepsy evaluation with video-EEG monitoring. In the study population: 16 of 35 patients had clonic features preceeding the PP; only 18 patients of 44 had an extratemporal lesion (with no description of the spacial relation to the motor cortex); only 5 of these 18 had a tumor, while none had ischemia as the underlying lesion; and only 4 of 44 patients had an unequivocal extratemporal seizure onset zone. While all these are typical features of patients with PP presenting to a neurologist, they are present only in a minority (or not at all) in the study population. The study seems valid in reaching conclusions for the population presented, but a generalization to the overall population presenting to the neurologist with a Todd’s paresis is not warranted on the basis of information presented, let alone the classification of this paper as a review implying a general overview of the subject matter reflected in the title.
Reply to Vroomen 3 August 2004
Paolo Gallmetzer, Abteilung für Klinsche Epilepsieforschung Universitatsklinik fur Neurologie, Wahringer Gurtel 18-20, A-1090 Vienna, Austria, Christoph Baumgartner Send Correspondence to journal: Re: Reply to Vroomen christoph.baumgartner{at}univie.ac.at Paolo Gallmetzer, et al.	We thank Dr. Vroomen for his interest in our study. We aimed to identify the typical clinical features of postictal paresis in patients with medically refractory epilepsy undergoing prolonged video-EEG monitoring. We also wanted to provide information on the clinical features of “pure” postictal paresis following epileptic seizures not confounded by other precipitating causes such as ischemia or tumor-related edema. Our patient population was therefore a selected one which was also clearly stated. Dr. Vroomen mentioned that the “typical” patient with a postictal paresis is a patient with an underlying structural lesion (tumor or cerebral ischemia) that has a relation to the motor cortex, that postictal paresis is often of longer duration and that patients with a postictal paresis typically do present with ictal clonic phenomena. This statement reflects Dr. Vroomen’s opinion and he does not cite published data. Postictal paresis of longer duration was reported in patients with a history of stroke. [1] In these patients, it may be difficult to distinguish a “pure epileptic” paresis from a “combined paresis” resulting from both ischemia and an epileptic cause. Postictal paresis was not confined to patients with a seizure onset in the motor cortex which actually represents one of our main findings, but our study population was too small to investigate a relationship between a specific seizure-onset zone and the incidence of postictal paresis. Clonic phenomena were the most common seen motor phenomena in our patients, occurring in 55.6% of all seizures (n = 40) and in 65.9% of all patients (n = 29) at least during some seizures. The incidence of clonic phenomena in our patients confirms a recent study where tonic or clonic phenomena were also found in about three-quarters of the patients showing postictal paresis.[2] References 1. Rolak LA, Rutecki P, Ashizawa T, Harati Y. Clinical features of Todd's post-epileptic paralysis. J Neurol Neurosurg Psychiatry 1992; 55:63-4. 2. Kellinghaus C, Kotagal P. Lateralizing value of Todd's palsy in patients with epilepsy. Neurology 2004; 62:289-291.