Replacement of electroencephalography with polysomnography in epilepsy for improved assessment: Need of the hour

Replacement of electroencephalography with polysomnography in epilepsy for improved assessment: Need of the hour

Epilepsy & Behavior 29 (2013) 422–423 Contents lists available at ScienceDirect Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh ...

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Epilepsy & Behavior 29 (2013) 422–423

Contents lists available at ScienceDirect

Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh

Letter to the Editor Replacement of electroencephalography with polysomnography in epilepsy for improved assessment: Need of the hour To the Editor: The diagnosis of epilepsy is essentially clinical, and EEG has, for a long time, remained the mainstay in investigating cases of epilepsy. A routine EEG provides supportive evidence for the diagnosis and classification of epilepsy, which, however, may not be adequate for the assessment of an epilepsy status that includes prognosis, severity of the epileptic state, risk of future seizures, and, more importantly, the possibility of existing or future intractability or drug resistance. In view of current advancements in medical knowledge and research, patients with epilepsy are probably entitled to know about the status of their epilepsy in greater detail than the mere diagnosis and classification of the disorder. Until today, EEG findings have failed to show a consistent relation with the severity or intractability of epilepsy [1]. Both severity and intractability are subjective or clinically assessed characteristics based mainly on the intensity, duration, and frequency of seizures and the failure of adequate and well-tolerated antiepileptic drug regimes. A routine EEG, therefore, has definite limitations especially regarding the ability to provide convincing evidence for the existent severity or intractability of epilepsy or possibility of its future intractable course. This brief paper attempts to justify the promotion of polysomnography (inclusive of a routine EEG) as a more important investigative tool than a mere routine EEG in assessing epilepsy status with a fair degree of accuracy and extent. Rapid eye movement (REM) sleep is well documented to exert a potent antiepileptic influence, which has been attributed mainly to its associated main components, i.e., ponto–geniculo–occipital (PGO) spikes and EEG desynchronization, the latter being a well-known antiepileptic state [2]; indeed, dissociation of EEG desynchronization that occurs in REM-sleep behavior disorder (RBD) has been suggested [3] to be a major sole factor in significantly increasing the incidence of epilepsy and interictal epileptiform discharges (IEDs) as observed in studies by researchers that also hypothesize that chronically altered REM sleep, which occurs in RBD, increases the chances of seizures in humans [4,5]. Dissociation of naturally occurring EEG desynchronization during REM sleep, thus, appears to cause significant reduction or even loss of the protective antiepileptic potential of REM sleep. Further, REM sleep is found to be decreased in several forms of severe and intractable epilepsy [6–9]; conversely, relief in intractable seizures from alternative therapies, namely, ketogenic diet, vagal nerve stimulation, and temporal lobe surgery, is found to be associated with an increase or restoration of REM sleep [10–12]. Thus, it may be postulated that an epileptic state can develop owing to failure or breakdown of a normal REM-sleep profile (which includes latency, duration components like PGO spikes, EEG desynchronization, and muscle atonia), the possibility of which cannot be ruled out altogether and warrants further insight into this causal–

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effect relationship, although, admittedly, this postulation may not be applicable in all cases of epilepsy. Largely based on these studies, REM sleep is, therefore, being proposed as a reliable biomarker of intractability in epilepsy [13]. Rapid eye movement-sleep profile can be best assessed by a simple and noninvasive polysomnographic recording, which, therefore, can yield far greater information compared with routine EEG in patients with epilepsy, information that can be vital in the detection and/or assessment of severity and intractability of the epileptic state or even predicting (to a variable extent) the possible occurrence of a future intractable course of epilepsy. Early detection of disruption of REM-sleep profile can act as an alert for an early intervention and/or surveillance of a possible future intractable course, which may decrease the chances of progression to frank intractability. Therefore, it is suggested that epilepsy status can be assessed more comprehensively by polysomnography (inclusive of a routine EEG) that is associated with an additional assessment of REM-sleep profile. For this reason, it is recommended that routine EEG be replaced with polysomnography as it offers a superior choice in the investigation of epilepsy cases. The work is original. Conflict of interest None to disclose. References [1] Selvitelli MF, Walker LM, Schomer DL, Chang BS. The relationship of interictal epileptiform discharges to clinical epilepsy severity: a study of routine electroencephalograms and review of the literature. J Clin Neurophysiol 2010;27(2):87–92. [2] Jaseja H. Mechanism of endogenous anti-epileptogenesis during rapid eye movement sleep. Med Hypotheses 2006;66(4):866. [3] Jaseja H. Endogenous anti-epileptogenic purpose of REM sleep in man: corroborative clinical neurophysiological evidence. Clin Neurophysiol 2009;120(4):840. [4] Manni R, Terzaghi M. REM behavior disorder associated with epileptic seizures. Neurology 2005;64:883–4. [5] Manni R, Terzaghi M, Zambrelli E. REM sleep behavior disorder and epileptic phenomena: clinical aspects of the comorbidity. Epilepsia 2006;47(Suppl. 5):78–81. [6] Nunes ML, Ferri R, Arzimanoglou A, Curxi L, Apple CC, Costa da Costa J. Sleep organization in children with partial refractory epilepsy. J Child Neurol 2003;18(11):763–6. [7] Selwa LM, Marzec ML, Chervin RD, Weatherwax KJ, Vaughn BV, Foldvary-Schaefer N, et al. Sleep staging and respiratory events in refractory epilepsy patients: is there a first night effect? Epilepsia 2008;49(12):2063–8. [8] Pereira AM, Bruni O, Ferri R, Palmini A, Nunes ML. The impact of epilepsy on sleep architecture during childhood. Epilepsia 2012;53(9):1519–25. [9] Kohyama J. Pathophysiology of West syndrome—consideration from sleep studies. In: Benjamin SM, editor. Focus of epilepsy research. New York: Nova Science Publishers; 2004. p. 79–104. [10] Hallbook T, Kohler S, Rosen I, Lundgren J. Effects of ketogenic diet on epileptiform activity in children with therapy resistant epilepsy. Epilepsy Res 2007;77:134–40. [11] Martinez A. Effect of vagus nerve stimulation on epilepsy-induced changes in the temporal organization of sleep in cats. Salud Mental 2012;35(2):147–55. [12] Serafini A, Kuate C, Gelisse P, Velizarova R, Gigli GL, Coubes P, et al. Sleep before and after temporal lobe epilepsy surgery. Seizure 2012;21:260–5. [13] Jaseja B, Jaseja H. Rapid eye movement (REM) sleep: a reliable biomarker of intractability in epilepsy. Epilepsy Behav 2013. http://dx.doi.org/10.1016/j.yebeh.2013. 06.027.

Letter to the Editor

Bhanu Jaseja Biotechnology Department, MITS, Gwalior, India Harinder Jaseja Physiology Department, G.R. Medical College, Gwalior, India Corresponding author at: 8, C-Block, Harishanker-puram, Lashkar, Gwalior 474009, M.P., India. E-mail address: [email protected]. 20 July 2013

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