Meditation and epilepsy: A still hung jury

Meditation and epilepsy: A still hung jury

Medical Hypotheses (2006) 67, 247–250 Meditation and epilepsy: A still hung jury Erik K. St. Louis a,*...

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Medical Hypotheses (2006) 67, 247–250

Meditation and epilepsy: A still hung jury Erik K. St. Louis


, Ephraim Philip Lansky



Department of Neurology, Iowa Comprehensive Epilepsy Program, University of Iowa Hospitals and Clinics and Carver College of Medicine, 200 Hawkins Drive, Iowa City, IA 52242, USA b Punisyn Pharmaceuticals, Haifa, Israel Received 17 February 2006; accepted 20 February 2006

Summary Meditation has been advocated as a treatment for several medical problems, including epilepsy. Conversely, concern has been raised that meditation may aggravate or even precipitate epilepsy. We present a case of new onset mesial temporal lobe epilepsy in a young woman meditator lacking other apparent risk factors for epilepsy as a springboard for a balanced discussion concerning the potential relationship between meditation and epilepsy, and a criticism of the current literature in this field. Prospective clinical studies of meditators with video-electroencephalography and clinical trials of meditation in refractory epilepsy patients are needed to resolve current controversies concerning meditation and epilepsy. c 2006 Elsevier Ltd. All rights reserved.

It has been hypothesized that the neural hypersynchrony accompanying the practice of meditation may lead to subsequent development of provoked seizures or epilepsy recently in this journal, while others have presented arguments attempting to refute this hypothesis [1–5]. Viewpoints on a potential relationship between meditation and epilepsy seem to represent two diametrical extremes: those speculating that behavioral meditative phenomena could represent provoked epileptic seizures resulting from chronic kindling of the human brain [1,2], and those from the meditation community who repudiate such a relationship based upon opposing speculative claims. Proponents of meditation argue that since meditation induces ketosis, which may increase brain c-amino * Corresponding author. Tel.: +1 319 356 7235; fax: +1 319 356 4505. E-mail address: [email protected] (E.K. St. Louis).

butyric acid (GABA, the principle inhibitory central nervous system neurotransmitter), meditation would be expected to inhibit epileptic seizures and possibly kindling, rather than aggravate or precipitate seizures [3]. Others have cast doubt on the idea that meditation may precipitate epilepsy, since they have not seen such cases following extensive personal experience with meditation in healthcare [4], and given that retrospective insurance data has suggested that meditation actually may decrease neurological hospital admissions (although this study did not specifically focus on epilepsy) [5]. One problem with the theoretical proposal that meditation precipitates epilepsy is that to date, no compelling, well-documented case of new onset epilepsy occurring in a meditating patient has been recognized. We now report a clinical case, which suggests a possible connection between meditation and epilepsy.

0306-9877/$ - see front matter c 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2006.02.039

248 An 18-year-old woman who had faithfully practiced transcendental meditation (TM) since childhood was evaluated for newly evolved spells. She lacked any previous medical, psychological, or psychiatric history, and particularly denied remote symptomatic risk factors for epilepsy such as febrile seizures, closed head injury, or meningoencephalitis, or a family history of epilepsy. Her spells were characterized by an initial uncomfortable epigastric sensation, progressing to staring and amnesia, or when the spells occurred nocturnally, thrashing in bed. These lasted a few minutes, and were followed by brief confusion, tongue biting, and urinary incontinence prior to a return to baseline. The spells had occurred four times over one year since onset. Investigations included a normal brain magnetic resonance image (MRI), and interictal EEG, which demonstrated left mid-temporal interictal epileptiform discharges. A therapeutic trial of oxcarbazepine (a drug of choice for partial epilepsy) resulted in complete control of her spells for six months, but then witnessed generalized tonic–clonic seizures occurred on three occasions following sleep deprivation and missed medication doses. She has been seizure-free for the last 6-months with faithful adherence to oxcarbazepine, and continues to practice TM. She has not experienced a spell during TM practice to her knowledge. This case report illustrates onset of mesial temporal lobe epilepsy in a lifelong meditator who lacked known risk factors for epilepsy. A causative association between her practice of TM and subsequent development of epilepsy cannot be established with certainty, and admittedly, this potential association may represent no more than chance. Perhaps the strongest argument against the possibility of this patient’s meditation causing or contributing to the development of her epilepsy is that she meditated chronically without developing epilepsy until late in adolescence. However, several mechanisms of brain injury incite human temporal lobe epileptogenesis by triggering a chronic cascade of longitudinal synaptic and axonal reorganization and hippocampal neuronogenesis [6], only to result in clinically overt seizures after the course of many years. Some might criticize the diagnosis of epilepsy in this patient, given that her spells could be psychogenic in nature. Definitive confirmation of a diagnosis of epilepsy would require ictal EEG recording of her habitual clinical spells. However, her clinical history is highly consistent with complex partial seizures of temporal lobe origin, interictal EEG findings strongly support localization of an epileptogenic focus in the left temporal lobe, and her reproducibly excellent clin-

St. Louis and Lansky ical response to empiric oxcarbazepine (and seizure recurrence with each episode of non-adherence) argues strongly for an epileptic etiology. In favor of a potential association between her meditative practice and epilepsy is the localization of her seizure focus to a limbic region of brain presumably involved in meditation. To our knowledge, this is the first well-documented case of new onset mesial temporal lobe epilepsy potentially associated with meditation to be reported in the literature. While many will reasonably argue that we have reached too far in drawing attention to a possible relationship between this patient’s meditative practice as an etiology for her partial epilepsy, repetitive entrainment of the limbic system into a state of physiological neural hypersynchrony by TM practice could eventually engender in vivo kindling and incite an epileptogenic zone in the mesial temporal lobe capable of autonomous, pathophysiological neuronal hypersynchrony, eventually begetting partial seizures. On the other hand, some would point to this case as evidence against an aggravating or triggering role of TM in epilepsy, since this patient with mesial temporal lobe epilepsy has noted no reliable provocation of seizures by her continuing practice of TM, and thus far, her epilepsy has been responsive to medication, not pharmacoresistant as one might expect if TM were playing a continuing role in aggravating her seizure focus. In our opinion, evidence to conclusively establish or disprove whether meditation precipitates acute provoked seizures or chronic epilepsy is currently lacking. While the idea that meditation produces cognitive kindling in the brain and causes seizures is both concerning and enticing, the current evidence that meditation and epilepsy are associated is superficial, speculative, and flawed. Many have argued that meditation invokes behavioral and electroencephalographic features of simple and complex partial seizures, such as psychic phenomena, an altered subjective state of awareness, and abnormal motor activity including myoclonus [1,2,7–12]. However, this hypothesis has remained at the level of conjecture. Prior reports of presumed seizures associated with meditative practice have suffered from incomplete reporting of clinical and electroencephalographic (EEG) features associated with the spells in question, [7–11] or worse, errant over-reaching interpretation of electroencephalographic features accompanying meditation. In one case, an EEG reported in the literature was interpreted as representing interictal or ictal epileptiform discharges, which when reviewed by one author, a board certi-

Meditation and epilepsy: A still hung jury fied electroencephalographer (eks), showed that the EEG waveforms reported as interictal spikes were muscle artifacts, and the purported temporal lobe seizure was probably instead a benign normal EEG rhythm, rhythmic mid-temporal theta of drowsiness (RMTD, or psychomotor variant), [8] although the 3 channel recording utilized is an inadequate montage for distinguishing epileptiform discharges [12]. A recent review in this journal raised concern that meditative EEG patterns resemble the characteristics of mesial temporal electrographic seizure activity. Nicholson [2] argued that the EEG activity of meditation, that of hypersynchronous, elevated amplitude, c frequency band activity distributed over the frontotemporal regions in a ‘‘hatband’’ or ‘‘crown’’ distribution, [13] is suggestive of the topography of electrographic seizure discharges reported in a subgroup of patients with partial epilepsy of mesial temporal lobe origin [14]. However, this logic is faulty, since several other non-epileptic, physiologic hypersynchronous neural patterns of EEG activation that have similar qualitative appearances to these patterns exist [15,16]. These previously reported meditationevoked EEG alterations lack the electroencephalographic sine qua non of a partial seizure, that of ictal spatiotemporal evolution, the transformation of a discharge into different EEG waveform morphologies, frequencies, and electrical field distributions over time, which occurs as a partial seizure evolves and propagates through the brain [17,18]. The EEG characteristics of amplitude, frequency, and electrical field distribution alone are inadequate to define EEG activity as an epileptic ictus. Demonstration of morphological and frequency variation and propagation beyond initial electrical field boundaries are the most telling characteristics to help confirm an electrographic event as a partial seizure [18]. The hypersynchronous, high voltage c frequency activity seen in experienced Tibetan monastic practitioners of meditation lacks spatiotemporal evolution, and is therefore unlikely to be an ictal seizure event [13]. Ideally, future studies of meditators utilizing ictal video-EEG monitoring to permit direct correlation of electrographic and behavioral phenomena should be carried out. Recently developed sophisticated EEG techniques utilizing mathematical frequency and spatial analysis for mere differentiation of ictal epileptiform rhythms from non-epileptic physiological rhythms add little to visual inspection. Subjective real time interpretation of the ictal EEG by an experienced clinical electroencephalographer remains the gold standard for interpretation of an ictal electrographic

249 seizure discharge. Future application of magnetoencephalography could provide complementary information to standard EEG, especially in detection of suspected neocortical seizure foci [19]. Meditation advocates reason that since previous treatment trials of meditative methods such as yoga in epilepsy patients demonstrated reduction in chronic seizure burden rather than seizure aggravation, meditation does not provoke epilepsy [20]. However, one should not reason that because meditation could benefit established epilepsy that meditation may not kindle brain in susceptible healthy individuals and lead to de novo epileptogenesis, and before advocating widespread adoption of meditation for chronic epilepsy patients, further evidence of its safety and more rigorous establishment of its efficacy would certainly be required from larger, prospective, controlled clinical trials. That meditation could improve epileptic seizure burden given its substantial efficacy in reducing physical and emotional stress is not surprising. The possibility of differential efficacy and safety in different epilepsy syndromes also needs to be considered, given the substantially different pathophysiologic mechanisms and evidence for differential efficacy for existing treatment modalities such as anti-epileptic drugs, vagus nerve stimulation, and epilepsy surgery. Pivotal clinical trials should be performed to determine the efficacy and safety of meditation in different epilepsy syndromes. Future studies of meditation and epilepsy would be best designed and conducted with four complementary goals. First, to determine whether meditation is associated with epilepsy, a large, population-based, cross-sectional retrospective cohort study should be performed. Second, to address whether meditation provokes de novo interictal epileptiform activity or ictal seizures acutely or chronically via kindling the healthy, non-epileptic brain, a prospective study of novice meditators without a history of epilepsy utilizing serial videoEEG recordings during meditation and sham meditation sessions should be carried out. Third, to explore whether meditative behavioral phenomena in experienced/expert meditators without known epilepsy are in actuality subtle simple partial seizures, ictal video-EEG recordings utilizing true temporal or sphenoidal electrode placements are necessary. Fourth and last, to determine whether meditation is safe and effective for improving clinical seizure burden in known epileptic patients, large, prospective, double-blind, randomized clinical trials comparing the effects of meditation vs. control sham techniques in different epilepsy syndromes, including primary idiopathic generalized epilepsy, mesial temporal lobe epilepsy, and other

250 partial epilepsy syndromes should be mounted. While designing a clinical study involving meditation is somewhat logistically difficult, concealing randomization between sham and meditation groups and blinding physician raters and EEG interpreters should limit bias and yield interpretable results. Well designed retrospective and prospective clinical studies, including population-based, epidemiological studies of meditation and epilepsy, and clinical trials in novices, experienced meditators, and subjects with epilepsy, can answer the persisting questions of whether meditation kindles human brain or precipitates epileptic seizures in susceptible individuals with or without a history of epilepsy. We believe the jury is still out on these issues, and call for unbiased research rather than further conjecture and personal opinion on these important public health questions.

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