Re: Mindfulness Meditation Research: Issues of Participant S
Posted: Fri Feb 22, 2019 4:14 am
Meditation may predispose to epilepsy: an insight into the alteration in brain environment induced by meditation
by Harinder Jaseja*
Physiology Department, G.R. Medical College, 8, 10-C-Block, Near Paliwal Health Club, Harishanker-puram, Lashkar, Gwalior 474009, MP, India
Received 31 August 2004; accepted 13 September 2004
c 2004 Elsevier Ltd. All rights reserved.
NOTICE: THIS WORK MAY BE PROTECTED BY COPYRIGHT
Summary
Stress-induced diseases in modern life are on an alarming rise not only in developed countries but also in developing ones. To alleviate stress, one practice that is being commonly and increasingly adapted to is meditation. Limited studies on meditation have reported occurrence of mental calmness along with apparently favorable changes in certain autonomic functional parameters like heart rate, blood pressure, respiration and skin resistance. Recently, meditation is also being practiced and advised for alleviation of epilepsy; however, very little work is available to comprehend effect and utility of meditation on epilepsy. Neuro-imaging and in-depth studies during the course and attainment of meditational state have revealed alteration in neuro-chemistry and neuro-physiology of brain environment that could favor epileptogenesis. The rise in brain glutamate and serotonin along with development of ‘hypersynchrony’ of EEG activity (which occur during the course and attainment of meditational state) are well documented to form the underlying basis of epilepsy. Each of the above-mentioned factors is individually capable of inducing susceptibility and decreasing threshold to epilepsy. Based on these changes in brain, this paper raises a grave possibility and risk of meditation in developing epilepsy or increasing the severity and frequency of attacks in an already epileptic state, contrary to the popular belief of its remedial role in alleviating epilepsy.
Introduction
There is global increase in stress and strain of today’s life, both at home front and job place. The global competitiveness and challenges of modern life are taking a great toll on physical and mental health that is being reflected by an alarming rise in stress induced diseases.
Counseling and/or drug therapy have not been much effective in relieving stress in most of the cases. In addition, these methods cannot be applicable in many situations. Also, in those cases where they have been able to produce significant relief, the effect has been short lived.
An increasing tendency towards adapting practice of meditation for relief of stress is being observed universally as it is devoid of side effects of drugs and great compromise with life style that one is used to. Meditation is a complex process, during the course and attainment of which, multiple changes in mental, neuro-hormonal and autonomic functions occur. These changes vary from being subtle to sometimes being easily perceptible by the meditator. Due to the complexity, mystique and fascination of the mental processes and changes associated with meditation, it still remains a phenomenon of great interest to researchers and shall continue to do so for several years to come.
The biological autonomic effects on heart rate, blood pressure, respiration and skin resistance have been studied to a significant extent. However, with the advent of neuro-imaging techniques like EEG, fMRI, PET and SPECT [1–5], the cerebral and mental processes associated with meditation have attracted much interest to researchers. Undoubtedly, it is these processes that form the underlying basis of the composite effect of meditation on body and mind.
Effects of meditation on brain
EEG changes
A number of investigators have studied EEG changes in normal meditators. The effects have mainly been on alpha rhythm as observed by Bagchi & Wenger [28] and Kasamatsu & Hirai [29]. In 1961, Anand et al. [30] observed increasing amplitude and slowing frequency of alpha rhythm, which gradually spread from its normal predominant locality i.e., occipital to frontal regions. Banquet [6] also found high amplitude alpha rhythm during meditation and coined the term ‘hypersynchrony’ [6,7]. It needs to be reminded that epileptic discharges are more appropriately known as ‘hypersynchronous’ discharges, which are due to an abnormally high synchronized firing of a neuronal aggregate. Banquet also noted development of theta frequencies during meditation. These low frequency, high amplitude EEG rhythms are generally present during meditation.
Effect on prefrontal and cingulate cortex
Neuro-imaging techniques have demonstrated increased activity in prefrontal (PFC) (mainly right side) and cingulate cortex (CC) [8–11] during meditation. This leads to production of the excitatory neurotransmitter, Glutamate in the brain. This hormone is used by PFC neurons to communicate among themselves and other brain structures [12]. There is continued increase in Glutamate with continued activity in PFC during the course of meditation process.
Effect on serotonin
It has been observed that Serotonin (5-HT) increases during meditation. Secretion is increased by stimulation of lateral hypothalamus and PFC [13] that invariably occurs during meditation. Several studies have demonstrated increased urinary excretion of Serotonin metabolites after meditation [14].
Effect on inter-hemispheric coherence
Kiloh et al. [15] observed increase in inter-hemispheric coherence, symmetry and synchronization of alpha rhythm during meditation.
Thus, the neuro-effects of meditation may be summarized to produce:
1. Increase in synchrony of EEG activity (hypersynchrony).
2. Increase in inter-hemispheric coherence of EEG activity.
3. Increase in brain Glutamate.
4. Increase in brain Serotonin.
There is overwhelming evidence of hypersynchrony predisposing to epilepsy. Hyperventilation causes synchrony and precipitates epilepsy [16]. It is a provocative technique during EEG recording. Sleep also is a provocative technique, a significant number of epileptics reveal inter-ictal epileptiform activity in their EEG only during sleep [17,18]. Hypersynchrony of sleep facilitates both initiation and propagation of partial seizures [17]. It is well known that NREM sleep causes increased susceptibility to epilepsy. Spiky epileptic discharge means more synchronisation of unit cell populations and Spike is caused by synchronisation of population group 1 neurons [19]. Spikes depict interictal epileptiform activity and their correlation with intracellular recordings shows that the former are associated with firing of action potentials [20].
Increase in inter-hemispheric coherence of EEG activity may contribute in its own way towards propagation and generalization of epileptic discharges. A focal discharge restricted to a localized region can tend to become widespread precariously. Corpus callostomy is a surgical procedure performed for control of un-controllable generalized seizures, the objective being to block inter-hemispheric transmission of epileptic potentials.
Glutamate is neuro-excitatory transmitter and widely implicated in epilepsy. The epileptic focus has been shown to contain more Glutamate than in normal state [21] and potassium-stimulated Glutamate release is more in cortical slices removed from epileptic patients than normal tissue [21].
Neurons in epileptic region exhibit paroxysmal depolarization shift (PDS) that is associated with a burst of action potentials [22]; interestingly, effect of Glutamate on NMDA receptors also produces a response similar to PDS [22] and a search for Glutamate antagonists as anti-epileptics is being promoted.
Serotonin also has been implicated in epileptogenesis and anti-serotonin are found to possess anti-convulsant properties [23,24]. 5-HT 2A receptor activation causes slow depolarisations and enhancement of excitatory signals such as Glutamate [25] and Cyproheptadine, which is 5-HT 2A blocker, has anti-convulsant activity [26].
Conclusion
Thus, each of the above-cited effects, which invariably occur at sometime during the course of meditation can present a potential risk for epileptogenesis and/or precipitating attack(s) in an epileptic patient. Needless to say, the concurrent presence of two or more of these effects can contribute tremendously to epileptogenesis, even to the extent of rendering a normal person epilepsy-prone.
Meditation is known to produce relaxation and epilepsy after relaxation is a well-known entity [27]. Meditation is presently being advised and resorted to for alleviating epilepsy; this paper clearly outlines the risk of enhancing the epileptic state during the course and attainment of meditation state.
However, further insight into the neuro-physiological and neuro-chemical avenues associated with meditation is definitely required. The epileptic proneness and incidence of epilepsy in regular meditators needs to be elucidated. Presently, however, caution may be exercised over the practice of meditation in patients prone to epilepsy. At least, epileptic patients seeking alleviation of their attacks through practice of meditation may be warned of the potential hazard outlined in the paper.
_______________
Notes:
* Tel.: +91 751 233 1147. E-mail address: dr_jaseja@yahoo.com.
0306-9877/$ - see front matter c 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2004.09.012
References
[1] Herzog H, Lele VR, Kuwert T, et al. Changed pattern of regional glucose metabolism during Yoga meditative relaxation. Neuropsychobiology 1990-1991;23:182–7.
[2] Lou HC, Kjaer TW, Friberg L,. et al. A 15O-H2O PET study of meditation and the resting state of normal consciousness. Human Brain Map 1999;7:98–105.
[3] Kjaer, Bertelsen, Piccini, Brooks, Alving, Lou, 2002.
[4] Newberg AB, Alavi A, Baime M,. et al. The measurement of regional blood flow during the complex cognitive task of meditation: a preliminary SPECT study. Psychiatr Res Neuroimaging 2001;106:113–22.
[5] Lazar SW, Bush G, Gollub RL,. et al. Functional brain mapping of the relaxation response and meditation. Neuroreport 2000;11:1581–5.
[6] Banquet JP. Spectral analysis of EEG in meditation. Electroencephal Clin Neurophysiol 1973;35:143–51.
[7] Banquet JP. EEG and meditation. Electroencephalography Clin Neurophysiol 1972;33:449.
[8] Ingvar DH. The will of the brain: cerebral correlates of willful acts. J Theor Biol 1994;171:7–12.
[9] Frith CD, Friston K, Liddle PF,. et al. Willed action and the prefrontal cortex in man. A study with PET. Proc R Soc Lond 1991;244:241–6.
[10] Posner MI, Peterson SE. The attention system of the human brain. Ann Rev Neurosci 1990;13:25–42.
[11] Pardo JV, Fox PT, Raichle ME. Localization of a human system for sustained attention by positron emission tomography. Nature 1991;349:61–4.
[12] Cheramy A, Romo R, Glowinski. Role of corticostriatal glutamatergic neurons in the presynaptic control of dopamine release. In: Sandler M, Feuerstein C, Scatton B et al, editors. Neurotransmitter interactions in the basal ganglia. New York: Raven Press; 1987.
[13] Olds ME, Forbes JL. The central basis of motivation, intracranial self-stimulation studies. Ann Rev Psychol 1981;32:523–74.
[14] Walton KG, Pugh ND, Gelderloos P, Macrae P. Stress reduction and preventing hypertension: preliminary support for a psychoneuroendocrine mechanism. J Altern Complement Med 1995;1:263–83.
[15] Kiloh LG, Osselton JW. Clinical electroencephalography. 4th ed. London: Butterworth; 1981.
[16] Handbook of electro-encephalography and clinical neurophysiology. vol. 13, part A. Amsterdam: Elsevier Scientific Publishing Company; 1975. p. 48–9.
[17] Herman ST, Walczak TS, Bazil CW. Neurology 2001;56:1453–9.
[18] Handbook of electro-encephalography and clinical neurophysiology. vol. 13, part A. Amsterdam: Elsevier Scientific Publishing Company; 1975. p. 31, 38.
[19] Fenwick P. The relationship between mind, brain and seizures. Arch Indian Psychiat 1994;1(1):3–6.
[20] Goodman and Gilman’s The pharmacological basis of therapeutics. 9th ed., International edn.; 1996. p. 465.
[21] Rang HP, Dale MM, Ritter JM. Pharmacology. 3rd ed. 1995. p. 599.
[22] Rang HP, Dale MM, Ritter JM. Pharmacology. 3rd ed. 1995. p. 598.
[23] Vimal Chandra. Ind J Pharmacol 1972;4(3):174–7.
[24] Bapat SK, Vimal Chandra. Ind J Pharmacol 1969;1(4):32–6.
[25] Goodman and Gilman’s. The pharmacological basis of therapeutics. 9th ed. International edn. 1996. p. 256.
[26] Satoskar, Kale, Bhandarkar’s. Pharmacology and pharmacotherapeutics. 16th ed. 1999, p. 318.
[27] Epilepsy News, Sleep and Epilepsy, Mohammed I. Zahoor produced by Sleep Research Laboratory, Wallace Mendelson, Director, The University of Chicago Hospitals.
[28] Bagchi BK, Wenger MA. Simultaneous EEG and other recordings during some yogic practices. Electroencephalogr Clin Neurophysiol 1958;10:193.
[29] Kasamatsu A, Hirai T. An electroencephalographic study on the zen medication. In: Tart, editor. Altered states of consciousness; 1969. p. 501–14.
[30] Anand BK, Chhina GS, Singh B. Some aspects of electroencephalographic studies in yogis. Electroencephalogr Clin Neurophysiol 1961;13:452–6.
by Harinder Jaseja*
Physiology Department, G.R. Medical College, 8, 10-C-Block, Near Paliwal Health Club, Harishanker-puram, Lashkar, Gwalior 474009, MP, India
Received 31 August 2004; accepted 13 September 2004
c 2004 Elsevier Ltd. All rights reserved.
NOTICE: THIS WORK MAY BE PROTECTED BY COPYRIGHT
YOU ARE REQUIRED TO READ THE COPYRIGHT NOTICE AT THIS LINK BEFORE YOU READ THE FOLLOWING WORK, THAT IS AVAILABLE SOLELY FOR PRIVATE STUDY, SCHOLARSHIP OR RESEARCH PURSUANT TO 17 U.S.C. SECTION 107 AND 108. IN THE EVENT THAT THE LIBRARY DETERMINES THAT UNLAWFUL COPYING OF THIS WORK HAS OCCURRED, THE LIBRARY HAS THE RIGHT TO BLOCK THE I.P. ADDRESS AT WHICH THE UNLAWFUL COPYING APPEARED TO HAVE OCCURRED. THANK YOU FOR RESPECTING THE RIGHTS OF COPYRIGHT OWNERS.
Summary
Stress-induced diseases in modern life are on an alarming rise not only in developed countries but also in developing ones. To alleviate stress, one practice that is being commonly and increasingly adapted to is meditation. Limited studies on meditation have reported occurrence of mental calmness along with apparently favorable changes in certain autonomic functional parameters like heart rate, blood pressure, respiration and skin resistance. Recently, meditation is also being practiced and advised for alleviation of epilepsy; however, very little work is available to comprehend effect and utility of meditation on epilepsy. Neuro-imaging and in-depth studies during the course and attainment of meditational state have revealed alteration in neuro-chemistry and neuro-physiology of brain environment that could favor epileptogenesis. The rise in brain glutamate and serotonin along with development of ‘hypersynchrony’ of EEG activity (which occur during the course and attainment of meditational state) are well documented to form the underlying basis of epilepsy. Each of the above-mentioned factors is individually capable of inducing susceptibility and decreasing threshold to epilepsy. Based on these changes in brain, this paper raises a grave possibility and risk of meditation in developing epilepsy or increasing the severity and frequency of attacks in an already epileptic state, contrary to the popular belief of its remedial role in alleviating epilepsy.
Introduction
There is global increase in stress and strain of today’s life, both at home front and job place. The global competitiveness and challenges of modern life are taking a great toll on physical and mental health that is being reflected by an alarming rise in stress induced diseases.
Counseling and/or drug therapy have not been much effective in relieving stress in most of the cases. In addition, these methods cannot be applicable in many situations. Also, in those cases where they have been able to produce significant relief, the effect has been short lived.
An increasing tendency towards adapting practice of meditation for relief of stress is being observed universally as it is devoid of side effects of drugs and great compromise with life style that one is used to. Meditation is a complex process, during the course and attainment of which, multiple changes in mental, neuro-hormonal and autonomic functions occur. These changes vary from being subtle to sometimes being easily perceptible by the meditator. Due to the complexity, mystique and fascination of the mental processes and changes associated with meditation, it still remains a phenomenon of great interest to researchers and shall continue to do so for several years to come.
The biological autonomic effects on heart rate, blood pressure, respiration and skin resistance have been studied to a significant extent. However, with the advent of neuro-imaging techniques like EEG, fMRI, PET and SPECT [1–5], the cerebral and mental processes associated with meditation have attracted much interest to researchers. Undoubtedly, it is these processes that form the underlying basis of the composite effect of meditation on body and mind.
Effects of meditation on brain
EEG changes
A number of investigators have studied EEG changes in normal meditators. The effects have mainly been on alpha rhythm as observed by Bagchi & Wenger [28] and Kasamatsu & Hirai [29]. In 1961, Anand et al. [30] observed increasing amplitude and slowing frequency of alpha rhythm, which gradually spread from its normal predominant locality i.e., occipital to frontal regions. Banquet [6] also found high amplitude alpha rhythm during meditation and coined the term ‘hypersynchrony’ [6,7]. It needs to be reminded that epileptic discharges are more appropriately known as ‘hypersynchronous’ discharges, which are due to an abnormally high synchronized firing of a neuronal aggregate. Banquet also noted development of theta frequencies during meditation. These low frequency, high amplitude EEG rhythms are generally present during meditation.
Effect on prefrontal and cingulate cortex
Neuro-imaging techniques have demonstrated increased activity in prefrontal (PFC) (mainly right side) and cingulate cortex (CC) [8–11] during meditation. This leads to production of the excitatory neurotransmitter, Glutamate in the brain. This hormone is used by PFC neurons to communicate among themselves and other brain structures [12]. There is continued increase in Glutamate with continued activity in PFC during the course of meditation process.
Effect on serotonin
It has been observed that Serotonin (5-HT) increases during meditation. Secretion is increased by stimulation of lateral hypothalamus and PFC [13] that invariably occurs during meditation. Several studies have demonstrated increased urinary excretion of Serotonin metabolites after meditation [14].
Effect on inter-hemispheric coherence
Kiloh et al. [15] observed increase in inter-hemispheric coherence, symmetry and synchronization of alpha rhythm during meditation.
Thus, the neuro-effects of meditation may be summarized to produce:
1. Increase in synchrony of EEG activity (hypersynchrony).
2. Increase in inter-hemispheric coherence of EEG activity.
3. Increase in brain Glutamate.
4. Increase in brain Serotonin.
There is overwhelming evidence of hypersynchrony predisposing to epilepsy. Hyperventilation causes synchrony and precipitates epilepsy [16]. It is a provocative technique during EEG recording. Sleep also is a provocative technique, a significant number of epileptics reveal inter-ictal epileptiform activity in their EEG only during sleep [17,18]. Hypersynchrony of sleep facilitates both initiation and propagation of partial seizures [17]. It is well known that NREM sleep causes increased susceptibility to epilepsy. Spiky epileptic discharge means more synchronisation of unit cell populations and Spike is caused by synchronisation of population group 1 neurons [19]. Spikes depict interictal epileptiform activity and their correlation with intracellular recordings shows that the former are associated with firing of action potentials [20].
Increase in inter-hemispheric coherence of EEG activity may contribute in its own way towards propagation and generalization of epileptic discharges. A focal discharge restricted to a localized region can tend to become widespread precariously. Corpus callostomy is a surgical procedure performed for control of un-controllable generalized seizures, the objective being to block inter-hemispheric transmission of epileptic potentials.
Glutamate is neuro-excitatory transmitter and widely implicated in epilepsy. The epileptic focus has been shown to contain more Glutamate than in normal state [21] and potassium-stimulated Glutamate release is more in cortical slices removed from epileptic patients than normal tissue [21].
Neurons in epileptic region exhibit paroxysmal depolarization shift (PDS) that is associated with a burst of action potentials [22]; interestingly, effect of Glutamate on NMDA receptors also produces a response similar to PDS [22] and a search for Glutamate antagonists as anti-epileptics is being promoted.
Serotonin also has been implicated in epileptogenesis and anti-serotonin are found to possess anti-convulsant properties [23,24]. 5-HT 2A receptor activation causes slow depolarisations and enhancement of excitatory signals such as Glutamate [25] and Cyproheptadine, which is 5-HT 2A blocker, has anti-convulsant activity [26].
Conclusion
Thus, each of the above-cited effects, which invariably occur at sometime during the course of meditation can present a potential risk for epileptogenesis and/or precipitating attack(s) in an epileptic patient. Needless to say, the concurrent presence of two or more of these effects can contribute tremendously to epileptogenesis, even to the extent of rendering a normal person epilepsy-prone.
Meditation is known to produce relaxation and epilepsy after relaxation is a well-known entity [27]. Meditation is presently being advised and resorted to for alleviating epilepsy; this paper clearly outlines the risk of enhancing the epileptic state during the course and attainment of meditation state.
However, further insight into the neuro-physiological and neuro-chemical avenues associated with meditation is definitely required. The epileptic proneness and incidence of epilepsy in regular meditators needs to be elucidated. Presently, however, caution may be exercised over the practice of meditation in patients prone to epilepsy. At least, epileptic patients seeking alleviation of their attacks through practice of meditation may be warned of the potential hazard outlined in the paper.
_______________
Notes:
* Tel.: +91 751 233 1147. E-mail address: dr_jaseja@yahoo.com.
0306-9877/$ - see front matter c 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2004.09.012
References
[1] Herzog H, Lele VR, Kuwert T, et al. Changed pattern of regional glucose metabolism during Yoga meditative relaxation. Neuropsychobiology 1990-1991;23:182–7.
[2] Lou HC, Kjaer TW, Friberg L,. et al. A 15O-H2O PET study of meditation and the resting state of normal consciousness. Human Brain Map 1999;7:98–105.
[3] Kjaer, Bertelsen, Piccini, Brooks, Alving, Lou, 2002.
[4] Newberg AB, Alavi A, Baime M,. et al. The measurement of regional blood flow during the complex cognitive task of meditation: a preliminary SPECT study. Psychiatr Res Neuroimaging 2001;106:113–22.
[5] Lazar SW, Bush G, Gollub RL,. et al. Functional brain mapping of the relaxation response and meditation. Neuroreport 2000;11:1581–5.
[6] Banquet JP. Spectral analysis of EEG in meditation. Electroencephal Clin Neurophysiol 1973;35:143–51.
[7] Banquet JP. EEG and meditation. Electroencephalography Clin Neurophysiol 1972;33:449.
[8] Ingvar DH. The will of the brain: cerebral correlates of willful acts. J Theor Biol 1994;171:7–12.
[9] Frith CD, Friston K, Liddle PF,. et al. Willed action and the prefrontal cortex in man. A study with PET. Proc R Soc Lond 1991;244:241–6.
[10] Posner MI, Peterson SE. The attention system of the human brain. Ann Rev Neurosci 1990;13:25–42.
[11] Pardo JV, Fox PT, Raichle ME. Localization of a human system for sustained attention by positron emission tomography. Nature 1991;349:61–4.
[12] Cheramy A, Romo R, Glowinski. Role of corticostriatal glutamatergic neurons in the presynaptic control of dopamine release. In: Sandler M, Feuerstein C, Scatton B et al, editors. Neurotransmitter interactions in the basal ganglia. New York: Raven Press; 1987.
[13] Olds ME, Forbes JL. The central basis of motivation, intracranial self-stimulation studies. Ann Rev Psychol 1981;32:523–74.
[14] Walton KG, Pugh ND, Gelderloos P, Macrae P. Stress reduction and preventing hypertension: preliminary support for a psychoneuroendocrine mechanism. J Altern Complement Med 1995;1:263–83.
[15] Kiloh LG, Osselton JW. Clinical electroencephalography. 4th ed. London: Butterworth; 1981.
[16] Handbook of electro-encephalography and clinical neurophysiology. vol. 13, part A. Amsterdam: Elsevier Scientific Publishing Company; 1975. p. 48–9.
[17] Herman ST, Walczak TS, Bazil CW. Neurology 2001;56:1453–9.
[18] Handbook of electro-encephalography and clinical neurophysiology. vol. 13, part A. Amsterdam: Elsevier Scientific Publishing Company; 1975. p. 31, 38.
[19] Fenwick P. The relationship between mind, brain and seizures. Arch Indian Psychiat 1994;1(1):3–6.
[20] Goodman and Gilman’s The pharmacological basis of therapeutics. 9th ed., International edn.; 1996. p. 465.
[21] Rang HP, Dale MM, Ritter JM. Pharmacology. 3rd ed. 1995. p. 599.
[22] Rang HP, Dale MM, Ritter JM. Pharmacology. 3rd ed. 1995. p. 598.
[23] Vimal Chandra. Ind J Pharmacol 1972;4(3):174–7.
[24] Bapat SK, Vimal Chandra. Ind J Pharmacol 1969;1(4):32–6.
[25] Goodman and Gilman’s. The pharmacological basis of therapeutics. 9th ed. International edn. 1996. p. 256.
[26] Satoskar, Kale, Bhandarkar’s. Pharmacology and pharmacotherapeutics. 16th ed. 1999, p. 318.
[27] Epilepsy News, Sleep and Epilepsy, Mohammed I. Zahoor produced by Sleep Research Laboratory, Wallace Mendelson, Director, The University of Chicago Hospitals.
[28] Bagchi BK, Wenger MA. Simultaneous EEG and other recordings during some yogic practices. Electroencephalogr Clin Neurophysiol 1958;10:193.
[29] Kasamatsu A, Hirai T. An electroencephalographic study on the zen medication. In: Tart, editor. Altered states of consciousness; 1969. p. 501–14.
[30] Anand BK, Chhina GS, Singh B. Some aspects of electroencephalographic studies in yogis. Electroencephalogr Clin Neurophysiol 1961;13:452–6.