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Pedunculopontine nucleus (PPN) stimulation in intractable epilepsy: Evidence-related programming
Epilepsy & Behavior 31 (2014) 56
Contents lists available at ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Letter to the Editor Pedunculopontine nucleus (PPN) stimulation in intractable epilepsy: Evidence-related programming
waves) during nighttime sleep. This programming can ensure EEG desynchronization, i.e., antiepileptic influence and environment for desired period(s) through the wake-sleep cycle to achieve significant seizure control with parallel improvement in quality of life.
To the Editor The work is original. Pedunculopontine nucleus stimulation (PPNS) has been recently proposed as an effective adjunctive therapy for patients with intractable epilepsy (IE) [1–3]. As with other forms of deep brain stimulation (DBS) therapy for advanced stages of diseases like Parkinson's disease (PD), obsessive–compulsive disorders and IE, programming of DBS constitutes an important step and factor in determining the efficacy and also the success of the therapy. This brief paper attempts to present relevant evidence that can aid in rational programming of the proposed PPNS in patients with IE for effective control of their seizures. The proposed PPNS in IE is essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep which has been reported to be enhanced by PPNS in several studies [4–7]. It has been suggested that the antiepileptic property of REM sleep is dual in nature and is based upon not only EEG-desynchronization but also on generation of ponto-geniculo-occipital (PGO) waves that constitute an important component of REM sleep [8]. Ponto-geniculo-occipital waves have also been recorded from human pons during and before REM sleep in a study of clinical effects of unilateral PPNS in patients with PD [9]. Degeneration of acetylcholine neurons (AChN) in PPN has been implicated in postural impairment found in patients with PD [10] for which PPNS has shown considerable success in the ongoing clinical trials [11]; by analogy, the degeneration of AChN in PPN observed in autopsy examinations of patients with West syndrome (WS) [12] may, therefore, constitute an additional important rationale in support of the postulation of PPNS in IE with reasonable hopes of successful control of seizures. The degeneration of AChN of PPN in West syndrome (WS) [12] has led the researchers to suggest a specific role of AChN in epileptogenesis and which may also account for possible postural impairment in patients with WS that may escape detection unless the possibility is borne in the clinicians' minds and specifically searched for. Low-frequency (10–25 Hz) stimulation of PPN as observed in daytime polysomnography has been found to promote alertness [7] that is associated with EEG desynchronization and, therefore, is capable of exercising antiepileptic influence [13]; PPN, otherwise, also plays an important role in maintenance of the cortical arousal during wakefulness [14]. Thus, from available evidence, it is suggested that PPNS programming may be designed to attain alertness (associated with EEG desynchronization) during daytime at low-frequency stimulation and REM sleep (associated with EEG desynchronization and PGO
1525-5050/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.yebeh.2013.11.015
Conflict of Interest None to disclose.
References [1] Jaseja H. Pedunculopontine nucleus stimulation: a novel adjunctive therapeutic approach in intractable epilepsy. Epilepsy Behav 2013;27(1):279. [2] Jaseja H. Pedunculopontine nucleus stimulation: potent therapeutic role in intractable epilepsy. Epilepsy Behav 2013;27(1):280. [3] Jaseja H. Pedunculopontine nucleus stimulation in intractable epilepsy: simulation of nature's anti-epileptic role and mechanism. Epilepsy Behav 2013;27(3):507. [4] Lim AS, Moro E, Lozano AM, Hamani C, Dostrovsky JO, Hutchison WD, et al. Selective enhancement of rapid eye movement sleep by deep brain stimulation of the human pons. Ann Neurol 2009;66(1):110–4. [5] Romigi A, Placidi F, Peppe A, Pierantozzi M, Izzi F, Brusa L, et al. Pedunculopontine nucleus stimulation influences REM sleep in Parkinson's disease. Eur J Neurol 2008;15:e64–5. [6] Allessandro S, Ceravolo R, Brusa L, Pierantozzi M, Costa A, Galati S, et al. Non-motor functions in parkinsonian patients implanted in the pedunculopontine nucleus: focus on sleep and cognitive domains. J Neurol Sci 2010;289:44–8. [7] Arnulf I, Ferraye M, Fraix V, Benabid AL, Chabardes S, Goetz L, et al. Sleep induced by stimulation in the human pedunculopontine nucleus area. Ann Neurol 2010;67:546–9. [8] Jaseja H. Functional components of REM sleep programmed to exert natural antiepileptogenic influence. Med Hypotheses 2007;68(5):1186–7. [9] Lim AS, Lozano AM, Moro E, Hamani C, Hutchison WD, Dostrovsky JO, et al. Characterization of REM-sleep associated ponto-geniculo-occipital waves in the human pons. Sleep 2007;30(7):823–7. [10] Müller ML, Albin RL, Kotagal V, Koeppe RA, Scott PJ, Frey KA, et al. Thalamic cholinergic innervations and postural sensory integration function in Parkinson's disease. Brain 2013;136(Pt 11):3282–9. [11] Thevathasan W, Coyne TJ, Hyam JA, Kerr G, Jenkinson N, Aziz TZ, et al. Pedunculopontine nucleus stimulation improves gait freezing in Parkinson disease. Neurosurgery 2011;69(6):1248–53 [discussion 1254]. [12] Hayashi M, Nakajima K, Miyata R, Tanuma N, Kodama T. Lesions of acetylcholine neurons in refractory epilepsy. ISRN Neurol 2012;2012:404263. [13] Peter F. The relationship between mind, brain and seizures. Arch Indian Psychiat 1994;1(1):3–6. [14] Amara AW, Watts RL, Walker HC. The effects of deep brain stimulation on sleep in Parkinson's disease. Ther Adv Neurol Disord 2011;4(1):15–24.
Harinder Jaseja Vellore EEG Center, Gwalior, India 8, C-Block, Harishanker-puram, Lashkar, Gwalior 474002, M.P., India. E-mail address: [email protected]. 8 November 2013
Contents lists available at ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Letter to the Editor Pedunculopontine nucleus (PPN) stimulation in intractable epilepsy: Evidence-related programming
waves) during nighttime sleep. This programming can ensure EEG desynchronization, i.e., antiepileptic influence and environment for desired period(s) through the wake-sleep cycle to achieve significant seizure control with parallel improvement in quality of life.
To the Editor The work is original. Pedunculopontine nucleus stimulation (PPNS) has been recently proposed as an effective adjunctive therapy for patients with intractable epilepsy (IE) [1–3]. As with other forms of deep brain stimulation (DBS) therapy for advanced stages of diseases like Parkinson's disease (PD), obsessive–compulsive disorders and IE, programming of DBS constitutes an important step and factor in determining the efficacy and also the success of the therapy. This brief paper attempts to present relevant evidence that can aid in rational programming of the proposed PPNS in patients with IE for effective control of their seizures. The proposed PPNS in IE is essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep which has been reported to be enhanced by PPNS in several studies [4–7]. It has been suggested that the antiepileptic property of REM sleep is dual in nature and is based upon not only EEG-desynchronization but also on generation of ponto-geniculo-occipital (PGO) waves that constitute an important component of REM sleep [8]. Ponto-geniculo-occipital waves have also been recorded from human pons during and before REM sleep in a study of clinical effects of unilateral PPNS in patients with PD [9]. Degeneration of acetylcholine neurons (AChN) in PPN has been implicated in postural impairment found in patients with PD [10] for which PPNS has shown considerable success in the ongoing clinical trials [11]; by analogy, the degeneration of AChN in PPN observed in autopsy examinations of patients with West syndrome (WS) [12] may, therefore, constitute an additional important rationale in support of the postulation of PPNS in IE with reasonable hopes of successful control of seizures. The degeneration of AChN of PPN in West syndrome (WS) [12] has led the researchers to suggest a specific role of AChN in epileptogenesis and which may also account for possible postural impairment in patients with WS that may escape detection unless the possibility is borne in the clinicians' minds and specifically searched for. Low-frequency (10–25 Hz) stimulation of PPN as observed in daytime polysomnography has been found to promote alertness [7] that is associated with EEG desynchronization and, therefore, is capable of exercising antiepileptic influence [13]; PPN, otherwise, also plays an important role in maintenance of the cortical arousal during wakefulness [14]. Thus, from available evidence, it is suggested that PPNS programming may be designed to attain alertness (associated with EEG desynchronization) during daytime at low-frequency stimulation and REM sleep (associated with EEG desynchronization and PGO
1525-5050/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.yebeh.2013.11.015
Conflict of Interest None to disclose.
References [1] Jaseja H. Pedunculopontine nucleus stimulation: a novel adjunctive therapeutic approach in intractable epilepsy. Epilepsy Behav 2013;27(1):279. [2] Jaseja H. Pedunculopontine nucleus stimulation: potent therapeutic role in intractable epilepsy. Epilepsy Behav 2013;27(1):280. [3] Jaseja H. Pedunculopontine nucleus stimulation in intractable epilepsy: simulation of nature's anti-epileptic role and mechanism. Epilepsy Behav 2013;27(3):507. [4] Lim AS, Moro E, Lozano AM, Hamani C, Dostrovsky JO, Hutchison WD, et al. Selective enhancement of rapid eye movement sleep by deep brain stimulation of the human pons. Ann Neurol 2009;66(1):110–4. [5] Romigi A, Placidi F, Peppe A, Pierantozzi M, Izzi F, Brusa L, et al. Pedunculopontine nucleus stimulation influences REM sleep in Parkinson's disease. Eur J Neurol 2008;15:e64–5. [6] Allessandro S, Ceravolo R, Brusa L, Pierantozzi M, Costa A, Galati S, et al. Non-motor functions in parkinsonian patients implanted in the pedunculopontine nucleus: focus on sleep and cognitive domains. J Neurol Sci 2010;289:44–8. [7] Arnulf I, Ferraye M, Fraix V, Benabid AL, Chabardes S, Goetz L, et al. Sleep induced by stimulation in the human pedunculopontine nucleus area. Ann Neurol 2010;67:546–9. [8] Jaseja H. Functional components of REM sleep programmed to exert natural antiepileptogenic influence. Med Hypotheses 2007;68(5):1186–7. [9] Lim AS, Lozano AM, Moro E, Hamani C, Hutchison WD, Dostrovsky JO, et al. Characterization of REM-sleep associated ponto-geniculo-occipital waves in the human pons. Sleep 2007;30(7):823–7. [10] Müller ML, Albin RL, Kotagal V, Koeppe RA, Scott PJ, Frey KA, et al. Thalamic cholinergic innervations and postural sensory integration function in Parkinson's disease. Brain 2013;136(Pt 11):3282–9. [11] Thevathasan W, Coyne TJ, Hyam JA, Kerr G, Jenkinson N, Aziz TZ, et al. Pedunculopontine nucleus stimulation improves gait freezing in Parkinson disease. Neurosurgery 2011;69(6):1248–53 [discussion 1254]. [12] Hayashi M, Nakajima K, Miyata R, Tanuma N, Kodama T. Lesions of acetylcholine neurons in refractory epilepsy. ISRN Neurol 2012;2012:404263. [13] Peter F. The relationship between mind, brain and seizures. Arch Indian Psychiat 1994;1(1):3–6. [14] Amara AW, Watts RL, Walker HC. The effects of deep brain stimulation on sleep in Parkinson's disease. Ther Adv Neurol Disord 2011;4(1):15–24.
Harinder Jaseja Vellore EEG Center, Gwalior, India 8, C-Block, Harishanker-puram, Lashkar, Gwalior 474002, M.P., India. E-mail address: [email protected]. 8 November 2013