Current Research on Local Field Potential Rhythms of Deep Brain Stimulation Indications
Chen Yue1 Qian Xing1 Hao Hongwei1# Li Luming1,2#*
1National Engineering Laboratory for Neuromodulation, Beijing 100084, China 2Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing 100093, China
Abstract：As a technology of neuromodulation, Deep Brain Stimulation (DBS) has become an established clinical treatment for brain disorders and opened a window of brain for neuroscience researchers. In this article, current treatment status and pathology hypothesis of 4 FDA-approved brain disorders are briefly introduced, including the Parkinson disease (PD), dystonia, essential tremor and obsessive compulsive disorder (OCD). The LFP theta, alpha, beta, gamma and other high frequency rhythms of the above diseases are summarized as well. Relevance between the LFP rhythms and clinical symptoms or behaviors is analyzed. The latest implantable LFP research tool and the real-time collection results are introduced. In conclusion, the LFP rhythms of DBS targets or related areas could reflect characteristics of different brain disorders. These electrophysiological rhythms will make the foundation for the pathological study, DBS mechanism exploration and theoretical development of neuromodulation. At last, based on the limits of the current researches, this article proposes some prospect of LFP rhythm study, which would be of great significance to the field of neuromodulation.
基金资助:国家自然科学基金大仪器专项(81527901);中央在京高校重大成果转化项目(Z151100003915123); 中国生物医学工程学会高级会员(Senior member, Chinese Society of Biomedical Engineering)
引用本文:
陈玥, 钱星, 郝红伟, 李路明. 脑深部刺激适应症局部场电位节律特征研究进展[J]. 中国生物医学工程学报, 2016, 35(5): 577-586.
Chen Yue Qian Xing Hao Hongwei Li Luming. Current Research on Local Field Potential Rhythms of Deep Brain Stimulation Indications. Chinese Journal of Biomedical Engineering, 2016, 35(5): 577-586.
[1] Perlmutter JS, Mink JW. Deep brain stimulation [J].Annual Review of Neuroscience, 2006, 29: 229-257. [2] 李路明,郝红伟. 植入式神经刺激器的现状与发展趋势[J]. 中国医疗器械杂志,2009,02:107-111. [3] Benabid AL, Pollak P, Hoffmann D, et al. Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus[J]. The Lancet, 1991, 337(8738): 403-406. [4] Logothetis NK. The underpinnings of the BOLD functional magnetic resonance imaging signal [J]. The Journal of Neuroscience, 2003, 23(10): 3963-3971. [5] Iadecola C. Neurovascular regulation in the normal brain and in Alzheimer′s disease [J]. Nature Reviews Neuroscience, 2004, 5(5): 347-360. [6] Shen H, Neuroscience: Tuning the brain [EB]. http://www.nature.com/news/neuroscience-tuning-the-brain-1.14900, 2014-03-19/2016-02-23. [7] Kandel ER, Schwartz JH, Jessell TM, et al. Principles of neural science [M] (5th Edition). Beijing: China Machine Press, 2015:996-1403. [8] Alexander GE, Crutcher MD. Functional architecture of basal ganglia circuits: neural substrates of parallel processing [J]. Trends in Neurosciences, 1990, 13(7): 266-271. [9] DeLong MR. Primate models of movement disorders of basal ganglia origin [J]. Trends in Neurosciences, 1990, 13(7): 281-285. [10] Brown P, Oliviero A, Mazzone P, et al. Dopamine dependency of oscillations between subthalamic nucleus and pallidum in Parkinson′s disease [J]. The Journal of Neuroscience, 2001, 21(3): 1033-1038. [11] Swann N, Poizner H, Houser M, et al. Deep brain stimulation of the subthalamic nucleus alters the cortical profile of response inhibition in the beta frequency band: A scalp EEG study in Parkinson′s disease[J]. The Journal of Neuroscience, 2011, 31(15): 5721-5729. [12] McCarthy MM, Moore-Kochlacs C, Gu X, et al. Striatal origin of the pathologic beta oscillations in Parkinson′s disease[J]. Proceedings of the National Academy of Sciences, 2011, 108(28): 11620-11625. [13] Ray NJ, Jenkinson N, Wang S, et al. Local field potential beta activity in the subthalamic nucleus of patients with Parkinson′s disease is associated with improvements in bradykinesia after dopamine and deep brain stimulation [J]. Experimental Neurology, 2008, 213(1): 108-113. [14] Kühn AA, Tsui A, Aziz T, et al. Pathological synchronisation in the subthalamic nucleus of patients with Parkinson′s disease relates to both bradykinesia and rigidity [J]. Experimental Neurology, 2009, 215(2): 380-387. [15] Kühn AA, Kempf F, Brücke C, et al. High-frequency stimulation of the subthalamic nucleus suppresses oscillatory β activity in patients with Parkinson′s disease in parallel with improvement in motor performance [J]. The Journal of Neuroscience, 2008, 28(24): 6165-6173. [16] Whitmer D, De Solages C, Hill B, et al. High frequency deep brain stimulation attenuates subthalamic and cortical rhythms in Parkinson′s disease[J]. Front Hum Neurosci, 2012, 6(155): 1-18. [17] Eusebio A, Thevathasan W, Gaynor LD, et al. Deep brain stimulation can suppress pathological synchronisation in parkinsonian patients[J]. Journal of Neurology, Neurosurgery & Psychiatry, 2011, 82(5): 569-573. [18] Grill WM, Snyder AN, Miocinovic S. Deep brain stimulation creates an informational lesion of the stimulated nucleus[J]. Neuroreport, 2004, 15(7): 1137-1140. [19] Priori A, Foffani G, Rossi L, et al. Adaptive deep brain stimulation (aDBS) controlled by local field potential oscillations[J]. Experimental Neurology, 2013, 245: 77-86. [20] Joundi R A, Brittain J S, Green A L, et al. Oscillatory activity in the subthalamic nucleus during arm reaching in Parkinson′s disease[J]. Experimental Neurology, 2012, 236(2): 319-326. [21] Quinn E J, Blumenfeld Z, Velisar A, et al. Beta oscillations in freely moving Parkinson′s subjects are attenuated during deep brain stimulation [J]. Movement Disorders, 2015, 30(13): 1750-1758. [22] Cassidy M, Mazzone P, Oliviero A, et al. Movement-related changes in synchronization in the human basal ganglia [J]. Brain, 2002, 125(6): 1235-1246. [23] Connolly AT, Muralidharan A, Hendrix C, et al. Local field potential recordings in a non-human primate model of Parkinsons disease using the Activa PC+S neurostimulator [J]. Journal of Neural Engineering, 2015, 12(6): 066012. [24] Kühn AA, Doyle L, Pogosyan A, et al. Modulation of beta oscillations in the subthalamic area during motor imagery in Parkinson′s disease[J]. Brain, 2006, 129(3): 695-706. [25] Qian X, Hao H, Ma B, et al. Implanted rechargeable electroencephalography (EEG) device [J]. Electronics Letters, 2014, 50(20): 1419-1421. [26] Stanslaski S, Afshar P, Cong P, et al. Design and validation of a fully implantable, chronic, closed-loop neuromodulation device with concurrent sensing and stimulation[J]. IEEE Transactions on Neural Systems and Rehabilitation Engineering, 2012, 20(4): 410-421. [27] Jenkinson N, Kühn AA, Brown P. Gamma oscillations in the human basal ganglia [J]. Experimental Neurology, 2013, 245: 72-76. [28] Beudel M, Little S, Pogosyan A, et al. Tremor reduction by deep brain stimulation is associated with gamma power suppression in Parkinson′s disease [J]. Neuromodulation: Technology at the Neural Interface, 2015, 18(5): 349-354. [29] Anzak A, Tan H, Pogosyan A, et al. Subthalamic nucleus activity optimizes maximal effort motor responses in Parkinson′s disease[J]. Brain, 2012, 135(9): 2766-2778. [30] Weinberger M, Hutchison WD, Lozano AM, et al. Increased gamma oscillatory activity in the subthalamic nucleus during tremor in Parkinson′s disease patients[J]. Journal of Neurophysiology, 2009, 101(2): 789-802. [31] Anzak A, Gaynor L, Beigi M, et al. Subthalamic nucleus gamma oscillations mediate a switch from automatic to controlled processing: a study of random number generation in Parkinson′s disease [J]. Neuroimage, 2013, 64: 284-289. [32] Foffani G, Priori A, Egidi M, et al. 300‐Hz subthalamic oscillations in Parkinson′s disease [J]. Brain, 2003, 126(10): 2153-2163. [33] zkurt T E, Butz M, Homburger M, et al. High frequency oscillations in the subthalamic nucleus: a neurophysiological marker of the motor state in Parkinson′s disease[J]. Experimental Neurology, 2011, 229(2): 324-331. [34] Blumenfeld Z, Bront-Stewart H. High frequency deep brain stimulation and neural rhythms in Parkinson′s disease [J]. Neuropsychology Review, 2015, 25(4): 384-397. [35] Thompson JA, Lanctin D, Ince NF, et al. Clinical implications of local field potentials for understanding and treating movement disorders [J]. Stereotactic and Functional Neurosurgery, 2014, 92(4): 251-263. [36] Beudel M, Brown P. Adaptive deep brain stimulation in Parkinson′s disease [J]. Parkinsonism & Related Disorders, 2016, 22: S123-S126. [37] Alonso-Frech F, Zamarbide I, Alegre M, et al. Slow oscillatory activity and levodopa-induced dyskinesias in Parkinson′s disease [J]. Brain, 2006, 129(7): 1748-1757. [38] Lewis SJG, Barker RA. A pathophysiological model of freezing of gait in Parkinson′s disease [J]. Parkinsonism & Related Disorders, 2009, 15(5): 333-338. [39] Redgrave P, Rodriguez M, Smith Y, et al. Goal-directed and habitual control in the basal ganglia: implications for Parkinson′s disease[J]. Nature Reviews Neuroscience, 2010, 11(11): 760-772. [40] Androulidakis AG, Mazzone P, Litvak V, et al. Oscillatory activity in the pedunculopontine area of patients with Parkinson′s disease[J]. Experimental Neurology, 2008, 211(1): 59-66. [41] Huebl J, Schoenecker T, Siegert S, et al. Modulation of subthalamic alpha activity to emotional stimuli correlates with depressive symptoms in Parkinson′s disease [J]. Movement Disorders, 2011, 26(3): 477-483. [42] Marco-Pallarés J, Münte T F, Rodríguez-Fornells A. The role of high-frequency oscillatory activity in reward processing and learning [J]. Neuroscience & Biobehavioral Reviews, 2015, 49: 1-7. [43] López-Azcárate J, Tainta M, Rodríguez-Oroz MC, et al. Coupling between beta and high-frequency activity in the human subthalamic nucleus may be a pathophysiological mechanism in Parkinson′s disease [J]. The Journal of Neuroscience, 2010, 30(19): 6667-6677. [44] Connolly AT, Jensen AL, Bello EM, et al. Modulations in oscillatory frequency and coupling in globus pallidus with increasing parkinsonian severity[J]. The Journal of Neuroscience, 2015, 35(15): 6231-6240. [45] 王宗宝,黄永志,张新静,等. 帕金森病患者局部场电位信号多频耦合特征分析[J]. 生物医学工程学杂志,2015,04:874-880. [46] Chen CC, Kühn AA, Trottenberg T, et al. Neuronal activity in globus pallidus interna can be synchronized to local field potential activity over 3-12 Hz in patients with dystonia [J]. Experimental Neurology, 2006, 202(2): 480-486. [47] Kühn AA, Brücke C, Schneider GH, et al. Increased beta activity in dystonia patients after drug-induced dopamine deficiency [J]. Experimental Neurology, 2008, 214(1): 140-143. [48] Lee J R, Kiss ZHT. Interhemispheric difference of pallidal local field potential activity in cervical dystonia [J]. Journal of Neurology, Neurosurgery & Psychiatry, 2013, 85(3): 306-310. [49] Neumann WJ, Huebl J, Brücke C, et al. Enhanced low-frequency oscillatory activity of the subthalamic nucleus in a patient with dystonia [J]. Movement Disorders, 2012, 27(8): 1063-1066. [50] Liu X, Wang S, Yianni J, et al. The sensory and motor representation of synchronized oscillations in the globus pallidus in patients with primary dystonia [J]. Brain, 2008, 131(6): 1562-1573. [51] Weinberger M, Hutchison WD, Alavi M, et al. Oscillatory activity in the globus pallidus internus: comparison between Parkinson′s disease and dystonia [J]. Clinical Neurophysiology, 2012, 123(2): 358-368. [52] Volkmann J, Mueller J, Deuschl G, et al. Pallidal neurostimulation in patients with medication-refractory cervical dystonia: a randomised, sham-controlled trial [J]. The Lancet Neurology, 2014, 13(9): 875-884. [53] 杨张凯,王学廉,汪鑫,等. 脑深部电刺激治疗肌张力障碍的疗效分析[J]. 中国临床神经外科杂志,2015,1:21-24. [54] Barow E, Neumann WJ, Brücke C, et al. Deep brain stimulation suppresses pallidal low frequency activity in patients with phasic dystonic movements [J]. Brain, 2014, 137(11): 3012-3024. [55] Singh A, Kammermeier S, Plate A, et al. Pattern of local field potential activity in the globus pallidus internum of dystonic patients during walking on a treadmill [J]. Experimental Neurology, 2011, 232(2): 162-167. [56] Brücke C, Huebl J, Schnecker T, et al. Scaling of movement is related to pallidal γ oscillations in patients with dystonia [J]. The Journal of Neuroscience, 2012, 32(3): 1008-1019. [57] Welter ML, Grabli D, Karachi C, et al. Pallidal activity in myoclonus dystonia correlates with motor signs [J]. Movement Disorders, 2015, 30(7): 992-996. [58] Elble RJ. What is essential tremor? [J]. Current Neurology and Neuroscience Reports. 2013, 13(6) :1-8. [59] Koller WC, Lyons KE, Wilkinson SB, et al. Long-term safety and efficacy of unilateral deep brain stimulation of the thalamus in essential tremor[J]. Movement Disorders, 2001, 16(3): 464-468. [60] 陈宁,孟凡刚,马羽,等. 丘脑底核脑深部电刺激治疗特发性震颤2例临床分析[J]. 立体定向和功能性神经外科杂志,2013,1:34-37. [61] Kane A, Hutchison WD, Hodaie M, et al. Enhanced synchronization of thalamic theta band local field potentials in patients with essential tremor [J]. Experimental Neurology, 2009, 217(1): 171-176. [62] Basha D, Dostrovsky J O, Rios A LL, et al. Beta oscillatory neurons in the motor thalamus of movement disorder and pain patients[J]. Experimental Neurology, 2014, 261: 782-790. [63] Marsden JF, Ashby P, Limousin-Dowsey P, et al. Coherence between cerebellar thalamus, cortex and muscle in man[J]. Brain, 2000, 123(7): 1459-1470. [64] Air EL, Ryapolova-Webb E, de Hemptinne C, et al. Acute effects of thalamic deep brain stimulation and thalamotomy on sensorimotor cortex local field potentials in essential tremor [J]. Clinical Neurophysiology, 2012, 123(11): 2232-2238. [65] Abramowitz JS, Taylor S, McKay D. Obsessive-compulsive disorder [J]. The Lancet, 2009, 374(9688): 491-499. [66] Greenberg BD, Malone DA, Friehs GM, et al. Three-year outcomes in deep brain stimulation for highly resistant obsessive\|compulsive disorder [J]. Neuropsychopharmacology, 2006, 31(11): 2384-2393. [67] Huff W, Lenartz D, Schormann M, et al. Unilateral deep brain stimulation of the nucleus accumbens in patients with treatment-resistant obsessive-compulsive disorder: Outcomes after one year[J]. Clinical Neurology and Neurosurgery, 2010, 112(2): 137-143. [68] Kohl S, Schnherr DM, Luigjes J, et al. Deep brain stimulation for treatment-refractory obsessive compulsive disorder: a systematic review [J]. BMC Psychiatry, 2014, 14(1): 214. [69] Bastin J, Polosan M, Piallat B, et al. Changes of oscillatory activity in the subthalamic nucleus during obsessive-compulsive disorder symptoms: two case reports [J]. Cortex, 2014, 60: 145-150. [70] Ewing SG, Grace AA. Long-term high frequency deep brain stimulation of the nucleus accumbens drives time-dependent changes in functional connectivity in the rodent limbic system [J]. Brain Stimulation, 2013, 6(3): 274-285. [71] Neumann WJ, Staub F, Horn A, et al. Deep brain recordings using an implanted pulse generator in Parkinson′s disease [J]. Neuromodulation: Technology at the Neural Interface, 2016, 19(1): 20-24. [72] Little S, Pogosyan A, Neal S, et al. Adaptive deep brain stimulation in advanced Parkinson disease [J]. Annals of Neurology, 2013, 74(3): 449-457. [73] Fasano A, Lozano AM. The FM/AM world is shaping the future of deep brain stimulation[J]. Movement Disorders, 2014, 29(2): 161-163. [74] Jia F, Guo Y, Wan S, et al. Variable frequency stimulation of subthalamic nucleus for freezing of gait in Parkinson′s disease[J]. Parkinsonism & Related Disorders, 2015, 21(12): 1471-1472.
