Deep Brain Stimulation Effective and Safe For Patients with Obsessive Compulsive Disorder and Comorbid Bipolar Disorder
Srikanta Kumar Sahoo1, Suvendu Narayan Mishra2, SaurjyaRanjan Das3, Jatindra Nath Mohanty4*
1Department of Neurology, IMS and Sum Hospital, SOA Deemed to be University, Bhubaneswar, India.
2Department of Psychiatry, IMS and Sum Hospital, SOA Deemed to be University, Bhubaneswar, India.
3Department of Anatomy, IMS and Sum Hospital, SOA Deemed to be University, Bhubaneswar, India.
4Medical Research Laboratory, IMS and Sum Hospital, SOA Deemed to be University, Bhubaneswar, India.
Abstract
Deep brain stimulation (DBS) is a successful treatment for unmanageable obsessive- compulsive disorder (OCD). Bipolar disorder (BD) is for the most part considered a contra- sign for DBS because of as often as possible detailed transient impulsivity or (hypo) insanity.
Inferior quality proof additionally recommends expanded positive reaction in hyper patients with bipolar confusion. There is negligible data in clinical writing identifying with intense unfriendly impacts related with the utilization of DBS in bipolar problem. Nonetheless, there is a shortage of proof concerning what befalls patients as far as backslide, reaction, or abatement, a long time after end of incitement. The utilization of DBS in patients with BD requires much more investigation. Nonetheless, present proof shows that it is viable for patients with bipolar sorrow. Its utilization in hyper people has not been very much explained. Further exploration ought to investigate its adequacy in hyper people; and particularly how to additionally refine the methodology to expand viability and diminish the danger of antagonistic occasions in patients with bipolar turmoil.
Keywords: Bipolar disorder, Deep brain stimulation, Mania, Depression, Unipolar depression.
Introduction
Over the top habitual problem (OCD) is a mental issue portrayed by fanatical considerations and urgent practices. Ordinary treatment alternatives for OCD are antidepressants and intellectual social treatment (CBT), however an expected 10% of patients are headstrong to these treatment choices [1]. Moreover, patients with OCD frequently have comorbid mental ailments [2]. The predominance of bipolar problem (BD) in patients with OCD is assessed to be 18.4% [3]. Elective medicines, other than CBT and drug, to oversee treatment headstrong OCD patients with comorbid BD are a neglected need. Albeit electroconvulsive treatment is powerful for the treatment of BD [4], the proof for ECT as a compelling treatment for OCD is
restricted [5]. Transcranial attractive incitement (TMS) is another type of treatment that has as of late been proposed for OCD. Be that as it may, the subsequent length of studies inspecting the impacts of OCD are not longer than 3 months, despite the fact that the constructive outcomes of TMS for OCD are known to be transient [6]. For BD, TMS doesn't appear to be successful [7].
Profound cerebrum incitement (DBS) includes implantation of cathodes and balance of explicit mind work. Following the principal preliminaries on DBS for OCD [8], a few investigations indicated that DBS focused at striatal zones is a compelling and safe treatment choice for patients with stubborn OCD [9]. All things considered, most involvement in DBS for OCD gets from clinical investigations, barring patients with genuine comorbid indications [10]. Most of studies rejected patients with comorbid bipolar confusion, in light of the expected danger of incitement actuated (hypo)mania [11]. Nonetheless, three examinations inspected adequacy and wellbeing of DBS for treatment safe melancholy (TRD) and incorporated a sum of 9 patients with BD II, focusing on the subcallosal cingulate [12]
ventral container/ventral striatum [12] and supero-horizontal part of the average forebrain pack [13]. DBS adequately smothered indications of despondency in patients with BD, while DBS caused hypomanic manifestations in just one case. Hypomanic side effects in this patient settled totally when incitement was stopped [12]. All in all, these examinations uphold the possibility that DBS is ok for patients with BD II, however experience is as yet restricted.A constraint of the previously mentioned examines, is that patients with BD I were barred for treatment with DBS [14]. Patients with BD II have just hypomanic scenes, while patients with BD I have a background marked by in any event one hyper scene. To our anxiety, just one case-report distributed the consequences of a patients with BD I that was effectively treated with DBS of the Cg 24/25 for burdensome indications [15]. No (hypo) hyper scenes happened following DBS for this situation. In any case, there is still restricted proof for the security of DBS in patients with a (co-sullen) BD I. Here, we present the consequences of 5 patients with OCD and comorbid BD I or II that got DBS of the ventral foremost appendage of the interior container (vALIC). The primary target of this investigation is to give fair-minded data as respects to the viability of DBS in the administration of BD.
Material and methods
We led a hunt on online information bases utilizing the catchphrases: bipolar turmoil, unipolar melancholy, profound mind incitement (DBS), madness, misery, and psychosurgery.
We included case reports, case arrangement, open-mark, single-daze, and randomized twofold visually impaired trick controlled investigations. The information sources were PubMed from MEDLINE, PsycINFO, COCHRANE, and EMBASE.
Eligibility Criteria
Studies that revealed results emerging from the utilization of DBS in sorrow, treatment-safe gloom, unipolar melancholy, madness, bipolar turmoil, or emotional issues were remembered for this examination. There were no constraints as respects the size of the subject populaces, explicit results of the investigates, and the chose study plans. Just examination papers in
English language were chosen. Arrangements of references of a few deliberate surveys were likewise utilized for filtering further references.
Inclination was killed by two autonomous commentators who screened the titles and edited compositions of the last determinations. Articles and papers that didn't meet the qualification standards were avoided. Official choices on the papers that were later included were made by the creators and commentators.
Exclusion Criteria
All the subsequent examinations from the chose sources were decreased by the end of studies that were not straightforwardly identified with the investigation of the utilization of DBS in sorrow, treatment-safe gloom, unipolar discouragement, bipolar despondency, craziness, or potentially bipolar confusion. Studies that examined the utilization of DBS in Tourette's condition, Parkinson's illness, Alzheimer's infection, or dependence were dispensed with.
Results and Discussion
In the treatment of the burdensome part of BD with DBS, there are four primary targets territories of the mind, which are the subcallosal cingulate cerebrum territory 25 (SCC- BA25), the Nucleus Accumbens (NAcc), the average forebrain group (MFB), and the ventral container/ventral striatum (VC/VS) [21-23]. Notwithstanding these, the parallel habenula (LHb), and the second rate thalamic peduncle (ITP) have likewise been demonstrated to be superb focuses for DBS [21,22]. The previous four fundamental targets have been demonstrated to be strong for DBS utilizing limited scope considers.
Be that as it may, there exists no standard randomized controlled preliminary to assess their similar efficacies. In assessing the treatment of sadness, reaction is estimated utilizing the Hamilton Depression Rating Scale (HDRS) as well as the Montgomery- Asberg Depression Rating Scale (MADRS). A 'reaction' alludes to a decrease of more prominent than or equivalent to half in either the HDRS or potentially MADRS or both, while 'abatement' alludes to a score of "nondepressed" on both of the two scoring frameworks [18].
Efficacy of DBS at the Subcallosal Cingulate (SCC-BA25)
The hugeness of the SCC (BA25) as a significant objective for DBS was first called attention to by uniting datasets which indicated the regulation of this territory will bring about a stimulant reaction and suggestive improvement in patients with both unipolar and bipolar sorrow [16]. It has the upside of not inclining patients with bipolar melancholy towards madness, a typical symptom of meds used to treat BD. Utilizing the SCC DBS, reaction rates somewhere in the range of 41% and 66% have been recorded inside 24-26 weeks, which later expanded to 64% to 92% following two to six years [17]. In this equivalent examination on patients with unipolar despondency, the abatement rate was somewhere in the range of 42% and 58%. These outcomes are exceptional for any type of treatment for bipolar melancholy. The capacity of SCC DBS to impact interest, state of mind, mystic uneasiness, suicidality, and center sleep deprivation simultaneously is a significant supporter of the checked improvement in the HDRS score. Thinking about the impact of DBS on bipolar despondency, in any case, 17
members were gone into an investigation in which they were at first treated with single- blinded incitement for about a month, and persistent dynamic incitement for an additional a half year [27]. Checking proceeded for a very long time after the beginning of dynamic incitement. There was a huge stimulant reaction of 42% and 65% following 6 and two years, separately; notwithstanding an improvement in capacity. The reduction rates were 18% and 58% inside a similar time spans [18]. None of the patients experienced unconstrained backslide, and there were no manifestations reminiscent of hypomania, insanity or hypermania. This outcome has additionally been duplicated in another investigation, demonstrating the capacity of DBS to viably treat bipolar confusion [18]. Adequacy of DBS at the mediocre thalamic peduncle (ITP)
The incitement of the ITP with DBS was first revealed for a situation investigation of a female patient with TRD that existed together with bulimia and marginal character issue [19]. A huge reaction was accomplished with ongoing incitement for almost two years.
Quite, she encountered a mellow resurgence of burdensome side effects when dynamic incitement was halted following eight months for a twofold visually impaired testing period. Negative impacts, for example, tachycardia, tension, dyspnea, nystagmus and perspiring were related with the intense ITP DBS (Table 1). Nonetheless, there were no recorded unfavorable impacts related with persistent incitement [20]. Likewise, examines have indicated the impact of central incitement of the LHb in two patients who had hard-headed misery, lethargic to prescriptions and ECT [21]. The two patients recorded huge decrease in their HDRS scores, despite the fact that suspension of incitement caused a quick backslide in the two cases, and which step by step settled with resumption of incitement. It was additionally brought up that the one of the patients required a voltage increment to 10.5V from 5V to arrive at full abatement; which proposes that there will be a quicker utilization of battery power and incessant changes in battery will be required [22]. In the two cases, there were no negative impacts with one or the other intense or ongoing incitement.
Table 1: Clinical studies on the use of DBS for unipolar depression and BD
Study Number/t
ype
Targ et
HDRS (%)
Follow -up period
Remark s
Mayberg et al.(2005) [47] 6
(unipolar)
SCC 55.0%
response
6mo
Lozano et al. (2008) [63];
Kennedy et al.(2011) [58] 20
(unipolar)
SCC 64.3%
response
72 mo
Holtzheimer et al.(2012) [27] 11
(unipolar) 7
(bipolar)
SCC 69.0%
response
24mo 92%
response
Malone et al.(2009) [30] 15
(unipolar)
VC/
VS
53.3%
response
48mo 40%
remission
Dougherty et al. (2014) [64] 30
(unipolar)
VC/
VS
23%
response
24 mo
Schlaepfer et al.(2013) [21] 7 (bipolar) MF B
- 6 mo
Bewernick et al.(2010) [34] 11
(unipolar)
NAc c
41.7%
response
48mo 9%
remission Jiménez et al.(2005) [22] 1
(unipolar)
ITP Remission N/R
No adve rse even ts Kiening et al.(2013) [36]; Knapp
et al.(2009) [62]; Sartorius et al.(2007) [37]
1
(unipolar)
LHb Remission N/R
Type signifies whether the form of depression is unipolar/bipolar; SCC =Subcallosal Cingulate; VC/VS
= Ventral Capsule/Ventral Striatum; MFB = Medial Forebrain Bundle; NAcc= Nucleus accumbens;
ITP = Inferior Thalamic Peduncle; mo= months; HDRS = Hamilton Depression Rating Scale; N/R = Not Reported.
The adequacy of the DBS in BD further reinforces the speculations that disposition problems are brought about by the pathologic interruption of neural organizations that moderate shifting parts of human passionate conduct. Confirmations presented through mind imaging from fMRI, PET outputs, and dispersion tractography have demonstrated decreased dim issue volume in the broadman region (BA) of the cerebrum in the orbital BA11 and BA47,and ventrolateral prefrontal cortex (PFC) BA45& BA47 [23]; prevalent transient gyrus; and back cingulate cortex in patients with BD [24]. These have been related with strange hardware, particularly inside the limbic-cortical-striatal-pallidal- thalamic (LCSPT) circuits [25]. The LCSPT circuit which has been related with passionate conduct is especially embroiled in the causation of melancholy. Since interruption of these circuits influences legitimate neural transmission through them, it is anything but difficult to relate how the brokenness can prompt the obsessive full of feeling states that are found in BD [26].
The subsequent neuroanatomical, neurophysio-consistent, neuropathological, and neurochemical variations from the norm that has been given confirmations meets under the neurocircuitry models of melancholy and craziness. The irregular releases and digestion in the amygdala, SCC, NAcc, and average thalamus frames the reasoning behind the use of DBS as a restorative methodology [27,28]. In straightforward terms, DBS acts to repress action in the dark/white issue that it invigorates, despite the fact that its component of activity has been demonstrated to be very more unpredictable [29]. Its outcomes rely to a great extent upon the area of cathodes in the cerebrum and the greatness of incitement.
Likewise, the adequacy of DBS additionally relies upon the degree of movement of the mind zone and the limit of DBS to successfully tweak this action [29].
The utilization of DBS has been inclined more towards patients with both unipolar and bipolar gloom, in which huge positive reaction has been noted when contrasted with madness [22]. Notwithstanding, a couple of studies additionally highlight its handiness
in patients with real bipolar problems [30]. Notwithstanding these investigations, there is a case report of a patient experiencing recalcitrant bipolar issue, substituting and logically demolishing melancholy and insanity, which was inert to pharmacotherapy, ECT, and even nerve incitement (VNS) [31]. The investigation revealed a 2.5 year subsequent abatement in the HRSD score from 32 to 8 following a half year of persistent incitement of the SCC with DBS.
A lot of studies have detailed huge outcomes with SCC DBS, highlighting the helpfulness of SCC regulation in treating both unipolar and bipolar emotional problems [32]. The SCC is a significant neural hardware for the guideline of temperament and has been set up as a huge objective for DBS in burdensome patients [33]. The outcomes so far recommends the positive job, the SCC (BA-25) can play in overseeing patients that include both hyper and burdensome scenes inside the setting of a bipolar issue considering the decreased danger of causing madness dissimilar to different DBS targets [34]. In any case, the moment plausibility of setting off hyper scenes in patients with unipolar sorrow actually should be thought of. This is on the grounds that one case report has revealed a female patient being overseen for OCD with DBS of the NAcc and the foremost appendage of the inside container, who accordingly displayed a hyper scene [35]. Transient lunacy has additionally been accounted for in a couple of different cases after the utilization of DBS [36].The reason for this incitement actuated insanity may have been brought about by spread of incitement from the objective locales to regions around the frontal and limbic districts [37]. The administration of BD with DBS requires further investigation of the mind regions which should be animated, so undesired side effects brought about by DBS can be forestalled.
The convenience of different DBS targets, for example, the VC/VS, NAcc, ITP, and LHb. All have revealed differing victories on patients with unipolar misery that can't be thought little of in patients with BD. Despite the fact that there have been insignificant examinations into their significance in overseeing BD patients, the achievement revealed with the Medial Forebrain Bundle (MFB) DBS in 6 out of 7 bipolar patients proposes the utilization of different DBS targets merits considering [38]. All these other potential objective zones have been appeared to share generous linkages inside their hardware, and they are additionally known to assume significant jobs in the pathophysiology of BD dependent on outcomes from neuroimaging, morphologic, and metabolic examinations [38].
By and large, these confirmations recommend that DBS is surely a viable treatment methodology for bipolar issues, despite the fact that it is slanted towards the treatment of gloom [39]. BD is a heterogeneous issue comprising of a wide scope of indication designs that have been appeared to emerge from at least one useless disposition affecting neural circuits [40]. All things considered, focusing on at least one of these hardware have brought about critical positive reaction in patients with unipolar misery just as those with bipolar problems, yet with expanded burdensome states. Better outcomes can be acquired with ideal incitement settings, more exact terminal situating, improved voltage choice, and adjustment of explicit microstructural targets [41,42]. It is hard to
completely express that DBS is powerful for the treatment of hyper states as there is restricted proof to back this up.
Conclusion
The utilization of DBS can carry genuinely necessary indicative help to the burdensome province of BP patients. Nonetheless, more examination actually should be done to show the viability of this treatment methodology that mixes neurosurgery with interventional psychiatry. Especially, the lack of data concerning the utilization of DBS in insanity focuses at the requirement for more case reports, visually impaired and randomized preliminaries to unmistakably build up the adequacy of DBS in hyper patients.
Additionally, the subject of which patients will profit maximally from DBS is yet to be set up. For this reason, enormous multicenter coordinated effort and trade of data to support improved patient determination for DBS is required.
Despite the fact that DBS is as yet considered as a type of test treatment for the present, its acknowledgment by driving figures in the field that are burdened with the assignment of creating conventions for its clinical use will help hurry its status as a suggested line of treatment for patients with mind-set full of feeling problems. It is trusted that it will continuously work its approach to turning out to be either a second-line or first-line treatment for burdensome condition of bipolar problem.
Reference
1. D. Denys. Pharmacotherapy of obsessive-compulsive disorder and obsessive- compulsive spectrum disordersPsychiatr. Clin. North Am., 29 (2006), pp. 553-584, 10.1016/j.psc.2006.02.013
2. C.F. Brady. Obsessive-compulsive disorder and common comorbiditiesJ. Clin.
Psychiatry, 75 (2014), p. e02, 10.4088/JCP.13023tx1c
3. A. Amerio, B. Stubbs, A. Odone, M. Tonna, C. Marchesi, S.N. GhaemiThe prevalence and predictors of comorbid bipolar disorder and obsessive-compulsive disorder: a systematic review and meta-analysisJ. Affect. Disord., 186 (2015), pp.
99-109, 10.1016/j.jad.2015.06.005.
4. G. Perugi, P. Medda, C. Toni, M.G. Mariani, C. Socci, M. Mauri. The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-state, mania and catatonic featuresCurr.
Neuropharmacol., 15 (2017), pp. 359-371.
5. L.F. Fontenelle, E.S.F. Coutinho, N.M. Lins-Martins, P.B. Fitzgerald, H. Fujiwara, M. Yucel. Electroconvulsive therapy for obsessive-compulsive disorder: a systematic reviewJ. Clin. Psychiatry, 76 (2015), pp. 949-957, 10.4088/JCP.14r09129.
6. A. Lusicic, K.R. Schruers, S. Pallanti, D.J. CastleTranscranial magnetic stimulation in the treatment of obsessive-compulsive disorder: current perspectivesNeuropsychiatr. Dis. Treat., 14 (2018), pp. 1721-1736, 10.2147/NDT.S121140.
7. F.A. KozelClinical repetitive transcranial magnetic stimulation for posttraumatic
stress disorder, generalized anxiety disorder, and bipolar disorder Psychiatr. Clin.
North Am., 41 (2018), pp. 433-446.
8. L. Gabriels, P. Cosyns, B. Nuttin, H. Demeulemeester, J. Gybels. Deep brain stimulation for treatment-refractory obsessive-compulsive disorder:
psychopathological and neuropsychological outcome in three cases. ActaPsychiatr.
Scand., 107 (2003), pp. 275-282.
9. P. Alonso, D. Cuadras, L. Gabriels, D. Denys, W. Goodman, B.D. Greenberg, F.
Jimenez-Ponce, J. Kuhn, D. Lenartz, L. Mallet, B. Nuttin, E. Real, C. Segalas, R.
Schuurman Du, S.T. Montcel, J.M. Menchon. Deep brain stimulation for obsessive-compulsive disorder: a meta-analysis of treatment outcome and predictors of response. PLoS ONE, 10 (2015), pp. 1-16.
10. D. Denys, M. Mantione, M. Figee, P. van den Munckhof, F. Koerselman, H.
Westenberg, A. Bosch, R. Schuurman. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorderArch. Gen.
Psychiatry, 67 (2010), pp. 1061-1068.
11. S. Kohl, D.M. Schönherr, J. Luigjes, D. Denys, U.J. Mueller, D. Lenartz, V.
Visser-Vandewalle, J. Kuhn. Deep brain stimulation for treatment-refractory obsessive compulsive disorder: a systematic review.BMC Psychiatry, 14 (2014), p.
214
12. D.A. Malone, D.D. Dougherty, A.R. Rezai, L.L. Carpenter, G.M. Friehs, E.N.
Eskandar, S.L. Rauch, S.A. Rasmussen, A.G. Machado, C.S. Kubu, A.R. Tyrka, L.H. Price, P.H. Stypulkowski, J.E. Giftakis, M.T. Rise, P.F. Malloy, S.P.
Salloway, B.D. Greenberg. Deep brain stimulation of the ventral capsule/ventral striatum for treatment-resistant depression. Biol. Psychiatry, 65 (2009), pp. 267- 275.
13. T.E. Schlaepfer, B.H. Bewernick, S. Kayser, B. Mädler, V.A. CoenenRapid effects of deep brain stimulation for treatment-resistant major depressionBiol. Psychiatry, 73 (2013), pp. 1204-1212.
14. C.V. Torres, E. Ezquiaga, M. Navas, M.A. GarcíaPallero, R.G. SolaLong-term results of deep brain stimulation of the subcallosal cingulate for medication- resistant bipolar I depression and rapid cycling bipolar ii depressionBiol.
Psychiatry, 81 (2017), pp.e33-e34.
15. Jiménez F, Velasco F, Salin-Pascual R, Hernández JA, Velasco M, Criales JL, et al. A patient with a resistant major depression disorder treated with deep brain stimulation in the inferior thalamic peduncle. Neurosurgery.2005;57:585–593.
16. Sartorius A, et al. Remission of major depression under deep brain stimulation of the lateral habenula in a therapy-refractory patient. Biol Psychiatry. 2010;67(2):e9–
e11.
17. Mayberg HS. Targeted electrode-based modulation of neural circuits for depression.J.Clin. Invest.2009;119:717–25
18. Price JL, DrevetsWC. 2010. Neurocirc- uitry of mood disorders. Neuropsychopha- rmacology.2010;35:192–216.
19. Riva-Posse P, Holtzheimer PE, Garlow SJ, Mayberg HS. Practical considerations
in the development and refinement of subcallosal cingulate white matter deep brain stimulation for the treatment resistant depression. WorldNeurosurg. 2012;pii:
S1878-8750.
20. Holtzheimer PE, Kelley ME, Gross RE, Filkowski MM, Garlow SJ, Barrocas A, et al.Subcallosal cingulate deep brain stimulation for treatment-resistant unipolar and bipolar depression. Arch Gen Psychiatry.2012;69:150-158.
21. Puigdemont D, Pérez-Egea R, Portella MJ, Molet J, de Diego‑Adeliño J, Gironell A, et al. Deep brain stimulation of the subcallosal cingulate gyrus: further evidence in treatment‑resistant major depression. Int J Neuropsychopharm- acol.2012;15:121-133.
22. Holtzheimer, PE, Mayberg, HS.Deepbrain stimulation for psychiatric disorders.Annu. Rev. Neurosci. 2011;34:289–307
23. Malone DA Jr, Dougherty DD, Rezai AR, Carpenter LL, Friehs GM, Eskandar EN, et al. Deep brain stimulation of the ventral capsule/ventral striatum for treatment- resistant depression. Biol Psychiatry. 2009;65:267-275.
24. Humphries MD, Prescott TJ. The ventral basal ganglia, a selection mechanism at the crossroads of space, strategy, and reward.Prog.Neurobiol.2010;90:385–417 25. Sesack SR, Grace AA. Cortico-basal ganglia reward
network: microcircuitry. Neuropsychopharmacology.2010;35:27– 47
26. Schlaepfer TE, Cohen MX, Frick C, Kosel M, Brodesser D, et al. Deep brain stimulation to reward circuitry alleviates anhedonia in refractory major depression.Neuropsychopharmacology.2008;33:368– 77
27. Bewernick BH, Hurlemann R, Matusch A, Kayser S, Grubert C, et al. Nucleus accumbens deep brain stimulation decreases ratings of depression and anxiety in treatment-resistant depression. Biol. Psychiatry.2010;67:110–16
28. Bewernick BH, Kayser S, Sturm V, SchlaepferTE.Longterm effects of nucleus accumbens deep brain stimulation in treatment-resistant depression: evidence for sustained efficacy. Neuropsychophar- macology.2012;37:1975–1985.
29. Kiening K, Sartorius A.A new translational target for deep brain stimulation to treat depression.EMBOMol Med.2013;5:1151–1153.
30. Sartorius A, HennFA.Deep brain stimulation of the lateral habenula in treatment resistant major depression.Med Hypotheses.2007;69:1305–1308.
31. Drevets WC, Price JL.Neuroimaging and neuropathological studies of mood disorders. In: Licinio JWM, ed. Biology of depression: from novel insights to therapeutic strategies. Weinheim: Wiley- VCH Verlag GmbH & Co; 2005
32. Lyoo IK, Kim MJ, Stoll AL, Demopulos CM, Parow AM, DagerSR,et al. Frontal lobe gray matter density decreases in bipolar I disorder. Biol Psychiatry.
2004;55:648–651.
33. Nugent AC, Milham MP, Bain EE, Mah L, Cannon DM, Marrett S, et al. Cortical abnormalities in bipolar disorder investigated with MRI and voxel-based morphometry. Neuroimage.2006;30:485– 497.
34. Drevets WC, Gadde K, Krishnan KRR. Neuroimaging studies of depression. In:
Charney DS, Nestler EJ, Bunney BS, eds. The neurobiological foundation of
mental illness, 2nd ed. New York: Oxford University Press; 2004.
35. Drevets WC, Videen TO, Price JL, Preskorn SH, Carmichael ST, RaichleME.A functional anatomical study of unipolar depression.JNeurosci. 1992;12:3628–3641.
36. 41. Drevets WC, Price JL,Furey ML. Brain structural and functional abnorm- alities in mood disorders: implications for neurocircuitry models of depression.
BrainStructFunct.2008;213:93–118.
37. Benabid AL, Pollak P, Gervason C, Hoffmann D, Gao DM, et al. Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus. Lancet.1991;337:403–6
38. Iremonger KJ, Anderson TR, Hu B, Kiss ZH. Cellular mechanisms preventing sustained activation of cortex during subcortical high-frequency stimulation. J.
Neurophysiol.2006;96:613–21
39. Chand SK, Nanda S, Rout E, Mohanty JN, Mishra R, Joshi RK. De novo sequencing and characterization of defensetranscriptome responsive to Pythiumaphanidermatum infection in Curcuma longa L. Physiological and Molecular Plant Pathology. 2016 Apr 1;94:27-37.
40. Mayberg HS, et al. Deep brain stimulation for treatment-resistant depression.
Neuron. 2005;45(5):651–660.
41. Drevets WC, Ongur D, Price JL. Neuroimaging abnormalities in the subgenualprefrontal cortex: implications for the pathophysiology of familial mood disorders. Mol Psychiatry. 1998;3(3):220– 226.
42. Haq IU, Foote KD, Goodman WK, Ricciuti N, Ward H, Sudhyadhom A, etal.Acase of mania following deep brain stimulation for obsessive compulsive disorder.
StereotactFunctNeurosurg. 2010;88:322–328
