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342 The APA Publishing Textbook of Mood Disorders, Second Edition
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resistant OCD is approved by the FDA according to the Humanitarian Device Exemption (U.S. Food and Drug Administration 2020).
Development
Since about the turn of the century, DBS has also been under investigation for the
treatment of treatment-resistant depression (TRD). Although it is approved for OCD,
DBS is not yet approved for TRD therapy by the FDA. As outlined in the introduction
to this chapter, depression is now conceptualized as a complex brain disorder involving several key brain circuits. Therefore, various potential structures within these circuits are under investigation as DBS targets for TRD (Drobisz and Damborská 2019).
The following targets have been studied most thoroughly (Döbrössy et al. 2021; Figure 20–3): subgenual cingulate gyrus (SCG), capsular targets (ALIC and ventral capsule/ventral striatum [VC/VS]), nucleus accumbens, and superolateral medial
forebrain bundle (slMFB).
Subgenual Cingulate Gyrus
Converging findings from clinical, anatomical, neurochemical, and functional imaging studies of depression, as well as studies using induced sadness in healthy subjects, resulted in a neuroanatomical model that describes depression as a “failure of
the coordinated interactions of a distributed network of limbic-cortical pathways”
(Mayberg 1997, p. 471). The SCG (also area Cg25 or Brodmann area 25) is highlighted
as a switching point in this network. The prominent position of the SCG led to the
hypothesis that high-frequency electrical stimulation of this area could result in a de
crease in depressive symptoms by decreasing SCG activity. The first positive results
with open-label stimulation (Mayberg et al. 2005) promoted further research on the
neuropathology and optimal stimulation target for treatment purposes.
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Capsular Targets: Anterior Limb of the Internal Capsule
and Ventral Capsule/Ventral Striatum
Unlike the SCG, the ALIC and VC/VS were chosen mainly based on clinical observations. Both targets form part of the striatum, which is involved in the cortico-striatothalamo-cortical (CSTC) network, seen as highly relevant in the pathophysiology of
OCD (Alexander et al. 1986; Karas et al. 2019). The VC/VS contains the ventral half
of the ALIC and impinges inferiorly on the VS (Greenberg et al. 2006). Due to their
extreme spatial and functional proximity, the ALIC and VC/VS are summarized as
capsular targets. Ablative procedures in the CSTC network have led to improvements
in OCD and in TRD in about 35%–70% of treated patients (Greenberg et al. 2003). In
addition to ablative procedures, DBS applied to CSTC targets has also improved OCD
symptoms (Alonso et al. 2015; Blomstedt et al. 2013). In two trials intending to treat
treatment-resistant OCD using DBS applied to the capsular targets, not only was a decrease in OCD symptoms reported, but also a decrease in depressive symptoms
(Greenberg et al. 2006; Nuttin et al. 2003). These observations, along with the antidepressant effects of ablative procedures, led to the first study on VC/VS stimulation in
TRD (Malone et al. 2009).
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FIGURE 20–3. Experimental targets for deep brain stimulation in treatment-resistant
depression.
To view this figure in color, see Plate 8 in Color Gallery in middle of book.
ALIC= anterior limb of the internal capsule; CG25=Brodmann area 25; NAcc=nucleus accumbens; SCG=
subgenual cingulate gyrus; slMFB=superolateral branch of the medial forebrain bundle; VCVS=ventral
capsule/ventral striatum.
Source. Adapted from Figure 2 (Volker A. Coenen, 2019; p. 92) in Döbrössy M, Ramanathan C, Ashouri
Vajari D, et al.: “Neuromodulation in Psychiatric Disorders: Experimental and Clinical Evidence for Re
ward and Motivation Network Deep Brain Stimulation: Focus on the Medial Forebrain Bundle.” European
Journal of Neuroscience 53(1):89–113, 2021. Available at: https://onlinelibrary.wiley.com/doi/10.1111/
ejn.14975. Accessed October 26, 2021. Copyright © 2020, The Authors, used under the terms of the Creative
Commons Attribution License.
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Nucleus Accumbens
The nucleus accumbens forms part of the VS and is therefore located very close to the
capsular stimulation targets. It is highly involved in processing reward and pleasure
information: neuronal activity and dopamine release increase in the nucleus accumbens during expectation and experience of rewards (Adinoff 2004; Doyon et al. 2005;
Schultz 2004), and increased VS activity is associated with induced euphoria (Aharon
et al. 2001; Drevets et al. 2001; Knutson et al. 2001). A translational study found that
long-term administration of an antidepressant could re-regulate activity of the nucleus
accumbens in socially stressed mice (Berton et al. 2006). Based on these findings, it has
been proposed that anhedonia—a key symptom of depression (American Psychiatric
Association 2013)—represents a lack of reward-motivated behavior and is related to
activity in the nucleus accumbens (Schlaepfer et al. 2008a). On a neuroanatomical
level, the nucleus accumbens is interconnected with other brain areas involved in
emotion processing, including the DBS target SCG, described earlier (Hamani et al.
2009; Vergani et al. 2016). It has therefore been concluded that stimulating the nucleus
accumbens would result in modulation of other parts of emotion-related networks as
well and would decrease anhedonia (Schlaepfer et al. 2008a).
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Superolateral Branch of the Medial Forebrain Bundle
Similar to the nucleus accumbens, the medial forebrain bundle is highly associated
with reward processing. It is located at the center of a distributed network that is con
sidered the neural substrate of the reward circuitry and has been studied thoroughly
in rodents (Wise 22005). This system—among others—is engaged in predicting and
computing rewards, initiating exploration, and eliciting hedonic consummatory be
havior (Carlezon and Chartoff 2007; Waraczynski 2006). Although well known in rodents, it was not until 2009 that the full structure of this network was visualized in
humans (Coenen et al. 2009). Using diffusion tensor imaging, a procedure based on
MRI analysis that allows imaging of fiber connections based on the anisotropy of the
brain tissue, it has been shown that the human medial forebrain bundle originates in
the ventral tegmental area and then splits into a lower and a superolateral branch.
The slMFB is of particular interest for DBS because of its neuroanatomical structure.
The superolateral branch “shears out laterally, under-crosses the thalamus and ascends
to the interior portion of the anterior limb of the internal capsule (ALIC)” (Coenen et
al. 2011, p. 1974). The slMFB also accesses the ventral striatum and the nucleus accum
bens directly, whereas direct connections with the white matter tracts surrounding the
SCG are seen inconsistently (Coenen et al. 2011). This neuroanatomical description
demonstrates the connecting position of the slMFB with the targets described earlier.
In a diffusion tensor imaging study of healthy subjects, it was demonstrated that the
historically most commonly chosen lesion targets for depression treatment are actu
ally interconnected by fiber tracts that are mainly part of the slMFB (Schoene-Bake et
al. 2010). In retrospect, this means that although these targets might have been se
lected for other reasons originally, the efficacy of the described DBS targets in TRD is
best explained by their shared involvement in the reward system. Because the slMFB
is a central connecting element in this system, it has been promoted as a stimulation
target in itself (Coenen et al. 2011; Schlaepfer et al. 2014).
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State of the Art
Table 20–A in the Appendix shows all published studies we know of that involved
stimulation of the DBS targets described earlier for the treatment of TRD and included
a response rate. The most commonly used clinician-rated instruments for assessing de
pression severity are the Hamilton Depression Rating Scale (HAM-D; Hamilton 1960)
and the Montgomery-Åsberg Depression Rating Scale (MADRS; Montgomery and
Åsberg 1979; Santor et al. 2006); different versions of the HAM-D may be used. Response is usually defined as greater than 50% improvement compared with baseline.
In general, a substantial rate of response and even remission is achieved—especially
in relation to the treatment-resistant illness in this population. Apparently, none of the
targets presented seems to be substantially superior to the others. Due to the small
number of RCTs, even a meta-analysis could not reliably determine a superior target
(Kisely et al. 2018). Despite the generally high response rates, predominantly in openlabel studies, response and remission rates vary substantially among studies and fluctuate over time. This is typical for studies with small sample sizes (Khan et al. 2018)
and indicates that RCTs and meta-analyses are needed for a better estimation of the
actual treatment efficacy. Although many study protocols set the end of study at 6 or
12 months (see Appendix Table 20–A), clinical long-term observations over many
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years have been reported in several publications. Thus, DBS for depression is a longterm treatment.
As mentioned, one of the great advantages of DBS over lesion procedures is that
sham-controlled trials become feasible. Therefore, after some very promising openlabel pilot trials and small
well-designed sham-controlled studies were started, with sample sizes determined
on the basis of power analyses (Dougherty et al. 2015; Holtzheimer et al. 2017). Un
fortunately, both studies were stopped after preliminary futility analyses did not find
significant group differences in depressive symptoms between sham and active stim
ulation.
Nevertheless, instead of discarding DBS as treatment for TRD due to these preliminary findings, we should seek explanations for the failed trials of Dougherty et al.
(2015 and Holtzheimer et al. (2017). First, these RCTs were highly underpowered.
Their sample sizes (30 and 90, respectively) were much smaller than expected (208
and 201, respectively) and made them quite unlikely to yield statistically significant
and replicable results (see Khan et al. 2018 for deeper insight into the problems of trial
design in antidepressant treatment). The lack of a significant group difference does not
necessarily point toward an ineffective treatment. Looking at the study design pre
sented in Dougherty et al. (2015), one can argue that a treatment duration of 4 months
before response assessment might be too brief in relation to the duration of illness in
this severely ill and treatment-resistant population (Schlaepfer 2015). Furthermore,
the time period for individual parameter adjustment was limited to a few days only,
which seems much too short for this complex intervention. On the other hand, pa
rameter adjustment in the study by Holtzheimer et al. (2017) followed a plan that
might have been too strict. Reaching a stable response can take time (Bergfeld et al.
2016), a factor that should be considered in future trial designs (Mayberg et al. 2016).
Beyond these issues, it is also questionable whether the commonly used outcome
parameters—the HAM-D and the MADRS—are sensitive enough for the assessment
of symptom changes in severe depression. The chronically severe depression in the
study population might result in ceiling effects. Therefore, DBS-specific measures of
severe depression are urgently needed (Schlaepfer 2015). Furthermore, the HAM-D
and MADRS are multidimensional measures that try to assess the whole depression
syndrome. Efficacy analyses usually focus on the sum score. Unfortunately, similar
sum scores can be achieved by a great number of unique symptom combinations and
thereby cover up the nuances of the present depression manifestation (Fried and
Nesse 2015). At the same time, a sum score reduction does not give any information
about which aspects of the illness actually did improve (Khan et al. 2018). To improve
interpretability, it therefore makes sense to look at single symptoms and to find mea
surements that contain fewer dimensions (Fried and Nesse 2015).
Finally, the HAM-D and MADRS actually ask for the patient’s depressive symptoms in the past week. Comparing depression severity at baseline and at an arbitrarily
chosen follow-up time point can be influenced by many variables other than treatment
and does not tell anything about the course of treatment response (Schlaepfer 2015).
For assessment of the whole process from baseline to end of study, the area under the
curve has been proposed (Bewernick et al. 2017b; Schlaepfer 2015); this measure is the
product of time and depression severity and contains all measuring points and
thereby gives information about stability of illness/response. Especially for studies
controlled trials (see Appendix Table 20–A), two large,
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with long-term follow-up, this seems to be a more meaningful outcome parameter
than the mere comparison between two points in time. In October 2018, a new largescale RCT on the treatment of TRD with DBS was started, taking into account the dif
ficulties of the studies by Dougherty et al. (2015) and Holtzheimer et al. (2017). The
stimulation target is the slMFB (clinical trial identifier NCT03653858). Although no
results have been reported yet, this study might be a milestone for DBS in TRD.
DBS has been in use for a while now, yet the exact mode of action remains unclear.
Different hypotheses on the electrochemical processes induced by DBS have been put
forward, the most common ones being direct inhibition of neural activity, direct exci
tation of neural activity, informational lesion, and synaptic filtering. These concepts
focus on the acute effects of DBS in movement disorders; for an explanation of these
concepts and the current evidence, see Lozano et al. (2019). Currently under investi
gation are neuroplastic changes induced by DBS in rodent models of depression (Falowski et al. 2011; Veerakumar et al. 2014).
Where does all this leave us? DBS is a promising treatment for depression with impressive results in open-label studies. Surprisingly, RCTs have not been as successful
so far. This might be at least partially related to methodological difficulties that
should be addressed in future studies. Further well-designed comparable studies on
treatment efficacy that allow for meta-analysis are therefore urgently needed. At the
same time, careful patient selection that considers individual risks is indispensable,
because DBS is an invasive procedure that comes with certain risks (see the next section, “Safety”). Several targets are under investigation, and at this point we cannot determine which is the most effective—neither in general nor in the individual case.
Generally, antidepressant effects may vary due to interactions of DBS target, param
eter settings, and individual clinical characteristics (Dandekar et al. 2018). Deeper insight into this relationship could be a basis for personalized treatment, which is why
clinical research should focus on single symptoms as well as on the whole syndrome.
Ultimately, a better understanding of the mode of action of DBS is needed to improve
target selection and parameter adjustment. So far, DBS should only be considered as
a treatment alternative once all approved and well-evaluated treatment procedures
have been exhausted. If this requirement is fulfilled, DBS, administered by an expert
team in the context of clinical studies, may offer a chance for significant illness im
provement.
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Safety
Like any other treatment, DBS is associated with side effects. These side effects can be
surgery-, stimulation-, or device-related. Broad overviews of adverse events reported
thus far in DBS for TRD are presented in reviews by Kisely et al. (2018) and Dandekar
et al. (2018). The main surgery-associated side effects are wound infection, erosion,
lead migration, device-related infection, and hemorrhage. These adverse effects may
be permanent but are transient in most cases. The incidence rate of hemorrhage in
functional neurosurgery (lesion procedures and DBS in general) is about 5.0% (Zrinzo
et al. 2012).
Stimulation-related adverse effects such as hypomanic symptoms, disinhibition,
restlessness, anxiety, sweating, or headaches are mostly transient (Kisely et al. 2018).
Parameter adjustment is required if adverse effects are persistent or experienced as
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stressful (Schlaepfer et al. 2014). Suicide attempts and completed suicides have been
reported as well (i.e., Bergfeld et al. 2016; Bewernick et al. 2010; Kennedy et al. 2011).
Because prospective studies indicate an increased risk of suicide in patients with TRD
(Oquendo et al. 2006), this should be expected and demonstrates the necessity of close
psychiatric supervision during studies and follow-up.
Symptom aggravation due to unintended (i.e., battery depletion) or planned (i.e.,
blinded stimulation) stimulation discontinuation has been reported (i.e., Bergfeld et
al. 2016; Holtzheimer et al. 2012; Kilian et al. 2019). Although one study did not find
clinical changes after a planned 48-hour stimulation discontinuation, metabolic
changes become apparent after this short time period (Martin-Blanco et al. 2015). These
findings support the hypothesis that continuous stimulation is essential for effective
treatment.
Besides these general adverse events, different stimulation targets seem to be associated with specific side effects (see Dandekar et al. 2018). Due to small sample sizes
and only partial data available from control groups, data on the efficacy and safety of
DBS in TRD must be considered preliminary.
Ethical Considerations
Applying DBS for TRD should be and is discussed in light of ethical principles. Quite
frequently, concerns regarding possible personality changes under DBS are voiced
(Grant et al. 2014; Hildt 2006; Synofzik and Schlaepfer 2008). To address these concerns, it is necessary to reflect on what is meant by the term personality—a question
that exceeds the scope of this chapter. In short, a quantitative analysis of personality
traits before and after DBS for TRD did not reveal any changes (Bewernick et al. 2018).
In qualitative analyses in DBS for Parkinson’s disease and OCD, patients occasionally
report feelings of strangeness or unfamiliarity with themselves (de Haan et al. 2015;
Gilbert et al. 2017; Schüpbach et al. 2006). At the same time, effective treatment of psychiatric disorders can be conceptualized as purposefully changing aspects of an individual’s personality (Synofzik and Schlaepfer 2008) and therefore leads to the question
of whether a change in personality is inevitably undesirable (Grant et al. 2014; Syn
ofzik and Schlaepfer 2008).
Regarding interpersonal relationships, poor social adjustment, especially in marital relationships and professional lives, has been reported after DBS for Parkinson’s
disease, despite the successful reduction of motor symptoms. This leads to the assumption that rapid improvement of a disabling condition might have a destabilizing
effect (Baertschi et al. 2019; Schüpbach et al. 2006) that should be taken into account
when informing patients about the potential risks and benefits of DBS and when defining outcome measures in studies on treatment efficacy, especially because very
rapid improvement of depressive symptomatology has been observed in DBS for
TRD (Schlaepfer et al. 2013). These considerations of DBS for psychiatric purposes are
extended by a body of literature (i.e., Grant et al. 2014; Kuhn et al. 2009; Synofzik and
Schlaepfer 2008) focused on the well-established principles of bioethical nonmaleficence, justice, and autonomy expounded by Beauchamp and Childress (2009). To ensure that these principles are not only discussed in general but also taken into account
in every individual case and in planning clinical trials, guidelines for patient selection
have been proposed (Nuttin et al. 2014).
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Without question, DBS remains an invasive treatment and comes with certain
risks. Thus, careful selection of patients and targets is important to ensure that pa
tients receive the best treatment available. Regarding risk-benefit estimations, it is an
advantage that surgery-related side effects are already well known due to the appli
cation of DBS in neurology (Kleiner-Fisman et al. 2006). Additionally, the side-effect
risks of DBS must be balanced against the immense burden of disease (Mrazek et al.
2014) and the side effects of alternative treatments such as electroconvulsive therapy
(Kolshus et al. 2017). As discussed earlier, depression is a complex syndrome. We
should therefore aim for individualized patient care that takes into account the individual depression manifestation (Fried and Nesse 2015) and assesses the best-fitting
DBS target. Ultimately, DBS pursues the same goal as all biological interventions for
depression—reestablishing the balance of brain circuits involved in maintaining de
pression in general and TRD in particular.
References
Aaronson ST, Carpenter LL, Conway CR, et al: Vagus nerve stimulation therapy randomized
to different amounts of electrical charge for treatment-resistant depression: acute and
chronic effects. Brain Stimul 6(4):631–640, 2013 23122916
Aaronson ST, Sears P, Ruvuna F, et al: A 5-year observational study of patients with treatment-
resistant depression treated with vagus nerve stimulation or treatment as usual: com
parison of response, remission, and suicidality. Am J Psychiatry 174(7):640–648, 2017
28359201
Accolla EA, Aust S, Merkl A, et al: Deep brain stimulation of the posterior gyrus rectus region
for treatment resistant depression. J Affect Disord 194:33–37, 2016 26802505
Adinoff B: Neurobiologic processes in drug reward and addiction. Harv Rev Psychiatry
12(6):305–320, 2004 15764467
Aharon I, Etcoff N, Ariely D, et al: Beautiful faces have variable reward value: fMRI and behav-
ioral evidence. Neuron 32(3):537–551, 2001 11709163
Alexander GE, DeLong MR, Strick PL: Parallel organization of functionally segregated circuits
linking basal ganglia and cortex. Annu Rev Neurosci 9(1):357–381, 1986 3085570
Alonso P, Cuadras D, Gabriëls L, et al: Deep brain stimulation for obsessive-compulsive disor-
der: a meta-analysis of treatment outcome and predictors of response. PLoS One
10(7):e0133591, 2015 26208305
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 5th
Edition. Arlington, VA, American Psychiatric Association, 2013
Armitage R, Husain M, Hoffmann R, et al: The effects of vagus nerve stimulation on sleep EEG
in depression: a preliminary report. J Psychosom Res 54(5):475–482, 2003 12726905
Baertschi M, Flores Alves Dos Santos J, Burkhard P, et al: The burden of normality as a model
of psychosocial adjustment after deep brain stimulation for Parkinson’s disease: a systematic investigation. Neuropsychology 33(2):178–194, 2019 30667249
Bajbouj M, Merkl A, Schlaepfer TE, et al: Two-year outcome of vagus nerve stimulation in treat-
ment-resistant depression. J Clin Psychopharmacol 30(3):273–281, 2010 20473062
Beauchamp TL, Childress JF: Principles of Biomedical Ethics, 6th Edition. New York, Oxford
University Press, 2009
Benabid AL, Pollak P, Louveau A, et al: Combined (thalamotomy and stimulation) stereotactic
surgery of the VIM thalamic nucleus for bilateral Parkinson disease. Appl Neurophysiol
50(1–6):344–346, 1987 3329873
Benabid AL, Pollak P, Gross C, et al: Acute and long-term effects of subthalamic nucleus stim-
ulation in Parkinson’s disease. Stereotact Funct Neurosurg 62(1–4):76–84, 1994 7631092
-
-
-
-
349 Vagus Nerve Stimulation and Deep Brain Stimulation
https://t.me/med1917
Ben-Menachem E: Vagus-nerve stimulation for the treatment of epilepsy. Lancet Neurol
1(8):477–482, 2002 12849332
Ben-Menachem E, Mañon-Espaillat R, Ristanovic R, et al: Vagus nerve stimulation for treatment
of partial seizures: 1. A controlled study of effect on seizures. Epilepsia 35(3):616–626, 1994
8026408
Bennabi D, Aouizerate B, El-Hage W, et al: Risk factors for treatment resistance in unipolar de-
pression: a systematic review. J Affect Disord 171:137–141, 2015 25305428
Bergfeld IO, Mantione M, Hoogendoorn ML, et al: Deep brain stimulation of the ventral ante-
rior limb of the internal capsule for treatment-resistant depression: a randomized clinical
trial. JAMA Psychiatry 73(5):456–464, 2016 27049915
Berry SM, Broglio K, Bunker M, et al: A patient-level meta-analysis of studies evaluating vagus
nerve stimulation therapy for treatment-resistant depression. Med Devices (Auckl) 6:17–
35, 2013 23482508
Berton O, Nestler EJ: New approaches to antidepressant drug discovery: beyond monoamines.
Nat Rev Neurosci 7(2):137–151, 2006 16429123
Berton O, McClung CA, DiLeone RJ, et al: Essential role of BDNF in the mesolimbic dopamine
pathway in social defeat stress. Science 311(5762):864–868, 2006 16469931
Bewernick BH, Hurlemann R, Matusch A, et al: Nucleus accumbens deep brain stimulation de-
creases ratings of depression and anxiety in treatment-resistant depression. Biol Psychiatry 67(2):110–116, 2010 19914605
Bewernick BH, Kayser S, Sturm V, et al: Long-term effects of nucleus accumbens deep brain
stimulation in treatment-resistant depression: evidence for sustained efficacy. Neuropsy
chopharmacology 37(9):1975–1985, 2012 22473055
Bewernick BH, Kayser S, Gippert SM, et al: Acute antidepressant effects of deep brain stimula-
tion—review and data from slMFB-stimulation. Personalized Medicine in Psychiatry 3:1–
7, 2017a. Available at: https://www.personalizedmedpsych.com/article/S24681717(17)30003-0/fulltext. Accessed October 26, 2021.
Bewernick BH, Kayser S, Gippert SM, et al: Deep brain stimulation to the medial forebrain bun-
dle for depression—long-term outcomes and a novel data analysis strategy. Brain Stimul
10(3):664–671, 2017b 28259544
Bewernick BH, Kilian HM, Schmidt K, et al: Deep brain stimulation of the supero-lateral branch
of the medial forebrain bundle does not lead to changes in personality in patients suffering
from severe depression. Psychol Med 48(16):2684–2692, 2018 29493478
Blomstedt P, Sjöberg RL, Hansson M, et al: Deep brain stimulation in the treatment of obses-
sive-compulsive disorder. World Neurosurg 80(6):e245–e253, 2013 23044000
Borders C, Hsu F, Sweidan AJ, et al: Deep brain stimulation for obsessive compulsive disorder:
a review of results by anatomical target. Ment Illn 10(2):7900, 2018 30542526
Carlezon WA Jr, Chartoff EH: Intracranial self-stimulation (ICSS) in rodents to study the neu-
robiology of motivation. Nat Protoc 2(11):2987–2995, 2007 18007634
Ce peda MS, Re ps J, Fife D, et al: F indi ng tr eatment-resistant depression in real-world data: how
a data-driven approach compares with expert-based heuristics. Depress Anxiety
35(3):220–228, 2018 29244906
Coenen VA, Honey CR, Hurwitz T, et al: Medial forebrain bundle stimulation as a patho-
physiological mechanism for hypomania in subthalamic nucleus deep brain stimulation
for Parkinson’s disease. Neurosurgery 64(6):1106–1114, discussion 1114–1115, 2009
19487890
Coenen VA, Schlaepfer TE, Maedler B, et al: Cross-species affective functions of the medial fore-
brain bundle-implications for the treatment of affective pain and depression in humans.
Neurosci Biobehav Rev 35(9):1971–1981, 2011 21184778
Coenen VA, Schlaepfer TE, Goll P, et al: The medial forebrain bundle as a target for deep brain
stimulation for obsessive-compulsive disorder. CNS Spectr 22(3):282–289, 2017 27268576
Coenen VA, Bewernick BH, Kayser S, et al: Superolateral medial forebrain bundle deep brain
stimulation in major depression: a gateway trial. Neuropsychopharmacology 44(7):1224–
1232, 2019 30867553
-
350 The APA Publishing Textbook of Mood Disorders, Second Edition
https://t.me/med1917
Conway CR, Sheline YI, Chibnall JT, et al: Cerebral blood flow changes during vagus nerve
stimulation for depression. Psychiatry Res 146(2):179–184, 2006 16510266
Conway CR, Sheline YI, Chibnall JT, et al: Brain blood-flow change with acute vagus nerve stim-
ulation in treatment-refractory major depressive disorder. Brain Stimul 5(2):163–171, 2012
22037127
Conway CR, Chibnall JT, Gebara MA, et al: Association of cerebral metabolic activity changes
with vagus nerve stimulation antidepressant response in treatment-resistant depression.
Brain Stimul 6(5):788–797, 2013 23485649
Daban C, Martinez-Aran A, Cruz N, et al: Safety and efficacy of vagus nerve stimulation in
treatment-resistant depression. A systematic review. J Affect Disord 110(1–2):1–15, 2008
18374988
Dandekar MP, Fenoy AJ, Carvalho AF, et al: Deep brain stimulation for treatment-resistant de-
pression: an integrative review of preclinical and clinical findings and translational implications. Mol Psychiatry 23(5):1094–1112, 2018 29483673
Davidson B, Giacobbe P, Mithani K, et al: Lack of clinical response to deep brain stimulation of
the medial forebrain bundle in depression. Brain Stimul 13(5):1268–1270, 2020 32540453
de Haan S, Rietveld E, Stokhof M, et al: Effects of deep brain stimulation on the lived experience
of obsessive-compulsive disorder patients: In-depth interviews with 18 patients. PLoS One
10(8):e0135524, 2015 26312488
Denys D, Mantione M, Figee M, et al: Deep brain stimulation of the nucleus accumbens for
treatment-refractory obsessive-compulsive disorder. Arch Gen Psychiatry 67(10):1061–
1068, 2010 20921122
Döbrössy M, Ramanathan C, Ashouri Vajari D, et al: Neuromodulation in psychiatric disor-
ders: experimental and clinical evidence for reward and motivation network deep brain
stimulation: focus on the medial forebrain bundle. European Journal of Neuroscience
53(1):89–113, 2021. Available at: https://onlinelibrary.wiley.com/doi/10.1111/ejn.14975.
Accessed October 26, 2021.
Dougherty DD, Rezai AR, Carpenter LL, et al: A randomized sham-controlled trial of deep
brain stimulation of the ventral capsule/ventral striatum for chronic treatment-resistant
depression. Biol Psychiatry 78(4):240–248, 2015 25726497
Doyon WM, Anders SK, Ramachandra VS, et al: Effect of operant self-administration of 10%
ethanol plus 10% sucrose on dopamine and ethanol concentrations in the nucleus ac
cumbens. J Neurochem 93(6):1469–1481, 2005 15935063
Drevets WC, Gautier C, Price JC, et al: Amphetamine-induced dopamine release in human ven-
tral striatum correlates with euphoria. Biol Psychiatry 49(2):81–96, 2001 11164755
Drobisz D, Damborská A: Deep brain stimulation targets for treating depression. Behav Brain
Res 359:266–273, 2019 30414974
Dunlop BW, Rajendra JK, Craighead WE, et al: Functional connectivity of the subcallosal cin-
gulate cortex and differential outcomes to treatment with cognitive-behavioral therapy or
antidepressant medication for major depressive disorder. Am J Psychiatry 174(6):533–545,
2017 28335622
Dunner DL, Rush AJ, Russell JM, et al: Prospective, long-term, multicenter study of the natu-
ralistic outcomes of patients with treatment-resistant depression. J Clin Psychiatry
67(5):688–695, 2006 16841617
Eitan R, Fontaine D, Benoît M, et al: One year double blind study of high vs low frequency sub-
callosal cingulate stimulation for depression. J Psychiatr Res 96:124–134, 2018 29032294
Elger G, Hoppe C, Falkai P, et al: Vagus nerve stimulation is associated with mood improve-
ments in epilepsy patients. Epilepsy Res 42(2–3):203–210, 2000 11074193
Englot DJ, Chang EF, Auguste KI: Vagus nerve stimulation for epilepsy: a meta-analysis of effi-
cacy and predictors of response. J Neurosurg 115(6):1248–1255, 2011 21838505
Falowski SM, Sharan A, Reyes BA, et al: An evaluation of neuroplasticity and behavior after
deep brain stimulation of the nucleus accumbens in an animal model of depression. Neurosurgery 69(6):1281–1290, 2011 21566538
Famm K, Litt B, Tracey KJ, et al: Drug discovery: a jump-start for electroceuticals. Nature
496(7444):159–161, 2013 23579662
-
351 Vagus Nerve Stimulation and Deep Brain Stimulation
https://t.me/med1917
Fenoy AJ, Schulz P, Selvaraj S, et al: Deep brain stimulation of the medial forebrain bundle: dis-
tinctive responses in resistant depression. J Affect Disord 203:143–151, 2016 27288959
Fenoy AJ, Schulz PE, Selvaraj S, et al: A longitudinal study on deep brain stimulation of the me-
dial forebrain bundle for treatment-resistant depression. Transl Psychiatry 8(1):111, 2018
29867109
Fife D, Feng Y, Wang MY-H, et al: Epidemiology of pharmaceutically treated depression and
treatment resistant depression in Taiwan. Psychiatry Res 252:277–283, 2017 28288438
Fried EI, Nesse RM: Depression sum-scores don’t add up: why analyzing specific depression
symptoms is essential. BMC Med 13(1):72, 2015 25879936
Galluccio L, Palazzo S, Santagati GE: Modeling signal propagation in nanomachine-to-neuron
communications. Nano Communication Networks 2(4):213–222, 2011. Available at: https://
www.sciencedirect.com/science/article/abs/pii/S1878778911000548?via%3Dihub. Accessed October 26, 2021.
Gemeinsamer-Bundesausschus: Qualitätsberichte der Krankenhäuser im XML-Format. 2014–
2019. 2021. Available at: https://www.g-ba.de/themen/qualitaetssicherung/
datenerhebung-zur-qualitaetssicherung/datenerhebung-qualitaetsbericht/. Accessed
October 2021.
George MS, Rush AJ, Marangell LB, et al: A one-year comparison of vagus nerve stimulation
with treatment as usual for treatment-resistant depression. Biol Psychiatry 58(5):364–373,
2005 16139582
Gilbert F, Goddard E, Viaña JNM, et al: I miss being me: phenomenological effects of deep brain
stimulation. AJOB Neurosci 8(2):96–109, 2017
Grant RA, Halpern CH, Baltuch GH, et al: Ethical considerations in deep brain stimulation for
psychiatric illness. J Clin Neurosci 21(1):1–5, 2014 24055023
Greenberg BD, Price LH, Rauch SL, et al: Neurosurgery for intractable obsessive-compulsive
disorder and depression: critical issues. Neurosurg Clin N Am 14(2):199–212, 2003
12856488
Greenberg BD, Malone DA, Friehs GM, et al: Three-year outcomes in deep brain stimulation
for highly resistant obsessive-compulsive disorder. Neuropsychopharmacology
31(11):2384–2393, 2006 16855529
Hamani C, Mayberg H, Snyder B, et al: Deep brain stimulation of the subcallosal cingulate gy-
rus for depression: anatomical location of active contacts in clinical responders and a suggested guideline for targeting. J Neurosurg 111(6):1209–1215, 2009 19480538
Hamilton M: A rating scale for depression. J Neurol Neurosurg Psychiatry 23(1):56–62, 1960
14399272
Handforth A, DeGiorgio CM, Schachter SC, et al: Vagus nerve stimulation therapy for partial-
onset seizures: a randomized active-control trial. Neurology 51(1):48–55, 1998 9674777
Harden CL, Pulver MC, Ravdin LD, et al: A pilot study of mood in epilepsy patients treated
with vagus nerve stimulation. Epilepsy Behav 1(2):93–99, 2000 12609137
Hariz MI, Blomstedt P, Zrinzo L: Deep brain stimulation between 1947 and 1987: the untold
story. Neurosurg Focus 29(2):E1, 2010 20672911
Henry TR: Therapeutic mechanisms of vagus nerve stimulation. Neurology 59 (6 suppl 4):S3–
S14, 2002 12270962
Henry TR, Bakay RA, Pennell PB, et al: Brain blood-flow alterations induced by therapeutic va-
gus nerve stimulation in partial epilepsy, II: prolonged effects at high and low levels of
stimulation. Epilepsia 45(9):1064–1070, 2004 15329071
Hildt E: Electrodes in the brain: some anthropological and ethical aspects of deep brain stimu-
lation. The International Review of Information Ethics 5(9):33–39, 2006. Available at:
https://informationethics.ca/index.php/irie/article/view/193. Accessed October 26,
2021.
Hodgkin AL, Huxley AF: A quantitative description of membrane current and its application
to conduction and excitation in nerve. J Physiol 117(4):500–544, 1952 1299123
Holtzheimer PE, Kelley ME, Gross RE, et al: Subcallosal cingulate deep brain stimulation for
treatment-resistant unipolar and bipolar depr
2012 22213770
ession. Arch Gen Psychiatry 69(2):150–158,
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