Deep brain stimulation: Difference between revisions

Deep brain stimulation
Deep brain stimulation
	DBS-probes shown in X-ray of the skull (white areas around maxilla and mandible represent metal dentures and are unrelated to DBS devices)
Specialty	Neurosurgery
MeSH	D046690
MedlinePlus	007453
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Deep brain stimulation (DBS) is a surgical procedure that implants a neurostimulator and electrodes which sends electrical impulses to specified targets in the brain responsible for movement control. The treatment is designed for a range of movement disorders such as Parkinson's disease, essential tremor, and dystonia, as well as for certain neuropsychiatric conditions like obsessive-compulsive disorder (OCD) and epilepsy.^[1] The exact mechanisms of DBS are complex and not entirely clear, but it is known to modify brain activity in a structured way.^[2]

DBS has been approved by the Food and Drug Administration as a treatment for essential tremor and Parkinson's disease (PD) since 1997.^[3] DBS was approved for dystonia in 2003,^[4] obsessive–compulsive disorder (OCD) in 2009, and epilepsy in 2018.^[5]^[6]^[7] DBS has been studied in clinical trials as a potential treatment for chronic pain, for various affective disorders, including major depression, for Alzheimer's Disease and drug addiction, among other brain disorders. It is one of few neurosurgical procedures that allow blinded studies.^[1]

As a first approximation, DBS is thought to mimic the clinical effects of lesioning^[8], likely by attenuating (pathologically elevated) information flow through affected brain networks^[9]. Thus, DBS is thought to create an 'informational lesion'^[10], which can be switched off by turning off the DBS device, i.e. is reversible. This is a strong advantage compared to actual brain lesions that are at times also surgically applied to similar targets in similar conditions and which are permanent.

Medical use

DBS is FDA approved or has FDA device exemptions for treatment of Parkinson's Disease, dystonia, Essential Tremor, obsessive-compulsive disorder and epilepsy. In Europe, beyond these indications, a CE mark exists for treatment of Alzheimer's Disease, and while there had been a device exemption for OCD, as well, this has not been renewed^[11]. All other indications are considered investigational, i.e. carried out within medical studies under IRB approval. The table below summarizes FDA approvals.


Indication	Approval Date	Details	DBS Target	Evidence	Source
Essential Tremor (or Parkinsonian Tremor)	July 31, 1997	The FDA approved DBS for the suppression of tremor in the upper extremity in patients with essential tremor.	Ventral intermediate nucleus of the thalamus (VIM)	The approval was based on clinical trials showing significant tremor reduction with thalamic DBS in patients with essential tremor, demonstrating long-term efficacy and safety. The key study is^[12].	FDA
Parkinson's Disease	January 14, 2002	Approved for advanced Parkinson’s disease symptoms not adequately controlled by medications.	Subthalamic nucleus (STN) or internal globus pallidus (GPi)	The key trial that led to approval is^[13]. Further large-scale randomized controlled trials such as^[14], demonstrated the superiority of DBS in the subthalamic nucleus compared to best medical therapy, improving motor function and quality of life.	FDA
Dystonia	April 15, 2003	Granted under a Humanitarian Device Exemption (HDE) for the treatment of chronic, intractable primary dystonia, including generalized and segmental dystonia, hemidystonia, and cervical dystonia in patients seven years of age or above.	Internal globus pallidus (GPi)	The key evidence came from smaller clinical trials under the Humanitarian Device Exemption, where DBS significantly improved motor function in patients with primary dystonia. Prominent trials include ^[15]^[16].	FDA
Obsessive-Compulsive Disorder	February 19, 2009	Approved under HDE for adjunctive treatment of severe, treatment-resistant OCD.	Nucleus Accumbens (NAc)	Initial approval came under HDE based on evidence from smaller, open-label trials, such as^[17], showing reductions in OCD symptoms in severe cases.	FDA
Epilepsy	April 27, 2018	Approved for bilateral stimulation of the anterior nucleus of the thalamus (ANT) as an adjunctive therapy to reduce the frequency of seizures in adults with partial-onset seizures.	Anterior nucleus of the thalamus (ANT)	The key evidence came from the SANTE trial^[18], demonstrating a significant reduction in seizure frequency in patients receiving DBS.	FDA

Parkinson's disease

DBS is used to manage some of the symptoms of Parkinson's disease that cannot be adequately controlled with medications.^[19]^[20] PD is treated by applying high-frequency (> 100 Hz) stimulation to target structures in the depth of the brain. Frequently used targets include the subthalamic nucleus (STN), internal pallidum (GPi) and ventrointermediate nucleus of the thalamus (VIM). The pedunculopontine nucleus has been used as an investigational target to treat freezing of gait.

DBS is recommended for people who have PD with motor fluctuations and tremors inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems.^[21] Four areas of the brain have been treated with neural stimulators in PD. Most DBS surgeries in routine practice target either the GPi or the STN, which, in prospective trials have been equally efficient in reducing motor symptoms^[22]^[23], likely due to a shared network being stimulated with either target^[24]. General differences between targets are not easy to summarize, but often include the following:

DBS of the GPi has been shown to reduce uncontrollable movements called dyskinesias. This may sometimes allow a patient to take adequate (additional) quantities of medications (especially levodopa), thus leading to better control of symptoms.
DBS of the subthalamic nucleus has a more sudden effect on tremor (while effect on tremor in GPi is sometimes delayed). Also, studies associated STN-DBS with reductions in dopaminergic medication.
DBS of the VIM is mainly used to reduce shaking movements (tremor), and hence is, if at all, used in tremor-dominant variants of PD (and also to treat Essential Tremor).
Some studies suggested efficacy for DBS of the PPN in reducing freezing of gait, but results have been mixed and the target is not routinely used.

Selection of the correct DBS target is a complicated process. Multiple clinical characteristics are used to select the target including – identifying the most troublesome symptoms, the dose of levodopa that the patient is currently taking, the effects and side-effects of current medications and concurrent problems. Decisions are often made in multidisciplinary teams at specialized institutions.

Essential Tremor

As the most common movement disorder^[25], ET was also the first indication to be approved for DBS (alongside Parkinsonian tremor). DBS electrodes are commonly targeted into the ventrointermediate nucleus of the thalamus (VIM) or ventrally adjacent areas that have been referred to as parts of the zona incerta, or posterior thalamic area. Recent metaanalytical evidence suggests that multiple targets along the circuitry of the cerebellothalamic pathway (also referred to as the dentatorubrothalamic or dentatothalamic tract) are similarly effective, i.e. modulating the cerebellar inflows into the thalamus may be key for therapeutic efficacy^[26]^[27], for a review see^[28]. Already in the first publication on the matter by the team of Alim Louis Benabid, it could be shown that frequencies above 100 Hz are most effective for cessation of tremor, while lower frequencies have less effect^[29]. In clinical practice, frequencies between 80 and 180 Hz are typically applied.

Dystonia

In dystonia, marked effects can be reached by targeting the GPi using high frequency DBS, with large randomized trials demonstrating improvements of ~45% within the first six months of treatment^[30]. Similar effects have been reported in open label trials that targeted the STN (but this target is investigational for dystonia)^[31].

Obsessive-Compulsive-Disorder

DBS for OCD was first attempted by the team of Bart Nuttin in 1999^[32]. Curiously, the year 1999 marked three innovations all published in the Lancet: The first attempt to treat Tourette's Syndrome by the team of Veerle Visser-Vandewalle^[33], the aforementioned trial by Nuttin and a trial reporting on bilateral stimulation of dystonia by Joachim Krauss and colleagues^[34]. Of these, the study by Visser-Vandewalle is considered the first modern-day indication of DBS in neuropsychiatric indication (Tourette's Syndrome), making the trial by Nuttin for OCD the second. DBS for OCD received a humanitarian device exemption from the FDA in 2009^[35]. In Europe, the CE Mark for Deep Brain Stimulation (DBS) for Obsessive-Compulsive Disorder (OCD) was active from 2009 to 2022 but not renewed thereafter, which was likely not motivated by a lack of evidence but by a lack of monetary interests, which has led to expert letters calling for a 'crisis of access' above and beyond Europe^[36]^[37].

Beyond the original target in the anterior limb of the internal capsule (ALIC)^[32], multiple target sites have been probed, such as the nucleus accumbens^[38] (sometimes subsumized with the ALIC as the ventral capsule/ventral striatum or VC/VS target^[39]), the bed nucleus of stria terminalis^[40], the inferior thalamic peduncle^[41] and the anteromedial portion of the STN^[42]. Within the ALIC region, large probabilistic mapping trials have identified two distinct sites of maximum efficacy^[43], one likely corresponding to 'hyperdirect' pathway inputs^[44] to the subthalamic nucleus and other midbrain regions, the other potentially corresponding to 'indirect' pathway projections within the same basal ganglia thalamocortical loop. A potential circuit structure that seems to combine most effective targets in both the ALIC and STN region has been identified and termed the OCD response tract^[45] by the group of Andreas Horn. Modulating this fiber tract system, which has been described as projections from dorsal anterior cingulate and ventrolateral prefrontal cortices to the subthalamic nucleus (and potentially other midbrain structures), as well as reciprocal thalamic projections to the same sites, has been robustly associated with optimal treatment response across multiple studies from various groups^[46]^[47]^[48]^[49]^[50]^[51].

Epilepsy

As many as 36.3% of epilepsy patients are drug-resistant.^[52] These patients are at risk for significant morbidity and mortality.^[53] In cases where surgery is not an option, neurostimulation such as DBS, as well as vagus nerve stimulation and responsive neurostimulation can be considered.^{[medical citation needed]} Targets other than the anterior nucleus of the thalamus have been studied for the treatment of epilepsy, such as the centromedian nucleus of the thalamus, the cerebellum and others.^[54]

Tourette syndrome

As mentioned above, the first DBS application for Tourette's Syndrome has been carried out by the team of Veerle Visser-Vandewalle in 1999^[55]. Building upon the ablative lesion cases carried out by Rolf Hassler and colleagues^[56], Visser-Vandewalle chose the intersection between the centromedian, parafascicular and ventrooralis internus nuclei of the thalamus as her DBS target. Authors reported that, after surgery, tics disappeared and "a change in the patient’s character occurred in that he had become much more kind-hearted." DBS has been used experimentally in treating adults with severe Tourette syndrome who do not respond to conventional treatment. Despite widely publicized early successes, DBS remains a highly experimental procedure for treating Tourette's, and more study is needed to determine whether long-term benefits outweigh the risks.^[57]^[58]^[59]^[60] The procedure is well tolerated, but complications include "short battery life, abrupt symptom worsening upon cessation of stimulation, hypomanic or manic conversion, and the significant time and effort involved in optimizing stimulation parameters".^[61]

The procedure is invasive and expensive and requires long-term expert care. Benefits for severe Tourette's are inconclusive, considering the less robust effects of this surgery seen in the Netherlands. Tourette's is more common in pediatric populations, tending to remit in adulthood, so, in general, this would not be a recommended procedure for use on children. It may not always be obvious how to utilize DBS for a particular person because the diagnosis of Tourette's is based on a history of symptoms rather than an examination of neurological activity. Due to concern over the use of DBS in Tourette syndrome treatment, the Tourette Association of America convened a group of experts to develop recommendations guiding the use and potential clinical trials of DBS for TS.^[62]

Robertson reported that DBS had been used on 55 adults by 2011, remained an experimental treatment at that time, and recommended that the procedure "should only be conducted by experienced functional neurosurgeons operating in centres which also have a dedicated Tourette syndrome clinic".^[58] According to Malone et al. (2006), "Only patients with severe, debilitating, and treatment-refractory illness should be considered; while those with severe personality disorders and substance-abuse problems should be excluded."^[61] Du et al. (2010) say, "As an invasive therapy, DBS is currently only advisable for severely affected, treatment-refractory TS adults".^[59] Singer (2011) says, "pending determination of patient selection criteria and the outcome of carefully controlled clinical trials, a cautious approach is recommended".^[57] Viswanathan et al. (2012) say DBS should be used for people with "severe functional impairment that cannot be managed medically".^[63]

Adaptive Deep Brain Stimulation

Adaptive of Closed Loop Deep Brain Stimulation is a technique in which a steering signal influences when, with which amplitude or at which electrode contacts the DBS system is activated. This steering signal can be a physiological sensing signal, which is typically either recorded from the same implanted electrode or a cortical electrode/ECoG strip/grid. Alternatively, signals from wearables, that e.g. detect symptoms such as tremor, may be used to guide stimulation across time. The concept of adaptive deep brain stimulation is as old as the concept of electrical stimulation of the brain, itself, i.e. originates in the 1950ies-1960ies and was implemented by early pioneers such as Carl-Wilhelm Sem-Jacobsen^[3], Natalia Bechtereva^[4], José Delgado^[5] or Robert Heath^[6]. The reason these scientists came up with the concept so early was out of necessity: At the time, chronic stimulation as carried out in open-loop (conventional) DBS applications was not technically possible using fully implanted devices, since the battery technology at the time was not ready to do so^[8]. With the advent of 'modern' DBS as implemented by the team of Alim Louis Benabid, for decades, chronic, open-loop DBS became the dominant application. Here, pulses are emitted to the brain tissue in a fixed frequency (often 130 Hz) without sensing brain signals or other forms of a steering signal.It took until the 2010s, after a demonstration of efficacy of aDBS in the macaque by the team of Hagai Bergman in 2011^[10], the first in-human application of aDBS was carried out by the team of Peter Brown in 2013^[9], followed by the team of Alberto Priori in the same year^[22]. Since then, several companies, including Medtronic and Newronika have begun developing commercial applications of closed-loop DBS.

Adverse effects

Arteriogram of the arterial supply that can hemorrhage during DBS implantation

DBS carries the risks of major surgery, with a complication rate related to the experience of the surgical team. The major complications include hemorrhage (1–2%) and infection (3–5%).^[64]

The potential exists for neuropsychiatric side effects after DBS, including apathy, hallucinations, hypersexuality, cognitive dysfunction, depression, and euphoria. However, these effects may be temporary and related to (1) incorrect placement of electrodes, (2) open-loop VS closed-loop stimulation, meaning a constant stimulation or an A.I. monitoring delivery system^[65] and (3) calibration of the stimulator, so these side effects are potentially reversible.^[66]

Because the brain can shift slightly during surgery, the electrodes can become displaced or dislodged from the specific location. This may cause more profound complications such as personality changes, but electrode misplacement is relatively easy to identify using CT scan. Also, surgery complications may occur, such as bleeding within the brain. After surgery, swelling of the brain tissue, mild disorientation, and sleepiness are normal. After 2–4 weeks, a follow-up visit is used to remove sutures, turn on the neurostimulator, and program it.^{[citation needed]}

Impaired swimming skills surfaced as an unexpected risk of the procedure; several Parkinson's disease patients lost their ability to swim after receiving deep brain stimulation.^[67]^[68]

Mechanisms

The exact mechanism of action of DBS is not known.^[69] A variety of hypotheses try to explain the mechanisms of DBS:^[70]^[71]

Depolarization blockade: Electrical currents block the neuronal output at or near the electrode site.
Synaptic inhibition: This causes an indirect regulation of the neuronal output by activating axon terminals with synaptic connections to neurons near the stimulating electrode.
Desynchronization of abnormal oscillatory activity of neurons
Antidromic activation either activating/blockading distant neurons or blockading slow axons^[2]

DBS represents an advance on previous treatments which involved pallidotomy (i.e., surgical ablation of the globus pallidus) or thalamotomy (i.e., surgical ablation of the thalamus).^[72] Instead, a thin lead with multiple electrodes is implanted in the globus pallidus, nucleus ventralis intermedius thalami, or subthalamic nucleus, and electric pulses are used therapeutically. The lead from the implant is extended to the neurostimulator under the skin in the chest area.^{[citation needed]}

Its direct effect on the physiology of brain cells and neurotransmitters is currently debated, but by sending high-frequency electrical impulses into specific areas of the brain, it can mitigate symptoms^[73] and directly diminish the side effects induced by PD medications,^[74] allowing a decrease in medications, or making a medication regimen more tolerable.^{[citation needed]}

Components and placement

The DBS system consists of three components: the implanted pulse generator (IPG), the lead, and an extension. The IPG is a battery-powered neurostimulator encased in a titanium housing, which sends electrical pulses to the brain that interfere with neural activity at the target site. The lead is a coiled wire insulated in polyurethane with four platinum-iridium electrodes and is placed in one or two different nuclei of the brain. The lead is connected to the IPG by an extension, an insulated wire that runs below the skin, from the head, down the side of the neck, behind the ear, to the IPG, which is placed subcutaneously below the clavicle, or in some cases, the abdomen.^[19] The IPG can be calibrated by a neurologist, nurse, or trained technician to optimize symptom suppression and control side effects.^[75]

DBS leads are placed in the brain according to the type of symptoms to be addressed. For non-Parkinsonian essential tremor, the lead is placed in either the ventrointermediate nucleus of the thalamus or the zona incerta;^[76] for dystonia and symptoms associated with PD (rigidity, bradykinesia/akinesia, and tremor), the lead may be placed in either the globus pallidus internus or the subthalamic nucleus; for OCD and depression to the nucleus accumbens; for incessant pain to the posterior thalamic region or periaqueductal gray; and for epilepsy treatment to the anterior thalamic nucleus.^{[citation needed]}

All three components are surgically implanted inside the body. Lead implantation may take place under local anesthesia or under general anesthesia ("asleep DBS"), such as for dystonia. A hole about 14 mm in diameter is drilled in the skull and the probe electrode is inserted stereotactically, using either frame-based or frameless stereotaxis.^[77] During the awake procedure with local anesthesia, feedback from the person is used to determine the optimal placement of the permanent electrode. During the asleep procedure, intraoperative MRI guidance is used for direct visualization of brain tissue and device.^[78] The installation of the IPG and extension leads occurs under general anesthesia.^[79] The right side of the brain is stimulated to address symptoms on the left side of the body and vice versa.^{[citation needed]}

Research

Chronic pain

Stimulation of the periaqueductal gray and periventricular gray for nociceptive pain, and the internal capsule, ventral posterolateral nucleus, and ventral posteromedial nucleus for neuropathic pain has produced impressive results with some people, but results vary. One study^[80] of 17 people with intractable cancer pain found that 13 were virtually pain-free and only four required opioid analgesics on release from hospital after the intervention. Most ultimately did resort to opioids, usually in the last few weeks of life.^[81] DBS has also been applied for phantom limb pain.^[82]

Major depression and obsessive-compulsive disorder

DBS has been used in a small number of clinical trials to treat people with severe treatment-resistant depression (TRD).^[83] A number of neuroanatomical targets have been used for DBS for TRD including the subgenual cingulate gyrus, posterior gyrus rectus,^[84] nucleus accumbens,^[85] ventral capsule/ventral striatum, inferior thalamic peduncle, and the lateral habenula.^[83] A recently proposed target of DBS intervention in depression is the superolateral branch of the medial forebrain bundle; its stimulation lead to surprisingly rapid antidepressant effects.^[86]

The small numbers in the early trials of DBS for TRD currently limit the selection of an optimal neuroanatomical target.^[83] Evidence is insufficient to support DBS as a therapeutic modality for depression; however, the procedure may be an effective treatment modality in the future.^[87] In fact, beneficial results have been documented in the neurosurgical literature, including a few instances in which people who were deeply depressed were provided with portable stimulators for self-treatment.^[88]^[89]^[90]

A systematic review of DBS for TRD and OCD identified 23 cases, nine for OCD, seven for TRD, and one for both. "[A]bout half the patients did show dramatic improvement" and adverse events were "generally trivial" given the younger age of the psychiatric population relative to the age of people with movement disorders.^[91] The first randomized, controlled study of DBS for the treatment of TRD targeting the ventral capsule/ventral striatum area did not demonstrate a significant difference in response rates between the active and sham groups at the end of a 16-week study.^[92] However, a second randomized controlled study of ventral capsule DBS for TRD did demonstrate a significant difference in response rates between active DBS (44% responders) and sham DBS (0% responders).^[93] Efficacy of DBS is established for OCD, with on average 60% responders in severely ill and treatment-resistant patients.^[94] Based on these results the Food and Drug Administration (FDA) has approved DBS for treatment-resistant OCD under a Humanitarian Device Exemption (HDE), requiring that the procedure be performed only in a hospital with specialist qualifications to do so.

DBS for TRD can be as effective as antidepressants and have good response and remission rates, but adverse effects and safety must be more fully evaluated. Common side effects include "wound infection, perioperative headache, and worsening/irritable mood [and] increased suicidality".^[95]

Other clinical applications

Results of DBS in people with dystonia, where positive effects often appear gradually over a period of weeks to months, indicate a role of functional reorganization in at least some cases.^[96] The procedure has been tested for effectiveness in people with epilepsy that is resistant to medication.^[97] DBS may reduce or eliminate epileptic seizures with programmed or responsive stimulation.^{[citation needed]}

DBS of the septal areas of persons with schizophrenia has resulted in enhanced alertness, cooperation, and euphoria.^[98] Persons with narcolepsy and complex-partial seizures also reported euphoria and sexual thoughts from self-elicited DBS of the septal nuclei.^[89]

Orgasmic ecstasy was reported with the electrical stimulation of the brain with depth electrodes in the left hippocampus at 3mA, and the right hippocampus at 1 mA.^[99]

In 2015, a group of Brazilian researchers led by neurosurgeon Erich Fonoff [pt] described a new technique that allows for simultaneous implants of electrodes called bilateral stereotactic procedure for DBS. The main benefits are less time spent on the procedure and greater accuracy.^[100]

In 2016, DBS was found to improve learning and memory in a mouse model of Rett syndrome.^[101] More recent (2018) work showed, that forniceal DBS upregulates genes involved in synaptic function, cell survival, and neurogenesis,^[102] making some first steps at explaining the restoration of hippocampal circuit function.

Epilepsy target

According to one long-term follow-up study, DBS targeting the anterior nucleus of the thalamus may be somewhat more effective for temporal lobe epilepsy, and efficacy may increase over time.^[103]^[104]

References

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External links

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[:0-3] "FDA approves brain implant to help reduce Parkinson's disease and essential tremor symptoms". FDA. Retrieved May 23, 2016. The first device, Medtronic's Activa Deep Brain Stimulation Therapy System, was approved in 1997 for tremor associated with essential tremor and Parkinson's disease.

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[:2-5] "Medtronic Receives FDA Approval for Deep Brain Stimulation Therapy for Medically Refractory Epilepsy" (Press release). Medtronic. 1 May 2018.

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@@ Line 27: / Line 27: @@
 DBS has been approved by the [[Food and Drug Administration]] as a treatment for essential tremor and [[Parkinson's disease]] (PD) since 1997.<ref name=":0">{{Cite web|url=https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm451152.htm|title= FDA approves brain implant to help reduce Parkinson's disease and essential tremor symptoms|website=FDA|access-date=May 23, 2016|quote=The first device, Medtronic's Activa Deep Brain Stimulation Therapy System, was approved in 1997 for tremor associated with essential tremor and Parkinson's disease.}}</ref> DBS was approved for [[dystonia]] in 2003,<ref name=":1">{{cite news | vauthors = Phillips S |title='Brain pacemaker' for a rare disorder |url=https://www.nbcnews.com/id/wbna19265007 |archive-url=https://web.archive.org/web/20210428014405/https://www.nbcnews.com/id/wbna19265007 |url-status=dead |archive-date=April 28, 2021 |work=NBC News |date=17 June 2007 }}</ref> obsessive–compulsive disorder (OCD) in 2009, and [[epilepsy]] in 2018.<ref name=":2">{{cite press release |title=Medtronic Receives FDA Approval for Deep Brain Stimulation Therapy for Medically Refractory Epilepsy |url=https://news.medtronic.com/2018-05-01-Medtronic-Receives-FDA-Approval-for-Deep-Brain-Stimulation-Therapy-for-Medically-Refractory-Epilepsy |publisher=Medtronic |date=1 May 2018 }}</ref><ref name=":3">{{cite web|url=https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm149529.htm|title=FDA Approves Humanitarian Device Exemption for Deep Brain Stimulator for Severe Obsessive-Compulsive Disorder|work=FDA}}</ref><ref name=gildenberg>{{cite journal | vauthors = Gildenberg PL | title = Evolution of neuromodulation | journal = Stereotactic and Functional Neurosurgery | volume = 83 | issue = 2–3 | pages = 71–79 | date = 2005 | pmid = 16006778 | doi = 10.1159/000086865 | s2cid = 20234898 }}</ref> DBS has been studied in clinical trials as a potential treatment for [[chronic pain]], for various affective disorders, including [[major depressive disorder|major depression]], for [[Alzheimer's disease|Alzheimer's Disease]] and [[drug addiction]], among other brain disorders. It is one of few neurosurgical procedures that allow [[Blind experiment|blinded studies]].<ref name="Kringelbach"/>
-As a first approximation, DBS is thought to mimic the clinical effects of [[lesioning]]<ref name=":4">{{cite book |title=Parkinson's Disease and Related Disorders, Part II |vauthors=Morris JG, Owler B, Hely MA, Fung VS |year=2007 |isbn=978-0-444-52893-3 |series=Handbook of Clinical Neurology |volume=84 |pages=459–478 |chapter=Hydrocephalus and structural lesions |doi=10.1016/S0072-9752(07)84055-3 |oclc=1132129865 |pmid=18808964}}</ref>, likely by attenuating (pathologically elevated) information flow through affected brain networks<ref name=":5">{{Cite journal |last=Hollunder |first=Barbara |last2=Ostrem |first2=Jill L. |last3=Sahin |first3=Ilkem Aysu |last4=Rajamani |first4=Nanditha |last5=Oxenford |first5=Simón |last6=Butenko |first6=Konstantin |last7=Neudorfer |first7=Clemens |last8=Reinhardt |first8=Pablo |last9=Zvarova |first9=Patricia |last10=Polosan |first10=Mircea |last11=Akram |first11=Harith |last12=Vissani |first12=Matteo |last13=Zhang |first13=Chencheng |last14=Sun |first14=Bomin |last15=Navratil |first15=Pavel |date=March 2024 |title=Mapping dysfunctional circuits in the frontal cortex using deep brain stimulation |url=https://www.nature.com/articles/s41593-024-01570-1 |journal=Nature Neuroscience |language=en |volume=27 |issue=3 |pages=573–586 |doi=10.1038/s41593-024-01570-1 |issn=1097-6256 |pmc=10917675 |pmid=38388734}}</ref>. Thus, DBS is thought to create an 'informational lesion'<ref name=":6">{{Cite journal |last=Grill |first=Warren M. |last2=Snyder |first2=Andrea N. |last3=Miocinovic |first3=Svjetlana |date=May 2004 |title=Deep brain stimulation creates an informational lesion of the stimulated nucleus: |url=http://journals.lww.com/00001756-200405190-00011 |journal=NeuroReport |language=en |volume=15 |issue=7 |pages=1137–1140 |doi=10.1097/00001756-200405190-00011 |issn=0959-4965}}</ref>, which can be switched off by turning off the DBS device, i.e. is reversible. This is a strong advantage compared to actual [[Stereotactic surgery|brain lesions]] that are at times also surgically applied to similar targets in similar conditions and which are permanent.
+As a first approximation, DBS is thought to mimic the clinical effects of [[lesioning]]<ref name=":4">{{cite book |title=Parkinson's Disease and Related Disorders, Part II |vauthors=Morris JG, Owler B, Hely MA, Fung VS |year=2007 |isbn=978-0-444-52893-3 |series=Handbook of Clinical Neurology |volume=84 |pages=459–478 |chapter=Hydrocephalus and structural lesions |doi=10.1016/S0072-9752(07)84055-3 |oclc=1132129865 |pmid=18808964}}</ref>, likely by attenuating (pathologically elevated) information flow through affected brain networks<ref name=":5">{{Cite journal |last1=Hollunder |first1=Barbara |last2=Ostrem |first2=Jill L. |last3=Sahin |first3=Ilkem Aysu |last4=Rajamani |first4=Nanditha |last5=Oxenford |first5=Simón |last6=Butenko |first6=Konstantin |last7=Neudorfer |first7=Clemens |last8=Reinhardt |first8=Pablo |last9=Zvarova |first9=Patricia |last10=Polosan |first10=Mircea |last11=Akram |first11=Harith |last12=Vissani |first12=Matteo |last13=Zhang |first13=Chencheng |last14=Sun |first14=Bomin |last15=Navratil |first15=Pavel |date=March 2024 |title=Mapping dysfunctional circuits in the frontal cortex using deep brain stimulation |journal=Nature Neuroscience |language=en |volume=27 |issue=3 |pages=573–586 |doi=10.1038/s41593-024-01570-1 |issn=1097-6256 |pmc=10917675 |pmid=38388734}}</ref>. Thus, DBS is thought to create an 'informational lesion'<ref name=":6">{{Cite journal |last1=Grill |first1=Warren M. |last2=Snyder |first2=Andrea N. |last3=Miocinovic |first3=Svjetlana |date=May 2004 |title=Deep brain stimulation creates an informational lesion of the stimulated nucleus |url=http://journals.lww.com/00001756-200405190-00011 |journal=NeuroReport |language=en |volume=15 |issue=7 |pages=1137–1140 |doi=10.1097/00001756-200405190-00011 |pmid=15129161 |issn=0959-4965}}</ref>, which can be switched off by turning off the DBS device, i.e. is reversible. This is a strong advantage compared to actual [[Stereotactic surgery|brain lesions]] that are at times also surgically applied to similar targets in similar conditions and which are permanent.
 == Medical use ==
 [[File:Prep for Deep Brain Stimulation.png|thumb|260px|An adult male undergoing pre-op preparation for deep brain stimulation]]
-[[Image:Parkinson surgery.jpg|thumb|260px|Insertion of electrode during surgery using a [[Stereotactic surgery|stereotactic frame]]]]DBS is FDA approved or has FDA device exemptions for treatment of Parkinson's Disease, dystonia, Essential Tremor, obsessive-compulsive disorder and epilepsy. In Europe, beyond these indications, a CE mark exists for treatment of Alzheimer's Disease, and while there had been a device exemption for OCD, as well, this has not been renewed<ref>{{Cite journal |last=Visser-Vandewalle |first=Veerle |last2=Andrade |first2=Pablo |last3=Mosley |first3=Philip E. |last4=Greenberg |first4=Benjamin D. |last5=Schuurman |first5=Rick |last6=McLaughlin |first6=Nicole C. |last7=Voon |first7=Valerie |last8=Krack |first8=Paul |last9=Foote |first9=Kelly D. |last10=Mayberg |first10=Helen S. |last11=Figee |first11=Martijn |last12=Kopell |first12=Brian H. |last13=Polosan |first13=Mircea |last14=Joyce |first14=Eileen M. |last15=Chabardes |first15=Stephan |date=2022-08 |title=Deep brain stimulation for obsessive–compulsive disorder: a crisis of access |url=https://www.nature.com/articles/s41591-022-01879-z |journal=Nature Medicine |language=en |volume=28 |issue=8 |pages=1529–1532 |doi=10.1038/s41591-022-01879-z |issn=1078-8956}}</ref>. All other indications are considered investigational, i.e. carried out within medical studies under IRB approval. The table below summarizes FDA approvals.
+[[Image:Parkinson surgery.jpg|thumb|260px|Insertion of electrode during surgery using a [[Stereotactic surgery|stereotactic frame]]]]DBS is FDA approved or has FDA device exemptions for treatment of Parkinson's Disease, dystonia, Essential Tremor, obsessive-compulsive disorder and epilepsy. In Europe, beyond these indications, a CE mark exists for treatment of Alzheimer's Disease, and while there had been a device exemption for OCD, as well, this has not been renewed<ref>{{Cite journal |last1=Visser-Vandewalle |first1=Veerle |last2=Andrade |first2=Pablo |last3=Mosley |first3=Philip E. |last4=Greenberg |first4=Benjamin D. |last5=Schuurman |first5=Rick |last6=McLaughlin |first6=Nicole C. |last7=Voon |first7=Valerie |last8=Krack |first8=Paul |last9=Foote |first9=Kelly D. |last10=Mayberg |first10=Helen S. |last11=Figee |first11=Martijn |last12=Kopell |first12=Brian H. |last13=Polosan |first13=Mircea |last14=Joyce |first14=Eileen M. |last15=Chabardes |first15=Stephan |date=August 2022 |title=Deep brain stimulation for obsessive–compulsive disorder: a crisis of access |url=https://www.nature.com/articles/s41591-022-01879-z |journal=Nature Medicine |language=en |volume=28 |issue=8 |pages=1529–1532 |doi=10.1038/s41591-022-01879-z |pmid=35840727 |issn=1078-8956}}</ref>. All other indications are considered investigational, i.e. carried out within medical studies under IRB approval. The table below summarizes FDA approvals.
 {| class="wikitable"
 |+
@@ Line 45: / Line 45: @@
 |The FDA approved DBS for the suppression of tremor in the upper extremity in patients with essential tremor.
 |Ventral intermediate nucleus of the thalamus (VIM)
-|The approval was based on clinical trials showing significant tremor reduction with thalamic DBS in patients with essential tremor, demonstrating long-term efficacy and safety. The key study is<ref>{{Cite journal |last=Benabid |first=A.L. |last2=Pollak |first2=P. |last3=Hoffmann |first3=D. |last4=Gervason |first4=C. |last5=Hommel |first5=M. |last6=Perret |first6=J.E. |last7=de Rougemont |first7=J. |last8=Gao |first8=D.M. |date=1991-02 |title=Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus |url=https://linkinghub.elsevier.com/retrieve/pii/014067369191175T |journal=The Lancet |language=en |volume=337 |issue=8738 |pages=403–406 |doi=10.1016/0140-6736(91)91175-T}}</ref>.
+|The approval was based on clinical trials showing significant tremor reduction with thalamic DBS in patients with essential tremor, demonstrating long-term efficacy and safety. The key study is<ref>{{Cite journal |last1=Benabid |first1=A.L. |last2=Pollak |first2=P. |last3=Hoffmann |first3=D. |last4=Gervason |first4=C. |last5=Hommel |first5=M. |last6=Perret |first6=J.E. |last7=de Rougemont |first7=J. |last8=Gao |first8=D.M. |date=February 1991 |title=Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus |url=https://linkinghub.elsevier.com/retrieve/pii/014067369191175T |journal=The Lancet |language=en |volume=337 |issue=8738 |pages=403–406 |doi=10.1016/0140-6736(91)91175-T|pmid=1671433 }}</ref>.
 |[https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfpma/pma.cfm?id=P960009 FDA]
 |-
@@ Line 52: / Line 52: @@
 |Approved for advanced Parkinson’s disease symptoms not adequately controlled by medications.
 |Subthalamic nucleus (STN) or internal globus pallidus (GPi)
-|The key trial that led to approval is<ref>{{Cite journal |date=2001-09-27 |title=Deep-Brain Stimulation of the Subthalamic Nucleus or the Pars Interna of the Globus Pallidus in Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa000827 |journal=New England Journal of Medicine |language=en |volume=345 |issue=13 |pages=956–963 |doi=10.1056/NEJMoa000827 |issn=0028-4793}}</ref>. Further large-scale randomized controlled trials such as<ref>{{Cite journal |last=Deuschl |first=Günther |last2=Schade-Brittinger |first2=Carmen |last3=Krack |first3=Paul |last4=Volkmann |first4=Jens |last5=Schäfer |first5=Helmut |last6=Bötzel |first6=Kai |last7=Daniels |first7=Christine |last8=Deutschländer |first8=Angela |last9=Dillmann |first9=Ulrich |last10=Eisner |first10=Wilhelm |last11=Gruber |first11=Doreen |last12=Hamel |first12=Wolfgang |last13=Herzog |first13=Jan |last14=Hilker |first14=Rüdiger |last15=Klebe |first15=Stephan |date=2006-08-31 |title=A Randomized Trial of Deep-Brain Stimulation for Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa060281 |journal=New England Journal of Medicine |language=en |volume=355 |issue=9 |pages=896–908 |doi=10.1056/NEJMoa060281 |issn=0028-4793}}</ref>, demonstrated the superiority of DBS in the subthalamic nucleus compared to best medical therapy, improving motor function and quality of life.
+|The key trial that led to approval is<ref>{{Cite journal |date=2001-09-27 |title=Deep-Brain Stimulation of the Subthalamic Nucleus or the Pars Interna of the Globus Pallidus in Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa000827 |journal=New England Journal of Medicine |language=en |volume=345 |issue=13 |pages=956–963 |doi=10.1056/NEJMoa000827 |pmid=11575287 |issn=0028-4793 |author1=Deep-Brain Stimulation for Parkinson's Disease Study Group |last2=Obeso |first2=J. A. |last3=Olanow |first3=C. W. |last4=Rodriguez-Oroz |first4=M. C. |last5=Krack |first5=P. |last6=Kumar |first6=R. |last7=Lang |first7=A. E. }}</ref>. Further large-scale randomized controlled trials such as<ref>{{Cite journal |last1=Deuschl |first1=Günther |last2=Schade-Brittinger |first2=Carmen |last3=Krack |first3=Paul |last4=Volkmann |first4=Jens |last5=Schäfer |first5=Helmut |last6=Bötzel |first6=Kai |last7=Daniels |first7=Christine |last8=Deutschländer |first8=Angela |last9=Dillmann |first9=Ulrich |last10=Eisner |first10=Wilhelm |last11=Gruber |first11=Doreen |last12=Hamel |first12=Wolfgang |last13=Herzog |first13=Jan |last14=Hilker |first14=Rüdiger |last15=Klebe |first15=Stephan |date=2006-08-31 |title=A Randomized Trial of Deep-Brain Stimulation for Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa060281 |journal=New England Journal of Medicine |language=en |volume=355 |issue=9 |pages=896–908 |doi=10.1056/NEJMoa060281 |issn=0028-4793}}</ref>, demonstrated the superiority of DBS in the subthalamic nucleus compared to best medical therapy, improving motor function and quality of life.
 |[https://www.accessdata.fda.gov/cdrh_docs/pdf/P960009S007a.pdf FDA]
 |-
@@ Line 59: / Line 59: @@
 |Granted under a Humanitarian Device Exemption (HDE) for the treatment of chronic, intractable primary dystonia, including generalized and segmental dystonia, hemidystonia, and cervical dystonia in patients seven years of age or above.
 |Internal globus pallidus (GPi)
-|The key evidence came from smaller clinical trials under the Humanitarian Device Exemption, where DBS significantly improved motor function in patients with primary dystonia. Prominent trials include <ref>{{Cite journal |last=Vidailhet |first=Marie |last2=Vercueil |first2=Laurent |last3=Houeto |first3=Jean-Luc |last4=Krystkowiak |first4=Pierre |last5=Benabid |first5=Alim-Louis |last6=Cornu |first6=Philippe |last7=Lagrange |first7=Christelle |last8=Tézenas du Montcel |first8=Sophie |last9=Dormont |first9=Didier |last10=Grand |first10=Sylvie |last11=Blond |first11=Serge |last12=Detante |first12=Olivier |last13=Pillon |first13=Bernard |last14=Ardouin |first14=Claire |last15=Agid |first15=Yves |date=2005-02-03 |title=Bilateral Deep-Brain Stimulation of the Globus Pallidus in Primary Generalized Dystonia |url=http://www.nejm.org/doi/10.1056/NEJMoa042187 |journal=New England Journal of Medicine |language=en |volume=352 |issue=5 |pages=459–467 |doi=10.1056/NEJMoa042187 |issn=0028-4793}}</ref><ref>{{Cite journal |last=Kupsch |first=Andreas |last2=Benecke |first2=Reiner |last3=Müller |first3=Jörg |last4=Trottenberg |first4=Thomas |last5=Schneider |first5=Gerd-Helge |last6=Poewe |first6=Werner |last7=Eisner |first7=Wilhelm |last8=Wolters |first8=Alexander |last9=Müller |first9=Jan-Uwe |last10=Deuschl |first10=Günther |last11=Pinsker |first11=Marcus O. |last12=Skogseid |first12=Inger Marie |last13=Roeste |first13=Geir Ketil |last14=Vollmer-Haase |first14=Juliane |last15=Brentrup |first15=Angela |date=2006-11-09 |title=Pallidal Deep-Brain Stimulation in Primary Generalized or Segmental Dystonia |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa063618 |journal=New England Journal of Medicine |language=en |volume=355 |issue=19 |pages=1978–1990 |doi=10.1056/NEJMoa063618 |issn=0028-4793}}</ref>.
+|The key evidence came from smaller clinical trials under the Humanitarian Device Exemption, where DBS significantly improved motor function in patients with primary dystonia. Prominent trials include <ref>{{Cite journal |last1=Vidailhet |first1=Marie |last2=Vercueil |first2=Laurent |last3=Houeto |first3=Jean-Luc |last4=Krystkowiak |first4=Pierre |last5=Benabid |first5=Alim-Louis |last6=Cornu |first6=Philippe |last7=Lagrange |first7=Christelle |last8=Tézenas du Montcel |first8=Sophie |last9=Dormont |first9=Didier |last10=Grand |first10=Sylvie |last11=Blond |first11=Serge |last12=Detante |first12=Olivier |last13=Pillon |first13=Bernard |last14=Ardouin |first14=Claire |last15=Agid |first15=Yves |date=2005-02-03 |title=Bilateral Deep-Brain Stimulation of the Globus Pallidus in Primary Generalized Dystonia |url=http://www.nejm.org/doi/10.1056/NEJMoa042187 |journal=New England Journal of Medicine |language=en |volume=352 |issue=5 |pages=459–467 |doi=10.1056/NEJMoa042187 |pmid=15689584 |issn=0028-4793}}</ref><ref>{{Cite journal |last1=Kupsch |first1=Andreas |last2=Benecke |first2=Reiner |last3=Müller |first3=Jörg |last4=Trottenberg |first4=Thomas |last5=Schneider |first5=Gerd-Helge |last6=Poewe |first6=Werner |last7=Eisner |first7=Wilhelm |last8=Wolters |first8=Alexander |last9=Müller |first9=Jan-Uwe |last10=Deuschl |first10=Günther |last11=Pinsker |first11=Marcus O. |last12=Skogseid |first12=Inger Marie |last13=Roeste |first13=Geir Ketil |last14=Vollmer-Haase |first14=Juliane |last15=Brentrup |first15=Angela |date=2006-11-09 |title=Pallidal Deep-Brain Stimulation in Primary Generalized or Segmental Dystonia |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa063618 |journal=New England Journal of Medicine |language=en |volume=355 |issue=19 |pages=1978–1990 |doi=10.1056/NEJMoa063618 |issn=0028-4793}}</ref>.
 |[https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfhde/hde.cfm?id=H020007 FDA]
 |-
@@ Line 66: / Line 66: @@
 |Approved under HDE for adjunctive treatment of severe, treatment-resistant OCD.
 |Nucleus Accumbens (NAc)
-|Initial approval came under HDE based on evidence from smaller, open-label trials, such as<ref>{{Cite journal |last=Nuttin |first=Bart J. |last2=Gabriëls |first2=Loes A. |last3=Cosyns |first3=Paul R. |last4=Meyerson |first4=Björn A. |last5=Andréewitch |first5=Sergej |last6=Sunaert |first6=Stefan G. |last7=Maes |first7=Alex F. |last8=Dupont |first8=Patrick J. |last9=Gybels |first9=Jan M. |last10=Gielen |first10=Frans |last11=Demeulemeester |first11=Hilde G. |date=2003-06 |title=Long-term Electrical Capsular Stimulation in Patients with Obsessive-Compulsive Disorder |url=https://journals.lww.com/00006123-200306000-00002 |journal=Neurosurgery |language=en |volume=52 |issue=6 |pages=1263–1274 |doi=10.1227/01.NEU.0000064565.49299.9A |issn=0148-396X}}</ref>, showing reductions in OCD symptoms in severe cases.
+|Initial approval came under HDE based on evidence from smaller, open-label trials, such as<ref>{{Cite journal |last1=Nuttin |first1=Bart J. |last2=Gabriëls |first2=Loes A. |last3=Cosyns |first3=Paul R. |last4=Meyerson |first4=Björn A. |last5=Andréewitch |first5=Sergej |last6=Sunaert |first6=Stefan G. |last7=Maes |first7=Alex F. |last8=Dupont |first8=Patrick J. |last9=Gybels |first9=Jan M. |last10=Gielen |first10=Frans |last11=Demeulemeester |first11=Hilde G. |date=June 2003 |title=Long-term Electrical Capsular Stimulation in Patients with Obsessive-Compulsive Disorder |url=https://journals.lww.com/00006123-200306000-00002 |journal=Neurosurgery |language=en |volume=52 |issue=6 |pages=1263–1274 |doi=10.1227/01.NEU.0000064565.49299.9A |pmid=12762871 |issn=0148-396X}}</ref>, showing reductions in OCD symptoms in severe cases.
 |[https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfhde/hde.cfm?id=375533 FDA]
 |-
@@ Line 73: / Line 73: @@
 |Approved for bilateral stimulation of the anterior nucleus of the thalamus (ANT) as an adjunctive therapy to reduce the frequency of seizures in adults with partial-onset seizures.
 |Anterior nucleus of the thalamus (ANT)
-|The key evidence came from the SANTE trial<ref>{{Cite journal |last=Fisher |first=Robert |last2=Salanova |first2=Vicenta |last3=Witt |first3=Thomas |last4=Worth |first4=Robert |last5=Henry |first5=Thomas |last6=Gross |first6=Robert |last7=Oommen |first7=Kalarickal |last8=Osorio |first8=Ivan |last9=Nazzaro |first9=Jules |last10=Labar |first10=Douglas |last11=Kaplitt |first11=Michael |last12=Sperling |first12=Michael |last13=Sandok |first13=Evan |last14=Neal |first14=John |last15=Handforth |first15=Adrian |date=2010-05 |title=Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy |url=https://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2010.02536.x |journal=Epilepsia |language=en |volume=51 |issue=5 |pages=899–908 |doi=10.1111/j.1528-1167.2010.02536.x |issn=0013-9580}}</ref>, demonstrating a significant reduction in seizure frequency in patients receiving DBS.
+|The key evidence came from the SANTE trial<ref>{{Cite journal |last1=Fisher |first1=Robert |last2=Salanova |first2=Vicenta |last3=Witt |first3=Thomas |last4=Worth |first4=Robert |last5=Henry |first5=Thomas |last6=Gross |first6=Robert |last7=Oommen |first7=Kalarickal |last8=Osorio |first8=Ivan |last9=Nazzaro |first9=Jules |last10=Labar |first10=Douglas |last11=Kaplitt |first11=Michael |last12=Sperling |first12=Michael |last13=Sandok |first13=Evan |last14=Neal |first14=John |last15=Handforth |first15=Adrian |date=May 2010 |title=Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy |url=https://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2010.02536.x |journal=Epilepsia |language=en |volume=51 |issue=5 |pages=899–908 |doi=10.1111/j.1528-1167.2010.02536.x |pmid=20331461 |issn=0013-9580}}</ref>, demonstrating a significant reduction in seizure frequency in patients receiving DBS.
 |[https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfpma/pma.cfm?id=P960009S219 FDA]
 |}
@@ Line 80: / Line 80: @@
 DBS is used to manage some of the symptoms of Parkinson's disease that cannot be adequately controlled with medications.<ref name=NINDS/><ref name="USDHHS">U.S. Department of Health and Human Services. [https://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/DeviceApprovalsandClearances/Recently-ApprovedDevices/ucm083894.htm FDA approves implanted brain stimulator to control tremors.] Retrieved February 10, 2015.</ref> PD is treated by applying high-frequency (> 100 Hz) stimulation to target structures in the depth of the brain. Frequently used targets include the [[subthalamic nucleus]] (STN), internal [[pallidum]] (GPi) and ventrointermediate nucleus of the [[thalamus]] (VIM). The [[pedunculopontine nucleus]] has been used as an investigational target to treat [[freezing of gait]].
-DBS is recommended for people who have PD with motor fluctuations and tremors inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe [[wikt:neuropsychiatric|neuropsychiatric]] problems.<ref name="pmid20937936">{{cite journal | vauthors = Bronstein JM, Tagliati M, Alterman RL, Lozano AM, Volkmann J, Stefani A, Horak FB, Okun MS, Foote KD, Krack P, Pahwa R, Henderson JM, Hariz MI, Bakay RA, Rezai A, Marks WJ, Moro E, Vitek JL, Weaver FM, Gross RE, DeLong MR | display-authors = 6 | title = Deep brain stimulation for Parkinson disease: an expert consensus and review of key issues | journal = Archives of Neurology | volume = 68 | issue = 2 | pages = 165 | date = February 2011 | pmid = 20937936 | pmc = 4523130 | doi = 10.1001/archneurol.2010.260 }}</ref> Four areas of the brain have been treated with neural stimulators in PD. Most DBS surgeries in routine practice target either the GPi or the STN, which, in prospective trials have been equally efficient in reducing motor symptoms<ref name=":7">{{Cite journal |last=Follett |first=Kenneth A. |last2=Weaver |first2=Frances M. |last3=Stern |first3=Matthew |last4=Hur |first4=Kwan |last5=Harris |first5=Crystal L. |last6=Luo |first6=Ping |last7=Marks |first7=William J. |last8=Rothlind |first8=Johannes |last9=Sagher |first9=Oren |last10=Moy |first10=Claudia |last11=Pahwa |first11=Rajesh |last12=Burchiel |first12=Kim |last13=Hogarth |first13=Penelope |last14=Lai |first14=Eugene C. |last15=Duda |first15=John E. |date=2010-06-03 |title=Pallidal versus Subthalamic Deep-Brain Stimulation for Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa0907083 |journal=New England Journal of Medicine |language=en |volume=362 |issue=22 |pages=2077–2091 |doi=10.1056/NEJMoa0907083 |issn=0028-4793}}</ref><ref>{{Cite journal |last=Odekerken |first=Vincent J.J. |last2=Boel |first2=Judith A. |last3=Schmand |first3=Ben A. |last4=de Haan |first4=Rob J. |last5=Figee |first5=M. |last6=van den Munckhof |first6=Pepijn |last7=Schuurman |first7=P. Richard |last8=de Bie |first8=Rob M.A. |last9=For the NSTAPS study group |last10=NSTAPS study group |last11=de Bie |first11=R.M.A. |last12=Bour |first12=L. |last13=Contarino |first13=M.F. |last14=de Haan |first14=R.J. |last15=Iwan |first15=M. |date=2016-02-23 |title=GPi vs STN deep brain stimulation for Parkinson disease: Three-year follow-up |url=https://www.neurology.org/doi/10.1212/WNL.0000000000002401 |journal=Neurology |language=en |volume=86 |issue=8 |pages=755–761 |doi=10.1212/WNL.0000000000002401 |issn=0028-3878}}</ref>, likely due to a shared network being stimulated with either target<ref>{{Cite journal |last=Sobesky |first=Leon |last2=Goede |first2=Lukas |last3=Odekerken |first3=Vincent J J |last4=Wang |first4=Qiang |last5=Li |first5=Ningfei |last6=Neudorfer |first6=Clemens |last7=Rajamani |first7=Nanditha |last8=Al-Fatly |first8=Bassam |last9=Reich |first9=Martin |last10=Volkmann |first10=Jens |last11=de Bie |first11=Rob M A |last12=Kühn |first12=Andrea A |last13=Horn |first13=Andreas |date=2022-03-29 |title=Subthalamic and pallidal deep brain stimulation: are we modulating the same network? |url=https://academic.oup.com/brain/article/145/1/251/6359209 |journal=Brain |language=en |volume=145 |issue=1 |pages=251–262 |doi=10.1093/brain/awab258 |issn=0006-8950}}</ref>. General differences between targets are not easy to summarize, but often include the following:
+DBS is recommended for people who have PD with motor fluctuations and tremors inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe [[wikt:neuropsychiatric|neuropsychiatric]] problems.<ref name="pmid20937936">{{cite journal | vauthors = Bronstein JM, Tagliati M, Alterman RL, Lozano AM, Volkmann J, Stefani A, Horak FB, Okun MS, Foote KD, Krack P, Pahwa R, Henderson JM, Hariz MI, Bakay RA, Rezai A, Marks WJ, Moro E, Vitek JL, Weaver FM, Gross RE, DeLong MR | display-authors = 6 | title = Deep brain stimulation for Parkinson disease: an expert consensus and review of key issues | journal = Archives of Neurology | volume = 68 | issue = 2 | pages = 165 | date = February 2011 | pmid = 20937936 | pmc = 4523130 | doi = 10.1001/archneurol.2010.260 }}</ref> Four areas of the brain have been treated with neural stimulators in PD. Most DBS surgeries in routine practice target either the GPi or the STN, which, in prospective trials have been equally efficient in reducing motor symptoms<ref name=":7">{{Cite journal |last1=Follett |first1=Kenneth A. |last2=Weaver |first2=Frances M. |last3=Stern |first3=Matthew |last4=Hur |first4=Kwan |last5=Harris |first5=Crystal L. |last6=Luo |first6=Ping |last7=Marks |first7=William J. |last8=Rothlind |first8=Johannes |last9=Sagher |first9=Oren |last10=Moy |first10=Claudia |last11=Pahwa |first11=Rajesh |last12=Burchiel |first12=Kim |last13=Hogarth |first13=Penelope |last14=Lai |first14=Eugene C. |last15=Duda |first15=John E. |date=2010-06-03 |title=Pallidal versus Subthalamic Deep-Brain Stimulation for Parkinson's Disease |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa0907083 |journal=New England Journal of Medicine |language=en |volume=362 |issue=22 |pages=2077–2091 |doi=10.1056/NEJMoa0907083 |pmid=20519680 |issn=0028-4793}}</ref><ref>{{Cite journal |last1=Odekerken |first1=Vincent J.J. |last2=Boel |first2=Judith A. |last3=Schmand |first3=Ben A. |last4=de Haan |first4=Rob J. |last5=Figee |first5=M. |last6=van den Munckhof |first6=Pepijn |last7=Schuurman |first7=P. Richard |last8=de Bie |first8=Rob M.A. |last9=For the NSTAPS study group |last10=NSTAPS study group |last11=de Bie |first11=R.M.A. |last12=Bour |first12=L. |last13=Contarino |first13=M.F. |last14=de Haan |first14=R.J. |last15=Iwan |first15=M. |date=2016-02-23 |title=GPi vs STN deep brain stimulation for Parkinson disease: Three-year follow-up |url=https://www.neurology.org/doi/10.1212/WNL.0000000000002401 |journal=Neurology |language=en |volume=86 |issue=8 |pages=755–761 |doi=10.1212/WNL.0000000000002401 |pmid=26819458 |issn=0028-3878}}</ref>, likely due to a shared network being stimulated with either target<ref>{{Cite journal |last1=Sobesky |first1=Leon |last2=Goede |first2=Lukas |last3=Odekerken |first3=Vincent J J |last4=Wang |first4=Qiang |last5=Li |first5=Ningfei |last6=Neudorfer |first6=Clemens |last7=Rajamani |first7=Nanditha |last8=Al-Fatly |first8=Bassam |last9=Reich |first9=Martin |last10=Volkmann |first10=Jens |last11=de Bie |first11=Rob M A |last12=Kühn |first12=Andrea A |last13=Horn |first13=Andreas |date=2022-03-29 |title=Subthalamic and pallidal deep brain stimulation: are we modulating the same network? |url=https://academic.oup.com/brain/article/145/1/251/6359209 |journal=Brain |language=en |volume=145 |issue=1 |pages=251–262 |doi=10.1093/brain/awab258 |issn=0006-8950}}</ref>. General differences between targets are not easy to summarize, but often include the following:
 * DBS of the GPi has been shown to reduce uncontrollable movements called [[dyskinesia]]s. This may sometimes allow a patient to take adequate (additional) quantities of medications (especially [[levodopa]]), thus leading to better control of symptoms.
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 === Essential Tremor ===
-As the most common movement disorder<ref>{{Cite web |title=Essential Tremor: Essential Facts for Patients |url=https://www.movementdisorders.org/MDS/Resources/Patient-Education/Essential-Tremor.htm |access-date=2024-09-22 |website=www.movementdisorders.org}}</ref>, ET was also the first indication to be approved for DBS (alongside Parkinsonian tremor). DBS electrodes are commonly targeted into the ventrointermediate nucleus of the thalamus (VIM) or ventrally adjacent areas that have been referred to as parts of the [[zona incerta]], or posterior thalamic area. Recent metaanalytical evidence suggests that multiple targets along the circuitry of the cerebellothalamic pathway (also referred to as the dentatorubrothalamic or dentatothalamic tract) are similarly effective, i.e. modulating the cerebellar inflows into the thalamus may be key for therapeutic efficacy<ref>{{Cite journal |last=Nowacki |first=Andreas |last2=Barlatey |first2=Sabry |last3=Al‐Fatly |first3=Bassam |last4=Dembek |first4=Till |last5=Bot |first5=Maarten |last6=Green |first6=Alexander L. |last7=Kübler |first7=Dorothee |last8=Lachenmayer |first8=M. Lenard |last9=Debove |first9=Ines |last10=Segura‐Amil |first10=Alba |last11=Horn |first11=Andreas |last12=Visser‐Vandewalle |first12=Veerle |last13=Schuurman |first13=Rick |last14=Barbe |first14=Michael |last15=Aziz |first15=Tipu Z. |date=2022-05 |title=Probabilistic Mapping Reveals Optimal Stimulation Site in Essential Tremor |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26324 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=602–612 |doi=10.1002/ana.26324 |issn=0364-5134}}</ref><ref>{{Cite journal |last=Neudorfer |first=Clemens |last2=Kroneberg |first2=Daniel |last3=Al‐Fatly |first3=Bassam |last4=Goede |first4=Lukas |last5=Kübler |first5=Dorothee |last6=Faust |first6=Katharina |last7=van Rienen |first7=Ursula |last8=Tietze |first8=Anna |last9=Picht |first9=Thomas |last10=Herrington |first10=Todd M. |last11=Middlebrooks |first11=Erik H. |last12=Kühn |first12=Andrea |last13=Schneider |first13=Gerd‐Helge |last14=Horn |first14=Andreas |date=2022-05 |title=Personalizing Deep Brain Stimulation Using Advanced Imaging Sequences |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26326 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=613–628 |doi=10.1002/ana.26326 |issn=0364-5134}}</ref>, for a review see<ref>{{Cite journal |last=Fox |first=Michael D. |last2=Deuschl |first2=Günther |date=2022-05 |title=Converging on a Neuromodulation Target for Tremor |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26361 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=581–584 |doi=10.1002/ana.26361 |issn=0364-5134}}</ref>. Already in the first publication on the matter by the team of Alim Louis Benabid, it could be shown that frequencies above 100 Hz are most effective for cessation of tremor, while lower frequencies have less effect<ref>{{Cite journal |last=Benabid |first=A.L. |last2=Pollak |first2=P. |last3=Hoffmann |first3=D. |last4=Gervason |first4=C. |last5=Hommel |first5=M. |last6=Perret |first6=J.E. |last7=de Rougemont |first7=J. |last8=Gao |first8=D.M. |date=1991-02 |title=Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus |url=https://linkinghub.elsevier.com/retrieve/pii/014067369191175T |journal=The Lancet |language=en |volume=337 |issue=8738 |pages=403–406 |doi=10.1016/0140-6736(91)91175-T}}</ref>. In clinical practice, frequencies between 80 and 180 Hz are typically applied.
+As the most common movement disorder<ref>{{Cite web |title=Essential Tremor: Essential Facts for Patients |url=https://www.movementdisorders.org/MDS/Resources/Patient-Education/Essential-Tremor.htm |access-date=2024-09-22 |website=www.movementdisorders.org}}</ref>, ET was also the first indication to be approved for DBS (alongside Parkinsonian tremor). DBS electrodes are commonly targeted into the ventrointermediate nucleus of the thalamus (VIM) or ventrally adjacent areas that have been referred to as parts of the [[zona incerta]], or posterior thalamic area. Recent metaanalytical evidence suggests that multiple targets along the circuitry of the cerebellothalamic pathway (also referred to as the dentatorubrothalamic or dentatothalamic tract) are similarly effective, i.e. modulating the cerebellar inflows into the thalamus may be key for therapeutic efficacy<ref>{{Cite journal |last1=Nowacki |first1=Andreas |last2=Barlatey |first2=Sabry |last3=Al-Fatly |first3=Bassam |last4=Dembek |first4=Till |last5=Bot |first5=Maarten |last6=Green |first6=Alexander L. |last7=Kübler |first7=Dorothee |last8=Lachenmayer |first8=M. Lenard |last9=Debove |first9=Ines |last10=Segura-Amil |first10=Alba |last11=Horn |first11=Andreas |last12=Visser-Vandewalle |first12=Veerle |last13=Schuurman |first13=Rick |last14=Barbe |first14=Michael |last15=Aziz |first15=Tipu Z. |date=May 2022 |title=Probabilistic Mapping Reveals Optimal Stimulation Site in Essential Tremor |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26324 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=602–612 |doi=10.1002/ana.26324 |pmid=35150172 |issn=0364-5134}}</ref><ref>{{Cite journal |last1=Neudorfer |first1=Clemens |last2=Kroneberg |first2=Daniel |last3=Al-Fatly |first3=Bassam |last4=Goede |first4=Lukas |last5=Kübler |first5=Dorothee |last6=Faust |first6=Katharina |last7=van Rienen |first7=Ursula |last8=Tietze |first8=Anna |last9=Picht |first9=Thomas |last10=Herrington |first10=Todd M. |last11=Middlebrooks |first11=Erik H. |last12=Kühn |first12=Andrea |last13=Schneider |first13=Gerd-Helge |last14=Horn |first14=Andreas |date=May 2022 |title=Personalizing Deep Brain Stimulation Using Advanced Imaging Sequences |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26326 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=613–628 |doi=10.1002/ana.26326 |pmid=35165921 |issn=0364-5134}}</ref>, for a review see<ref>{{Cite journal |last1=Fox |first1=Michael D. |last2=Deuschl |first2=Günther |date=May 2022 |title=Converging on a Neuromodulation Target for Tremor |url=https://onlinelibrary.wiley.com/doi/10.1002/ana.26361 |journal=Annals of Neurology |language=en |volume=91 |issue=5 |pages=581–584 |doi=10.1002/ana.26361 |pmid=35362142 |issn=0364-5134}}</ref>. Already in the first publication on the matter by the team of Alim Louis Benabid, it could be shown that frequencies above 100 Hz are most effective for cessation of tremor, while lower frequencies have less effect<ref>{{Cite journal |last1=Benabid |first1=A.L. |last2=Pollak |first2=P. |last3=Hoffmann |first3=D. |last4=Gervason |first4=C. |last5=Hommel |first5=M. |last6=Perret |first6=J.E. |last7=de Rougemont |first7=J. |last8=Gao |first8=D.M. |date=February 1991 |title=Long-term suppression of tremor by chronic stimulation of the ventral intermediate thalamic nucleus |url=https://linkinghub.elsevier.com/retrieve/pii/014067369191175T |journal=The Lancet |language=en |volume=337 |issue=8738 |pages=403–406 |doi=10.1016/0140-6736(91)91175-T|pmid=1671433 }}</ref>. In clinical practice, frequencies between 80 and 180 Hz are typically applied.
 === Dystonia ===
-In dystonia, marked effects can be reached by targeting the GPi using high frequency DBS, with large randomized trials demonstrating improvements of ~45% within the first six months of treatment<ref>{{Cite journal |last=Kupsch |first=Andreas |last2=Benecke |first2=Reiner |last3=Müller |first3=Jörg |last4=Trottenberg |first4=Thomas |last5=Schneider |first5=Gerd-Helge |last6=Poewe |first6=Werner |last7=Eisner |first7=Wilhelm |last8=Wolters |first8=Alexander |last9=Müller |first9=Jan-Uwe |last10=Deuschl |first10=Günther |last11=Pinsker |first11=Marcus O. |last12=Skogseid |first12=Inger Marie |last13=Roeste |first13=Geir Ketil |last14=Vollmer-Haase |first14=Juliane |last15=Brentrup |first15=Angela |date=2006-11-09 |title=Pallidal Deep-Brain Stimulation in Primary Generalized or Segmental Dystonia |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa063618 |journal=New England Journal of Medicine |language=en |volume=355 |issue=19 |pages=1978–1990 |doi=10.1056/NEJMoa063618 |issn=0028-4793}}</ref>. Similar effects have been reported in open label trials that targeted the STN (but this target is investigational for dystonia)<ref>{{Cite journal |last=Hollunder |first=Barbara |last2=Ostrem |first2=Jill L. |last3=Sahin |first3=Ilkem Aysu |last4=Rajamani |first4=Nanditha |last5=Oxenford |first5=Simón |last6=Butenko |first6=Konstantin |last7=Neudorfer |first7=Clemens |last8=Reinhardt |first8=Pablo |last9=Zvarova |first9=Patricia |last10=Polosan |first10=Mircea |last11=Akram |first11=Harith |last12=Vissani |first12=Matteo |last13=Zhang |first13=Chencheng |last14=Sun |first14=Bomin |last15=Navratil |first15=Pavel |date=2024-03 |title=Mapping dysfunctional circuits in the frontal cortex using deep brain stimulation |url=https://www.nature.com/articles/s41593-024-01570-1 |journal=Nature Neuroscience |language=en |volume=27 |issue=3 |pages=573–586 |doi=10.1038/s41593-024-01570-1 |issn=1097-6256 |pmc=PMC10917675 |pmid=38388734}}</ref>.
+In dystonia, marked effects can be reached by targeting the GPi using high frequency DBS, with large randomized trials demonstrating improvements of ~45% within the first six months of treatment<ref>{{Cite journal |last1=Kupsch |first1=Andreas |last2=Benecke |first2=Reiner |last3=Müller |first3=Jörg |last4=Trottenberg |first4=Thomas |last5=Schneider |first5=Gerd-Helge |last6=Poewe |first6=Werner |last7=Eisner |first7=Wilhelm |last8=Wolters |first8=Alexander |last9=Müller |first9=Jan-Uwe |last10=Deuschl |first10=Günther |last11=Pinsker |first11=Marcus O. |last12=Skogseid |first12=Inger Marie |last13=Roeste |first13=Geir Ketil |last14=Vollmer-Haase |first14=Juliane |last15=Brentrup |first15=Angela |date=2006-11-09 |title=Pallidal Deep-Brain Stimulation in Primary Generalized or Segmental Dystonia |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa063618 |journal=New England Journal of Medicine |language=en |volume=355 |issue=19 |pages=1978–1990 |doi=10.1056/NEJMoa063618 |issn=0028-4793}}</ref>. Similar effects have been reported in open label trials that targeted the STN (but this target is investigational for dystonia)<ref>{{Cite journal |last1=Hollunder |first1=Barbara |last2=Ostrem |first2=Jill L. |last3=Sahin |first3=Ilkem Aysu |last4=Rajamani |first4=Nanditha |last5=Oxenford |first5=Simón |last6=Butenko |first6=Konstantin |last7=Neudorfer |first7=Clemens |last8=Reinhardt |first8=Pablo |last9=Zvarova |first9=Patricia |last10=Polosan |first10=Mircea |last11=Akram |first11=Harith |last12=Vissani |first12=Matteo |last13=Zhang |first13=Chencheng |last14=Sun |first14=Bomin |last15=Navratil |first15=Pavel |date=March 2024 |title=Mapping dysfunctional circuits in the frontal cortex using deep brain stimulation |journal=Nature Neuroscience |language=en |volume=27 |issue=3 |pages=573–586 |doi=10.1038/s41593-024-01570-1 |issn=1097-6256 |pmc=10917675 |pmid=38388734}}</ref>.
 {{Expand section}}
 === Obsessive-Compulsive-Disorder ===
-DBS for OCD was first attempted by the team of [[Bart Nuttin]] in 1999<ref name=":8">{{Cite journal |last=Nuttin |first=Bart |last2=Cosyns |first2=Paul |last3=Demeulemeester |first3=Hilde |last4=Gybels |first4=Jan |last5=Meyerson |first5=Björn |date=1999-10 |title=Electrical stimulation in anterior limbs of internal capsules in patients with obsessive-compulsive disorder |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673699023764 |journal=The Lancet |language=en |volume=354 |issue=9189 |pages=1526 |doi=10.1016/S0140-6736(99)02376-4}}</ref>. Curiously, the year 1999 marked three innovations all published in [[the Lancet]]: The first attempt to treat Tourette's Syndrome by the team of [[Veerle Visser-Vandewalle]]<ref>{{Cite journal |last=Vandewalle |first=V |last2=van der Linden |first2=Chr |last3=Groenewegen |first3=Hj |last4=Caemaert |first4=J |date=1999-02 |title=Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673698059649 |journal=The Lancet |language=en |volume=353 |issue=9154 |pages=724 |doi=10.1016/S0140-6736(98)05964-9}}</ref>, the aforementioned trial by Nuttin and a trial reporting on bilateral stimulation of dystonia by Joachim Krauss and colleagues<ref>{{Cite journal |last=Krauss |first=Joachim K |last2=Pohle |first2=Thomas |last3=Weber |first3=Sabine |last4=Ozdoba |first4=Christoph |last5=Burgunder |first5=Jean-Marc |date=1999-09 |title=Bilateral stimulation of globus pallidus internus for treatment of cervical dystonia |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673699800221 |journal=The Lancet |language=en |volume=354 |issue=9181 |pages=837–838 |doi=10.1016/S0140-6736(99)80022-1}}</ref>. Of these, the study by Visser-Vandewalle is considered the first modern-day indication of DBS in neuropsychiatric indication (Tourette's Syndrome), making the trial by Nuttin for OCD the second. DBS for OCD received a humanitarian device exemption from the FDA in 2009<ref>{{Cite web |title=FDA Humanitarian Device Exemption Approval for OCD |url=https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfhde/hde.cfm?id=375533}}</ref>. In Europe, the CE Mark for Deep Brain Stimulation (DBS) for Obsessive-Compulsive Disorder (OCD) was active from 2009 to 2022 but not renewed thereafter, which was likely not motivated by a lack of evidence but by a lack of monetary interests, which has led to expert letters calling for a 'crisis of access' above and beyond Europe<ref>{{Cite journal |last=Visser-Vandewalle |first=Veerle |last2=Andrade |first2=Pablo |last3=Mosley |first3=Philip E. |last4=Greenberg |first4=Benjamin D. |last5=Schuurman |first5=Rick |last6=McLaughlin |first6=Nicole C. |last7=Voon |first7=Valerie |last8=Krack |first8=Paul |last9=Foote |first9=Kelly D. |last10=Mayberg |first10=Helen S. |last11=Figee |first11=Martijn |last12=Kopell |first12=Brian H. |last13=Polosan |first13=Mircea |last14=Joyce |first14=Eileen M. |last15=Chabardes |first15=Stephan |date=2022-08 |title=Deep brain stimulation for obsessive–compulsive disorder: a crisis of access |url=https://www.nature.com/articles/s41591-022-01879-z |journal=Nature Medicine |language=en |volume=28 |issue=8 |pages=1529–1532 |doi=10.1038/s41591-022-01879-z |issn=1078-8956}}</ref><ref>{{Cite journal |last=Mosley |first=Philip E |last2=Velakoulis |first2=Dennis |last3=Farrand |first3=Sarah |last4=Marsh |first4=Rodney |last5=Mohan |first5=Adith |last6=Castle |first6=David |last7=Sachdev |first7=Perminder S |date=2022-05 |title=Deep brain stimulation for treatment-refractory obsessive-compulsive disorder should be an accepted therapy in Australia |url=http://journals.sagepub.com/doi/10.1177/00048674211031482 |journal=Australian & New Zealand Journal of Psychiatry |language=en |volume=56 |issue=5 |pages=430–436 |doi=10.1177/00048674211031482 |issn=0004-8674}}</ref>.
+DBS for OCD was first attempted by the team of [[Bart Nuttin]] in 1999<ref name=":8">{{Cite journal |last1=Nuttin |first1=Bart |last2=Cosyns |first2=Paul |last3=Demeulemeester |first3=Hilde |last4=Gybels |first4=Jan |last5=Meyerson |first5=Björn |date=October 1999 |title=Electrical stimulation in anterior limbs of internal capsules in patients with obsessive-compulsive disorder |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673699023764 |journal=The Lancet |language=en |volume=354 |issue=9189 |pages=1526 |doi=10.1016/S0140-6736(99)02376-4}}</ref>. Curiously, the year 1999 marked three innovations all published in [[the Lancet]]: The first attempt to treat Tourette's Syndrome by the team of [[Veerle Visser-Vandewalle]]<ref>{{Cite journal |last1=Vandewalle |first1=V |last2=van der Linden |first2=Chr |last3=Groenewegen |first3=Hj |last4=Caemaert |first4=J |date=February 1999 |title=Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673698059649 |journal=The Lancet |language=en |volume=353 |issue=9154 |pages=724 |doi=10.1016/S0140-6736(98)05964-9|pmid=10073521 }}</ref>, the aforementioned trial by Nuttin and a trial reporting on bilateral stimulation of dystonia by Joachim Krauss and colleagues<ref>{{Cite journal |last1=Krauss |first1=Joachim K |last2=Pohle |first2=Thomas |last3=Weber |first3=Sabine |last4=Ozdoba |first4=Christoph |last5=Burgunder |first5=Jean-Marc |date=September 1999 |title=Bilateral stimulation of globus pallidus internus for treatment of cervical dystonia |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673699800221 |journal=The Lancet |language=en |volume=354 |issue=9181 |pages=837–838 |doi=10.1016/S0140-6736(99)80022-1|pmid=10485734 }}</ref>. Of these, the study by Visser-Vandewalle is considered the first modern-day indication of DBS in neuropsychiatric indication (Tourette's Syndrome), making the trial by Nuttin for OCD the second. DBS for OCD received a humanitarian device exemption from the FDA in 2009<ref>{{Cite web |title=FDA Humanitarian Device Exemption Approval for OCD |url=https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfhde/hde.cfm?id=375533}}</ref>. In Europe, the CE Mark for Deep Brain Stimulation (DBS) for Obsessive-Compulsive Disorder (OCD) was active from 2009 to 2022 but not renewed thereafter, which was likely not motivated by a lack of evidence but by a lack of monetary interests, which has led to expert letters calling for a 'crisis of access' above and beyond Europe<ref>{{Cite journal |last1=Visser-Vandewalle |first1=Veerle |last2=Andrade |first2=Pablo |last3=Mosley |first3=Philip E. |last4=Greenberg |first4=Benjamin D. |last5=Schuurman |first5=Rick |last6=McLaughlin |first6=Nicole C. |last7=Voon |first7=Valerie |last8=Krack |first8=Paul |last9=Foote |first9=Kelly D. |last10=Mayberg |first10=Helen S. |last11=Figee |first11=Martijn |last12=Kopell |first12=Brian H. |last13=Polosan |first13=Mircea |last14=Joyce |first14=Eileen M. |last15=Chabardes |first15=Stephan |date=August 2022 |title=Deep brain stimulation for obsessive–compulsive disorder: a crisis of access |url=https://www.nature.com/articles/s41591-022-01879-z |journal=Nature Medicine |language=en |volume=28 |issue=8 |pages=1529–1532 |doi=10.1038/s41591-022-01879-z |pmid=35840727 |issn=1078-8956}}</ref><ref>{{Cite journal |last1=Mosley |first1=Philip E |last2=Velakoulis |first2=Dennis |last3=Farrand |first3=Sarah |last4=Marsh |first4=Rodney |last5=Mohan |first5=Adith |last6=Castle |first6=David |last7=Sachdev |first7=Perminder S |date=May 2022 |title=Deep brain stimulation for treatment-refractory obsessive-compulsive disorder should be an accepted therapy in Australia |url=http://journals.sagepub.com/doi/10.1177/00048674211031482 |journal=Australian & New Zealand Journal of Psychiatry |language=en |volume=56 |issue=5 |pages=430–436 |doi=10.1177/00048674211031482 |pmid=34263654 |issn=0004-8674}}</ref>.
-Beyond the original target in the [[anterior limb of the internal capsule]] (ALIC)<ref name=":8" />, multiple target sites have been probed, such as the [[nucleus accumbens]]<ref>{{Cite journal |last=Denys |first=Damiaan |last2=Mantione |first2=Mariska |last3=Figee |first3=Martijn |last4=van den Munckhof |first4=Pepijn |last5=Koerselman |first5=Frank |last6=Westenberg |first6=Herman |last7=Bosch |first7=Andries |last8=Schuurman |first8=Rick |date=2010-10-04 |title=Deep Brain Stimulation of the Nucleus Accumbens for Treatment-Refractory Obsessive-Compulsive Disorder |url=http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/archgenpsychiatry.2010.122 |journal=Archives of General Psychiatry |language=en |volume=67 |issue=10 |pages=1061 |doi=10.1001/archgenpsychiatry.2010.122 |issn=0003-990X}}</ref> (sometimes subsumized with the ALIC as the ventral capsule/ventral striatum or VC/VS target<ref>{{Cite journal |last=Greenberg |first=B D |last2=Gabriels |first2=L A |last3=Malone |first3=D A |last4=Rezai |first4=A R |last5=Friehs |first5=G M |last6=Okun |first6=M S |last7=Shapira |first7=N A |last8=Foote |first8=K D |last9=Cosyns |first9=P R |last10=Kubu |first10=C S |last11=Malloy |first11=P F |last12=Salloway |first12=S P |last13=Giftakis |first13=J E |last14=Rise |first14=M T |last15=Machado |first15=A G |date=2010-01 |title=Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: worldwide experience |url=https://www.nature.com/articles/mp200855 |journal=Molecular Psychiatry |language=en |volume=15 |issue=1 |pages=64–79 |doi=10.1038/mp.2008.55 |issn=1359-4184 |pmc=PMC3790898 |pmid=18490925}}</ref>), the [[bed nucleus of stria terminalis]]<ref>{{Cite journal |last=Luyten |first=L |last2=Hendrickx |first2=S |last3=Raymaekers |first3=S |last4=Gabriëls |first4=L |last5=Nuttin |first5=B |date=2016-09 |title=Electrical stimulation in the bed nucleus of the stria terminalis alleviates severe obsessive-compulsive disorder |url=https://www.nature.com/articles/mp2015124 |journal=Molecular Psychiatry |language=en |volume=21 |issue=9 |pages=1272–1280 |doi=10.1038/mp.2015.124 |issn=1359-4184}}</ref>, the [[inferior thalamic peduncle]]<ref>{{Cite journal |last=Jiménez-Ponce |first=Fiacro |last2=Velasco-Campos |first2=Francisco |last3=Castro-Farfán |first3=Guillermo |last4=Nicolini |first4=Humberto |last5=Velasco |first5=Ana Luisa |last6=Salín-Pascual |first6=Rafael |last7=Trejo |first7=David |last8=Criales |first8=José Luis |date=2009-12 |title=PRELIMINARY STUDY IN PATIENTS WITH OBSESSIVE-COMPULSIVE DISORDER TREATED WITH ELECTRICAL STIMULATION IN THE INFERIOR THALAMIC PEDUNCLE |url=https://journals.lww.com/01787389-200912001-00026 |journal=Operative Neurosurgery |language=en |volume=65 |issue=6 |pages=ons203–ons209 |doi=10.1227/01.NEU.0000345938.39199.90 |issn=2332-4252}}</ref> and the anteromedial portion of the [[Subthalamic nucleus|STN]]<ref>{{Cite journal |last=Mallet |first=Luc |last2=Polosan |first2=Mircea |last3=Jaafari |first3=Nematollah |last4=Baup |first4=Nicolas |last5=Welter |first5=Marie-Laure |last6=Fontaine |first6=Denys |last7=Montcel |first7=Sophie Tezenas du |last8=Yelnik |first8=Jérôme |last9=Chéreau |first9=Isabelle |last10=Arbus |first10=Christophe |last11=Raoul |first11=Sylvie |last12=Aouizerate |first12=Bruno |last13=Damier |first13=Philippe |last14=Chabardès |first14=Stephan |last15=Czernecki |first15=Virginie |date=2008-11-13 |title=Subthalamic Nucleus Stimulation in Severe Obsessive–Compulsive Disorder |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa0708514 |journal=New England Journal of Medicine |language=en |volume=359 |issue=20 |pages=2121–2134 |doi=10.1056/NEJMoa0708514 |issn=0028-4793}}</ref>. Within the ALIC region, large probabilistic mapping trials have identified two distinct sites of maximum efficacy<ref>{{Cite journal |last=Meyer |first=Garance M. |last2=Hollunder |first2=Barbara |last3=Li |first3=Ningfei |last4=Butenko |first4=Konstantin |last5=Dembek |first5=Till A. |last6=Hart |first6=Lauren |last7=Nombela |first7=Cristina |last8=Mosley |first8=Philip |last9=Akram |first9=Harith |last10=Acevedo |first10=Nicola |last11=Borron |first11=Benjamin M. |last12=Chou |first12=Tina |last13=Castaño Montoya |first13=Juan Pablo |last14=Strange |first14=Bryan |last15=Barcia |first15=Juan A. |date=2024-07 |title=Deep Brain Stimulation for Obsessive-Compulsive Disorder: Optimal Stimulation Sites |url=https://linkinghub.elsevier.com/retrieve/pii/S0006322323017857 |journal=Biological Psychiatry |language=en |volume=96 |issue=2 |pages=101–113 |doi=10.1016/j.biopsych.2023.12.010 |pmc=PMC11190041 |pmid=38141909}}</ref>, one likely corresponding to [[Basal ganglia|'hyperdirect' pathway]] inputs<ref>{{Cite journal |last=Li |first=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |url=https://www.nature.com/articles/s41467-020-16734-3 |journal=Nature Communications |language=en |volume=11 |issue=1 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=PMC7335093 |pmid=32620886}}</ref> to the subthalamic nucleus and other midbrain regions, the other potentially corresponding to [[Indirect pathway|'indirect' pathway]] projections within the same [[Basal ganglia|basal ganglia thalamocortical loop]]. A potential circuit structure that seems to combine most effective targets in both the ALIC and STN region has been identified and termed the [[OCD response tract]]<ref>{{Cite journal |last=Li |first=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |url=https://www.nature.com/articles/s41467-020-16734-3 |journal=Nature Communications |language=en |volume=11 |issue=1 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=PMC7335093 |pmid=32620886}}</ref> by the group of [[Andreas Horn]]. Modulating this fiber tract system, which has been described as projections from [[Anterior cingulate cortex|dorsal anterior cingulate]] and [[Ventrolateral prefrontal cortex|ventrolateral prefrontal]] cortices to the [[subthalamic nucleus]] (and potentially other [[midbrain]] structures), as well as reciprocal [[Thalamus|thalamic]] projections to the same sites, has been robustly associated with optimal treatment response across multiple studies from various groups<ref>{{Cite journal |last=Li |first=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |url=https://www.nature.com/articles/s41467-020-16734-3 |journal=Nature Communications |language=en |volume=11 |issue=1 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=PMC7335093 |pmid=32620886}}</ref><ref>{{Cite journal |last=van der Vlis |first=Tim A.M. Bouwens |last2=Ackermans |first2=Linda |last3=Mulders |first3=Anne E.P. |last4=Vrij |first4=Casper A. |last5=Schruers |first5=Koen |last6=Temel |first6=Yasin |last7=Duits |first7=Annelien |last8=Leentjens |first8=Albert F.G. |date=2021-02 |title=Ventral Capsule/Ventral Striatum Stimulation in Obsessive-Compulsive Disorder: Toward a Unified Connectomic Target for Deep Brain Stimulation? |url=https://linkinghub.elsevier.com/retrieve/pii/S1094715921000891 |journal=Neuromodulation: Technology at the Neural Interface |language=en |volume=24 |issue=2 |pages=316–323 |doi=10.1111/ner.13339 |pmc=PMC7986682 |pmid=33368876}}</ref><ref>{{Cite journal |last=Johnson |first=Kara A. |last2=Duffley |first2=Gordon |last3=Foltynie |first3=Thomas |last4=Hariz |first4=Marwan |last5=Zrinzo |first5=Ludvic |last6=Joyce |first6=Eileen M. |last7=Akram |first7=Harith |last8=Servello |first8=Domenico |last9=Galbiati |first9=Tommaso F. |last10=Bona |first10=Alberto |last11=Porta |first11=Mauro |last12=Meng |first12=Fan-Gang |last13=Leentjens |first13=Albert F.G. |last14=Gunduz |first14=Aysegul |last15=Hu |first15=Wei |date=2021-10 |title=Basal Ganglia Pathways Associated With Therapeutic Pallidal Deep Brain Stimulation for Tourette Syndrome |url=https://linkinghub.elsevier.com/retrieve/pii/S2451902220303475 |journal=Biological Psychiatry: Cognitive Neuroscience and Neuroimaging |language=en |volume=6 |issue=10 |pages=961–972 |doi=10.1016/j.bpsc.2020.11.005 |pmc=PMC8864935 |pmid=33536144}}</ref><ref>{{Cite journal |last=Mosley |first=Philip E. |last2=Windels |first2=François |last3=Morris |first3=John |last4=Coyne |first4=Terry |last5=Marsh |first5=Rodney |last6=Giorni |first6=Andrea |last7=Mohan |first7=Adith |last8=Sachdev |first8=Perminder |last9=O’Leary |first9=Emily |last10=Boschen |first10=Mark |last11=Sah |first11=Pankaj |last12=Silburn |first12=Peter A. |date=2021-03-29 |title=A randomised, double-blind, sham-controlled trial of deep brain stimulation of the bed nucleus of the stria terminalis for treatment-resistant obsessive-compulsive disorder |url=https://www.nature.com/articles/s41398-021-01307-9 |journal=Translational Psychiatry |language=en |volume=11 |issue=1 |doi=10.1038/s41398-021-01307-9 |issn=2158-3188 |pmc=PMC8007749 |pmid=33782383}}</ref><ref>{{Cite journal |last=Baldermann |first=Juan Carlos |last2=Schüller |first2=Thomas |last3=Kohl |first3=Sina |last4=Voon |first4=Valerie |last5=Li |first5=Ningfei |last6=Hollunder |first6=Barbara |last7=Figee |first7=Martijn |last8=Haber |first8=Suzanne N. |last9=Sheth |first9=Sameer A. |last10=Mosley |first10=Philip E. |last11=Huys |first11=Daniel |last12=Johnson |first12=Kara A. |last13=Butson |first13=Christopher |last14=Ackermans |first14=Linda |last15=Bouwens van der Vlis |first15=Tim |date=2021-11 |title=Connectomic Deep Brain Stimulation for Obsessive-Compulsive Disorder |url=https://linkinghub.elsevier.com/retrieve/pii/S000632232101461X |journal=Biological Psychiatry |language=en |volume=90 |issue=10 |pages=678–688 |doi=10.1016/j.biopsych.2021.07.010}}</ref><ref>{{Cite journal |last=Gadot |first=Ron |last2=Li |first2=Ningfei |last3=Shofty |first3=Ben |last4=Avendano-Ortega |first4=Michelle |last5=McKay |first5=Sarah |last6=Bijanki |first6=Kelly R. |last7=Robinson |first7=Meghan E. |last8=Banks |first8=Garrett |last9=Provenza |first9=Nicole |last10=Storch |first10=Eric A. |last11=Goodman |first11=Wayne K. |last12=Horn |first12=Andreas |last13=Sheth |first13=Sameer A. |date=2024-07 |title=Tractography-Based Modeling Explains Treatment Outcomes in Patients Undergoing Deep Brain Stimulation for Obsessive-Compulsive Disorder |url=https://linkinghub.elsevier.com/retrieve/pii/S0006322323000458 |journal=Biological Psychiatry |language=en |volume=96 |issue=2 |pages=95–100 |doi=10.1016/j.biopsych.2023.01.017 |pmc=PMC10387502 |pmid=36948900}}</ref>.
+Beyond the original target in the [[anterior limb of the internal capsule]] (ALIC)<ref name=":8" />, multiple target sites have been probed, such as the [[nucleus accumbens]]<ref>{{Cite journal |last1=Denys |first1=Damiaan |last2=Mantione |first2=Mariska |last3=Figee |first3=Martijn |last4=van den Munckhof |first4=Pepijn |last5=Koerselman |first5=Frank |last6=Westenberg |first6=Herman |last7=Bosch |first7=Andries |last8=Schuurman |first8=Rick |date=2010-10-04 |title=Deep Brain Stimulation of the Nucleus Accumbens for Treatment-Refractory Obsessive-Compulsive Disorder |url=http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/archgenpsychiatry.2010.122 |journal=Archives of General Psychiatry |language=en |volume=67 |issue=10 |pages=1061 |doi=10.1001/archgenpsychiatry.2010.122 |pmid=20921122 |issn=0003-990X}}</ref> (sometimes subsumized with the ALIC as the ventral capsule/ventral striatum or VC/VS target<ref>{{Cite journal |last1=Greenberg |first1=B D |last2=Gabriels |first2=L A |last3=Malone |first3=D A |last4=Rezai |first4=A R |last5=Friehs |first5=G M |last6=Okun |first6=M S |last7=Shapira |first7=N A |last8=Foote |first8=K D |last9=Cosyns |first9=P R |last10=Kubu |first10=C S |last11=Malloy |first11=P F |last12=Salloway |first12=S P |last13=Giftakis |first13=J E |last14=Rise |first14=M T |last15=Machado |first15=A G |date=January 2010 |title=Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: worldwide experience |journal=Molecular Psychiatry |language=en |volume=15 |issue=1 |pages=64–79 |doi=10.1038/mp.2008.55 |issn=1359-4184 |pmc=3790898 |pmid=18490925}}</ref>), the [[bed nucleus of stria terminalis]]<ref>{{Cite journal |last1=Luyten |first1=L |last2=Hendrickx |first2=S |last3=Raymaekers |first3=S |last4=Gabriëls |first4=L |last5=Nuttin |first5=B |date=September 2016 |title=Electrical stimulation in the bed nucleus of the stria terminalis alleviates severe obsessive-compulsive disorder |url=https://www.nature.com/articles/mp2015124 |journal=Molecular Psychiatry |language=en |volume=21 |issue=9 |pages=1272–1280 |doi=10.1038/mp.2015.124 |pmid=26303665 |issn=1359-4184}}</ref>, the [[inferior thalamic peduncle]]<ref>{{Cite journal |last1=Jiménez-Ponce |first1=Fiacro |last2=Velasco-Campos |first2=Francisco |last3=Castro-Farfán |first3=Guillermo |last4=Nicolini |first4=Humberto |last5=Velasco |first5=Ana Luisa |last6=Salín-Pascual |first6=Rafael |last7=Trejo |first7=David |last8=Criales |first8=José Luis |date=December 2009 |title=Preliminary Study in Patients with Obsessive-Compulsive Disorder Treated with Electrical Stimulation in the Inferior Thalamic Peduncle |url=https://journals.lww.com/01787389-200912001-00026 |journal=Operative Neurosurgery |language=en |volume=65 |issue=6 |pages=ons203–ons209 |doi=10.1227/01.NEU.0000345938.39199.90 |pmid=19934996 |issn=2332-4252}}</ref> and the anteromedial portion of the [[Subthalamic nucleus|STN]]<ref>{{Cite journal |last1=Mallet |first1=Luc |last2=Polosan |first2=Mircea |last3=Jaafari |first3=Nematollah |last4=Baup |first4=Nicolas |last5=Welter |first5=Marie-Laure |last6=Fontaine |first6=Denys |last7=Montcel |first7=Sophie Tezenas du |last8=Yelnik |first8=Jérôme |last9=Chéreau |first9=Isabelle |last10=Arbus |first10=Christophe |last11=Raoul |first11=Sylvie |last12=Aouizerate |first12=Bruno |last13=Damier |first13=Philippe |last14=Chabardès |first14=Stephan |last15=Czernecki |first15=Virginie |date=2008-11-13 |title=Subthalamic Nucleus Stimulation in Severe Obsessive–Compulsive Disorder |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa0708514 |journal=New England Journal of Medicine |language=en |volume=359 |issue=20 |pages=2121–2134 |doi=10.1056/NEJMoa0708514 |issn=0028-4793}}</ref>. Within the ALIC region, large probabilistic mapping trials have identified two distinct sites of maximum efficacy<ref>{{Cite journal |last1=Meyer |first1=Garance M. |last2=Hollunder |first2=Barbara |last3=Li |first3=Ningfei |last4=Butenko |first4=Konstantin |last5=Dembek |first5=Till A. |last6=Hart |first6=Lauren |last7=Nombela |first7=Cristina |last8=Mosley |first8=Philip |last9=Akram |first9=Harith |last10=Acevedo |first10=Nicola |last11=Borron |first11=Benjamin M. |last12=Chou |first12=Tina |last13=Castaño Montoya |first13=Juan Pablo |last14=Strange |first14=Bryan |last15=Barcia |first15=Juan A. |date=July 2024 |title=Deep Brain Stimulation for Obsessive-Compulsive Disorder: Optimal Stimulation Sites |url=https://linkinghub.elsevier.com/retrieve/pii/S0006322323017857 |journal=Biological Psychiatry |language=en |volume=96 |issue=2 |pages=101–113 |doi=10.1016/j.biopsych.2023.12.010 |pmc=11190041 |pmid=38141909|pmc-embargo-date=July 15, 2025 }}</ref>, one likely corresponding to [[Basal ganglia|'hyperdirect' pathway]] inputs<ref>{{Cite journal |last1=Li |first1=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |journal=Nature Communications |language=en |volume=11 |issue=1 |page=3364 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=7335093 |pmid=32620886|bibcode=2020NatCo..11.3364L }}</ref> to the subthalamic nucleus and other midbrain regions, the other potentially corresponding to [[Indirect pathway|'indirect' pathway]] projections within the same [[Basal ganglia|basal ganglia thalamocortical loop]]. A potential circuit structure that seems to combine most effective targets in both the ALIC and STN region has been identified and termed the [[OCD response tract]]<ref>{{Cite journal |last1=Li |first1=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |journal=Nature Communications |language=en |volume=11 |issue=1 |page=3364 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=7335093 |pmid=32620886|bibcode=2020NatCo..11.3364L }}</ref> by the group of [[Andreas Horn]]. Modulating this fiber tract system, which has been described as projections from [[Anterior cingulate cortex|dorsal anterior cingulate]] and [[Ventrolateral prefrontal cortex|ventrolateral prefrontal]] cortices to the [[subthalamic nucleus]] (and potentially other [[midbrain]] structures), as well as reciprocal [[Thalamus|thalamic]] projections to the same sites, has been robustly associated with optimal treatment response across multiple studies from various groups<ref>{{Cite journal |last1=Li |first1=Ningfei |last2=Baldermann |first2=Juan Carlos |last3=Kibleur |first3=Astrid |last4=Treu |first4=Svenja |last5=Akram |first5=Harith |last6=Elias |first6=Gavin J. B. |last7=Boutet |first7=Alexandre |last8=Lozano |first8=Andres M. |last9=Al-Fatly |first9=Bassam |last10=Strange |first10=Bryan |last11=Barcia |first11=Juan A. |last12=Zrinzo |first12=Ludvic |last13=Joyce |first13=Eileen |last14=Chabardes |first14=Stephan |last15=Visser-Vandewalle |first15=Veerle |date=2020-07-03 |title=A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder |journal=Nature Communications |language=en |volume=11 |issue=1 |page=3364 |doi=10.1038/s41467-020-16734-3 |issn=2041-1723 |pmc=7335093 |pmid=32620886|bibcode=2020NatCo..11.3364L }}</ref><ref>{{Cite journal |last1=van der Vlis |first1=Tim A.M. Bouwens |last2=Ackermans |first2=Linda |last3=Mulders |first3=Anne E.P. |last4=Vrij |first4=Casper A. |last5=Schruers |first5=Koen |last6=Temel |first6=Yasin |last7=Duits |first7=Annelien |last8=Leentjens |first8=Albert F.G. |date=February 2021 |title=Ventral Capsule/Ventral Striatum Stimulation in Obsessive-Compulsive Disorder: Toward a Unified Connectomic Target for Deep Brain Stimulation? |journal=Neuromodulation: Technology at the Neural Interface |language=en |volume=24 |issue=2 |pages=316–323 |doi=10.1111/ner.13339 |pmc=7986682 |pmid=33368876}}</ref><ref>{{Cite journal |last1=Johnson |first1=Kara A. |last2=Duffley |first2=Gordon |last3=Foltynie |first3=Thomas |last4=Hariz |first4=Marwan |last5=Zrinzo |first5=Ludvic |last6=Joyce |first6=Eileen M. |last7=Akram |first7=Harith |last8=Servello |first8=Domenico |last9=Galbiati |first9=Tommaso F. |last10=Bona |first10=Alberto |last11=Porta |first11=Mauro |last12=Meng |first12=Fan-Gang |last13=Leentjens |first13=Albert F.G. |last14=Gunduz |first14=Aysegul |last15=Hu |first15=Wei |date=October 2021 |title=Basal Ganglia Pathways Associated With Therapeutic Pallidal Deep Brain Stimulation for Tourette Syndrome |journal=Biological Psychiatry: Cognitive Neuroscience and Neuroimaging |language=en |volume=6 |issue=10 |pages=961–972 |doi=10.1016/j.bpsc.2020.11.005 |pmc=8864935 |pmid=33536144}}</ref><ref>{{Cite journal |last1=Mosley |first1=Philip E. |last2=Windels |first2=François |last3=Morris |first3=John |last4=Coyne |first4=Terry |last5=Marsh |first5=Rodney |last6=Giorni |first6=Andrea |last7=Mohan |first7=Adith |last8=Sachdev |first8=Perminder |last9=O’Leary |first9=Emily |last10=Boschen |first10=Mark |last11=Sah |first11=Pankaj |last12=Silburn |first12=Peter A. |date=2021-03-29 |title=A randomised, double-blind, sham-controlled trial of deep brain stimulation of the bed nucleus of the stria terminalis for treatment-resistant obsessive-compulsive disorder |journal=Translational Psychiatry |language=en |volume=11 |issue=1 |page=190 |doi=10.1038/s41398-021-01307-9 |issn=2158-3188 |pmc=8007749 |pmid=33782383}}</ref><ref>{{Cite journal |last1=Baldermann |first1=Juan Carlos |last2=Schüller |first2=Thomas |last3=Kohl |first3=Sina |last4=Voon |first4=Valerie |last5=Li |first5=Ningfei |last6=Hollunder |first6=Barbara |last7=Figee |first7=Martijn |last8=Haber |first8=Suzanne N. |last9=Sheth |first9=Sameer A. |last10=Mosley |first10=Philip E. |last11=Huys |first11=Daniel |last12=Johnson |first12=Kara A. |last13=Butson |first13=Christopher |last14=Ackermans |first14=Linda |last15=Bouwens van der Vlis |first15=Tim |date=November 2021 |title=Connectomic Deep Brain Stimulation for Obsessive-Compulsive Disorder |url=https://linkinghub.elsevier.com/retrieve/pii/S000632232101461X |journal=Biological Psychiatry |language=en |volume=90 |issue=10 |pages=678–688 |doi=10.1016/j.biopsych.2021.07.010|pmid=34482949 }}</ref><ref>{{Cite journal |last1=Gadot |first1=Ron |last2=Li |first2=Ningfei |last3=Shofty |first3=Ben |last4=Avendano-Ortega |first4=Michelle |last5=McKay |first5=Sarah |last6=Bijanki |first6=Kelly R. |last7=Robinson |first7=Meghan E. |last8=Banks |first8=Garrett |last9=Provenza |first9=Nicole |last10=Storch |first10=Eric A. |last11=Goodman |first11=Wayne K. |last12=Horn |first12=Andreas |last13=Sheth |first13=Sameer A. |date=July 2024 |title=Tractography-Based Modeling Explains Treatment Outcomes in Patients Undergoing Deep Brain Stimulation for Obsessive-Compulsive Disorder |journal=Biological Psychiatry |language=en |volume=96 |issue=2 |pages=95–100 |doi=10.1016/j.biopsych.2023.01.017 |pmc=10387502 |pmid=36948900}}</ref>.
 === Epilepsy ===
@@ Line 109: / Line 109: @@
 {{further|Management of Tourette syndrome}}
-As mentioned above, the first DBS application for Tourette's Syndrome has been carried out by the team of [[Veerle Visser-Vandewalle]] in 1999<ref>{{Cite journal |last=Vandewalle |first=V |last2=van der Linden |first2=Chr |last3=Groenewegen |first3=Hj |last4=Caemaert |first4=J |date=1999-02 |title=Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673698059649 |journal=The Lancet |language=en |volume=353 |issue=9154 |pages=724 |doi=10.1016/S0140-6736(98)05964-9}}</ref>. Building upon the ablative lesion cases carried out by [[Rolf Hassler]] and colleagues<ref>{{Cite journal |last=Hassler |first=Rolf |title=raitement stéréotaxique des tics et cris inarticulés ou coprolaliques considérés comme phénomene d’obsession motrice au cours de la maladie de Gilles de la Tourette |journal=Rev Neurol |publication-date=1970}}</ref>, Visser-Vandewalle chose the intersection between the centromedian, parafascicular and ventrooralis internus nuclei of the thalamus as her DBS target. Authors reported that, after surgery, tics disappeared and "a change in the patient’s character occurred in that he had become much more kind-hearted." DBS has been used experimentally in treating adults with severe [[Tourette syndrome]] who do not respond to conventional treatment. Despite widely publicized early successes, DBS remains a highly [[Biomedical research|experimental]] procedure for treating Tourette's, and more study is needed to determine whether long-term benefits outweigh the risks.<ref name=Singer2011>{{cite book |doi=10.1016/B978-0-444-52014-2.00046-X |chapter=Tourette syndrome and other tic disorders |title=Hyperkinetic Movement Disorders |series=Handbook of Clinical Neurology |year=2011 | vauthors = Singer HS |volume=100 |pages=641–657 |pmid=21496613 |isbn=978-0-444-52014-2 }} Also see {{cite journal | vauthors = Singer HS | title = Tourette's syndrome: from behaviour to biology | journal = The Lancet. Neurology | volume = 4 | issue = 3 | pages = 149–159 | date = March 2005 | pmid = 15721825 | doi = 10.1016/S1474-4422(05)01012-4 | s2cid = 20181150 }}</ref><ref name=Robertson2011>{{cite journal | vauthors = Robertson MM | title = Gilles de la Tourette syndrome: the complexities of phenotype and treatment | journal = British Journal of Hospital Medicine | volume = 72 | issue = 2 | pages = 100–107 | date = February 2011 | pmid = 21378617 | doi = 10.12968/hmed.2011.72.2.100 }}</ref><ref name=Du2010>{{cite journal | vauthors = Du JC, Chiu TF, Lee KM, Wu HL, Yang YC, Hsu SY, Sun CS, Hwang B, Leckman JF | display-authors = 6 | title = Tourette syndrome in children: an updated review | journal = Pediatrics and Neonatology | volume = 51 | issue = 5 | pages = 255–264 | date = October 2010 | pmid = 20951354 | doi = 10.1016/S1875-9572(10)60050-2 | doi-access = free }}</ref><ref>[[Tourette Association of America|Tourette Syndrome Association]]. [https://web.archive.org/web/20051122154536/http://tsa-usa.org/news/DBS-Statement.htm Statement: Deep Brain Stimulation and Tourette Syndrome.] Retrieved November 22, 2005.</ref> The procedure is well tolerated, but complications include "short battery life, abrupt symptom worsening upon cessation of stimulation, hypomanic or manic conversion, and the significant time and effort involved in optimizing stimulation parameters".<ref name=Malone>{{cite book |chapter=Behavioral neurosurgery |pages=241–247 |chapter-url={{Google books|hhE74A1fTQkC|page=241|plainurl=yes}} |pmid=16536372 | vauthors = Walkup JT, Mink JW, Hollenbeck PJ |title=Tourette Syndrome |series=Advances in Neurology |date=2006 |volume=99 |publisher=Lippincott Williams & Wilkins |isbn=978-0-7817-9970-6 }}</ref>
+As mentioned above, the first DBS application for Tourette's Syndrome has been carried out by the team of [[Veerle Visser-Vandewalle]] in 1999<ref>{{Cite journal |last1=Vandewalle |first1=V |last2=van der Linden |first2=Chr |last3=Groenewegen |first3=Hj |last4=Caemaert |first4=J |date=February 1999 |title=Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus |url=https://linkinghub.elsevier.com/retrieve/pii/S0140673698059649 |journal=The Lancet |language=en |volume=353 |issue=9154 |pages=724 |doi=10.1016/S0140-6736(98)05964-9|pmid=10073521 }}</ref>. Building upon the ablative lesion cases carried out by [[Rolf Hassler]] and colleagues<ref>{{Cite journal |last=Hassler |first=Rolf |title=raitement stéréotaxique des tics et cris inarticulés ou coprolaliques considérés comme phénomene d'obsession motrice au cours de la maladie de Gilles de la Tourette |journal=Rev Neurol |publication-date=1970}}</ref>, Visser-Vandewalle chose the intersection between the centromedian, parafascicular and ventrooralis internus nuclei of the thalamus as her DBS target. Authors reported that, after surgery, tics disappeared and "a change in the patient’s character occurred in that he had become much more kind-hearted." DBS has been used experimentally in treating adults with severe [[Tourette syndrome]] who do not respond to conventional treatment. Despite widely publicized early successes, DBS remains a highly [[Biomedical research|experimental]] procedure for treating Tourette's, and more study is needed to determine whether long-term benefits outweigh the risks.<ref name=Singer2011>{{cite book |doi=10.1016/B978-0-444-52014-2.00046-X |chapter=Tourette syndrome and other tic disorders |title=Hyperkinetic Movement Disorders |series=Handbook of Clinical Neurology |year=2011 | vauthors = Singer HS |volume=100 |pages=641–657 |pmid=21496613 |isbn=978-0-444-52014-2 }} Also see {{cite journal | vauthors = Singer HS | title = Tourette's syndrome: from behaviour to biology | journal = The Lancet. Neurology | volume = 4 | issue = 3 | pages = 149–159 | date = March 2005 | pmid = 15721825 | doi = 10.1016/S1474-4422(05)01012-4 | s2cid = 20181150 }}</ref><ref name=Robertson2011>{{cite journal | vauthors = Robertson MM | title = Gilles de la Tourette syndrome: the complexities of phenotype and treatment | journal = British Journal of Hospital Medicine | volume = 72 | issue = 2 | pages = 100–107 | date = February 2011 | pmid = 21378617 | doi = 10.12968/hmed.2011.72.2.100 }}</ref><ref name=Du2010>{{cite journal | vauthors = Du JC, Chiu TF, Lee KM, Wu HL, Yang YC, Hsu SY, Sun CS, Hwang B, Leckman JF | display-authors = 6 | title = Tourette syndrome in children: an updated review | journal = Pediatrics and Neonatology | volume = 51 | issue = 5 | pages = 255–264 | date = October 2010 | pmid = 20951354 | doi = 10.1016/S1875-9572(10)60050-2 | doi-access = free }}</ref><ref>[[Tourette Association of America|Tourette Syndrome Association]]. [https://web.archive.org/web/20051122154536/http://tsa-usa.org/news/DBS-Statement.htm Statement: Deep Brain Stimulation and Tourette Syndrome.] Retrieved November 22, 2005.</ref> The procedure is well tolerated, but complications include "short battery life, abrupt symptom worsening upon cessation of stimulation, hypomanic or manic conversion, and the significant time and effort involved in optimizing stimulation parameters".<ref name=Malone>{{cite book |chapter=Behavioral neurosurgery |pages=241–247 |chapter-url={{Google books|hhE74A1fTQkC|page=241|plainurl=yes}} |pmid=16536372 | vauthors = Walkup JT, Mink JW, Hollenbeck PJ |title=Tourette Syndrome |series=Advances in Neurology |date=2006 |volume=99 |publisher=Lippincott Williams & Wilkins |isbn=978-0-7817-9970-6 }}</ref>
 The procedure is invasive and expensive and requires long-term expert care. Benefits for severe Tourette's are inconclusive, considering the less robust effects of this surgery seen in the [[Netherlands]]. Tourette's is more common in [[pediatric]] populations, tending to remit in adulthood, so, in general, this would not be a recommended procedure for use on children. It may not always be obvious how to utilize DBS for a particular person because the diagnosis of Tourette's is based on a history of symptoms rather than an examination of neurological activity. Due to concern over the use of DBS in [[management of Tourette syndrome|Tourette syndrome treatment]], the [[Tourette Association of America]] convened a group of experts to develop recommendations guiding the use and potential [[clinical trials]] of DBS for TS.<ref>{{cite journal | vauthors = Mink JW, Walkup J, Frey KA, Como P, Cath D, Delong MR, Erenberg G, Jankovic J, Juncos J, Leckman JF, Swerdlow N, Visser-Vandewalle V, Vitek JL | display-authors = 6 | title = Patient selection and assessment recommendations for deep brain stimulation in Tourette syndrome | journal = Movement Disorders | volume = 21 | issue = 11 | pages = 1831–1838 | date = November 2006 | pmid = 16991144 | doi = 10.1002/mds.21039 | hdl-access = free | author14 = Tourette Syndrome Association | s2cid = 16353255 | hdl = 2027.42/55891 }}</ref>