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Year : 2017  |  Volume : 65  |  Issue : 1  |  Page : 103--104

Neuromodulation in Tourette's syndrome

Milind Deogaonkar 
 Department of Neurosurgery, Ohio State University Wexner Medical Center, Columbus, OH, USA

Correspondence Address:
Dr. Milind Deogaonkar
Department of Neurosurgery, Ohio State University Wexner Medical Center, Columbus, OH, 43210

How to cite this article:
Deogaonkar M. Neuromodulation in Tourette's syndrome.Neurol India 2017;65:103-104

How to cite this URL:
Deogaonkar M. Neuromodulation in Tourette's syndrome. Neurol India [serial online] 2017 [cited 2020 Oct 21 ];65:103-104
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Full Text

Psychiatric and neuropsychiatric disorders such as Tourette's syndrome are difficult to treat. The complexity is even more pronounced in surgical treatments of these disorders as the outcomes are not black and white but multiple shades of gray. In addition, there is an additional ethical burden that accompanies any such intervention. Nevertheless, the quest to treat psychiatric disorders and modify human behavior using neurosurgical interventions dates back to the early part of the last century. However, owing to a lack of understanding of the pathophysiology of the disease and effects of intervention, the outcomes were at the best ambiguous. Technological advances in understanding neural circuitry, advanced imaging, safer tools of stereotaxy, and the advent of reversible neuromodulation in the form of deep brain stimulation (DBS) have emboldened our forays in psychiatric neurosurgery in recent years.

With a better understanding of the pathophysiology and neural circuits involved in these disorders, it is now possible to delineate a clear anatomical “target” or “targets.” The role of cortico-striato-thalamo-cortical (CSTC) circuit and the parallel functionally segregated “motor,” “oculomotor,” “dorsolateral prefrontal,” “anterior cingulate,” and “lateral orbitofrontal” loops linking basal ganglia and cortex via the thalamus is well established in psychiatric disorders.[1] To develop appropriate surgical intervention for disorders such as Tourette's syndrome, it is prudent to understand the pathophysiology of the neural substrate associated with it. Unlike the pathogenesis of movement disorders, which is usually associated with hyper- or hypoactivity of a single surgical target/circuit, the pathogenesis of psychiatric disorders is more complex and involve dysregulation between multiple neural circuits/centers or targets. Considering this multicircuit model, the primary abnormality is the dysrhythmia of basal ganglia and limbic striatal circuits that control the output of the orbitofrontal and anterior cingulate cortex as well as the medial, dorsomedial, and anterior thalamic nuclei.[2] Because these are the three components of this multicircuit model of Tourette's syndrome, the targets could be medial thalamus [centromedian-parafascicular (CMPf) complex], globus pallidus interna (anteromedial which is more limbic, or posteroventral), globus pallidus externa or anterior limb of internal capsule [or ventral capsule/ventral striatum (Vc/Vs)], which carries the reciprocal positive feedback loop from the orbital and prefrontal cortex to the dorsomedial nucleus of thalamus. All these targets are incorporated in the circuit of Papez that originates at the hippocampal formation to the mammillary bodies via the fornix, which projects via the mammilothalamic tracts to the anterior thalamic nuclei and then connects the anterior cingulate and striatal nucleus accumbens.[3]

Vandewalle et al., first reported DBS treatment for Tourette syndrome in 1999.[4] In this report, they modulated the medial thalamus. After that, various centers have used the globus pallidus internus, the anterior limb of internal capsule/nucleus accumbens, the globus pallidus externus, and the subthalamic nucleus as targets with significant clinical benefit. Nevertheless, the best target has not yet been identified. We have used CM-Pf as well as anterior limb of internal capsule/nucleus accumbens as targets in 6 patients of Tourette's syndrome with good clinical outcomes.

Going forward, in psychiatric neuromodulation, in diseases such as Tourette's syndrome, important points to consider are

Standardization of targets, inclusion criteria, and treatment of comorbid conditions [5]Need to follow a sequence of safety measures and ethical considerations to ensure proper execution and favorable outcomeA multispecialty team that is proficient in DBS as well as psychiatric disorder managementDesigning more robust hardware to reduce hardware-related complications in patients with predominantly motor ticsUse of adoptive stimulation or closed loop systems as the symptoms are paroxysmal.[5]

With technological advances and increased understanding of the basic pathophysiology of psychiatric disorders, it is likely that more precise targets will be unveiled in the near future. Advances in stimulation paradigms, directional leads, and availability of adaptive stimulation devices will help in maximizing the clinical benefits, while minimizing the risks/side effects associated with DBS. An interdisciplinary approach with strict ethical considerations needs to be implemented in managing these difficult-to-treat disorders. With appropriate use of technology and strict adherence to protocols, we are likely to ameliorate the symptoms and improve the lives of patients suffering from these refractory psychiatric disorders.


1Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu Rev Neurosci 1986;9:357-81.
2Rauch SL. Neuroimaging and neurocircuitry models pertaining to the neurosurgical treatment of psychiatric disorders. Neurosurg Clin N Am 2003;14:213-23.
3Papez JW. A proposed mechanism of emotion. 1937. J Neuropsychiatry Clin Neurosci 1995;7:103-12.
4Vandewalle V, van der Linden C, Groenewegen HJ, Caemaert J. Stereotactic treatment of Gilles de la Tourette syndrome by high frequency stimulation of thalamus. Lancet 1999;353:724.
5Andrade P, Visser-Vandewalle V. DBS in Tourette syndrome: Where are we standing now? J Neur Transm 2016;123:791-6.