Deep brain stimulation in movement disorders

Michael S Okun MD (Dr. Okun of the University of Florida has no relevant financial relationships to disclose.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released May 9, 1996; last updated December 6, 2016; expires December 6, 2019

Overview

The authors briefly review the basic knowledge regarding the surgical treatment known as deep brain stimulation (DBS) as applied to movement disorders such as Parkinson disease, essential tremor, dystonia, and Tourette syndrome. In this article, the authors address patient selection, the surgical procedure, programming, and postoperative medical management in DBS for these disorders. The authors also cover clinical outcomes and prognosis following DBS and update on some of the latest technological innovations.

Key points

 

• DBS is an FDA-approved therapy for Parkinson disease, tremor, and dystonia. The goal of DBS is to improve quality of life and ability to function.

 

• In Parkinson disease, DBS is considered when patients have intolerable wearing-off, motor fluctuations, or dyskinesias despite optimal medical management or, alternatively, have partially responsive or unresponsive tremor.

 

• In essential tremor, DBS is considered when patients have tremor that is disabling and unresponsive or partially responsive to medical therapies.

 

• In dystonia, DBS is considered in patients with significant disability who have failed medical therapy and in some cases botulinum toxin injections.

 

• Dementia and untreated depression are contraindications to DBS.

 

• An interdisciplinary team approach should be used to choose patients for DBS and a risk-benefit ratio should be used to decide on surgery.

Historical note and terminology

Surgical treatments for movement disorders were applied to human patients as early as the 1930s. Victor Horseley was a neurosurgeon who applied cortical motor strip resection to address the symptoms of athetosis and tremor. This approach, however, proved to be suboptimal, as interruption of the pyramidal pathways resulted in weakness and intolerable long-term side effects. Later, in the 1930s and 1940s, partial cordectomies were used as a technique to treat tremor, and cerebral pedunculotomies were utilized for choreoathetosis and hemiballismus. Morbidity was unfortunately unacceptably high with these early procedures. By the 1950s, surgeons had largely abandoned motor tract lesioning.

The next era of movement disorders surgery evolved to direct targeting of brain structures and there was a shift from the pyramidal motor tracts to the basal ganglia. Russell Meyers, who had earlier attempted anterior caudate resections to treat postencephalitic tremor, was an early proponent of a more focused surgical approach. He reported a case where he took a transventricular approach and removed the anterior two thirds of the caudate nucleus. The results were impressive, as tremor was abolished. Unfortunately, long-term follow-up of the caudate resection revealed disabling hyperkinetic movements, and the Meyers open transventricular approach was abandoned.

The most important evolution for the surgical treatment of movement disorders came with the introduction of frame-based surgery. Spiegel and Wycis used a frame to stereotactically guide lesions in a series of patients operated in the 1940s, which decreased mortality compared to the previously reported suboptimal open craniotomy approaches.

Two decades following the introduction of the head frame, Rolf Hassler, Irving Cooper, and several other neurosurgeons would begin reporting the benefits of this approach in a larger series of patients. Early reports detailed 3 potential surgical targets for the treatment of Parkinsonian tremor: the midbrain peduncles and tegmentum; the thalamus; and the pallidofugal pathways. Later in the same decade, J L Pool attempted to treat a patient's depression by implanting an electrode into her caudate nucleus. Unfortunately, there was a lack of detailed pre- and postoperative analysis on this patient, and deep brain stimulation for movement disorders would not be widely adopted for several more decades.

Irving Cooper and Rolf Hassler championed the idea that neurosurgical targeting should be based on brain anatomy and functional connectivity. The appreciation of this philosophy was cemented when Irving Cooper accidentally ligated the anterior choroidal artery in a patient with Parkinson disease and observed dramatic symptomatic improvement (reported in 1954). Following similar observations, Cooper introduced reversible “chemotomy” of the pallidum, and he used this approach as an operative screening tool to decide whether or not to place a permanent lesion. Cooper would temporarily “deactivate” the globus pallidus by injecting procaine and confirm benefits prior to ligating the anterior choroidal artery. Cooper would later use a double lumen catheter, and he also moved from pallidum to thalamus in some cases. His early reports detailed an ability to visualize the target area by injecting dye, and he reported his use of alcohol injection or cryotherapy for ultimate lesioning of an area. Radiofrequency test lesions and micro- as well as macroelectrode stimulation were later introduced as methods for functional localization of targets and as aids for better defining target accuracy. Heat, electricity, ultrasound, and focal gamma radiation would all be employed as ablative techniques over the next 3 decades.

A number of neurosurgeons started ablating the ventrolateral thalamus in the region of the nucleus ventralis intermedius and ventralis oralis anterior/ventralis oralis posterior nuclei (VOA-VOP) as a technique to relieve tremor and rigidity and also to address more complex symptoms such as choreoathetosis, hemiballismus, and possibly even the symptoms of Parkinson disease. Hassler reported that stimulation of the pallidum could elicit dystonia at low frequencies whereas, conversely, he observed improvement at higher stimulation frequencies. As smaller and better-placed surgical lesions became more feasible, new targets emerged including the centromedian nucleus, the posterior limb of the internal capsule, the subthalamic nucleus, and deep cerebellar nuclei. Additionally, the refined localization of previous targets also improved outcomes.

Though lesioning was effective, problems were increasingly evident with this approach. The technique was irreversible and could produce side effects and lead to morbidity. Bilateral lesions could lead to speech, swallowing, cognitive, and pseudobulbar effects. Surgery quickly fell out of favor for Parkinson disease with the introduction of levodopa therapy in the late 1960s. Surgical therapy would however reemerge in the early 1980s after it was realized that long-term exposure to levodopa could result in debilitating on-off fluctuations as well as dyskinesia, and that some tremors could not be addressed with levodopa.

The modern era of ablation reemerged with Laitenen, and stimulation was introduced as a result of the basic science work of Mahlon DeLong and the observations by Professor Benabid in human patients. Benabid observed that high frequency test stimulation during lesion localization for an ablative procedure could result in a reduction of tremor. His idea that prolonged or chronic thalamic stimulation could persistently suppress tremor resulted in the adoption of chronic DBS. DBS was quickly adapted and applied as a treatment for movement disorders, neuropsychiatric conditions, epilepsy, and pain. The implantation of deep brain stimulators provided an alternative to lesioning that was reversible, was adjustable, and the procedure could be performed bilaterally without unacceptable speech, swallowing, and cognitive side effects. DeLong and Benabid received the 2014 Lasker prize for their work on basal ganglia and also on the development of DBS (Okun 2014).

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