OBJECTIVE Contemporary theories of the pathophysiology of movement disorders emphasize abnormal oscillatory activity in basal ganglia-thalamocortical loops, but these have been studied in humans mainly using depth recordings. Recording from the surface of the cortex using electrocorticography (ECoG) provides a much higher amplitude signal than depth recordings, is less susceptible to deep brain stimulation (DBS) artifacts, and yields a surrogate measure of population spiking via “broadband gamma” (50–200 Hz) activity. Therefore, a technical approach to movement disorders surgery was developed that employs intraoperative ECoG as a research tool. METHODS One hundred eighty-eight patients undergoing DBS for the treatment of movement disorders were studied under an institutional review board–approved protocol. Through the standard bur hole exposure that is clinically indicated for DBS lead insertion, a strip electrode (6 or 28 contacts) was inserted to cover the primary motor or prefrontal cortical areas. Localization was confirmed by the reversal of the somatosensory evoked potential and intraoperative CT or 2D fluoroscopy. The ECoG potentials were recorded at rest and during a variety of tasks and analyzed offline in the frequency domain, focusing on activity between 3 and 200 Hz. Strips were removed prior to closure. Postoperative MRI was inspected for edema, signal change, or hematoma that could be related to the placement of the ECoG strip. RESULTS One hundred ninety-eight (99%) strips were successfully placed. Two ECoG placements were aborted due to resistance during the attempted passage of the electrode. Perioperative surgical complications occurred in 8 patients, including 5 hardware infections, 1 delayed chronic subdural hematoma requiring evacuation, 1 intraparenchymal hematoma, and 1 venous infarction distant from the site of the recording. None of these appeared to be directly related to the use of ECoG. CONCLUSIONS Intraoperative ECoG has long been used in neurosurgery for functional mapping and localization of seizure foci. As applied during DBS surgery, it has become an important research tool for understanding the brain networks in movement disorders and the mechanisms of therapeutic stimulation. In experienced hands, the technique appears to add minimal risk to surgery.

We investigated the potential of deep brain stimulation (DBS) in the central nucleus of the amygdala (CeA) in rats to modulate functional reward mechanisms. The CeA is the major output of the amygdala with direct connections to the hypothalamus and gustatory brainstem, and indirect connections with the nucleus accumbens. Further, CeA has been shown to be involved in learning, emotional integration, reward processing, and regulation of feeding. We hypothesized that DBS, which is used to treat movement disorders and other brain dysfunctions, might block reward motivation. In rats performing a lever pressing task to obtain sugar pellet rewards, we stimulated the CeA and control structures, and compared stimulation parameters. During CeA stimulation, animals stopped working for rewards and rejected freely available rewards. Taste reactivity testing during DBS exposed aversive reactions to normally liked sucrose tastes and even more aversive taste reactions to normally disliked quinine tastes. Interestingly, given the opportunity, animals implanted in the CeA would self-stimulate with 500 ms trains of stimulation at the same frequency and current parameters as continuous stimulation that would stop reward acquisition. Neural recordings during DBS showed that CeA neurons were still active and uncovered inhibitory-excitatory patterns after each stimulus pulse indicating possible entrainment of the neural firing with DBS. In summary, DBS modulation of CeA may effectively usurp normal neural activity patterns to create an “information lesion” that not only decreased motivational “wanting” of food rewards, but also blocked “liking” of rewards.

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Cluster headache, a trigeminal autonomic cephalgia, is a syndrome involving unilateral head pain associated with autonomic symptoms. The diagnosis is clinical. The pathophysiology of cluster headache is unknown. It is believed to involve the trigeminal nerve and ganglion, with autonomic dysfunction and vascular irritability. Initial treatment is with parenteral triptans and inhaled oxygen. Preventive agents include topiramate, verapamil, and lithium. Occipital nerve blocks and stimulation have been effective in small studies. Surgery is limited to those patients that have persistent, chronic cluster headache with a minimum of three attacks per week, despite treatment with at least three preventative agents. Deep brain stimulation of the posterior hypothalamus has been shown to be effective in the treatment of chronic cluster headache.

Diabetic neuropathy may cause numbness and burning pain in a distal, symmetric distribution, typically involving the hands and feet. Management is with improved glucose control and treatment with tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors, and anti-epileptics. Surgical treatment is reserved for those patients with severe symptoms, with significantly impaired quality of life, for whom medications have not provided significant relief. There is evidence that spinal cord stimulation can provide a significant reduction in pain. A temporary trial of stimulation should be performed prior to permanent implantation. Leads may be placed in the epidural space percutaneously or via laminectomy and are connected to an internal pulse generator. Complications are typically device related. Treatment of device infection may require device removal.

Geniculate neuralgia is a rare syndrome of episodic, lancinating pain located within the ear canal. There may be a trigger point within the canal and associated with disorders of tearing, taste, and salivation. It is important to distinguish geniculate neuralgia from other causes of inner ear pain, including structural lesions and glossopharyngeal or trigeminal neuralgia. MRI may show vascular conflict with CN VII/VIII complex. Typical treatment is with carbamazepine. Surgery is reserved for those patients who have an incomplete response to medication. Surgery is directed at microvascular decompression of the CN VII/VIII complex with or without sectioning of the nervus intermedius. The entry zones of CN IX and X may also be explored. Complications and management are discussed.