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Pain


Gamma Knife Radiosurgery for Trigeminal Neuralgia—A Review Edward A Monaco III, MD, PhD,1


Hideyuki Kano, MD, PhD,2 Ali Kooshkabadi, MD1


and L Dade Lunsford, MD3 1. Resident; 2. Research Assistant Professor; 3. Professor, Department of Neurological Surgery, University of Pittsburgh Medical Center


Abstract


Gamma knife radiosurgery (GKRS) evolved from the vision of Lars Leksell as a method of bloodless surgery for treating a wide variety of intracranial pathologies. Since the first GKRS procedure for trigeminal neuralgia (TN) in the early 1970s, thousands of medically refractory patients have been treated, with good results. GKRS has become a first-line treatment for medically refractory TN along with microvascular decompression and percutaneous rhizotomy. GKRS offers the advantages of minimal invasiveness and extremely low risk. When recommending a surgical treatment modality for medically refractory TN, one must consider patient preferences, procedural risks, medical comorbidities, and the success rates of the various approaches. In this context, we review the role of GKRS in the treatment of medically refractory TN.


Keywords Trigeminal neuralgia, gamma knife, stereotactic radiosurgery, tic douloureux, facial pain


Disclosure: The authors have no conflicts of interest to declare. Received: November 17, 2011 Accepted: December 19, 2011 Citation: US Neurology, 2011;7(2):149–53 Correspondence: L Dade Lunsford, MD, Department of Neurological Surgery, University of Pittsburgh Medical Center Presbyterian Hospital, Suite B-400, 200 Lothrop Street, Pittsburgh, PA 15213. E: lunsfordld@upmc.edu


What is Trigeminal Neuralgia?


Trigeminal neuralgia (TN) is a vexing clinical problem for a number of reasons, not least of which is clearly defining its clinical spectrum. A commonly accepted definition of TN is that of a facial pain syndrome in which a patient experiences brief, episodic, and sharp attacks of pain in the distribution of the trigeminal nerve. These painful attacks are typically unilateral but can rarely be bilateral. Painful attacks are often brought on by triggers including chewing or touching the affected dermatome. Atypical TN includes more lingering or non-episodic constant pain that does not have the typical tactile triggers. Moreover, atypical facial pain, often bilateral, can present in the context of somatoform disorders in which no organic cause can be identified. Finally, one or more of these different types of pain can be present in the same patient at the same time. It is important to distinguish between these different types of facial pain because their etiologies are probably different, and thus their treatments as well.


Burchiel’s recent classification scheme, with minor modifications, links the nature of the trigeminal pain with possible mechanisms (see Table 1).1 In this scheme, what has been known as tic douloureux or typical (type 1) TN is characterized by primarily episodic painful attacks located in the distribution of the trigeminal nerve branches. When constant or lingering pain is the predominant feature but there are additional episodic features, the syndrome is called type 2 TN. These idiopathic forms are distinguished from the deafferentation pain syndromes caused by either unintentional (i.e. accidental trauma) or intentional (purposeful surgical injury to the nerve) damage to the trigeminal nerve. Facial pain following a herpes zoster outbreak falls into this condition as well. These latter conditions are


© TOUCH BRIEFINGS 2011


associated with demonstrable trigeminal sensory loss. Finally, somatoform facial pain is labeled atypical facial pain, and is characterized by its bilaterality, as well as presence of pain well outside of the innervation of the trigeminal nerve. Unless otherwise specified, this article is focused on the paroxysmal trigeminal pain syndromes including types 1 and 2 TN as well as TN caused by multiple sclerosis (MS). None of the therapies covered in this article has meaningful benefit for constant or deafferentation facial pain.


Although TN has an annual incidence of 27 per 100,000,2 the mechanism


underlying its episodic facial pain remains incompletely understood. In many patients, it is related to vascular compression of the trigeminal nerve by branches of the superior cerebellar artery3,4


or, less commonly, adjacent


veins. How this mediates pain transmission is not clear, but it has been postulated that vascular compression results in local demyelination and axonopathy, which results in ephaptic transmission between the damaged heavily myelinated fibers and the smaller unmyelinated pain fibers.5


This


finding has led to the use of microvascular decompression (MVD) surgery as a primary treatment for TN, one that attacks the etiology in a significant number of patients. Patients with MS suffer from TN at a rate several-fold higher than the general population (2 %).6


trigeminal system due to the underlying autoimmune phenomenon is implicated, but whether ephaptic transmission or hyperexcitability of the trigeminal nucleus actually causes the episodic pain remains unproven.7


Because TN in MS does not feature vascular compression as its cause, it requires a different treatment approach. Finally, deafferentation syndromes of the trigeminal nerve are the result of nerve injury, not simply


149


Demyelination along the


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