JOURNAL ARTICLE

Operative findings and outcomes of microvascular decompression for trigeminal neuralgia in 35 patients affected by multiple sclerosis

Giovanni Broggi, Paolo Ferroli, Angelo Franzini, Vittoria Nazzi, Laura Farina, Loredana La Mantia, Clara Milanese
Neurosurgery 2004, 55 (4): 830-8; discussion 838-9
15458591

OBJECTIVE: The concept of vascular compression of the trigeminal root as the main etiological factor in idiopathic trigeminal neuralgia has achieved widespread acceptance, and microvascular decompression (MVD) is a well-established surgical procedure for its treatment. Multiple sclerosis (MS) has long been considered to be an absolute contraindication to MVD because of the supposed exclusive causative role of a demyelinating lesion affecting the trigeminal root entry zone. Magnetic resonance imaging preoperative identification of suspicious vessels along the cisternal course of the trigeminal nerve in MS patients raises the question of a possible causative role of vascular compression in MS patients.

METHODS: We describe magnetic resonance imaging findings, surgical findings, and outcomes in 35 MS patients who underwent MVD for medically intractable trigeminal neuralgia. Results were assessed by clinical follow-up and periodic phone surveys. The mean follow-up was 44 months (range, 6-108 mo).

RESULTS: Magnetic resonance imaging revealed the presence of demyelinating lesions affecting the brainstem trigeminal pathways of the painful side in 26 (74%) of 35 patients. During surgery, severe neurovascular compression at the trigeminal root entry zone was found in 16 (46%) of 35 patients. The long-term outcome was excellent in 39%, good in 14%, fair in 8%, and poor in 39% of patients. No statistically significant prognostic factor predicting good outcome could be found. There was no mortality, with a 2.5% long-term morbidity rate (facial nerve palsy in one patient).

CONCLUSION: Results of MVD in trigeminal neuralgia MS patients are much less satisfactory than in the idiopathic group, indicating that central mechanisms play a major role in pain genesis.

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