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Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression.
J Neurosurg. 1994 Jul; 81(1):1-9.JN

Abstract

Thirty-one (2%) of 1404 consecutive patients with typical trigeminal neuralgia who underwent microvascular decompression between 1972 and 1993 were found to have vascular compression by the vertebral artery (VA) or the basilar artery (BA). Compared to the remaining 1373 patients, this subgroup was older (mean age 62 vs. 55 years, p < 0.001), was predominantly male (68% vs. 39%, p < 0.002), demonstrated left-sided predominance (65% vs. 39%, p < 0.002), was more likely to be hypertensive (65% vs. 18%, p < 0.001), and was more likely to have ipsilateral hemifacial spasm (16% vs. 0.6%, p < 0.001). The trigeminal nerve was compressed by the VA in 18 cases (the VA alone in three and the VA plus other vessels in 15), the BA in 12 cases (the BA alone in four and the BA plus other vessels in eight), and the vertebrobasilar junction in one case. Twenty-nine of the 31 patients underwent vascular decompression of the trigeminal nerve, one had a complete trigeminal root section, and one underwent partial root section with vascular decompression of the remaining nerve. All 31 patients were pain-free, off medication immediately after surgery, and this pain-free, medication-free status was maintained at 1 year after surgery in 96% of cases, at 3 years in 92%, and at 10 years in 86%, based on life-table analysis. Minor trigeminal hypesthesia/hypalgesia was present preoperatively in 52%. New or worsened minor hypesthesia/hypalgesia developed in 41% of patients, while transient diplopia as well as hearing loss developed in 23% and 13% in the overall series, respectively. No patient developed major trigeminal sensory loss or masseter weakness after vascular decompression alone. There was no operative mortality. Vascular decompression is an effective treatment for patients with trigeminal neuralgia who have vertebrobasilar compression of the trigeminal nerve. Patients should be warned that decompression of a tortuous vertebrobasilar system carries a higher risk of mild trigeminal dysfunction, diplopia, and hearing loss than standard microvascular decompression.

Authors+Show Affiliations

Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pennsylvania.No affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

8207508

Citation

Linskey, M E., et al. "Microvascular Decompression for Trigeminal Neuralgia Caused By Vertebrobasilar Compression." Journal of Neurosurgery, vol. 81, no. 1, 1994, pp. 1-9.
Linskey ME, Jho HD, Jannetta PJ. Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. J Neurosurg. 1994;81(1):1-9.
Linskey, M. E., Jho, H. D., & Jannetta, P. J. (1994). Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. Journal of Neurosurgery, 81(1), 1-9.
Linskey ME, Jho HD, Jannetta PJ. Microvascular Decompression for Trigeminal Neuralgia Caused By Vertebrobasilar Compression. J Neurosurg. 1994;81(1):1-9. PubMed PMID: 8207508.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. AU - Linskey,M E, AU - Jho,H D, AU - Jannetta,P J, PY - 1994/7/1/pubmed PY - 1994/7/1/medline PY - 1994/7/1/entrez SP - 1 EP - 9 JF - Journal of neurosurgery JO - J Neurosurg VL - 81 IS - 1 N2 - Thirty-one (2%) of 1404 consecutive patients with typical trigeminal neuralgia who underwent microvascular decompression between 1972 and 1993 were found to have vascular compression by the vertebral artery (VA) or the basilar artery (BA). Compared to the remaining 1373 patients, this subgroup was older (mean age 62 vs. 55 years, p < 0.001), was predominantly male (68% vs. 39%, p < 0.002), demonstrated left-sided predominance (65% vs. 39%, p < 0.002), was more likely to be hypertensive (65% vs. 18%, p < 0.001), and was more likely to have ipsilateral hemifacial spasm (16% vs. 0.6%, p < 0.001). The trigeminal nerve was compressed by the VA in 18 cases (the VA alone in three and the VA plus other vessels in 15), the BA in 12 cases (the BA alone in four and the BA plus other vessels in eight), and the vertebrobasilar junction in one case. Twenty-nine of the 31 patients underwent vascular decompression of the trigeminal nerve, one had a complete trigeminal root section, and one underwent partial root section with vascular decompression of the remaining nerve. All 31 patients were pain-free, off medication immediately after surgery, and this pain-free, medication-free status was maintained at 1 year after surgery in 96% of cases, at 3 years in 92%, and at 10 years in 86%, based on life-table analysis. Minor trigeminal hypesthesia/hypalgesia was present preoperatively in 52%. New or worsened minor hypesthesia/hypalgesia developed in 41% of patients, while transient diplopia as well as hearing loss developed in 23% and 13% in the overall series, respectively. No patient developed major trigeminal sensory loss or masseter weakness after vascular decompression alone. There was no operative mortality. Vascular decompression is an effective treatment for patients with trigeminal neuralgia who have vertebrobasilar compression of the trigeminal nerve. Patients should be warned that decompression of a tortuous vertebrobasilar system carries a higher risk of mild trigeminal dysfunction, diplopia, and hearing loss than standard microvascular decompression. SN - 0022-3085 UR - https://www.unboundmedicine.com/medline/citation/8207508/Microvascular_decompression_for_trigeminal_neuralgia_caused_by_vertebrobasilar_compression_ DB - PRIME DP - Unbound Medicine ER -