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Mark R. McLaughlin, Peter J. Jannetta, Brent L. Clyde, Brian R. Subach, Christopher H. Comey and Daniel K. Resnick

Object

Microvascular decompression has become an accepted surgical technique for the treatment of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and other cranial nerve rhizopathies. The senior author (P.J.J.) began performing this procedure in 1969 and has performed more than 4400 operations. The purpose of this article is to review some of the nuances of the technical aspects of this procedure.

Methods

A review of 4415 operations shows that numerous modifications to the technique of microvascular decompression have occurred during the last 29 years. Of the 2420 operations performed for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia before 1990, cerebellar injury occurred in 21 cases (0.87%), hearing loss in 48 (1.98%), and cerebrospinal fluid (CSF) leakage in 59 cases (2.44%). Of the 1995 operations performed since 1990, cerebellar injuries declined to nine cases (0.45%), hearing loss to 16 (0.8%), and CSF leakage to 37 (1.85%) (p < 0.01, test for equality of distributions). The authors describe slight variations made to maximize surgical exposure and minimize potential complications in each of the six principal steps of this operation. These modifications have led to decreasing complication rates in recent years.

Conclusions

Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.

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Mark R. McLaughlin, Peter J. Jannetta, Brent L. Clyde, Brian R. Subach, Christopher H. Comey and Daniel K. Resnick

Object. Microvascular decompression has become an accepted surgical technique for the treatment of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and other cranial nerve rhizopathies. The senior author (P.J.J.) began performing this procedure in 1969 and has performed more than 4400 operations. The purpose of this article is to review some of the nuances of the technical aspects of this procedure.

Methods. A review of 4415 operations shows that numerous modifications to the technique of microvascular decompression have occurred during the last 29 years. Of the 2420 operations performed for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia before 1990, cerebellar injury occurred in 21 cases (0.87%), hearing loss in 48 (1.98%), and cerebrospinal fluid (CSF) leakage in 59 cases (2.44%). Of the 1995 operations performed since 1990, cerebellar injuries declined to nine cases (0.45%), hearing loss to 16 (0.8%), and CSF leakage to 37 (1.85% p < 0.01, test for equality of distributions). The authors describe slight variations made to maximize surgical exposure and minimize potential complications in each of the six principal steps of this operation. These modifications have led to decreasing complication rates in recent years.

Conclusions. Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.

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Daniel K. Resnick and Peter J. Jannetta

✓ A 37-year-old woman underwent microvascular decompression of the superior vestibular nerve for disabling positional vertigo. Immediately following the operation, she noted severe and spontaneous gagging and dysphagia. Multiple magnetic resonance images were obtained but failed to demonstrate a brainstem lesion and attempts at medical management failed. Two years later she underwent exploration of the posterior fossa. At the second operation, the vertebral artery as well as the posterior inferior cerebellar artery were noted to be compressing the vagus nerve. The vessels were mobilized and held away from the nerve with Teflon felt. The patient's symptoms resolved immediately after the second operation and she has remained symptom free. The authors hypothesize that at least one artery was shifted at the time of her first operation, or immediately thereafter, which resulted in vascular compression of the vagus nerve. To the authors' knowledge, this is the first reported case of a hyperactive gagging response treated with microvascular decompression. The case also illustrates the occurrence of a possibly iatrogenic neurovascular compression syndrome.

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Peter J. Jannetta, Mark R. Mclaughlin and Kenneth F. Casey

Vascular compression of the trigeminal nerve in the cerebellopontine angle is now generally accepted as the primary source or “trigger” causing trigeminal neuralgia. A clear clinicopathological association exists in the neurovascular relationship. In general, pain in the third division of the trigeminal nerve is caused by rostral compression, pain in the second division is caused by medial or more distant compression, and pain in the first division is caused by caudal compression.

This discussion of the surgical technique includes details on patient position, placement of the incision and craniectomy, microsurgical exposure of the supralateral cerebellopontine angle, visualization of the trigeminal nerve and vascular pathological features, microvascular decompression, and wound closure. Nuances of the technique are best learned in the company of a surgeon who has a longer experience with this procedure.

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Peter J. Jannetta

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Raymond F. Sekula Jr., Edward M. Marchan, Parviz Baghai, Peter J. Jannetta and Matthew R. Quigley

✓ Acute disseminated encephalomyelitis (ADEM), also known as postinfectious encephalomyelitis, is an immunologically mediated demyelinating disorder affecting the central nervous system that typically occurs after infection or vaccination. The prognosis of ADEM is generally favorable. In a small subset of patients with ADEM, however, fulminant cerebral edema requiring neurosurgical intervention will develop. Few recommendations are available to help the neurosurgeon in dealing with such cases. In this report, the authors present the case of a patient with ADEM in whom central brain herniation developed secondary to medically intractable cerebral edema. The authors review the salient features of the disease and suggest a role for neurosurgeons in cases of fulminant ADEM.