Evolution of oculomotor nerve paresis after endovascular coiling of posterior communicating artery aneurysms: a neuro-ophthalmological perspective.

OBJECTIVE: Guglielmi detachable coil treatment is becoming an accepted alternative to microsurgical clipping for select intracerebral aneurysms. Resolution of oculomotor nerve paresis (ONP) after endovascular packing was claimed to be complete in two prior series, with three and six cases. We describe the evolution of ONP after Guglielmi detachable coil treatment of posterior communicating artery aneurysms, and we search for endovascular and patient factors correlated with the degree of functional nerve recovery. METHODS: Twelve cases of ONP attributable to posterior communicating artery aneurysms were treated with Guglielmi detachable coils between 1999 and 2002. Eleven patients were available for follow-up monitoring. The degree of ONP was recorded at admission, at discharge, after 3 months, and at yearly intervals thereafter. The size of the aneurysm, the duration of ONP before coiling, the degree of coiling, age, and the presence of other microvascular risk factors were correlated with the degree of nerve recovery. RESULTS: Complete resolution of ONP did not occur in any of the 11 cases in this series. However, residual oculomotor nerve deficits did not cause diplopia with primary gaze for 10 of 11 patients. Clinically significant ptosis did not persist for any of the patients. The pupil remained minimally affected in all cases. CONCLUSION: Although mass effect remains after endovascular packing, oculomotor nerve dysfunction improves comparably to the recovery observed after surgical clipping. Contrary to previous reports, typical residual oculomotor nerve deficits persist. Older age and the presence of microvascular risk factors seem to be detrimental to ONP recovery.

Trigeminal neuralgia: the role of self-sustaining discharge in the trigeminal ganglion.

Idiosyncrasies of trigeminal neuralgia provide both clues and constraints on candidate hypotheses concerning the underlying neural mechanism. After reviewing the key clinical aspects of the disease, we propose here a novel hypothesis based on recent findings from experimental nerve-injury preparations. The hypothesis states that trigger stimuli set off bursts of activity in a small cluster of trigeminal ganglion (TRG) neurons that have been rendered hyperexcitable as a result of TRG or trigeminal root damage. Activity then spreads from this "TRG ignition focus" to encompass more widespread portions of the ganglion. After a brief period of autonomous firing (seconds to minutes), activity is quenched and a refractory period is initiated by an intrinsic suppressive (hyperpolarizing) process engaged as a result of the rapid firing. The primary abnormality resides in the TRG and trigeminal root, rather than in the skin or the CNS. Because of this, sensation is essentially normal between periods of ectopic paroxysmal TRG discharge.

The effect of glycerol on autotomy. An experimental model of neuralgia pain.

Autotomy in nerve injured rats has been put forward as an animal model in a broad range of chronic neuralgic pain. We have examined the effect of glycerol, a new and promising therapeutic agent for trigeminal neuralgia, on this animal model. A single dose of glycerol, alcohol or saline was injected directly into experimental sciatic nerve neuromas in rats via a chronically implanted cannula. Injections were made either at the time of nerve injury or 2 weeks afterwards. Both forms of glycerol treatment caused a significant reduction in autotomy behavior relative to saline. Alcohol also suppressed autotomy, but it was less effective than glycerol.