2007NeurosurgeryRequires access

Outcome of Oculomotor Nerve Palsy from Posterior Communicating Artery Aneurysms

Nassir M. Mansour, Kishor A. Choudhari

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Abstract

To the Editor: We read with interest the article by Chen et al. (2), who analyzed 13 patients with posterior communicating artery aneurysms and third nerve palsy. They compared the outcome of endovascular coiling versus surgical clipping. The result of their analysis favors surgical clipping over endovascular coiling. Half of their patients presented with subarachnoid hemorrhage; the other half presented with only mass effect. We notice that the most important aspect that has significant bearing on the outcome, i.e., the etiopathogenic mechanism of the third nerve palsy was not analyzed in this timely study. There are four different mechanisms that can be postulated in cases of aneurysmal third nerve palsy: 1) the direct “pressure effect” of the aneurysm upon the nerve, 2) the “pulsating/ throbbing” effect of the aneurysm, 3) the “irritating” effect of the subarachnoid blood in patients with ruptured aneurysms, and 4) a “combination” of one or more of the above. We think that the final outcome is as much a function of the pathogenic mechanism of the third nerve palsy as of the treatment modality selected. In our experience, surgical clipping and, thereby, decompression of the nerve is a preferable method of treatment if the size and site of the aneurysm indicate that the nerve is simply mechanically compressed. On the contrary, if the effect is thought to be solely owing to irritation by subarachnoid blood with a small aneurysm not in direct apposition with the nerve, endovascular intervention should ideally produce comparable results to that of surgery. Perhaps the major dilemma regarding decision-making arises in cases in which the third nerve palsy is thought to be purely owing to the “pulsatility” effect alone. In theory, if this is an isolated cause, endovascular obliteration of the aneurysm should produce satisfactory results. However, in the absence of robust supportive data, we prefer to err on the surgical side for such cases and have not been disappointed so far. Although our own observations are entirely in agreement with the authors' conclusions in general, unless the pathogenic mechanism responsible for the oculomotor nerve palsy is taken into consideration, we doubt if a multicenter study such as that suggested by the authors will produce meaningful results. Nassir Mansour Kishor A. Choudhari Belfast, United Kingdom

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To the Editor: We read with interest the article by Chen et al. (2), who analyzed 13 patients with posterior communicating artery aneurysms and third nerve palsy. They compared the outcome of endovascular coiling versus surgical clipping. The result of their analysis favors surgical clipping over endovascular coiling. Half of their patients presented with subarachnoid hemorrhage; the other half presented with only mass effect. We notice that the most important aspect that has significant bearing on the outcome, i.e., the etiopathogenic mechanism of the third nerve palsy was not analyzed in this timely study. There are four different mechanisms that can be postulated in cases of aneurysmal third nerve palsy: 1) the direct “pressure effect” of the aneurysm upon the nerve, 2) the “pulsating/ throbbing” effect of the aneurysm, 3) the “irritating” effect of the subarachnoid blood in patients with ruptured aneurysms, and 4) a “combination” of one or more of the above. We think that the final outcome is as much a function of the pathogenic mechanism of the third nerve palsy as of the treatment modality selected. In our experience, surgical clipping and, thereby, decompression of the nerve is a preferable method of treatment if the size and site of the aneurysm indicate that the nerve is simply mechanically compressed. On the contrary, if the effect is thought to be solely owing to irritation by subarachnoid blood with a small aneurysm not in direct apposition with the nerve, endovascular intervention should ideally produce comparable results to that of surgery. Perhaps the major dilemma regarding decision-making arises in cases in which the third nerve palsy is thought to be purely owing to the “pulsatility” effect alone. In theory, if this is an isolated cause, endovascular obliteration of the aneurysm should produce satisfactory results. However, in the absence of robust supportive data, we prefer to err on the surgical side for such cases and have not been disappointed so far. Although our own observations are entirely in agreement with the authors' conclusions in general, unless the pathogenic mechanism responsible for the oculomotor nerve palsy is taken into consideration, we doubt if a multicenter study such as that suggested by the authors will produce meaningful results. Nassir Mansour Kishor A. Choudhari Belfast, United Kingdom

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Available abstract

To the Editor: We read with interest the article by Chen et al. (2), who analyzed 13 patients with posterior communicating artery aneurysms and third nerve palsy. They compared the outcome of endovascular coiling versus surgical clipping. The result of their analysis favors surgical clipping over endovascular coiling. Half of their patients presented with subarachnoid hemorrhage; the other half presented with only mass effect. We notice that the most important aspect that has significant bearing on the outcome, i.e., the etiopathogenic mechanism of the third nerve palsy was not analyzed in this timely study. There are four different mechanisms that can be postulated in cases of aneurysmal third nerve palsy: 1) the direct “pressure effect” of the aneurysm upon the nerve, 2) the “pulsating/ throbbing” effect of the aneurysm, 3) the “irritating” effect of the subarachnoid blood in patients with ruptured aneurysms, and 4) a “combination” of one or more of the above. We think that the final outcome is as much a function of the pathogenic mechanism of the third nerve palsy as of the treatment modality selected. In our experience, surgical clipping and, thereby, decompression of the nerve is a preferable method of treatment if the size and site of the aneurysm indicate that the nerve is simply mechanically compressed. On the contrary, if the effect is thought to be solely owing to irritation by subarachnoid blood with a small aneurysm not in direct apposition with the nerve, endovascular intervention should ideally produce comparable results to that of surgery. Perhaps the major dilemma regarding decision-making arises in cases in which the third nerve palsy is thought to be purely owing to the “pulsatility” effect alone. In theory, if this is an isolated cause, endovascular obliteration of the aneurysm should produce satisfactory results. However, in the absence of robust supportive data, we prefer to err on the surgical side for such cases and have not been disappointed so far. Although our own observations are entirely in agreement with the authors' conclusions in general, unless the pathogenic mechanism responsible for the oculomotor nerve palsy is taken into consideration, we doubt if a multicenter study such as that suggested by the authors will produce meaningful results. Nassir Mansour Kishor A. Choudhari Belfast, United Kingdom

Key concepts: Medicine, Clipping (morphology), Oculomotor nerve palsy, Subarachnoid hemorrhage, Surgery, Aneurysm, Posterior communicating artery, Palsy

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