Anosmia after anterior communicating artery aneurysm endovascular treatment
Pathogenesis
The cause of anosmia after coiling for ruptured aneurysms remains elusive; severity of the initial hemorrhage or long lasting hydrocephalus may be contributing factors 1).
In patients with subarachnoid hemorrhage (SAH), anosmia has mainly been reported after surgery for anterior communicating artery aneurysms. Olfactory dysfunction after SAH caused by rupture of the ACoA are very frequent and were present in both treatment groups (aneurysmal clip placement and coil embolization).
Cerebral vasospasm and frontal lobe lesions are related to worse performance on an olfactory testing in patients undergoing endovascular coil embolization 2).
Both clip treatment and SAH contribute to the occurrence of anosmia, with different chances of improvement. Olfactory dysfunction occurs in almost all patients on the side of surgery and can occur subclinically after coil deployment 3).
Its occurrence after coiling suggests not only damage to the olfactory nerve by clipping but also that the SAH itself plays a role in its pathogenesis 4).
Case series
Bor et al. interviewed all patients who resumed independent living after SAH treated with coiling between 1997 and 2007. We assessed by means of logistic regression analyses whether risk of anosmia was influenced by site of the ruptured aneurysm, neurological condition on admission, amount of extravasated blood, hydrocephalus, and treatment for hydrocephalus.
Of 197 patients, 35 (18%; 95%CI:12 to 23) experienced anosmia. Anosmia had improved in 23 (66%) of them; in 20 the recovery had been complete after a median period of 6 weeks (SD +/-6.5). Intraventricular hemorrhage was a risk factor for anosmia (OR 2.4; 95%CI:1.0 to 5.9). Anterior aneurysm location (OR 1.1; 95%CI:0.5 to 2.3) and high amount of extravasated blood (OR 0.9; 95%CI:0.4 to 2.1) were not related to anosmia.
Anosmia occurs after coiling in 1 of every 6 SAH patients, but has a good prognosis in most patients. The cause of anosmia after coiling for ruptured aneurysms remains elusive; severity of the initial hemorrhage or long lasting hydrocephalus may be contributing factors. 5).
Martin et al. studied whether and how frequently patients with ACoA aneurysms present with smell identification deficits in 2 treatment groups (endovascular and surgical treatment).
Methods: A prospective study was conducted of patients with SAH caused by ruptured ACoAs and who had a Glasgow Outcome Scale score of 1 or 2, in comparison with a control group matched by age and sex. Olfactory function was assessed using the University of Pennsylvania Smell Identification Test (UPSIT).
Results: A total of 39 patients were enrolled. A marked olfactory impairment was observed in patients with ruptured ACoAs compared with the control group (p < 0.001). Seventeen patients with ruptured ACoAs (44%) compared with 1 patient in the control group (3%) showed a smell identification deficit according to performance on the UPSIT (p < 0.001). Both groups that underwent treatment presented with olfactory impairment. Ten (59%) of 17 patients who underwent aneurysmal clip placement versus 6 (28.5%) of 21 patients who underwent coil embolization scored below the 25th percentile on the UPSIT, and surgical patients also performed worse than endovascular patients (p = 0.048). The authors observed a worse performance on the olfactory test in patients subjected to endovascular coil embolization when cerebral vasospasm (p = 0.037) or frontal cerebral lesions (p = 0.009) were present. This difference was not observed in patients who underwent surgery.
Conclusions: Olfactory disorders after SAH caused by rupture of the ACoA are very frequent and were present in both treatment groups. Cerebral vasospasm and frontal lobe lesions are related to worse performance on an olfactory test in patients undergoing endovascular coil embolization 6).
To discriminate between the effects of aneurysmal rupture and treatment, Moman et al. assessed the occurrence of anosmia after clipping and coiling of unruptured aneurysms as well as after the coiling of ruptured aneurysms.
Methods: The authors interviewed patients in whom an unruptured aneurysm was treated by clipping (32 cases) or endovascular coiling (26 cases) as well as patients with SAH who underwent coil therapy (32 cases). A geographically defined subset of 20 patients per group was invited to undergo olfactory testing.
Results: Nine clip-treated patients (28% [95% CI 14-47%]) in the unruptured group reported having anosmia, and no coil-treated patient in the unruptured group (95% [CI 0-13%]) reported having anosmia; in the SAH group, 7 patients (22% [95% CI 9-40%]) reported having anosmia. Anosmia had improved over time in 3 of the clip-treated patients and in all but 1 of the patients with SAH. Examination revealed olfactory disturbance in 13 (65% [95% CI 41-85%]) of the clip-treated and 8 (42% [95% CI 20-67%]) of the coil-treated patients with unruptured aneurysms, and also in 7 (35% [95% CI 15-59%]) coil-treated patients with SAH. In 20 patients who underwent clip therapy for unruptured aneurysms, 19 (95% [95% CI 75-100%]) had olfactory dysfunction on the side ipsilateral to surgery (anosmia reported by 8 of them).
Conclusions: Both clip treatment and SAH contribute to the occurrence of anosmia, with different chances of improvement. Olfactory dysfunction occurs in almost all patients on the side of surgery and can occur subclinically after coil deployment. 7).
Wermer et al. studied the prevalence, predisposing factors (aneurysm site and type of treatment), impact, and prognosis of anosmia in patients with SAH.
Of the patients with SAH who resumed independent living, we included all patients treated by coiling between 1997 and 2003 and a sample of patients treated by clipping between 1985 and 2001. Patients underwent structured interviews regarding the presence and duration of anosmia. The impact of anosmia was scored using a visual analog scale ranging from 0 (no influence) to 100 (the worst thing that ever happened to them). Risk factors for anosmia were assessed by logistic regression analysis.
Overall, 89 of the 315 interviewed patients (28%; 95% confidence interval [CI], 23-34%) reported anosmia after SAH (mean follow-up period, 7.4 yr), including 10 (15%) of the 67 coiled patients and 79 (32%) of the 248 clipped patients. The median visual analog scale impact score was 53 (range, 0-100). In 20 of the 89 patients (23%; 95% CI, 15-33), the symptoms had improved over time. Risk factors for anosmia were treatment by clipping (odds ratio [OR], 2.7; 95% CI, 1.3-5.7) and anterior communicating artery aneurysms (OR, 2.0; 95% CI, 1.2-3.3).
Anosmia after SAH has a high prevalence, considerable impact, and poor prognosis. Its occurrence after coiling suggests not only damage to the olfactory nerve by clipping but also that the SAH itself plays a role in its pathogenesis. 8)
Nozaki et al. described a patient with bilateral persistent primitive olfactory arteries associated with an unruptured saccular aneurysm on the left persistent primitive olfactory artery. Seven reported cases with this anomalous artery including ours are reviewed and classified into two variants. This anomalous artery arises from the terminal portion of the internal carotid artery and courses anteromedially along the ipsilateral olfactory tract and makes a hair-pin curve posterior to the olfactory bulb, becoming the distal anterior cerebral artery (variant 1) or the ethmoidal artery (variant 2). Out of 7 reported cases, 4 cases are associated with saccular aneurysms. The aneurysm in variant 1 is located on the hair-pin curve at which an apparent arterial branch is sometimes absent. Two patients suffer from anosmia. Persistent primitive olfactory artery should be kept in mind because of its high association with intracranial saccular aneurysms and unique clinical presentation. 9).