Primary TN is more commonly seen in older patients. Neurovascular compression in the elderly is likely related to arteriosclerosis, given the increasing prevalence of arteriosclerosis with age. Arteriosclerosis gradually changes the shape and conformation of the vessel, potentially causing neurovascular compression [6]. This relationship may also explain the higher incidence of arterial neurovascular compression in older TN patients. Our case was different, whereby a giant intracavernous carotid aneurysm was found impinging on the trigeminal nerve causing pain over the maxillary distribution of the left trigeminal nerve.
Intracranial aneurysms causing facial pain may have multiple locations, including supraclinoid ICA, anterior ICA, vertebrobasilar, posterior-cerebral (PCA), cavernous ICA, and trigeminal artery [7, 8]. Intracavernous carotid aneurysms are commonly complicated by cranial nerve palsies, particularly oculomotor nerve, trochlear nerve, ophthalmic and maxillary branches of the trigeminal nerve, and the abducens nerve, which transverse the cavernous sinus [9]. Despite that, they rarely cause isolated trigeminal nerve palsy but have been found to cause isolated abducens, oculomotor or trochlear nerve palsy [5, 10]. In our case, the cranial nerve involved is solely the trigeminal nerve causing constant sharp facial pain ipsilateral to the giant left ICA intracavernous aneurysm.
Diagnosis of TN warrants imaging in all cases, especially if clinical suspicions are towards the presence of compressive (vascular on non-vascular) or inflammatory lesions of the trigeminal nerve. Imaging is particularly crucial if the pain is refractory to initial medical management or if the presentation is atypical [1]. The presence of the giant left ICA aneurysm in our patient explains why the facial pain became unresponsive towards pregabalin. Other possible secondary causes of TN include arteriovenous malformations, cerebellopontine angle tumours, nasopharyngeal tumours, and multiple sclerosis [1]. These conditions can be excluded utilizing imaging, particularly MRI.
Several challenges were encountered while managing this case. Improvement of symptoms shown towards initial medical treatment with pregabalin was seen progressed to refractory after a few months. Failure of medical treatment leads to endovascular treatment, which would reduce the risk of rupture and the formation of carotid–cavernous fistula and, at the same time, relieve the facial pain. Despite effective cannulation utilizing microwire, the key obstacle in our case that led to procedure failure was the difficulty in getting the microcatheter (for stent deployment) into the internal carotid artery distal to the aneurysm. Attempts to flip micro-guidewire within the aneurysm to provide support for the microcatheter were likewise unsuccessful.
Although pregabalin showed a reduction in the early treatment period, the first-line treatment in classic TNs (neurovascular compression) is pharmacological therapy with carbamazepine or oxcarbazepine [11]. The same drugs have also been suggested in secondary TNs, although placebo-controlled trials are lacking [11]. Other alternatives include baclofen, lamotrigine, pimozide, gabapentin, pregabalin, levetiracetam, botulinum toxin Type A and phenytoin [11]. The endovascular approach is the preferred method for the treatment of intracavernous carotid aneurysms. The introduction of flow-diverter stents has been shown safe and effective with very low mortality (0–0.44%) and morbidity rates (2.3–3.1%) with nearly 100% occlusion rates [12]. Another strategy that can be used is ICA occlusion with or without bypass utilizing balloon test occlusion (BTO) test before the procedure to assess tolerability of ICA occlusion [12].
