Though the concept of vascular compression has been adopted for hemifacial spasm and trigeminal neuralgia, contradictory results have been reported about the relationship between VCS and neuro-otologic symptoms. Īn improvement in dysfunctional hyperactivity of the 8th cranial nerve was detected after microvascular decompression, which favored relation to the existence of a vascular loop. Impaired blood flow through the vascular loop as a direct result of neurovascular compression was suggested to result in reduced vascular perfusion of the cochlea and vestibule leading to dysfunction. It was also proposed that the arterial elongation and brain “sag” related to the aging process may result in cranial nerve cross-compression in the CPA. The pulsatile vascular compression may result in nerve demyelination and/or fixation of the artery to the nerve by arachnoid adhesions. assumed that the proximity between the AICA and the nerves within the narrowed space of the IAC possibly produce nerve conduction disturbance due to the applied mechanical pressure via atheromatous, tortuous, or pulsating vessels. Various explanations were assumed to explain the impaired nerve’s function as an effect of vascular compression. Initially, the hypothesis of VCS was suggested by McKenzie in 1936 and later, discussed by Jannetta in 1975, to refer to cranial nerve dysfunction. This pathology is described as vascular compression syndrome (VCS) which is caused by direct contact between a blood vessel and a cranial nerve. It has been proposed that compression of the vestibulocochlear nerve (8th cranial nerve) by a vascular loop of the anterior inferior cerebellar artery (AICA) could be the causative factor resulting in the otologic symptom. However, in absence of inner ear disease, the exact cause is not always recognized. Tinnitus, sensorineural hearing loss (SNHL), and vertigo are common audio-vestibular symptoms and they are well-known classic triad in inner ear disease involving the membranous labyrinth. Therefore, presence of vascular loops in contact with the 8th cranial nerve is not certainly considered pathological but possibly to be a normal anatomical coincidental finding. No possible role of the presence of vascular loop/contact was identified in causing tinnitus, deafness, or vertigo as evaluated by 3D-CISS sequence. No statistically significant association was detected between the presence of different grades of vascular loop or types of vascular contact and any of the studied audio-vestibular symptoms. All MRI examinations were performed by using a 3 T (Magnetom Verio 3 T Siemens Medical Solutions, Erlangen, Germany). The non-symptomatic ears in the patients were added to the healthy control group. The healthy control group with no symptoms in either ear, n = 60 (120 ears): 32 females and 28 males. The study included 98 patients (196 ears) 51 females and 47 males with audio-vestibular dysfunction symptoms in isolation or combined 40 patients with tinnitus, 50 with sensory neural hearing loss, and 32 with vertigo. We aimed to evaluate the association of audio-vestibular symptoms with the presence of vascular loops and vascular contact in cerebellopontine angle (CPA) and the internal auditory canal (IAC) using 3Tesla MRI. This high sensitivity is a result of its inherent ability to accentuate the T2 values between cerebrospinal fluid (CSF) and adjacent anatomical or pathological structures. Three-dimensional (3D) constructive interference in steady state (CISS) is a fully refocused gradient-echo magnetic resonance imaging (MRI) sequence that has high sensitivity in evaluation of the cranial nerves. Some studies show that the etiology could be related to the presence of a vascular loop in contact with the 8th cranial nerve. Many diseases are associated with these symptoms however, the exact cause is not always identified. Tinnitus, sensory neural hearing loss (SNHL), and vertigo are common audio-vestibular symptoms.
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