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 . Tinnitus it can be classified as pulsatile and non-pulsatile or objective and subjective. Pulsatile tinnitus is less common than non-pulsatile and can be due to vascular tumour such as glomus or vascular abnormality. AICA loops in the cerebellopontine cistern have been implied in causing auditory and vestibular symptoms, as well as hemifacial spasm, resulting from compression of the VII and VIII cranial nerves.
The vessels can be classified according to their anatomic location:
type I: lying only in the CPA, but not entering the internal auditory canal (IAC)
type II: entering, but not extending >50% of the length of the IAC
type III: entering and extending >50% of the length of the IAC
It is important to evaluate the presence of vascular contact and the angulation of eighth cranial nerve at the contact point, as specific signs of vascular compression.
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. This pathology is described as vascular compression syndrome (VCS) which is caused by direct contact between a blood vessel and a cranial nerve. Initially, the hypothesis of VCS was suggested by McKenzie in 1936 and later, discussed by Jannetta in 1975, to refer to cranial nerve dysfunction.[1]
Vestibulocochlear compression syndrome
Microvascular compression of the vestibulocochlear nerve is known to cause disabling tinnitus and vertigo. Abnormal ABR, brief spells of vertigo, unilateral sensorineural hearing loss, abnormal vestibular findings, continuous tinnitus, hearing loss, abnormal electronystagmogram, and other findings have been reported to be diagnostic for neurovascular compression of the eighth cranial nerve.
Microscopic view of the longitudinal loop that the small branch from the AICA made around the facial nerve.
Pathophysiology
Various explanations were assumed to explain the impaired nerve’s function as an effect of vascular compression. Early in 1945, Sunderland et al. 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 [2]. The pulsatile vascular compression may result in nerve demyelination and/or fixation of the artery to the nerve by arachnoid adhesions [3]. 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 [4]. 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 [5].
An improvement in dysfunctional hyperactivity of the 8th cranial nerve was detected after microvascular decompression, which favored relation to the existence of a vascular loop .[5] 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 .[6]
Investigations
Highly sensitive MRI techniques have made it possible to investigate the relationship between intracranial vessels and nerves in a non-invasive manner. Volumetric sequences with strong T2 weighting (constructive interference in steady state imaging, fast imaging employing steady-state acquisition, and balanced fast-field echo imaging) present advantages over conventional angiographic examinations, given that, in addition to being non-invasive.
Different types of vascular contact in CISS images of the CPA and IAC with white arrows pointing to the vascular loop and the black arrows pointing to the corresponding 8th cranial nerve. (a) no contact, (b) direct contact, and (c) direct contact with mild angulation
Treatment
Microvascular decompression (MVD) of the vestibulocochlear nerve has been reported to be an efficient treatment option with high success rates of up to 80% for several vestibulocochlear compression syndromes. MVD for the vestibulocochlear nerve has successfully been performed for vessels compressing the nerve over its entire segment in the cerebellopontine angle. Several studies reported a complete recovery or marked improvement of subjective symptoms in 100% of the patients with vertigo and 65.5% of the patients with tinnitus. However, it is still difficult to consider neurovascular compression of the eighth cranial nerve as a major cause of disabling vertigo and tinnitus.
References
1.Jannetta PJ (1975) Neurovascular cross-compression in patients with hyperactive dysfunction symptoms of the eighth cranial nerve. Surg Forum 26:467–469
2.Applebaum EL, Valvassori GE (1984) Auditory and vestibular system findings in patients with vascular loops in the internal auditory canal. The Annals of otology, rhinology & laryngology Supplement 112:63–70
3.Jannetta PJ (1980) Neurovascular compression in cranial nerve and systemic disease. Ann Surg 192:518–525
4.Brunsteins DB, Ferreri AJ (1990) Microsurgical anatomy of VII and VIII cranial nerves and related arteries in the cerebellopontine angle. Surgical and radiologic anatomy : SRA 12:259–265
5.Jannetta PJ (1997) Outcome after microvascular decompression for typical trigeminal neuralgia, hemifacial spasm, tinnitus, disabling positional vertigo, and glossopharyngeal neuralgia (honored guest lecture). Clin Neurosurg 44:331–383
6.Nowe V, De Ridder D, Van de Heyning PH, Wang XL, Gielen J, Van Goethem J et al (2004) Does the location of a vascular loop in the cerebellopontine angle explain pulsatile and non-pulsatile tinnitus? Eur Radiol 14:2282–2289