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Vascular loops at the Cerebellopontine angle: Is there a correlation with tinnitus?




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.