Neurovascular conflicts of cerebellopontine angle are rare pathologies that can affect the fifth, seventh, eighth, and the ninth cranial nerves, they share the same pathophysiological mechanisms and benefit from the MRI contribution for their demonstration. Their surgical treatment is based on a microsurgical vascular decompression [1].

The aim of this study is to describe the various clinical and paraclinical aspects of neurovascular conflict of the cochleovestibular nerve and the therapeutic modalities through two cases: one revealed by unilateral tinnitus, another by a retrocochlear SNHL.

A 29-year-old patient, with no medical history, consulted for the exploration of an hypoacusis evolving since childhood and worsening gradually, with intermittent tinnitus and no notion of dizziness.

The otoscopic examination showed normal eardrums, vestibular exam showed no spontaneous or induced nystagmus, neither segmental deviation. The exploration of the other cranial nerves showed no neurological deficit and the rest of the ENT examination was without abnormalities.

The pure-tone audiometry showed right-sided sensorineural hearing loss with downward curve and an average hearing loss of 60db. Auditory evoked potentials of the brain stem have objectified an increase in latency of the right V wave, a prolonged I-V interval compared to the opposite side with interaural difference of 0.46ms.

This retrocochlear deafness motivated the realization of MRI of the EAC and the brain stem, which revealed a neurovascular conflict of the left cochleovestibular nerve, highlighted by a vascular loop of the antero-inferior cerebellar artery intersecting at right angle the nerve path in the internal auditory pore (Figure 1).

Microsurgical vascular decompression was decided in collaboration with neurosurgeons, but the patient refused any surgery.

A 26-year-old male with no medical history, consulted for isolated left-sided tinnitus without hearing loss or dizziness. Otoscopic and vestibular exams were normal as well as the rest of the ENT and other cranial pair examination.

The pure-tone audiometry and auditory evoked potentials showed normal hearing with no interval’s changes or latencies.

MRI of internal auditory canal and cerebellopontine angle in T2 sequence showed a vascular crossing of the left antero-inferior cerebral artery with the cochleovestibular nerve in the auditory meatus.

The patient was referred to the neurosurgery department for a microsurgical decompression and was lost of view.

The cranial nerves vascular compression syndrome or neurovascular conflict (NVC) includes a number of entities [3] that share between them:

• The anatomical site: cerebellopontine angle.
• The pathophysiological mechanism: an irritant thorn in contact with the root of the cranial nerve.
• Radiological exploration by the MRI.
• The therapeutic principle of decompressing the nerve and isolating the offensive vessel.

The Cerebellopontine angle is an anatomical region whose content is essentially neurovascular. Cranial nerves cross it straightly, and the vessels describe very variable and sinuous paths [6].

The anatomical contiguity between vascular and neural structures seems essential to the genesis of a NVC, but the mechanical effect is not sufficient in itself to explain it. The effect of the vascular beat against the nerve wall locally modifies its histological structure and physiological behavior [1].

Schematically, there are three competing theories to explain the pathophysiology of NVC [4] :

• The ephaptic theory: which stipulates a short circuit between axons at the level of conflict, the supposed seat of this ephaptic transmission is the Root Entry Zone (REZ).
• The nuclear theory: This supposes the aggression of nerve nuclei and beyond the nervous discharges in the direction of normal conduction.
• The mixed theory: admitting the existence of the two previous effects.

Clinical manifestations attributed to the VIIIth cranial nerve NVC are three: disabling positional vertigo, unilateral pulsatile tinnitus or steam jet tinnitus; and progressive unilateral sensorineural hearing loss [1].

Auditory evoked potentials of brainstem allow evoking retrocochlear origin of deafness in the presence of an isolated I wave, a lengthening of the I-V interval beyond 0,43ms with interaural difference of 0.3 mS [5].

MRI is the key exam in case of suspicion of a vascular compression of the cochleovestibular nerve. Radiological criterias of NVC are essentially the determination of conflict place (REZ), the deformation of neural structures and the orthogonal path of the vessel compared to the nerve path [1]. The MR angiography allows by the study of native cuts to better define the involved vessel. For the eighth cranial pair, arterial conflicts involve primarily the antero inferior cerebellar artery (AICA) [4].

The treatment of NVC is based on microsurgical vascular decompression. The surgical indication is based on a combination of clinical signs, abnormalities of AEP and neurovascular conflict on MRI. The approach is retrosigmoid and the principle of this decompression is to mobilize the responsible vessel and maintain it far from the involved nerve with a Teflon sponge which plays the role of insulation. The endoscopic control allows checking the right place of teflon and the absence of any residual contact [2].

The major risk during this decompression is the nerve damage, intraoperative monitoring of AEP represents a preventive alert of direct nerve trauma [2].

Neurovascular conflict involving the cochleovestibular nerve benefits from the contribution of the MRI which became essential, especially in front of progressive retrocochlear sensorineural hearing loss, unilateral tinnitus or disabling vertigo. It provides an important mapping for the surgical treatment based on a microsurgical vascular decompression.