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27.04.2016
Introduction: The vascular compression by redundant vessels under the VIII cranial nerves has been studied since the 80's, and many authors proposed correlations between the compression and the otoneurological findings (vertigo, tinnitus, hypoacusis, audiometry and electrophysiological findings).
INTRODUCTIONVascular compression by anomalous or redundant vessels over cranial nerves, and the establishment of statistically relevant correlation between compression and the neurological symptoms have been studied by several authors since the 1930'sVascular loop causing compression of the 5th cranial nerve resulting in trigeminal neuralgia was firstly suggested by DANDY in 1934 (1), and later, by GARDNER and MIKLOS (2) in 1959. Neurotology findings in patients with diagnosis of vascular loop of cranial nerves VIII in magnetic resonance imaging. Objective: Analyze and correlate the different signs and otoneurological symptoms, the audiological findings and its incidence over individuals with Vascular Loop (VL) diagnosis of VIII cranial nerves by magnetic resonance imaging (MRI). This concept was then extensively expanded to try to explain disorders of various cranial nerves. Mendes2, Ronaldo Vosguerau3, Marcos Mocellin4, Maria Theresa Costa Ramos de Oliveira3, Heloisa Nardi Koerner3. Method: Retrospective study through the analysis of medical records of 47 patients attended in the otoneurology clinic of Clinical Hospital of UFPR. These presentations are known as compressive syndromes, which include hemifacial spasms, glossopharyngeal neuralgia, geniculate neuralgia, and, more recently, a syndrome of the compression of the vestibule-cochlear nerve. Though MCKENZIE (3) suggested in 1936 that the Meniere Disease might be caused by an abnormal relation of the anterior inferior cerebellar artery (AICA) with the 8th cranial nerve, this concept was not reintroduced until 1975, when JANETTA (4) proposed that the redundant arterial loops at the cerebellar angle point (CAP) might interfere with the eight cranial pair resulting in symptoms of grave vertigo, tinnitus and auditory sensory neural loss. Results: The tinnitus was the most frequent symptom, in 83% of the patients, followed by hypoacusis (60%) and vertigo (36%).
All pathophysiological theories are based on a common theme: a redundant vessel adhering to a cranial nerve causing chronic ectopic excitation. The audiometry presented alterations in 89%, the brainstem evoked auditory potential in 33% and the vecto-electronystagmography in 17% of the patients.
Was not found statistically significant relation between the buzz or hypoacusis, and the presence of VL in MRI. It was suggested that this pathological procedure was restricted to the entrance area of the cranial nerve root, that being the junction area between central and peripheral myelin, where defects might occur. Only 36% of patients had complaints of vertigo, the main symptom described in theory of vascular compression of the VIII pair of nerve. LANG showed that the central segment of the 8th cranial pair has a length of 10mm (6 to 15 mm) and an intracisternal length of 15mm (8,5 to 22mm).
As in the audiometry and in brainstem evoked auditory potential was not found a statistically significant relation between the exam and the presence of the VL in the RMI. He found the transition area of the eight cranial nerve varying from the brainstem to the bottom of the Inner Auditory Canal (IAC). Conclusion: The results show independence between the findings of the RMI, clinical picture and audiological results (p>0,05) suggesting that there are no exclusive and direct relation between the diagnosis of vascular loop in the MRI and the clinical picture matching.


The known histology would be consistent with the occurrence of a syndrome of neurovascular compression of the eight cranial nerve, in any point of the trajectory, since the brainstem to the IAC. The existence of Vascular Compression Syndromes (VCS), and especially here with the compression of the VIII pair, was initially inferred by analogy to the hemifacial spasm syndrome, in which is well accepted that the cause is an aberrant vessel compressing the nerve. JANNETTA and MOLLER (5), from Pittsburgh, EUA, were the pioneers in the diagnosis and treatment of this disease. However, in other vascular compression syndromes proposed by the same authors (trigeminal neuralgia, glossopharyngeal neuralgia, etc.) they were not related and accepted as consequence of the vascular compression.
Though the goal was to separate the effect of the vessel over the nerve, other authors (6, 7) questioned if this procedure would simply damage the structure of the VIII pair, or was totally unjustified. Thus, despite countless articles published about this condition, the mere existence of VCS is still questioned. VCS's symptoms are unspecific and can easily be found in other conditions such as Meniere Disease, migraine or just innate movement intolerance. AEPB findings proposed by MOLLER (9) as characteristic of VCS would not be considered by many authors, such as SCHWABER and HALL (6, 7). The variability of vascular anatomy of the CAP and the inner auditory canal (IAC) in normal people contributed to the controversy around the concept of vascular compression syndromes.
Both post-mortem and radiologic studies investigated the place of the vascular loop formed by AICA in CAP (12, 13, 14).
The results showed considerable discrepancies, though all studies indicate that vascular loops would enter on IAC in a minority of patients.In essence, VCS of the VIII pair is a syndrome of vestibular symptoms (quick vertigo, combined with intolerance to moviment) and audiological symptoms that respond to treatment with medications for neuralgia (carbamazepine) and where other similar causes (Meniere, migraine) had been removed. The vertigo of VP is triggered by head movements and is not fatigable, as in patiants with VPPB, and its symptoms are not relieved with the use of vestibular suppressors (5). In VP patients don't have fluctuating hearing loss, characteristic of Meniere's disease.Both computerized axial tomography (CAT) and magnetic resonance (MR) with vascular loop findings still haven't proved to be specific as diagnostic aid, but new types of MR, such as FT-FISS may be more specific. An abnormal AEPB on the side of the symptoms supports the diagnostic, but a normal exam does not exclude it. Thus, the definite diagnostic is achieved only after surgical exploration, with follow-up cure.
They were submitted to the following complementary tests: audiometry, vectoelectronystagmography and AEPB, and they all had Magnetic Resonance exams with images consistent with Vascular Loop of the VIII cranial pair (Figure 1). We found that, compared with the otoneurological symptoms, the tinnitus was the most frequent, being present in 39 (83%) of the patients, followed by hypoacusis, in 28 (59,6%) and vertigo, in 17 (36,2%) of the patients.Tinnitus was present in 39 (83%) of the patients, most commonly bilaterally.
Eight patients (17%) did not complain of tinnitus.Hypoacusis appeared in 28 (59,6%) patients, with the remaining 19 (40,4%) without the complaint.
Vertigo appeared in 17 (36,2%) of patients, with 30 (63,8%) without this complaint.The audiometry presented alterations in 89,4% of the patients, with bilateral losses as the most frequent.


To the left, 5 patients (10,6%) had tinnitus and loop at the same side, and of the 19 patients with bilateral complaint, 11 (23,4%) had MR imaging of bilateral vascular loop. Eight patients (17%) of the study did not complain of tinnitus and presented vascular loop on the MR. There is independence between the localization of the vascular loop and the side of the perceived tinnitus. There is also independence between the localization of the vascular loop and the mere presence of tinnitus, independently of the side perceived, as well as the typo of tinnitus perceived, pulsatile or not.Relating the complaint of hypoacusis to the side of the loop, five out of thirteen patients with vascular loop to the right side presented hypoacusis on the same side, only one patient out of nine with vascular loop to the left side reported hypoacusis also to the left and nine out of twenty-five with bilateral loop also reported bilateral hypoacusis. There is independence both between the localization of the vascular loop and the side of the perceived hypoacusis and between the presence of vascular loop and the symptomology of hypoacusis, independently of the side it was perceived on.Regarding the audiometric results, four of the thirteen patients with vascular loop to the right presented altered audiometry of the same side, two out of nine patients with vascular loop to the left had altered audiometry to the left and sixteen of the twenty-five with bilateral loop also presented bilaterally altered audiometry.
Distribution of the AEBP results.DISCUSSIONWe observed that in the symptoms presented by patients, regarding both tinnitus and hypoacusis, there is no statistically significance between the symptom and the presence of vascular loop on the MR, be it in relation to the side perceived, or even by the mere presence of the symptom.
In tinnitus, even isolating only cases of pulsatile type, theoretically the one that would relate the most with the vascular loop, we noticed that the independence remains, and there is no direct relation between loop and tinnitus. This is also confirmed by the small number of patients of the study (7, or 14,8%) with complaint of pulsatile tinnitus.These findings corroborate those of MAKINS (15), who did not see any significant difference regarding the presence of vascular loop, between ears with signals and symptoms and healthy ears, suggesting that the presence of vascular loop on the MR is not pathologic, but an exam finding.
This independence remained in the analysis of audiologic exams (audiometry and AEBP), where the presence of vascular loop on the MR also did not present a statistically significance with the data from the audiologic exams. This reinforces the symptomatological findings, in this case without the subjectivity inherent to the symptoms. Response of trigeminal neuralgia to decompression of sensory root: discussion of cause of trigeminal neuralgia. Intracranial division of the vestibular portion of the auditory nerve for Meniere's disease.
Neurovascular cross-compression in patients with hyperactive dysfunction of the eighth cranial nerve. Moon I, Hain TC Delayed Quick Spins following Vestibular Nerve Section Respond to Anticonvulsant Medication.
Responsible Doctor of the Ambulatory of Otoneurology of the Otorhinolaryngology Service of Hospital de Clinicas of Universidade Federal do Parana.3) Radiologist Medical Doctor.
Doctor of the AID - Advanced Image Diagnosis - Curitiba - PR.4) Doctor in Otorhinolaryngology.



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