Surgical Anatomy of the Labyrinthine and Subarcuate Arteries and Clinical Implications.

OBJECTIVE: To study the surgical anatomy of the labyrinthine artery (LA) and the subarcuate artery (SA), their anatomic relationships, and clinical implications, as injury of the LA can result in hearing loss. METHODS: Ten formalin-fixed, latex-colored specimens were studied (20 sides). After retrosigmoid craniotomy and neurovascular dissection under microscopic magnification, 4-mm 0° and 30° endoscopic lenses were used to improve visualization. Results were statistically analyzed. RESULTS: The LA was a constant artery that followed the vestibulocochlear nerve into the internal auditory canal. The SA was an inconstant artery that ended in the dura mater around the subarcuate fossa in 35% of cases. The LA originated from the anterior inferior cerebellar artery in 89.3% of specimens and from the basilar artery in 10.7% of specimens. The SA branched off from the anterior inferior cerebellar artery when present. The origin of the LA was inferomedial to the vestibulocochlear nerve in most cases (71.4%), whereas the SA was usually lateral (70%). The distal portion of the LA was inferomedial to the vestibulocochlear nerve in 71.4% of cases. The distal portion of the SA was superolateral to the nerve in all cases (P < 0.00001). CONCLUSIONS: Knowledge of the different trajectory and anatomic relationship of the LA and the SA with the vestibulocochlear nerve is of paramount importance to differentiate them during surgery. The LA is usually inferomedial to the vestibulocochlear nerve at its distal and proximal aspects, whereas the SA usually originates lateral and ends superolateral to the nerve.

Ruptured intrameatal AICA aneurysms--a report of two cases and review of the literature.

BACKGROUND: Aneurysms of the distal part of the anterior-inferior cerebellar artery (AICA) are rare. Most are located in the cerebellopontine angle close to the internal auditory meatus. To our knowledge, only 13 patients with the aneurysm located inside the internal auditory meatus have been reported in the literature. METHOD AND FINDINGS: We present two cases of ruptured intrameatal AICA aneurysms that were treated in our center in the past year. The locations and clinical manifestations are discussed and all 13 previously published cases are reviewed. CONCLUSION: Exposure and decompression of all structures in the internal auditory meatus, careful manipulation of the nerves and vessels, temporary trapping of the aneurysm, and careful dissection of the neck to avoid partial clipping are the essential steps when treating intrameatal AICA aneurysms to reduce the risk of postoperative neurological deficits.

Acute vertigo and sensorineural hearing loss from infarction of the vestibulocochlear nerve: A case report.

RATIONALE: Acute unilateral audiovestibulopathy is a common neurotological syndrome. Differential diagnoses of acute unilateral audiovestibulopathy include viral infection, vascular insults, and tumors. Regarding vascular causes, ischemic stroke in the anterior inferior cerebellar artery (AICA) territory is known to be the leading cause of acute audiovestibular loss. Previous reports of AICA infarction with audiovestibulopathy failed to demonstrate magnetic resonance imaging (MRI)-positive vestibulocochlear infarctions. Only 1 report demonstrated acute infarction involving the vestibulocochlear nerve on diffusion weighted imaging (DWI)-MRI. PATIENT CONCERNS: A 67 year old man complained of sudden left hearing loss and vertigo. The patient showed left horizontal gaze-evoked nystagmus (GEN) and the head impulse test (HIT) was positive on the left side. Videonystagmography revealed spontaneous rebound nystagmus toward the right side; head-shaking nystagmus toward the right side. The patient presented with left caloric paresis (20.1%). Pure tone audiometry (PTA) revealed severe sensorineural hearing loss on the left side. DIAGNOSIS: MRI of temporal bone showed multifocal acute infarctions in the left inferior cerebellum. Moreover, images revealed tiny infarctions along the left vestibulocochlear nerve and the cochlea, implying acute vestibulocochlear nerve and labyrinthine infarction. There was no evidence of steno-occlusion of major cerebral vessels on MR angiography. INTERVENTIONS: Immediate stroke management was done. OUTCOMES: Neurological symptoms gradually improved after 3 to 5 days. LESSONS: We present a case illustrating a rare but significant finding of vestibulocochlear nerve infarction revealed by DWI-MRI. Prompt imaging protocol enabled the detection of significant findings in this patient with acute unilateral audiovestibulopathy. Clinicians should be aware of the vestibulocochlear nerve and labyrinth on MRI in patients with cerebellar stroke.

Is microvascular compression of the vestibulocochlear nerve a cause of unilateral hearing loss?

OBJECTIVES: We sought to confirm earlier findings in the literature that microvascular compression of the vestibulocochlear nerve might cause unilateral sensorineural hearing loss. We measured the length and width of the internal auditory canal (IAC) to investigate a possible association between a narrow porus, the presence of an anterior inferior cerebellar artery (AICA) loop, and the development of a microvascular compression syndrome. METHODS: We performed a prospective blinded analysis of 167 magnetic resonance imaging scans of the cerebellopontine angle. The presence of an AICA loop was scored. We analyzed these 167 patients for unilateral sensorineural hearing loss, which was defined as an interaural difference of 20 dB at 1 frequency or 10 dB at 2 or more frequencies. Furthermore, the width and length of the IAC on magnetic resonance imaging were measured. RESULTS: An AICA loop was identified in 94% of the 167 patients. There were 196 type I loops, 106 type II loops, and 14 type III loops. Sixty-six patients had unexplained unilateral hearing loss. There was no association between type II and III vascular loops, the width of the IAC, and unilateral hearing loss (p > .05). CONCLUSIONS: In this study we found no association between the depth of extension of the AICA loop into the IAC and the presence of unilateral hearing loss.

Internal auditory artery infarction: clinicopathologic correlation.

OBJECTIVE: To study the pathophysiology of labyrinthine infarction. BACKGROUND: The syndrome of sudden onset vertigo or hearing loss is commonly attributed to inner ear vascular disease, yet histologic studies of isolated labyrinthine infarction in humans have been rare and have not included a complete examination of the vertebrobasilar vascular system. METHODS: Temporal bones, brainstem, cerebellum, and the supplying blood vessels were subjected to gross and microscopic postmortem examinations in a 92-year-old woman who had a sudden onset of vertigo and hearing loss in the right ear 7 years before death. RESULTS: There were prominent atherosclerotic changes at the vertebrobasilar junction, but the internal auditory artery and its branches were patent on both sides. Histologic studies showed degenerative changes in the cochlea and vestibular labyrinth on the right. The posterior canal ampulla and saccular macule were relatively preserved showing partial areas of intact sensory epithelium with underlying nerve fibers. The right vestibulocochlear nerve showed a fibrotic scar and multiple patchy areas of degeneration. These findings are most consistent with a transient period of reduced perfusion of the internal auditory artery. CONCLUSION: The partial sparing of the inferior vestibular labyrinth may indicate a decreased vulnerability to ischemia because of its better collateral blood supply.

P-glycoprotein expression in capillary endothelial cells of the 7th and 8th nerves of guinea pig in relation to blood-nerve barrier sites.

Expression of P-glycoprotein (P-gp) was detected by immunohistochemical staining and Western blot analysis in the peripheral nerves (7th and 8th nerves) of the guinea pig using anti-P-gp monoclonal antibody C219. P-gp was detected in the capillary endothelial cells of these nerves. Immunoreactivity in these nerves was similar to that in the brain. Besides these nerves, positive staining was observed in the sciatic nerve, although immunoreactivity was somewhat lower than that of the 7th and 8th nerves. The present investigation suggested that P-gp in the endothelial cells of the peripheral nerves might play a very important role as a part of the blood-nerve barrier function, since P-ag acts as an extension pump in these cells.

Microsurgical relationships of the anterior inferior cerebellar artery and the facial-vestibulocochlear nerve complex.

The relationship of the anterior inferior cerebellar artery (AICA) to the facial (7th) and vestibulocochlear (8th) nerves was studied using 3x to 20x magnification in 50 cerebellopontine angles (CPAs) from 25 adult cadavers. The AICA originated from the basilar artery as a single (72% of the CPAs), duplicate (26%), or triplicate (2%) artery. Each of the 50 CPAs had one or more arterial trunks that coursed in close proximity to the 7th and 8th cranial nerves and thus were said to be nerve-related. The nerve-related arterial trunks were divided into three segments based on their relationship to the nerves and meatus: the premeatal, meatal, and postmeatal segments. The meatal segment projected to the meatus or into the canal in 64% of the CPAs. In relation to the nerves, the premeatal segment was most commonly anteroinferior, the meatal segment was inferior, and the postmeatal segment was posteroinferior. The nerve-related branches of the AICA gave rise to internal auditory arteries in 100% of the 50 CPAs, recurrent perforating arteries in 82%, and the subarcuate artery in 72%. The internal auditory and recurrent perforating arteries arose most commonly from the premeatal segment, and the subarcuate artery arose most commonly from the postmeatal segment. There were one to four internal auditory arteries per CPA, zero to three recurrent perforating arteries, and zero or one subarcuate artery. The effects of occlusion of the nerve-related arteries and their involvement in conditions treated by neurosurgeons are reviewed.

Deterioration of auditory evoked potentials during cerebellopontine angle manipulations. An interpretation based on an experimental model in dogs.

Evoked action potentials from the internal auditory meatus portion of the cochlear nerve (IAM-EAP's) and brain-stem auditory evoked potentials (BAEP's) from the vertex were simultaneously recorded during cerebellopontine angle (CPA) manipulations (retractions of the cerebellar hemisphere and the cochlear nerve) in dogs. The BAEP changes noted in these dogs were the same as those seen in patients. The IAM-EAP's showed graded deterioration related to BAEP changes. The results are as follows: Prolongation of the I-V interpeak latency of BAEP's, the most common finding during CPA manipulations, is the reflection of prolongation of the I-II interpeak latency, which is caused by conduction impairment or block of the nerve impulses between the extracranial portion of the cochlear nerve and the brain stem. The operative manipulations representing stretch or compression injury to the cochlear nerve in the CPA leads to an acute traumatic cranial nerve root lesion--a retrocochlear lesion. The obliteration of all BAEP components including wave I cannot be caused by conduction block. This is caused by occlusion of the internal auditory artery. Wave I of the BAEP's and the P1-N1 complex of the IAM-EAP's are important indicators of cochlear blood flow during surgical intervention. As possible causes of internal auditory artery obstruction, mechanical distortion of the relationship between the anterior inferior cerebellar artery (AICA) and the internal auditory artery at the junctional portion, mechanical vasospasm of the AICA-internal auditory artery complex, and ensuing no-reflow phenomena are discussed. Evoked action potentials are expected to be a useful intraoperative real-time monitor during CPA surgery that can detect rapid changes derived from cochlear artery insufficency. The real-time aspects can overcome some of the disadvantages of BAEP monitoring.

Neurovascular decompression of the eighth cranial nerve in patients with hemifacial spasm and incidental tinnitus: an alternative way to study tinnitus.

OBJECT: The authors sought to clarify the clinical characteristics of tinnitus resulting from neurovascular compression (NVC) of the eighth cranial nerve. METHODS: The authors explored the eighth cranial nerve in the cerebellopontine cistern during neurovascular decompression (NVD) of the facial nerve in 10 patients with hemifacial spasm who suffered from incidental tinnitus on the same side. The diagnosis of NVC of the eighth cranial nerve was confirmed in all patients. This condition was found in only seven of 114 patients with hemifacial spasm alone, indicating that NVC of the eighth cranial nerve is one of the causes of tinnitus (p < 0.001, chi-square test). The tinnitus resolved or was markedly improved after NVD of the eighth cranial nerve in eight patients (80%). Both pulsatile and continuous tinnitus responded well to NVD. All patients experienced various degrees of sensorineural hearing disturbance, but other neurotological examinations provided poor diagnostic value. CONCLUSIONS: It is the authors' opinion that sensorineural hearing loss and positive findings on magnetic resonance imaging are the most reliable evidence for the presence of tinnitus caused by NVC of the eighth cranial nerve.

Ultrastructure of astrocytes in the transitional region of the human eighth cranial nerve.

The nerve root segment where the transition from central to peripheral nervous tissue occurs is referred to as the transitional region (TR). Part of the TR is a continuation of the subpial glial limiting membrane (SGLM) which covers the surface of the brain. To assess the physiological and pathophysiological roles of astrocytes in the TR of the human eighth cranial nerve, electron microscopy was performed on surgically resected specimens of the eight cranial nerve root obtained from patients with cerebellopontine angle tumors. The astrocytic glial dome was sharply bounded by a basement membrane and was mainly composed of the bodies and processes of fibrous astrocytes. Desmosomes and gap junctions were found between these astrocytic processes. Half-desmosomes were found on the edge of the astrocytic glial dome and at the luminal surface of the perivascular glial limiting membrane. These ultrastructural features indicate that the astrocytes of the TR might have some motility capacity that allows adjustment to changes in the pressure exerted by the vessels, the peripheral nervous tissue, and the cerebrospinal fluid. In addition, it is also suggested that lack of structures linking the central and peripheral portions of the nerve and the abrupt change of nerve composition at the TR might predispose this area to injury by tractional forces or pathologic conditions such as tumor or arterial compression.