Hearing preservation and intraoperative auditory brainstem response and cochlear nerve compound action potential monitoring in the removal of small acoustic neurinoma via the retrosigmoid approach.

OBJECTIVE: Hearing preservation is the main focus of small acoustic neurinoma (AN) removal. Refinement of intraoperative auditory monitoring may improve postoperative hearing. We have introduced a newly designed intracranial electrode enabling continuous monitoring of the cochlear nerve compound action potential (CNAP). We performed simultaneous monitoring of the auditory brainstem response (ABR) and CNAP during retrosigmoid small AN removal, and clarified the surgical outcome and the usefulness of CNAP monitoring. METHODS: Twenty-two consecutive patients with a small AN underwent retrosigmoid tumour removal with attempting hearing preservation. ABR and CNAP were simultaneously monitored during tumour removal. RESULTS: AN was totally removed in all patients without facial palsy. Preservation rate of useful and serviceable hearing was 82% and 91%, respectively. During microsurgical tumour removal, various surgical equipments and procedures intensified artefacts of ABR, and reliable ABR monitoring with distinct wave V was obtained in 9/22 patients. Unaffected by artefacts, reliable CNAP monitoring was obtained more frequently (in 20/22 patients) than ABR (p = 0.0005). CNAP on completion of tumour removal predicted hearing preservation with no false positive or negative (100% sensitivity and 100% specificity). CNAP changed dynamically and stepwise with surgical manipulations. CONCLUSION: The retrosigmoid approach using auditory monitoring for a small AN can accomplish total tumour removal with an excellent hearing preservation rate. CNAP provides reliable auditory monitoring more frequently than ABR, reflects the intraoperative auditory function almost in real-time, predicts postoperative hearing with excellent sensitivity and specificity, and is more useful for monitoring in the removal of small AN with hearing preservation.

Alterations in regional cerebral blood flow following brain injury in the rat.

To elucidate the temporal changes in regional cerebral blood flow (rCBF) after experimental traumatic brain injury, serial rCBF measurements were made during a 24-h period following fluid-percussion (F-P) traumatic brain injury in the rat. Brain injury of 2.2 atm was induced over the left parietal cortex and serial measurements of rCBF were performed using the radiolabeled microsphere method. rCBF values were obtained prior to injury and at 15 and 30 min and 1, 2, 4, and 24 h postinjury. At 15 min postinjury, there was a profound, wide-spread reduction in rCBF in all brain regions studied (p less than 0.05). At 30 min and 1 h postinjury, all brain regions except pons-medulla and cerebellum showed significantly reduced rCBF compared to the preinjury values (p less than 0.05). By 2 h postinjury, however, a significant focal reduction of rCBF was observed only in the cerebral tissue surrounding the trauma site (p less than 0.05); rCBF in the remaining brain regions had recovered to the preinjury levels. By 4 h postinjury, rCBF had returned to normal in all brain regions studied. This recovery of rCBF was still evident at 24 h postinjury. The present study demonstrates that, following the experimental traumatic brain injury in the rat, (a) an initial global suppression of rCBF occurs up to 1 h postinjury; (b) at the trauma site, a more persistent focal reduction of rCBF occurs; and (c) these alterations in rCBF after trauma dissolve by 4 h postinjury.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of traumatic brain injury on regional cerebral blood flow in rats as measured with radiolabeled microspheres.

To clarify the effect of experimental brain injury on regional CBF (rCBF), repeated rCBF measurements were performed using radiolabeled microspheres in rats subjected to fluid-percussion traumatic brain injury. Three consecutive microsphere injections in six uninjured control rats substantiated that the procedure induces no significant changes in hemodynamic variables or rCBF. Animals were subjected to left parietal fluid-percussion brain injury of moderate severity (2.1-2.4 atm) and rCBF values were determined (a) prior to injury and 15 min and 1 h following injury (n = 7); and (b) prior to injury and 30 min and 2 h following injury (n = 7). At 15 min post injury, there was a profound reduction of rCBF in all brain regions studied (p less than 0.01). Although rCBF in the hindbrain had recovered to near-normal by 30 min post injury, rCBF in both injured and contralateral (uninjured) forebrain areas remained significantly suppressed up to 1 h post injury. At 2 h post injury, recovery of rCBF to near-normal values was observed in all brain regions except the focal area of injury (left parietal cortex) where rCBF remained significantly depressed (p less than 0.01). This prolonged focal oligemia at the injury site was associated with the development of reproducible cystic necrosis in the left parietotemporal cortex at 4 weeks post injury. Our results demonstrate that acute changes in rCBF occur following experimental traumatic brain injury in rats and that rCBF remains significantly depressed up to 2 h post injury in the area circumscribing the trauma site.

Traumatic brain injury in the rat: characterization of a lateral fluid-percussion model.

Experimental fluid-percussion models produce brain injury by rapidly injecting saline into the closed cranium. In the present study we characterize the physiological, histopathological and neurological responses to mechanical brain injury in the rat produced by lateral fluid-percussion injury of graded severity. Physiological experiments (n = 105) demonstrated that all levels of injury produced an acute and transient systemic hypertension and bradycardia. Acute hypertension followed by significant hypotension occurred at higher magnitudes of injury. Post-injury suppression of electroencephalographic amplitude was related to the severity of injury. An increase in slow wave (delta/theta) electroencephalographic activity with a concomitant decrease in alpha/beta electroencephalographic activity were observed only at moderate and high magnitude of injury and were correlated with a worsened neurological outcome (r = 0.84; P less than 0.05) and increased mortality (r = 0.66; P less than 0.05). Alterations in brainstem auditory-evoked potentials were also observed only at the higher levels of injury. Histopathological analysis revealed that the extent of post-injury hemorrhage, cavitation and vascular disruption (as measured by extravasation of Evans Blue dye) was greater at the higher magnitudes of injury. Neurological scoring performed over a 4-week post-injury period demonstrated that lateral fluid-percussion brain injury produces a chronic neurological deficit that is directly related to the severity of injury. Survival was also significantly reduced at the higher magnitudes of injury. These data demonstrate that the lateral model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may therefore be a useful experimental model for the study of the pathophysiology of traumatic brain injury.

Magnesium deficiency exacerbates and pretreatment improves outcome following traumatic brain injury in rats: 31P magnetic resonance spectroscopy and behavioral studies.

The biochemical mechanisms mediating delayed or secondary tissue injury after central nervous system trauma remain speculative. We have demonstrated previously that traumatic brain injury in rats causes a rapid decline in tissue intracellular free magnesium [Mg]f and total magnesium [Mg]t concentrations, which were significantly correlated with injury severity. In order to examine the relationship between magnesium and traumatic brain injury, we assessed whether (1) magnesium deficiency exacerbates or (2) magnesium treatment improves posttraumatic outcome following fluid-percussion brain injury (2.0-2.4 atm) in rats. Animals placed on magnesium-deficient diet for 14 days showed a 15% decrease in brain [Mg]f as measured by phosphorus (31P) magnetic resonance spectroscopy (MRS). Magnesium deficiency significantly exacerbated neurologic dysfunction and increased mortality following injury when compared to normally fed saline-treated controls. Conversely, pretreatment with magnesium sulfate (0.1 mEq) 15 min before brain injury prevented the fall in [Mg]f observed by 31P MRS in saline-treated animals and significantly improved both cellular bioenergetic state and chronic posttraumatic neurologic outcome. These combined observations suggest that alterations in brain [Mg]f after trauma may play a role in the pathophysiology of traumatic brain injury.

Magnesium protects against neurological deficit after brain injury.

The biochemical factors that mediate secondary or delayed damage to the central nervous system (CNS) remain speculative. We have recently demonstrated that brain injury in rats causes a rapid decline in brain intracellular free magnesium (Mg2+) and total magnesium concentrations that is significantly correlated with the severity of injury. In order to further investigate the relationship between Mg2+ and brain injury, we examined the effect of Mg2+ treatment on posttraumatic neurological outcome following fluid-percussion brain injury (2.0 atm) in rats. Since administration of ATP-MgCl2 has been shown to be beneficial in a variety of models of organ ischemia, we also examined the efficacy of ATP-MgCl2 or ATP alone in the treatment of experimental brain injury. Animals treated with low (12.5 mumol) or high (125 mumol) dose MgCl2 at 30 min postinjury showed a significant dose-dependent improvement in neurological function when compared to saline-treated controls. Treatment with ATP-MgCl2 (12.5 mumol) or ATP alone (12.5 mumol) caused no significant improvement in chronic neurological outcome. MgCl2-treated animals showed no change in postinjury mean arterial blood pressure (MAP), whereas animals treated with either ATP-MgCl2 or ATP alone showed a transient but significant fall in MAP (P less than 0.01) during the drug-infusion period. Our results suggest that postinjury treatment with MgCl2 is effective in limiting the extent of neurological dysfunction following experimental traumatic brain injury in the rat.

Effects of intravascular volume expansion on cerebral blood flow in patients with ruptured cerebral aneurysms.

To clarify the effect of intravascular volume expansion on cerebral blood flow (CBF) in patients after subarachnoid hemorrhage (SAH), we performed 55 pairs of regional CBF measurements using the xenon-133 inhalation method before and after volume expansion in 35 patients with ruptured cerebral aneurysms. CBF was calculated as the hemispheric mean value of the initial slope index. To accomplish volume expansion, we transfused 500 ml of 5% human serum albumin in half an hour. After volume expansion with albumin, the hemoglobin value decreased significantly (P less than 0.005). Volume expansion did not change the mean arterial blood pressure. During the first 2 weeks after SAH, CBF decreased significantly after volume expansion (P less than 0.005). During the 3rd week after SAH and subsequently to the 4th week after SAH, volume expansion produced no change in CBF. In patients with symptomatic vasospasm, CBF decreased significantly after volume expansion (P less than 0.005). In patients without symptomatic vasospasm, volume expansion produced no change in CBF. The results of this study suggest that increasing the intravascular volume above normal by volume expansion does not increase CBF or reverse symptomatic vasospasm.

Vasospasm and regional cerebral blood flow (rCBF) in patients with ruptured intracranial aneurysm: serial rCBF studies with the xenon-133 inhalation method.

To clarify the relationship of vasospasm to the reduction of cerebral blood flow (CBF) and the delayed ischemic neurological deficit, serial rCBF studies with the use of the xenon-133 inhalation method were conducted in 35 postoperative patients with ruptured intracranial aneurysms. The CBF was calculated as an initial slope index (ISI) derived from the desaturation curve of each head probe, and the hemispheric mean value of the ISI (mean ISI) was calculated in both hemispheres. The mean ISI in the hemisphere ipsilateral to the operation was low compared to that of the contralateral hemisphere. In relation to the presence of vasospasm, angiographic findings were classified into the following five types: diffuse, peripheral, proximal-severe, proximal-mild, and no spasm. Patients with vasospasm of the diffuse, peripheral, and proximal-severe types showed a markedly decreased mean ISI, and vasospasm of the diffuse type caused the greatest degree of reduction. The mean ISI of the patients who developed delayed ischemic neurological deficit (DIND) due to vasospasm was significantly decreased (37.4 +/- 4.6) compared to that of the patients who did not develop DIND (52.2 +/- 5.6). None of 3 cases of no spasm and only 1 of 14 cases of proximal-mild spasm developed DIND. On the other hand, all of 4 cases of diffuse, 2 of 3 cases of peripheral, and 2 of 6 cases of proximal-severe spasm developed DIND. Thus, if these three types of vasospasm are joined together as severe vasospasm, 8 of 13 cases with severe vasospasm developed DIND. These results suggest that severe vasospasm causes a reduction of CBF and that the reduced CBF brings about DIND.

Effects of acute ethanol intoxication on experimental brain injury in the rat: neurobehavioral and phosphorus-31 nuclear magnetic resonance spectroscopy studies.

Using the lateral fluid-percussion model of experimental brain injury in the rat, the authors investigated the effect of acute ethanol (EtOH) intoxication on cardiovascular changes, neurological motor deficits, brain bioenergetics, and mortality associated with traumatic brain injury. Two hours after gastric administration of EtOH (low dose in 20 animals, 1.5 g/kg; high dose in 28, 3.0 g/kg) or saline (equal volume), animals were subjected to a fluid-percussion brain injury centered over the left parietal cortex. These injuries were of either moderate (X = 2.2 atm; 10 animals/treatment) or high severity (X = 3.0 atm; 18 animals/saline, 10 animals/low-dose EtOH, and 18 animals/high-dose EtOH). Neurological motor function was evaluated daily over a 1-week period, while a subset of eight animals receiving high-dose EtOH and subjected to brain injury of high severity were monitored for 4 hours using phosphorus-31 nuclear magnetic resonance spectroscopy to determine intracellular pH, free magnesium, and brain cytosolic phosphorylation potential. A significant (p < 0.05) and prolonged (up to 1 hour) hypotension was observed in animals pretreated with either low- or high-dose EtOH. Neither low-dose (blood-EtOH concentration = 110 +/- 40 mg/dl) nor high-dose (blood-EtOH = 340 +/- 70 mg/dl) EtOH had any effect on survival or neurological motor function after moderate brain injury. Following severe brain injury, animals pretreated with high-dose (blood-EtOH concentration = 352 +/- 65 mg/dl) EtOH showed a significantly increased mortality and markedly worsened neurological deficits at 24 hours postinjury. Following injury, free magnesium and cytosolic phosphorylation potential declined in both groups by approximately 50% to 60%, with no significant differences between groups with respect to these variables. In contrast, brain intracellular pH in the EtOH-treated animals was consistently higher than in the control group after injury. These data suggest that prior exposure to EtOH, particularly at high concentrations, may have detrimental effects on neurobehavioral function and survival in the acute period (up to 24 hours) after severe brain injury, and may be associated with posttraumatic cerebral alkalosis.

Recovery of hearing after removal of a large jugular foramen schwannoma: report of two cases.

BACKGROUND: Although hearing loss is a common presenting symptom of jugular foramen schwannoma (JFS), recovery of hearing after tumor removal has rarely been reported. We report two cases of a large JFS presenting with severe hearing loss and recovering normal hearing after tumor removal. METHODS AND RESULTS: Two patients complaining of progressive hearing loss each proved to have a large JFS involving the posterior fossa. The hearing losses, which exceeded 90 dB, were not associated with dysfunction of the 9th, 10th, or 11th cranial nerves. Schwannomas were removed by a suboccipital retrosigmoid approach, preserving labyrinthine structures. The vestibulocochlear nerve, stretched and displaced rostrally by the tumor, was preserved with surrounding arachnoidal tissue. Soon after surgery, recovery of hearing began; normal hearing was restored within 3 months. CONCLUSIONS: In a case of JFS with severe hearing loss, normal hearing may be attainable by tumor removal using a retrosigmoid approach that preserves labyrinthine structures. The arachnoidal tissue separating the vestibulocochlear nerve from the schwannoma is important to hearing preservation.

Diffuse white matter changes caused by dural arteriovenous fistula.

We present two patients with progressive dementia who showed diffuse white matter changes on magnetic resonance imaging (MRI) associated with dural arteriovenous fistula (DAVF) involving the transverse-sigmoid sinuses. Angiography of both patients revealed that DAVF was associated with multiple occlusive changes in the dural venous sinus. The associated occlusive changes isolated the straight sinus and the DAVF from the other venous sinuses, and concentrated the drainage of the DAVF in the straight sinus. We postulate that the venous hypertension of the straight sinus resulted in the venous ischemia of the white matter, diffuse white matter changes on MRI, and progressive neurological signs including dementia. Treatment of the DAVF reversed white matter changes and neurological signs. Associated with the venous sinus occlusions, the DAVF caused dementia with diffuse white matter changes due to the venous ischemia.

Effects of decompressive craniectomy on regional cerebral blood flow in severe head trauma patients.

The effect of decompressive craniectomy on regional cerebral blood flow (rCBF) was investigated in five patients with severe head trauma who underwent decompressive craniectomy. Repeated rCBF studies using single photon emission computed tomography with 99mtechnetium-hexamethylpropyleneamine oxime observed that a hyperperfusion area (focal CBF increase) occurred in the decompressed brain within 24 hours after decompressive craniectomy. The hyperperfusion area in the decompressed brain enlarged and increased in severity by 1 week after surgery. However, it attenuated and disappeared by 1 month after surgery. The chronology of the hyperperfusion area corresponded to the change in the swelling of decompressed brain observed by x-ray computed tomography. Patient consciousness showed a significant and progressive improvement in the postoperative 1 month period. Decompressive craniectomy may cause a focal CBF increase in the decompressed brain related to the beneficial effect in patients with acute severe head trauma.

Types of traumatic brain injury and regional cerebral blood flow assessed by 99mTc-HMPAO SPECT.

To investigate the relationship between focal and diffuse traumatic brain injury (TBI) and regional cerebral blood flow (rCBF), rCBF changes in the first 24 hours post-trauma were studied in 12 severe head trauma patients using single photon emission computed tomography (SPECT) with 99mtechnetium-hexamethyl propyleneamine oxime. Patients were classified as focal or diffuse TBI based on x-ray computed tomographic (X-CT) findings and neurological signs. In six patients with focal damage, SPECT demonstrated 1) perfusion defect (focal severe ischemia) in the brain region larger than the brain contusion by X-CT, 2) hypoperfusion (focal CBF reduction) in the brain region without abnormality by X-CT, and 3) localized hyperperfusion (focal CBF increase) in the surgically decompressed brain after decompressive craniectomy. Focal damage may be associated with a heterogeneous CBF change by causing various focal CBF derangements. In six patients with diffuse damage, SPECT revealed hypoperfusion in only one patient. Diffuse damage may be associated with a homogeneous CBF change by rarely causing focal CBF derangements. The type of TBI, focal or diffuse, determines the type of CBF change, heterogeneous or homogeneous, in the acute severe head trauma patient.

Sigmoid sinus dural arteriovenous malformation resulting from jugular foramen schwannoma--case report.

A 69-year-old male presented with a jugular foramen schwannoma occluding the sigmoid sinus and associated with sigmoid sinus dural arteriovenous malformation. The patient presented with dizziness and pulsatile tinnitus following an extended period of hearing loss beginning several years before. Both lesions were resected successfully after transarterial embolization of the malformation. The sequence of symptom development suggests the dural sinus thrombosis caused the dural arteriovenous malformation.

Preoperative assessment of trigeminal neuralgia and hemifacial spasm using constructive interference in steady state-three-dimensional Fourier transformation magnetic resonance imaging.

Results of microvascular decompression (MVD) for trigeminal neuralgia (TN) and hemifacial spasm (HFS) may be improved by accurate preoperative assessment of neurovascular relationships at the root entry/exit zone (REZ). Constructive interference in steady state (CISS)-three-dimensional Fourier transformation (3DFT) magnetic resonance (MR) imaging was evaluated for visualizing the neurovascular relationships at the REZ. Fourteen patients with TN and eight patients with HFS underwent MR imaging using CISS-3DFT and 3D fast inflow with steady-state precession (FISP) sequences. Axial images of the cerebellopontine angle (CPA) obtained by the two sequences were reviewed to assess the neurovascular relationships at the REZ of the trigeminal and facial nerves. Eleven patients subsequently underwent MVD. Preoperative MR imaging findings were related to surgical observations and results. CISS MR imaging provided excellent contrast between the cranial nerves, small vessels, and cerebrospinal fluid (CSF) in the CPA. CISS was significantly better than FISP for delineating anatomic detail in the CPA (trigeminal and facial nerves, petrosal vein) and abnormal neurovascular relationships responsible for TN and HFS (vascular contact and deformity at the REZ). Preoperative CISS MR imaging demonstrated precisely the neurovascular relationships at the REZ and identified the offending artery in all seven patients with TN undergoing MVD. CISS MR imaging has high resolution and excellent contrast between cranial nerves, small vessels, and CSF, so can precisely and accurately delineate normal and abnormal neurovascular relationships at the REZ in the CPA, and is a valuable preoperative examination for MVD.

Prevention of cerebrospinal fluid leakage and delayed loss of preserved hearing after vestibular schwannoma removal: reconstruction of the internal auditory canal in the suboccipital transmeatal approach--technical note.

The suboccipital transmeatal approach uses packing of a muscle or fat graft into the internal auditory canal (IAC) to prevent postoperative cerebrospinal fluid (CSF) leakage. However, preserved hearing after removal of vestibular schwannomas may decline over time because of the progressive constriction of cochlear vascular supply due to scarring of the IAC. We propose a surgical technique for IAC reconstruction, which separates the preserved cochlear nerve and vasculature from the graft, and regains the CSF space in the IAC. Prior to the drilling of the posterior wall of the IAC, the dura mater of the petrous bone forming the posterior wall of the IAC is harvested for IAC reconstruction. After completion of tumor removal, a "roof" of the IAC is reconstructed using the dura mater, and a muscle or fat graft soaked with fibrin glue is placed on the "roof" of the IAC. The IAC was reconstructed using this technique in 26 consecutive patients with vestibular schwannomas who underwent tumor removal via the suboccipital transmeatal approach. Postoperative magnetic resonance imaging confirmed the regained CSF space in the IAC. No delayed hearing loss occurred in four patients with preserved hearing. No CSF leakage occurred after surgery. This new technique of IAC reconstruction may prevent delayed hearing loss as well as postoperative CSF leakage after removal of vestibular schwannomas via the suboccipital transmeatal approach.

Long-term follow-up of cerebral blood flow in patients with ruptured cerebral aneurysm.

The xenon-133 inhalation technique was used to make three measurements of regional cerebral blood flow (CBF) in 34 patients with ruptured cerebral aneurysm: in the acute period (less than 14 days) after subarachnoid hemorrhage, in the subacute period (15-30 days), and in the chronic period (12-24 months). The hemispheric mean value of initial slope index was used as the mean CBF. The clinical outcomes were classified into good recovery (GR) (24 cases), moderate disability (MD) (5), and severe disability (SD) (5) on the Glasgow Outcome Scale. In all periods, the mean CBF significantly correlated with the outcome. GR patients had the highest mean CBF, MD patients the intermediate mean CBF, and SD patients the lowest mean CBF. GR patients had a near-normal mean CBF by the chronic period, while SD patients showed no significant CBF recovery throughout the course.

Isolated metastases of adenocarcinoma in the bilateral internal auditory meatuses mimicking neurofibromatosis type 2--case report.

A 56-year-old male with a history of lung cancer presented with isolated metastases of adenocarcinoma in the bilateral internal auditory meatuses (IAMs), mimicking the bilateral acoustic schwannomas of neurofibromatosis type 2, and manifesting as rapidly worsening tinnitus and bilateral hearing loss. Magnetic resonance imaging showed small tumors in both IAMs with no sign of leptomeningeal metastasis. The preoperative diagnosis was neurofibromatosis type 2. Both tumors were removed and the histological diagnoses were adenocarcinoma. Neuroimaging differentiation of a solitary metastatic IAM tumor from a benign tumor is difficult, although rapidly progressive eighth cranial nerve dysfunction suggests a malignant process. Metastases should be considered as a rare diagnostic possibility in a patient with small tumors in both IAMs.

Angioarchitecture related to hemorrhage in cerebral arteriovenous malformations.

A retrospective study was conducted to determine the angioarchitecture related to hemorrhage in patients with cerebral arteriovenous malformations (AVMs), who underwent conservative treatment and long-term follow-up. The average observation period was 9.3 years, and the annual bleeding rate was estimated at 3.6%. In all cases angiographic findings were reviewed in detail. The average AVM grade by Spetzler-Martin was 3.5. Higher bleeding rate was observed in large AVM (5.4%) compared with small (2.1%) or medium AVM (2.9%). Deep venous drainage (8.6%/year) was strongly correlated to hemorrhage. Concerning location of nidus, hemorrhage was frequently found in insular, callosal, and cerebellar AVMs. Venous ectasia, feeder aneurysm, and external carotid supply were commonly demonstrated on angiograms. Comparison of annual bleeding rate revealed that AVMs with intranidal aneurysm (8.5%) and venous stenosis (5.5%) had a high propensity to hemorrhage. Therapeutic strategy should be focused on these potentially hazardous lesions by the use of endovascular embolization or stereotactic radiosurgery, even if surgical resection is not indicated.

[Acoustic neurinoma located exclusively in cerebellopontine angle cistern ("cisternal" acoustic neurinoma): a case report].

This is a case report of acoustic neurinoma which was located exclusively in the cerebellopontine angle (CPA) cistern and which did not extend into the internal auditory meatus ("cisternal" acoustic neurinoma). The 43-year-old female patient had signs of the left trigeminal nerve impairment including left face neuralgia. However, she did not have any neurootological symptom. No abnormal bony changes in the internal auditory meatus (IAM) were found by high-resolution bone-window CT. MRI showed a left CPA tumor of 25mm not extending into the IAM. The tumor was totally removed by the lateral suboccipital approach. It originated from the vestibular nerve medial to the porus acusticus and was located exclusively in the CPA cistern. No tumor extension into the IAM was confirmed. The cochlear nerve was involved in the tumor capsule and could not be preserved. The pathological diagnosis was that it was a neurilemmoma. Early diagnosis of "cisternal" acoustic neurinoma is difficult because it does not show neurootological symptoms in the early stage. The lateral suboccipital approach is appropriate for the removal of a "cisternal" acoustic neurinoma. However, in spite of the good preoperative hearing, the preservation of hearing is difficult because of the large tumor size.