Acoustic neurinoma presenting as subarachnoid hemorrhage

1974 ◽  
Vol 41 (3) ◽  
pp. 391-393 ◽  
Author(s):  
Kevin McCoyd ◽  
Kevin D. Barron ◽  
Robert J. Cassidy
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cranial Nerve ◽  
Acoustic Neurinoma ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Fine Print

✓An acute subarachnoid hemorrhage arising from a neurinoma of the eighth cranial nerve is reported.

Chronic subdural hematoma presenting as spontaneous subarachnoid hemorrhage

1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Clinical Findings ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.

Recurrent subarachnoid hemorrhage complicating cerebral arterial ectasia

1981 ◽  
Vol 55 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Steven J. Goldstein ◽  
Phillip A. Tibbs
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cranial Nerve ◽  
Review Of The Literature ◽  
Radiographic Findings ◽  
Content Type ◽  
Clinical Complications ◽  
Cranial Nerve Palsies ◽  
Arterial Ectasia ◽  
Fine Print

✓ A case of subarachnoid hemorrhage (SAH) complicating cerebral arterial ectasia is reported. While ischemia and cranial nerve palsies are commonly associated with this condition, review of the literature reveals that SAH is exceedingly rare. The pathogenesis, radiographic findings, and clinical complications of cerebral arterial ectasia are discussed.

Failure of a Heifetz aneurysm clip

1982 ◽  
Vol 57 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Ram Kossowsky ◽  
Manuel Dujovny ◽  
Nir Kossovsky ◽  
Yves Keravel
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Stress Corrosion ◽  
Fracture Mechanism ◽  
Intergranular Corrosion ◽  
Content Type ◽  
Aneurysm Clip ◽  
Stress Load ◽  
Highly Sensitive ◽  
Acute Subarachnoid Hemorrhage ◽  
Fine Print

✓ A 16-year-old girl died from an acute subarachnoid hemorrhage following the fracture of a blade of a Heifetz aneurysm clip. The clip was manufactured from 17-7PH steel, which on metallurgical testing was found to be highly sensitive to intergranular corrosion. The fracture mechanism was stress corrosion, brought on by the combination of a stress load, an electrolytic environment, and a susceptible steel.

Endovascular management of dissecting vertebrobasilar artery aneurysms in patients presenting with acute subarachnoid hemorrhage

2005 ◽  
Vol 103 (4) ◽  
pp. 649-655 ◽  
Author(s):  
Ichiro Yuki ◽  
Yuichi Murayama ◽  
Fernando Viñuela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Dissecting Aneurysm ◽  
Endovascular Techniques ◽  
Recurrent Hemorrhage ◽  
Content Type ◽  
Vertebrobasilar Artery ◽  
Acute Subarachnoid Hemorrhage ◽  
Grade Ii ◽  
Dissecting Aneurysms ◽  
Fine Print

Object. The authors report on a series of 29 patients presenting with acute subarachnoid hemorrhage (SAH) related to the rupture of a vertebrobasilar dissecting aneurysm. Special attention was focused on embolization techniques and immediate and midterm anatomical and clinical outcomes. Methods. Between March 1994 and January 2003, 29 patients presented with acute SAH caused by the rupture of a vertebrobasilar dissecting aneurysm. Eleven patients (37.9%) had Hunt and Hess Grade I SAH, four (13.8%) Grade II, six (20.7%) Grade III, five (17.2%) Grade IV, and three (10.3%) Grade V. Aneurysms were classified into five groups based on lesion location, and treatment courses were decided. All patients except two were treated by endovascular trapping of the aneurysm with concomitant occlusion of the involved vertebral artery (VA). No technical or clinical complication was observed in 28 patients (97%). Aneurysm perforation occurred during the procedure in one patient (3%). There was evidence of aneurysm recanalization in one patient. One patient with Hunt and Hess Grade IV SAH and two patients with Grade V SAH died. One patient died of respiratory infection 1 year after aneurysm trapping. One patient presented with a recurrent hemorrhage 1 month after treatment and died. Overall morbidity and mortality rates were 13.8 and 17.2%, respectively. Conclusions. Twenty-nine patients with acute SAH due to rupturing of vertebrobasilar dissecting aneurysms were treated using endovascular techniques. In most cases, endovascular trapping of the aneurysm and concomitant occlusion of the VA was technically and clinically successful.

Microvascular decompression for cochlear symptoms

2000 ◽  
Vol 93 (3) ◽  
pp. 421-426 ◽  
Author(s):  
Tomomi Okamura ◽  
Yasushi Kurokawa ◽  
Norio Ikeda ◽  
Seisho Abiko ◽  
Makoto Ideguchi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Cochlear Nerve ◽  
Auditory Brainstem Responses ◽  
Neurovascular Compression ◽  
Minimal Risk ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Fine Print

Object. The object of this study was to evaluate the efficacy of a new neurovascular decompression technique in relieving symptoms of cochlear nerve dysfunction.Methods. Nineteen patients with slowly progressive hearing loss, low-frequency fluctuating hearing loss, and high-pitched tinnitus due to neurovascular compression (NVC) of the eighth cranial nerve in a triangular space between the seventh and eighth cranial nerves (the VII–VIII triangle) of the cerebellopontine angle (CPA) were treated using a new technique for microvascular decompression that was developed by anatomical study in 24 cadaver specimens of the CPA. In 12 of 19 patients the anterior inferior cerebellar artery (AICA) was observed to cause compression in the VII–VIII triangle and this vessel was easily mobilized medially for placement of a silicone sponge or Teflon cushion between the compressing artery and nerve. Postoperatively, hearing loss of 20 dB or more that was present in 11 of the 19 patients with NVC improved by more than 5 dB in seven (64%), including the patient with the most severe hearing loss. Of 18 patients presenting with tinnitus preoperatively, eight (44%) had no tinnitus and an additional nine (for a total of 94%) had good improvement in tinnitus after surgery and at long-term follow up.Conclusions. The microvascular decompression technique described is highly successful in treating symptoms due to direct or indirect compression of the cochlear nerve, with minimal risk of complications. Recordings of auditory brainstem responses confirmed the clinical diagnosis of NVC of the eighth cranial nerve and correlated with clinical results after microvascular decompression of the cochlear nerve.

Microanatomical variations in the cerebellopontine angle associated with vestibular schwannomas (acoustic neuromas): a retrospective study of 1006 consecutive cases

2000 ◽  
Vol 92 (1) ◽  
pp. 70-78 ◽  
Author(s):  
Prakash Sampath ◽  
David Rini ◽  
Donlin M. Long
Keyword(s):  
Cranial Nerve ◽  
Anatomical Location ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Middle Fossa Approach ◽  
Group Iii ◽  
Common Location ◽  
Group I ◽  
Cerebellar Artery ◽  
Fine Print

Object. Great advances in neuroimaging, intraoperative cranial nerve monitoring, and microsurgical technique have shifted the focus of acoustic neuroma surgery from prolonging life to preserving cranial nerve function in patients. An appreciation of the vascular and cranial nerve microanatomy and the intimate relationship between neurovascular structures and the tumor is essential to achieve optimum results. In this paper the authors analyze the microanatomical variations in location of the facial and cochlear nerves in the cerebellopontine angle (CPA) associated with acoustic neuromas and, additionally, describe the frequency of involvement of surrounding neural and vascular structures with acoustic tumors of varying size. The authors base these findings on their experience with 1006 consecutive patients who underwent surgery via a retrosigmoid or translabyrinthine approach.Methods. Between July 1969 and January 1998, the senior author (D.M.L.) performed surgery in 1022 patients for acoustic neuroma: 705 (69%) via the retrosigmoid (suboccipital); 301 (29%) via the translabyrinthine; and 16 (2%) via the middle fossa approach. Patients undergoing the middle fossa approach were excluded from the study. The remaining 1006 patients were subdivided into three groups based on tumor size: Group I tumors (609 patients [61%]) were smaller than 2.5 cm; Group II tumors (244 patients [24%]) were between 2.5 and 4 cm; and Group III tumors (153 patients [15%]) were larger than 4 cm. The senior author's operative notes were analyzed for each patient. Relevant cranial nerve and vascular “involvement” as well as anatomical location with respect to the tumor in the CPA were noted. “Involvement” was defined as adherence between neurovascular structure and tumor (or capsule), for which surgical dissection was required to free the structure. Seventh and eighth cranial nerve involvement was divided into anterior, posterior, and polar (around the upper or lower pole) locations. Anterior and posterior locations were further subdivided into upper, middle, or lower thirds of the tumor.The most common location of the seventh cranial nerve (facial) was the anterior middle third of the tumor for all groups, although a significant number were found on the anterior superior portion. The posterior location was exceedingly rare (< 1%). Interestingly, patients with smaller tumors (Group I) had an incidence (3.4%) of the seventh cranial nerve passing through the tumor itself, equal to that of patients with larger tumors. The most common location of the eighth cranial nerve complex was the anterior inferior portion of the tumor. Not surprisingly, larger tumors (Group III) had a higher incidence of involvement of fourth cranial nerve (41%), fifth cranial nerve (100%), ninth—11th cranial nerve complex (99%), and 12th cranial nerve (31%), as well as superior cerebellar artery (79%), anterior inferior cerebellar artery (AICA) trunk (91.5%), AICA branches (100%), posterior inferior cerebellar artery (PICA) trunk (59.5%), PICA branches (79%), and the vertebral artery (VA) (93.5%). A small number of patients in Group III also had AICA (3.3%), PICA (3.3%), or VA (1.3%) vessels within the tumor itself.Conclusions. In this study, the authors show the great variation in anatomical location and involvement of neurovascular structures in the CPA. With this knowledge, they present certain technical lessons that may be useful in preserving nerve function during surgery and, in doing so, hope to provide neurosurgeons and neurootologists with valuable information that may help to achieve optimum outcomes in patients.

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

1998 ◽  
Vol 88 (2) ◽  
pp. 232-236 ◽  
Author(s):  
Hiroshi Ryu ◽  
Seiji Yamamoto ◽  
Kenji Sugiyama ◽  
Kenichi Uemura ◽  
Michihiko Nozue
Keyword(s):  
Hemifacial Spasm ◽  
Cranial Nerve ◽  
Diagnostic Value ◽  
Sensorineural Hearing ◽  
Neurovascular Compression ◽  
Eighth Cranial Nerve ◽  
Chi Square ◽  
Content Type ◽  
Neurovascular Decompression ◽  
Fine Print

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.

Eighth nerve lipoma

1980 ◽  
Vol 53 (3) ◽  
pp. 397-400 ◽  
Author(s):  
William C. Mattern ◽  
Robert E. Blattner ◽  
James Werth ◽  
Robert Shuman ◽  
Solomon Bloch ◽  
...  
Keyword(s):  
Cranial Nerve ◽  
Cerebellopontine Angle ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Postoperative Course ◽  
Eighth Nerve ◽  
Clinical Diagnostic ◽  
The Right ◽  
Fine Print

✓ A case of lipoma of the right eighth cranial nerve in the cerebellopontine angle (CPA) is presented. The patient had a clinical, diagnostic, surgical, and postoperative course similar to that of patients with other small CPA tumors. The literature on this rare CPA tumor is reviewed and discussed.

Acoustic neurinoma presenting as subarachnoid hemorrhage

1978 ◽  
Vol 49 (4) ◽  
pp. 602-604 ◽  
Author(s):  
Robert K. Gleeson ◽  
John F. Butzer ◽  
Oliver D. Grin
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acoustic Neurinoma ◽  
Content Type ◽  
Fine Print

✓ A case of an acoustic neurinoma presenting as a subarachnoid hemorrhage is described. This is the second such case in the literature.

Cortical cellular response in acute subarachnoid hemorrhage

1980 ◽  
Vol 52 (4) ◽  
pp. 456-462 ◽  
Author(s):  
Otakar R. Hubschmann ◽  
David Kornhauser
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cellular Response ◽  
Initial Step ◽  
Cellular Level ◽  
Cortical Cells ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Cellular Dysfunction ◽  
K Release ◽  
Fine Print

✓ Acute subarachnoid hemorrhage (SAH) over the cerebral cortex causes single or multiple waves of cellular depolarization, which may occur in a self-propagating, reverberating fashion. This process is characterized by a massive K+ release and transient depression in electrocortical activity. The K+ levels in the extracellular space reach magnitudes known to substantially affect the membrane potentials of neurons and glia, and may cause a release of neurotransmitters from depolarized presynaptic terminals. The release of K+ may be the initial step in the development of cellular edema and, together with a multitude of other chemical and biochemical changes taking place at the cellular level, may underlie the loss of autoregulation. Cortical cells rather than blood vessels are the primary targets in the initial stages of SAH, and ischemia does not play a causal role in the pathogenesis of cellular dysfunction during this stage.

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