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Background: Geniculate ganglion or nervus intermedius neuraigia is an unusual condition resulting in deep ear pain with or without signs of atypical trigeminal neuralgia, deep face, or throat pain. This article describes an experience with 14 patients who came to the neurosurgical service at the University of Pittsburgh Medical Center with a diagnosis of geniculate neuralgia., Methods: After failing conservative treatment and after undergoing neurologic, otologic, and dental evaluations, these 14 patients underwent 20 intracranial procedures consisting of retromastoid craniectomies with microvascular decompression of cranial nerves V, IX, and X with section of the nervus intermedius in most cases., Results: At operation, vascular compression of the nerves and nervus intermedius was found, which implicated vascular compression as an etiology of this disorder. Initially, 10 of 14 patients had an excellent outcome (71.5%), 3 experienced partial relief (21.5%), and there was 1 failure (7%). Ten patients were available for long-term (> 12 months) follow-up. Of these 10, 3 retained the excellent result (30%), 6 experienced partial relief (60%), and there was 1 failure (10%). Complications included one transient facial paresis, one facial numbness, one paresis of cranial nerves IX and X, one chemical meningitis, two cerebrospinal fluid leaks, and one superficial wound infection. Of those that fell from the excellent to partial category, this usually involved a return of atypical facial pain, but otalgia remained resolved., Conclusions: Overall, good results (with excellent or partial relief) were found long term for 90% of patients in this series. The authors recommend microvascular decompression of cranial nerves V, IX, and X with nervus intermedius section for the treatment of geniculate neuralgia.

This report describes a patient with sudden sensorineural hearing loss who was found to have a megadolichoectasia vertebrobasilar system that appeared to be causing compression of the ipsilateral facial and vestibulocochlear nerves. The patient was treated conservatively for 4 months, during which time no hearing returned. He then underwent microvascular decompression of the affected nerves. At surgery, marked compression of the cranial nerves VII-VIII complex and the pons was observed. Postoperatively, the patient experienced a gradual return of useful hearing. We suggest that vascular compression may be a rare, but treatable, cause of sensorineural hearing loss.

In a companion paper (Ann Surg 1985; 201(3):391-398), clinical data which suggest that neurogenic hypertension may be caused by arterial compression of the left medulla oblongata was presented. A chronic pathophysiologic animal model of neurogenic hypertension using a substitute for arterial pulsation, the neurovascular compression simulator (NCS), was developed. This paper presents data that demonstrate how development of hypertension in a nonhuman primate baboon (5 subject animals, 5 control animals) can be caused by the NCS, and the blood pressure can subsequently return to normal following cessation of NCS activity. These experiments show that pulsatile compression of the left ventrolateral medulla oblongata results in cardiovascular changes consistent with the sequence found in human neurogenic hypertension. Arteriosclerosis and arterial ectasia in the human contribute to arterial elongation and looping at the base of the brain. An arterial loop, by causing pulsatile compression of neural structures, elicits an increase in blood pressure initiated by an increase in cardiac output. This may be due to interference with the autonomic control of the heart and/or by alteration of the relative capacitance of the vascular system.

Considerable concern with cranial nerve syndromes has often required detailed information of the relationship between the vertebrobasilar system and the brainstem. The obvious invasiveness of conventional vertebral angiography poses the question of whether computed tomography (CT) might serve as a satisfactory technique or even as a sufficient diagnostic method. During a 12 month period, 12 of 250 patients with cranial nerve syndromes were diagnosed by CT as having vertebrobasilar ectasia. This communication correlates the clinical symptomatology with angiography and CT and presents evidence that CT alone can prove satisfactory.

Cerebral blood flow mapping with the xenon-enhanced/CT method has become a useful clinical tool in the management of patients with occlusive cerebral vascular disease. Studies involving 4-5 minutes of inhaling a xenon/oxygen mixture (less than or equal to 35%) can now be performed routinely with acceptable patient tolerance and compliance. Four cases with acute and chronic ischemic injuries are reported here to illustrate the manner in which this method has been used to characterize flow pattern in such patients and the relevance of this flow information to clinical patient management.

Electrophysiologic recordings were made from patients with hemifacial spasm (HFS) during microvascular decompression (MVD) operations to see if spasm and synkinesis are caused by ephaptic transmission at the site of lesion (root entry zone [REZ] of the facial nerve). The response from the orbicularis oculi muscle to electrical stimulation of the marginal mandibular nerve had a 2.2-msec longer latency (average of 16 patients) than the sum of the conduction times of the parts of the facial nerve that would be involved if the response was the result of ephaptic transmission at the REZ of the seventh cranial nerve. Similar results were obtained when the zygomatic branch of the facial nerve was stimulated. These results indicate that the facial motonucleus is involved in HFS.

An in-vivo experiment was developed to identify the biorheological properties of the spinal cord of puppies under uriaxial deformation. For strain less than 4.5%, the ratio between stress and strain was about 2.65 x 106 dyne/limbs of the puppies were recoverable after the spinal cord segment at L1 was stretched once by 10-50%.

Hemifacial spasm is usually an isolated symptom resulting from facial nerve root compression. Three patients had, in addition, tinnitus, hearing loss, facial sensory loss, diminished gag reflex, dysphagia, and dysarthria. Acoustic reflexes were abnormal, and facial nerve conduction studies showed evidence of ephaptic transmission and ectopic excitation. Brain CT and metrizamide cisternography were normal. Surgical exploration showed compression of cranial nerve roots by posterior inferior cerebellar artery branches. After decompression, symptoms abated, and electrical signs of hemifacial spasm disappeared. Vascular compression of nerve roots in the cerebellopontine recess may cause multiple cranial neuropathy.

Although an extensive literature exists concerning essential arterial hypertension, the primary etiology has been unclear. Arterial compression of the left lateral medulla oblongata by looping arteries of the base of the brain was seen incidently in 51 of 53 hypertensive patients who underwent left retromastoid craniectomy and microvascular decompression for unrelated cranial nerve dysfunctions. Such compression was not noted in normotensive patients. Treatment by vascular decompression of the medulla was performed in 42 of the 53 patients. Relief in the hypertension was seen in 32 of the patients and improvement in four. Arteriosclerosis and arterial ectasia contribute to arterial elongation and looping. If pulsatile compression of the left lateral medulla occurs, hypertension may develop as a consequence of an imbalance in the neural control systems that normally regulate blood pressure. The hypertension may further contribute to arterial elongation, providing a vicious circle of pathophysiologic changes.

We studied 59 patients with hemifacial spasm before decompression of the facial nerve in the cerebellopontine angle. Fifty-three patients were reexamined 1 week later, and 30 patients after 2 to 8 months. Within 1 week, ephaptic transmission disappeared in 23% and changed from bidirectional to unidirectional in 45%. After-discharges disappeared in 64% and were mild in 34%. Synkinesis after supraorbital nerve stimulation disappeared in 53%, and the blink reflex amplitude became normal. After 2 to 8 months, ephaptic transmission was abolished in 73% and unidirectional in 17%. After-discharges and synkinesis disappeared in 90%, and the latency of the blink reflex decreased. It is concluded that decompression stops ectopic/ ephaptic excitation due to decrease in the interstitial resistance, and enables remyelination.

Brain retraction and induced hypotension are surgical adjuncts capable of compromising cerebral blood flow. To evaluate their effects upon brain function, cortical evoked potentials, neurological status and cortical histological changes were determined as a function of graded levels of brain retractor and systemic perfusion pressure in the dog. Somatosensory evoked potentials recorded from the site of application of brain retraction showed a decrement as a function of both the amount of retraction pressure and the systemic perfusion pressure. An electrode distant from the retractor site showed similar, though reduced and more variable changes in amplitude. For higher levels of brain retractor pressure, induced hypotension to 50 mm Hg systemic perfusion pressure produced greater reductions in evoked potentials than in normotensive subjects. It was demonstrated that a reduction of 50% of the evoked potential amplitude after sixty minutes brain retraction signaled, with high probability, the occurrence of postoperative sensory and/or motor deficits and cortical histopathology. It was concluded that cortical evoked potentials represent a reliable indicator of the functional effects produced by applied cortical retraction pressure at several levels of systemic perfusion pressure. It was suggested that the recording of evoked potentials would prove most useful during neurosurgical procedures employing induced hypotension and brain retraction.

A method for locating the facial nerve during removal of medium to large acoustic tumors is described. The method consists of stimulating the tumor mass with short rectangular pulses of monopolar, constant voltage and then presenting the electrical responses from the facial muscles through a loudspeaker. In this way, regions of the tumor where there is no nerve present can be identified and large parts of the tumor removed safely and quickly. Monitoring spontaneous electromyogram (EMG) activity was used to reduce the risk of damaging the facial nerve when parts of medium to large acoustic tumors adhering to the nerve were removed from 20 patients operated upon consecutively by the same surgeon. Only 1 patient lost facial function with the nerve intact anatomically. Nine patients had normal function immediately after the operation and had no detectable weakness upon discharge 6-8 days later, 4 patients had weakness which was resolved, and 6 patients had partial loss of facial function at the time of discharge. The same method may be used to identify the facial nerve during other operations in which this structure is at risk.

The ideal operation for acoustic neurinoma would not only provide total excision without injury to the brain stem and with preservation of facial nerve function, but would also allow retention of useful hearing in those patients who come to operation with intact hearing function. Documented preservation of useful hearing in the rather extensive literature concerning acoustic neurinomas is rare. An operative technique has been developed utilizing a retromastoid approach, brain stem auditory-evoked potentials and direct auditory monitoring, facial nerve electromyography, and microsurgical techniques that have enabled us to preserve useful hearing in three and some hearing in two of six consecutive patients who had preoperative hearing. Rules regarding preservation and criteria regarding documentation of hearing preservation are outlined.

As we age, our arteries elongate and our brains "sag." As a consequence of these processes, redundant arterial loops and bridging or intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebellopontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. Symptoms of trigeminal or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory) and some cases of "essential" hypertension are caused by these vessels compressing cranial nerves V, IX--X, VII, VIII, and left X and medulla oblongata. Using microsurgical techniques, the symptoms may be relieved by vascular decompression, findings and results in 695 paients are briefly reviewed and correlated. A chronic primate model of "essential" hypertension is briefly described.

Four cases illustrating low-velocity penetrating injuries from foreign bodies are presented. The importance of formal intracranial exposure is emphasized. When used in these four cases, all patients had good recoveries. In children, penetration of the brain is likely because of the fragility of the orbital roof. The English-language literature on penetrating intracranial foreign bodies is also reviewed.