A clinical study of ocular motor nerve functions after petroclival meningioma resection.

BACKGROUND: Ocular motor dysfunction is one of the most common postoperative complications of petroclival meningioma. However, its incidence, recovery rate, and independent risk factors remain poorly explored. METHODS: A prospective analysis of 31 petroclival meningiomas was performed. Operative approaches were selected by utilizing a new 6-region classification of petroclival meningiomas we proposed. Two scores were used to evaluate the functions of the oculomotor and abducens nerves. Pearson correlation analysis and binary logistic regression analysis were used to identify independent risk factors for intraoperative oculomotor and abducens nerve injury. RESULTS: Postoperative new-onset dysfunctions in the pupillary light reflex and eye/eyelid movements as well as abducens paralysis were detected in eight (25.8%), ten (32.3%) and twelve (38.7%) cases, respectively. Their corresponding recovery rates after 6 months of follow-up were 75% (6/8), 80% (8/10), and 83.3% (10/12), respectively, and their mean times to start recovery were 4.03, 2.43, and 2.5 months, respectively. Tumor invasion into the suprasellar region/sphenoid sinus was the only risk factor for dysfunctions in both the pupillary light reflex (p = 0.001) and eye/eyelid movements (p = 0.002). Intraoperative utilization of the infratrigeminal interspace was the only risk factor for dysfunction in eyeball abduction movement (p = 0.004). CONCLUSIONS: Dysfunctions of the oculomotor and abducens nerves recovered within 6 months postoperatively. Tumor extension into the suprasellar region/sphenoid sinus was the only risk factor for oculomotor nerve paralysis. Eye/eyelid movements were more sensitive than the pupillary light reflex in reflecting nerve dysfunctions. Intraoperative utilization of the infratrigeminal interspace was the only risk factor for abducens nerve paralysis.

Facial reanimation according to the postresection defect during lateral skull base surgery.

The vast majority of benign tumors of the cerebellopontine angle, temporal bone, and parotid gland can be successfully resected without permanent injury to the facial nerve. Malignant tumors or recurrent disease may require facial nerve sacrifice, especially if preoperative facial paresis is present. This article will present case examples of the various methods to reconstruct facial animation after lateral skull base resections that require sacrifice of cranial nerve VII, and the associated mimetic facial musculature. Facial mimetic outcome after reanimation was graded using the House-Brackmann scale. Primary neurorrhaphy or interposition grafting may be performed when both the proximal and distal portions of the facial nerve are available and viable facial musculature is present. If only the distal facial nerve and viable facial musculature are available, a split hypoglossal to facial nerve anastomosis is used. A proximal facial nerve to microvascular free flap is performed when the proximal facial nerve is available without distal nerve or viable musculature. A cross-facial to microvascular free flap is performed when the proximal and distal facial nerve and facial musculature are unavailable. The above methods resulted in a House-Brackmann score of III/VI in all case examples postoperatively. The method of facial reanimation used depends on the availability of viable proximal facial nerve, the location of healthy, tumor-free distal facial nerve, and the presence of functioning facial mimetic musculature.

Avoiding injury to the abducens nerve during expanded endonasal endoscopic surgery: anatomic and clinical case studies.

BACKGROUND: Understanding the course of the most medially located parasellar cranial nerve, the abducens, becomes critical when performing an expanded endonasal approach. OBJECTIVE: We report an anatomoclinical study of the abducens nerve and describe relevant surgical nuances to avoid its injury. METHODS: Ten anatomic specimens were dissected using endoscopes attached to an high-definition camera. A series of anatomic measurements and relationships of the abducens nerve were noted. Illustrative clinical cases are described to translate those findings into practice. RESULTS: Cisternal, interdural, gulfar, and cavernous segments of the abducens were identified intracranially. The mean distance from the vertebrobasilar junction (VBJ) to the pontomedullary sulcus (PMS) was 4 mm; horizontal distance between both abducens nerves at the PMS was 10 mm, and between both abducens at the interdural segment was 18.5 mm. The upper limit of the lacerum segment of the internal carotid artery was at the same level of the dural entry point of the sixth cranial nerve posteriorly. The sellar floor at the sphenoid sinus marks the level of the gulfar segment in the craniocaudal axis. At the superior orbital fissure, the abducens nerve and V2 were at an average vertical distance of 11.5 mm. CONCLUSION: Anatomic landmarks to localize the abducens nerve intraoperatively, such as the VBJ for the transclival approach, the lacerum segment of the carotid, and the sellar floor for the medial petrous apex approach, and V2 for Meckel's cave approach, are reliable and complementary to the use of intraoperative electrophysiological monitoring.

Development of cranial nerve palsy shortly after endosaccular embolization for asymptomatic cerebral aneurysm: report of two cases and literature review.

CLINICAL DESCRIPTION: We report two cases of asymptomatic cerebral aneurysm in which cranial nerve palsy (CNP) developed shortly after symbolization. The CNP occurred immediately in case 1, but case 2 showed the CNP 30 h after symbolization. Although both aneurysms had increased in size on follow-up angiography, case 2 who showed dome re canalization resulted in progressive CNP deterioration. CONCLUSION: These findings suggest that the CNP may result not only from mechanical compression by coils but also from inflammation induced by perpendicular thrombosis, and that the prognosis of the CNP may be influenced by dome re canalization. This complication should be kept in mind in treatment for asymptomatic aneurysms adjacent to the cranial nerves.

Activation of c-Jun and ATF-2 in primate motor cranial nerve nuclei is not associated with apoptosis following axotomy.

Nerve transection induces complex changes in gene regulation and expression that can have profound phenotypic effects on the fate of axotomized neurons. The transcription factors c-Jun and ATF-2 (activating transcription factor-2) are components of a regulatory network that mediates survival, regeneration, and apoptosis following axotomy in rodents. The activation and function of c-Jun and ATF-2 after nerve injury have not been examined in primates. Using a novel model of cranial nerve injury in baboons, we have examined the temporality of c-Jun activation (phosphorylation) in cranial nerve (CN) III and CN VI neurons and ATF-2 activation in CN VI neurons at 2, 4, and 9 days post-injury by immunohistochemistry. Furthermore, we have addressed whether the activation of these factors is associated with apoptosis by the TUNEL assay. We report that activated c-Jun is present in CN III and CN VI neurons ipsilateral to axotomy at 2, 4, and 9 days post-injury, but not in neurons contralateral to injury. Additionally, CN VI neurons ipsilateral to injury at 4 and 9 days contain activated ATF-2. Furthermore, no evidence of TUNEL reactivity was observed in either nucleus, regardless of laterality, at any of the examined time points. These findings suggest that activation of both c-Jun and ATF-2 does not mediate apoptosis in axotomized primate CN III and CN VI neurons at time points up to 9 days. This report serves as a basic inquiry into the neuronal response to cranial nerve injury in primates.

Subtenon injection of botulinum toxin for treatment of traumatic sixth nerve palsy.

PURPOSE: Subtenon injection of botulinum toxin may produce results similar to intramuscular injection of the medial rectus muscle for the treatment of acute traumatic sixth nerve palsy. This study was designed to evaluate the clinical efficacy of subtenon injection and to compare our results with those in previously published reports. METHODS: During 3 years at a single institution, 13 patients with traumatic sixth nerve palsy of less than 6 months' duration were treated with subtenon injection of botulinum toxin. The deviation angles before and after injection were recorded. A distance esotropia of less than 10 prism diopters (PD) in the primary position or absence of diplopia at 3 months was defined as recovery. RESULTS: Of the 13 patients treated, 11 (84.5%) had unilateral palsy and 2 (15.4%) had bilateral palsy. The average pre-injection deviation was 39.5 PD of esotropia, and the average post-injection deviation was 17.0 PD. Seven patients experienced recovery and regained binocular single vision; the overall recovery rate was 53.8% (unilateral, 63.6%; bilateral, 0%). Six patients did not recover and subsequently underwent strabismus surgery. CONCLUSION: Patients with traumatic sixth nerve palsy treated with subtenon injection of botulinum toxin showed higher recovery rates than did most patients treated with conservative measures in published reports. The result of subtenon injection of botulinum toxin without electromyography (EMG) guidance was comparable to that obtained using EMG-guided intramuscular injection of botulinum toxin. Patients with unilateral palsy demonstrated a better recovery rate than did patients with bilateral palsy.

Intra-Operative electromyographic monitoring of extra-ocular motor nerves (Nn. III, VI) in skull base surgery.

BACKGROUND: Extraocular motor nerves (Nn. III, IV, VI) are at risk of damage during skull base surgery. A new recording technique was employed in 18 patients suffering from various skull base tumours in order to extend intra-operative EMG monitoring to the extra-ocular muscles. METHODS: Selective intra-operative EMG recordings were obtained from extra-ocular muscles by placement of single-shafted bipolar needle electrodes under the guidance of B-mode ultrasound to visualise the needle tip within the target muscle in the orbital cavity. FINDINGS: Following bipolar electrical stimulation, the oculomotor nerve (N.III) was intra-operatively identified in 5 out of 7 cases, and the abducens nerve (N.VI) in 12 out of 18 cases. Postoperative (3-6 months) oculomotor nerve function remained unchanged in 5 and improved in 2 patients. No permanent deterioration was observed. Abducens nerve function deteriorated in two patients and improved in one case, but remained unchanged in 15 cases. No side effects occurred. There was neither any distinct relation of ocular motor nerve function to the kind and extent of SMA ("spontaneous muscle activity") patterns, nor could such relationship be detected with concern to neurophysiological parameters (latencies, amplitudes) of electrically evoked CMAP ("compound muscle action potentials"). INTERPRETATION: The EMG technique proposed proved to be mainly effective as a mapping tool for intra-operative localisation and identification of ocular motor nerves in skull base surgery. However, the predictive value of conventional neurophysiological parameters for clinical outcome, seems to be rather poor. Further studies on a larger number of patients are therefore required to develop new quantification techniques which enable an intra-operative prediction of ocular motor nerve deficits. Further efforts are also necessary to extend this technique to the trochlear nerve.

Predictors of nonrecovery in acute traumatic sixth nerve palsy and paresis.

PURPOSE: To evaluate whether nonrecovery from acute traumatic sixth nerve palsy could be predicted from demographic factors or palsy characteristics. DESIGN: Prospective, observational case series SETTING: Multicenter (academic and private practices). OUTCOME MEASURE: Nonrecovery, defined as the presence of diplopia in primary position or more than 10 prism diopters of distance esotropia in primary position at 6 months after onset. METHODS: Using data from a previously described cohort of 84 eligible patients with acute traumatic sixth nerve palsy, we performed multivariate analyses of demographic factors and palsy characteristics. RESULTS: Nonrecovery at 6 months after onset was associated with a complete palsy (adjusted risk ratio, 9.11; 95% confidence interval [CI], 2.77-14.84) and with a bilateral palsy or paresis (adjusted risk ratio, 2.53; 95% CI, 0.98-4.29). The choice of conservative management (observation, prism, or patch) versus acute injection of Botulinum toxin (within 3 months of injury) did not influence final recovery. CONCLUSIONS: In acute traumatic sixth nerve palsy or paresis, failure to recover by 6 months after onset was associated independently with inability to abduct past midline at presentation and bilaterality. Although the overall recovery rate is high in acute traumatic sixth nerve palsy or paresis, a complete or bilateral case has a poor prognosis and is more likely to need strabismus surgery.