Electromyographic evaluation of functional electrical stimulation to injured oculomotor nerve

Functional electrical stimulation delivered early after injury to the proximal nerve stump has been proposed as a therapeutic approach for enhancing the speed and specificity of axonal regeneration following nerve injury. In this study, the injured oculomotor nerve was stimulated functionally by an implantable electrode. Electromyographic monitoring of the motor unit potential of the inferior oblique muscle was conducted for 12 weeks in two injury groups, one with and one without electric stimulation. The results revealed that, at 2, 4, 6, 8 weeks after functional electric stimulation of the injured oculomotor nerve, motor unit potentials significantly increased, such that amplitude was longer and spike duration gradually shortened. These findings indicate that the injured oculomotor nerve has the potential for regeneration and repair, but this ability is not sufficient for full functional recovery to occur. Importantly, the current results indicated that recovery and regeneration of the injured oculomotor nerve can be promoted with functional electrical stimulation.

Electrical stimulation promotes regeneration of injured oculomotor nerves in dogs

Functional recovery after oculomotor nerve injury is very poor. Electrical stimulation has been shown to promote regeneration of injured nerves. We hypothesized that electrical stimulation would improve the functional recovery of injured oculomotor nerves. Oculomotor nerve injury models were created by crushing the right oculomotor nerves of adult dogs. Stimulating electrodes were positioned in both proximal and distal locations of the lesion, and non-continuous rectangular, biphasic current pulses （0.7 V, 5 Hz） were administered 1 hour daily for 2 consecutive weeks. Analysis of the results showed that electrophysiological and morphological recovery of the injured oc- ulomotor nerve was enhanced, indicating that electrical stimulation improved neural regeneration. Thus, this therapy has the potential to promote the recovery of oculomotor nerve dysfunction.

Establishment of a beagle dog model of oculomotor nerve injury

The oculomotor nerves of beagle dogs received electrical stimulation at 0.3-2.0 V. After recording compound muscle action potentials of the inferior oblique muscle, the oculomotor nerve was quickly cut off and a direct end-to-end anastomosis was then performed. As a result, the stimulating elec-trode was smoothly inserted and placed, and ideal bioelectrical signals of the interior oblique muscle were acquired. After oculomotor nerve injury, compound muscle action potentials of the inferior oblique muscle were significantly decreased in beagle dogs. These findings suggest that an animal model of oculomotor nerve injury was successfully established for electrophysiological studies.

Regenerating nerve fiber innervation of extraocular muscles and motor functional changes following oculomotor nerve injuries at different sites

In the present study, the oculomotor nerves were sectioned at the proximal （subtentorial） and distal （superior orbital fissure） ends and repaired. After 24 weeks, vestibulo-ocular reflex evaluation confirmed that the regenerating nerve fibers following oculomotor nerve injury in the superior orbital fissure had a high level of specificity for innervating extraocular muscles. The level of functional recovery of extraocular muscles in rats in the superior orbital fissure injury group was remarkably superior over that in rats undergoing oculomotor nerve injuries at the proximal end （subtentorium）. Horseradish peroxidase retrograde tracing through the right superior rectus muscle showed that the distribution of neurons in the nucleus of the oculomotor nerve was directly associated with the injury site, and that crude fibers were badly damaged. The closer the site of injury of the oculomotor nerve was to the extraocular muscle, the better the recovery of neurological function was. The mechanism may be associated with the aberrant number of regenerated nerve fibers passing through the injury site.

Nomogram model for predicting oculomotor nerve palsy in patients with intracranial aneurysm

AIM:To explore the risk factors of oculomotor nerve palsy(ONP)in patients with intracranial aneurysm(IA)and develop a nomogram model for predicting ONP of IA patients.METHODS:A total of 329 IA patients were included.Logistic regression analysis was applied to identify independent factors,which were then integrated into the nomogram model.The performance of the nomogram model was evaluated by calibration cur ve,receiver operating curve(ROC),and decision curve analysis.RESULTS:Univariate and multivariate logistic regression analysis indicated posterior communicating artery(PCo A)aneur ysm[hazard ratio(HR)=17.13,P<0.001]and aneurysm diameter(HR=1.31,P<0.001)were independent risk factors of ONP in IA patients.Based on the results of logistic regression analysis,a nomogram model for predicting the ONP in IA patients was constructed.The calibration curve indicated the nomogram had a good agreement between the predictions and observations.The nomogram showed a high predictive accuracy and discriminative ability with an area under the curve(AUC)of 0.863.The decision curve analysis showed that the nomogram was powerful in the clinical decision.PCo A aneurysm(HR=3.38,P=0.015)was identified to be the only independent risk factor for ONP severity.CONCLUSION:PCo A aneurysm and aneurysm diameter are independent risk factors of ONP in IA patients.The nomogram established is performed reliably and accurately for predicting ONP.PCo A aneurysm is the only independent risk factor for ONP severity.

Prevalence of nerve-vessel contact at cisternal segments of the oculomotor nerve in asymptomatic patients evaluated with magnetic resonance images

Background Some studies indicated that cases of idiopathic oculomotor nerve palsy can be explained by vascular compression of the oculomotor nerve. Vascular contact with or compression to the cisternal segment of the oculomotor nerve has been reported frequently in asymptomatic individuals. In this study, we retrospectively analyzed the relationship between the oculomotor nerve＇s cisternal segment and adjacent arteries in asymptomatic patients and the prevalence of this occurrence via magnetic resonance imaging （MRI）. Method MRI of bilateral oculomotor nerves in 93 asymptomatic patients were reviewed. The oculomotor nerve-artery relationship was evaluated and classified from levels 1 to 3, representing the degrees of contact on oblique transverse and oblique sagittal reconstructed MRI. Prevalence of the nerve-artery relationship at each level was described. The correlation between the nerve-vessel relationship （levels） and the age was analyzed by Spearman＇s rank correlation analysis. Results Cisternal segment of the oculomotor nerve did not have contact with any artery （level 1） in 27.4% （51/186） nerves. One hundred nerves made contact with at least one artery （level 2）, but their shapes or configurations were not changed; 35 nerves （18.8%） were displaced or distorted due to artery compression （level 3）. The posterior cerebral artery had the greatest incidence of making contact with or compressing the cisternal segment of the oculomotor nerve （58.1%）. No significant correlation between nerve-vessel relationship （levels） and the age was found in this study. Conclusions Whether oculomotor nerve contact with or compression by one or more arteries is of high prevalence in asymptomatic individuals as evidenced by MRI examination. There is no correlation with individual age. Discretion should be used when making an etiological diagnosis of vascular compression for patients with oculomotor nerve palsy. Further investigation of other causes is warranted.

Acquired ptosis associated with oculomotor and contralateral facial nerve synkinesis： the first reported case

Dear Editor,Evidence of oculomotor nerve（ON）synkinesis is a common occurrence following both acquired and congenital III nerve palsy[1].It is generally accepted that aberrant regeneration is the likely aetiology of synkinesis in acquired III nerve palsy,following intracranial aneurysm,trauma,

Microvascular decompression for a patient with oculomotor palsy caused by posterior cerebral artery compression:A case report and literature review

BACKGROUND Aneurysm compression,diabetes,and traumatic brain injury are well-known causative factors of oculomotor nerve palsy(ONP),while cases of ONP induced by neurovascular conflicts have rarely been reported in the medical community.Here,we report a typical case of ONP caused by right posterior cerebral artery(PCA)compression to increase neurosurgeons’awareness of the disease and reduce misdiagnosis and recurrence.CASE SUMMARY A 54-year-old man without a known medical history presented with right ONP for the past 5 years.The patient presented to the hospital with right ptosis,diplopia,anisocoria(rt 5 mm,lt 2.5 mm),loss of duction in all directions,abduction,and light impaired pupillary reflexes.Magnetic resonance angiography and computed tomography venography examinations showed no phlebangioma,aneurysm,or intracranial lesion.After conducting oral glucose tolerance and prostigmin tests,diabetes and myasthenia gravis were excluded.Cranial nerve magnetic resonance imaging showed that the right PCA loop was in direct contact with the cisternal segment of the right oculomotor nerve(ON).Microvascular decompression(MVD)of the culprit vessel from the ON through a right subtemporal craniotomy was carried out,and the ONP symptoms were significantly relieved after 3 mo.CONCLUSION Vascular compression of the ON is a rare pathogeny of ONP that may be refractory to drug therapy and ophthalmic strabismus surgery.MVD is an effective treatment for ONP induced by neurovascular compression.

Validity and reliability of the Ocular Motor Nerve Palsy Scale

Objective and accurate assessment of the degree of ocular motor nerve palsy is helpful not only in the evaluation of prognosis, but also for the screening of treatment methods. However, there is currently no comprehensive measure of its severity. In this study, we designed the Ocular Motor Nerve Palsy Scale and investigated its validity and reliability. Six experts were invited to grade and evaluate the scale. The study recruited 106 patients with a definite diagnosis of unilateral isolated ocular motor nerve palsy. Three physicians evaluated the patients using the scale. One of the three physicians evaluated the patients again after 24 hours. The content validity index（CVI） and factor analysis were used to analyze the scale＇s construct validity. The intraclass correlation coefficient and Cronbach＇s alpha were used to evaluate the inter-rater and test-retest reliability and the internal consistency. The CVI results（I-CVI = 1.0, S-CVI = 0.9, Pc = 0.016, K＊ = 1） indicated good content validity. Factor analysis extracted two common factors that accounted for 85.2% of the variance. Furthermore, the load value of each component was above 0.8, indicating good construct validity. The Ocular Motor Nerve Palsy Scale was found to be highly reliable, with an inter-rater reliability intraclass correlation coefficient of 0.965（P 0.01）, a test-retest reliability intraclass correlation coefficient of 0.976（P 0.01）, and Cronbach＇s alpha values of 0.63–0.70. In conclusion, the Ocular Motor Nerve Palsy Scale with good validity and reliability can be used to quantify the severity of ocular motor nerve palsy. This study was registered at Chinese Clinical Trial Registry（registration number： Chi CTR-OOC-17010702）.

A standardized method to create peripheral nerve injury in dogs using an automatic non-serrated forceps

This study describes a method that not only generates an automatic and standardized crush injury in the skull base, but also provides investigators with the option to choose from a range of varying pressure revels. We designed an automatic, non-serrated forceps that exerts a varying force of 0 to 100 g and lasts for a defined period of 0 to 60 seconds. This device was then used to generate a crush injury to the right oculomotor nerve of dogs with a force of 10 g for 15 seconds, resulting in a deficit in the pupil-light reflex and ptosis. Further testing of our model with Toluidine-blue staining demonstrated that, at 2 weeks post-surgery disordered oculomotor nerve fibers, axonal loss, and a thinner than normal myelin sheath were visible. Electrophysiological examination showed occasional spontaneous potentials. Together, these data verified that the model for oculomotor nerve injury was successful, and that the forceps we designed can be used to establish standard mechanical injury models of peripheral nerves.

Neurotization of oculomotor,trochlear and abducent nerves in skull base surgery

Objective To anatomically reconstruct the oculomotor nerve, trochlear nerve, and abducent nerve by skull base surgery. Methods Seventeen cranial nerves (three oculomotor nerves, eight trochlear nerves and six abducent nerves) were injured and anatomically reconstructed in thirteen skull base operations during a period from 1994 to 2000. Repair techniques included end-to-end neurosuture or fibrin glue adhesion, graft neurosuture or fibrin glue adhesion. The relationships between repair techniques and functional recovery and the related factors were analyzed.Results Functional recovery began from 3 to 8 months after surgery. During a follow-up period of 4 months to 6 years, complete recovery of function was observed in 6 trochlear nerves (75%) and 4 abducent nerves (67%), while partial functional recovery was observed in the other cranial nerves including 2 trochlear nerves, 2 abducent nerves, and 3 oculomotor nerves.Conclusions Complete or partial functional recovery could be expected after anatomical neurotization of an injured oculomotor, trochlear or abducent nerve. Our study demonstrated that, in terms of functional recovery, trochlear and abducent nerves are more responsive than oculomotor nerves, and that end-to-end reconstruction is more efficient than graft reconstruction. These results encourage us to perform reconstruction for a separated cranial nerve as often as possible during skull base surgery.