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.

Damage to the inferior oblique muscle branch of the oculomotor nerve: a complication during orbital fat decompression.

PURPOSE: To present patients who suffered damage to the inferior oblique muscle branch of the oculomotor nerve during orbital fat decompression. METHODS: This study was a retrospective chart review of all patients who underwent orbital decompression surgery between April 2009 and June 2016 by the authors. RESULTS: Among 414 sides from 226 consecutive patients who underwent orbital decompression, the inferior oblique muscle branch was injured in two sides (0.5%) of two patients. Both patients showed hypotropia and incyclotropia immediately after surgery. Within 6 months of injury, ocular deviation on primary gaze had mostly resolved after conservative treatment. None of the patients underwent strabismus surgery. Postoperative computed tomographic images demonstrated that the affected branch was indistinct 3-4 mm posterior to the inferior oblique muscle. CONCLUSIONS: This report indicates that injury to the inferior oblique muscle nerve branch can occur at a point posterior to the inferior oblique muscle during orbital fat decompression; however, the resulting ocular deviation improves considerably within 6 months of injury.

Oculomotor Cognitive Control Abnormalities in Australian Rules Football Players with a History of Concussion.

This study used oculomotor, cognitive, and multi-modal magnetic resonance imaging (MRI) measures to assess for neurological abnormalities in current asymptomatic amateur Australian rules footballers (i.e., Australia's most participated collision sport) with a history of sports-related concussion (SRC). Participants were 15 male amateur Australian rules football players with a history of SRC greater than 6 months previously, and 15 sex-, age-, and education-matched athlete control subjects that had no history of neurotrauma or participation in collision sports. Participants completed a clinical interview, neuropsychological measures, and oculomotor measures of cognitive control. MRI investigation involved structural imaging, as well as diffusion tensor imaging and resting-state functional MRI sequences. Despite no group differences on conventional neuropsychological tests and multi-modal MRI measures, Australian rules football players with a history of SRC performed significantly worse on an oculomotor switch task: a measure of cognitive control that interleaves the response of looking towards a target (i.e., a prosaccade) with the response of looking away from a target (i.e., an antisaccade). Specifically, Australian footballers performed significantly shorter latency prosaccades and found changing from an antisaccade trial to a prosaccade trial (switch cost) significantly more difficult than control subjects. Poorer switch cost was related to poorer performance on a number of neuropsychological measures of inhibitory control. Further, when comparing performance on the cognitively more demanding switch task with performance on simpler, antisaccade/prosaccades tasks which require a single response, Australian footballers demonstrated a susceptibility to increased cognitive load, compared to the control group who were unaffected. These initial results suggest that current asymptomatic amateur Australian rules football players with a history of SRC may have persisting, subtle, cognitive changes, which are demonstrable on oculomotor cognitive measures. Future studies are required in order to further elucidate the full nature and clinical relevance of these findings.

Quantification and analysis of saccadic and smooth pursuit eye movements and fixations to detect oculomotor deficits.

Assessment of deficits in oculomotor function may be useful to detect visuomotor impairments due to a closed head injury. Systematic analysis schemes are needed to reliably quantify oculomotor deficits associated with oculomotor impairment via brain trauma. We propose a systematic, automated analysis scheme using various eye-tracking tasks to assess oculomotor function in a cohort of adolescents with acute concussion symptoms and aged-matched healthy controls. From these data we have evidence that these methods reliably detect oculomotor deficits in the concussed group, including reduced spatial accuracy and diminished tracking performance during visually guided prosaccade and self-paced saccade tasks. The accuracy and tracking deficits are consistent with prior studies on oculomotor function, while introducing novel discriminatory measures relative to fixation assessments - methodologically, a less complicated measure of performance - and thus represent a reliable and simple scheme of detection and analysis of oculomotor deficits associated with brain injury.

Traumatic avulsion of the oculomotor nerve documented by high-resolution magnetic resonance imaging.

Autopsy studies have described definitive traumatic avulsion of the oculomotor nerve from the brainstem; however, detailed characterization of mechanisms and localization of traumatic nerve injury has yet to be definitively described in vivo. We report the case of a 13-year-old girl in whom high-resolution magnetic resonance imaging confirmed irreversible injury to the left oculomotor nerve after trauma.

Isolated traumatic neurogenic ptosis with delayed recovery.

PURPOSE: To describe the entity of isolated neurogenic ptosis due to presumed tractional injury to the nerve of innervation of the levator palpebrae superioris, with recovery occurring over a period up to 6 months. METHODS: Retrospective case review. RESULTS: Three cases of presumed neurapraxic injury to the nerve of innervation to the levator palpebrae superioris are described. Two cases had a clear history of traction to the upper eyelid. There was no evidence of damage to other extraocular muscles or their nerves of innervation in 2 cases and mild transient superior rectus underaction in 1. Maximal recovery occurred over a period of up to 6 months. CONCLUSIONS: Traumatic neurapraxic injury to the nerve of innervation to the levator palpebrae superioris may occur in certain types of upper eyelid injury, most notably when there is significant forward traction applied to the upper eyelid. Although recovery may occur within weeks, as previously described, this series illustrates that recovery may take up to 6 months.

Clinical features and functional recovery of traumatic isolated oculomotor nerve palsy in mild head injury with sphenoid fracture.

OBJECT: The aim of this study was to provide information about long-term functional outcome in patients with isolated oculomotor nerve palsy following minor head injury and to discuss surgical treatment of these patients, especially those with accompanying sphenoid fracture. METHODS: A retrospective analysis was made of 26 patients with traumatic isolated oculomotor nerve palsy. The severity of oculomotor nerve palsy and the functional recovery were evaluated based on extraocular muscle movement, eyelid movement, and pupil size. On average, patients were evaluated 3.6 days after the initial injury, and the average follow-up period was 14.2 months (range 3 months-2 years). RESULTS: Twenty men and six women were enrolled in this study. The most common cause of trauma was motor vehicle accident in 17 (65.4%) of 26. Among all the recorded symptoms, internal ophthalmoplegia was most frequently seen. The recovery rates of ptosis, external ophthalmoplegia, and internal ophthalmoplegia were 95% (19 of 20 patients), 83.3% (15 of 18 patients), and 50% (13 of 26 patients), respectively. The 6 patients with sphenoid fracture underwent surgical decompression of the superior orbital fissure, after which all patients experienced recovery from ptosis and external ophthalmoplegia and 66.7% (4 of 6 patients) recovered from internal ophthalmoplegia. CONCLUSIONS: Limited eye movement may be a major factor that negatively affects functional recovery after mild head injury. Sphenoid fracture might be one of the potential mechanisms involved in traumatic isolated oculomotor nerve palsy after mild head injury. Surgical decompression should be considered when there is evidence of bone compression of the superior orbital fissure.

Sinquinesis óculomotora: dos casos de pacientes excepcionales / Oculomotor synkinesis: two cases excepcional patients

Las sinquinesis son movimientos simultáneos o coordinados en secuencia de mivimientos de músculos suplidos por diferentes nervios o por ramas independientes del mismo nervio que ocurren luego de la recuperación de una lesión axonal periferica; son debidos a la dirección errónea ("misdirection") que toman algunos axones hacia otros músculos que no constituyen su objetivo o blanco; así, cuando el paciente intenta mover algunos músculos, ocurren contracciones involuntarias en otros, no esperadas anatómicamente. Es una suerte de recableado mal realizado y confuso. En las dos pacientes que constituyen nuestro informe, ocurrieron alteraciones óculomotoras excepcionales. En la primera de 60 años portadora de un aneurisma gigante del senocavernoso izquierdo, la sinquinesis nerviosa aberrante ocurrió entre los nervios craneales tercero y sexto. En la segunda de 22 años a quien se resecó un osteocondroma gigante de la fosa media derecha, desarrolló una parálisis total del tercer nerviocraneal con sinquinesis trigémino-oculomotora entre el músculo pterigoideo derecho y el elevador del párpado superior; así como también entre el tercero (recto inferior) y sexto nervios (recto externo) ipsolateral. Se revisa la literatura al respecto.

Synkinesis are simultaneous or coordinated sequential movements of muscles that are supplied by different nerves or have independent nerve branches. They occur after the recovery a peripheral axonal injury. They are due to axons taking a wrong direction ("misdirection") towards muscles that do not constitute their objetives or targets. Thus, when the patient attempts to move a muscle, other muscles show anatomically unexpected involuntary contractions. It is a sort of confusing rewiring. Our report is based on the exceptional oculomotor alterations that occurred in two patients. In the first patient, a 60 years-old female carrying a giant aneurysm of the left cavernous sinus, the aberrant nerve synkinesis ocurred between the third and sixth cranial nerves. In the second patient, a 22 year-old female to whom was resected a giant osteochondroma of the right middle fossa, developed a total paralysis of the third cranial nerve with trigeminal oculomotor synkinesis between the right pterygoid muscle and the elevator of the upper eyelid; as well as between the inferior rectus and ipsilateral external rectus. We review the literature on the subject.

Intraoperative oculomotor nerve monitoring predicts outcome following clipping of posterior communicating artery aneurysms.

Valid parameters do not exist to predict oculomotor nerve palsy (ONP, ptosis and/or diplopia) intraoperatively. In 49 operations involving 46 patients with posterior communicating artery aneurysms, the oculomotor nerves were stimulated after the aneurysms were clipped. A quantitative analysis of evoked compound muscle action potential (CMAP) parameters (stimulus threshold, amplitude and latency) from the levator palpebrae superioris (LPS) muscle was performed. Absolute values of CMAP amplitude statistically correlated with initial and long-term oculomotor nerve function (ONF) after surgery (p<0.05). In addition, subarachnoid hemorrhage (SAH) significantly influenced the CMAP threshold (p<0.05). Monitoring of LPS muscle activity is valuable in the assessment of ONF, and the CMAP amplitude of LPS may be a reliable predictor of ONF. Moreover, SAH has an impact on the parameters of the LPS CMAP.

Aberrant regeneration of the third cranial nerve.

BACKGROUND: Aberrant regeneration of the third cranial nerve is most commonly due to its damage by trauma. CASE: A ten-month old child presented with the history of a fall from a four-storey building. She developed traumatic third nerve palsy and eventually the clinical features of aberrant regeneration of the third cranial nerve. The adduction of the eye improved over time. She was advised for patching for the strabismic amblyopia as well. CONCLUSION: Traumatic third nerve palsy may result in aberrant regeneration of the third cranial nerve. In younger patients, motility of the eye in different gazes may improve over time.

Grado de desviación en posición primaria de la mirada (PPM) en lesión del III y VI nervio / Degree of deviation in primary position in III and VI nerve injury

Objetivo: Evaluar las características en el grado de desviación en las lesiones del II y VI nervio, para establecer correlación entre cada una de las situaciones clínicas. Materiales y métodos: Se estudiaron expedientes de pacientes con lesión del III y VI nervio en el Hospital Nuestra Señora de La Luz, desde enero de 2000 hasta enero de 2005. En todos los pacientes se realizó examen oftalmológico completo, donde se evidenciara limitación de -4 ó mayor en III nervio, y limitación de la abducción de -4 ó mayor en VI nervio. Resultados: Se analizaron 71 expedientes, 31 con lesión del III nervio (11 con parálisis, 20 con paresia); 40 con lesión del VI nervio (16 con parálisis y 24 con paresia). En cuanto a la desviación media y la moda según el grado de limitación, se evidenció mayor desviación en la lesión del III nervio. Conclusiones: Las desviaciones horizontales encontradas cuando existe daño al III nervio son en general de mayor magnitud que las encontradas cuando existe daño al VI nervio.

Purpose: To evaluate characteristics in the amount of deviation in III and VI nerve palsies, to establish a correlation between each one of clinical situations. Methods: Retrospective study where the files of patients with the diagnosis of III or VI nerve injury in the Hospital Nuestra Señora de La Luz were reviewed from january of 2000 to january of 2005. All patients had a complete ophthalmologic evaluation, in whitch the deviation was noticed, and in those with an affection of the III nerve the limitation of the adduction went from -4 or more, and in those with de VI nerve affected, the limitation of the abduction went from -4 or more. Results: 71 patients were included, 31 with III nerve injury and 40 with VI nerve injury. Conclusions: Horizontal deviations found in III nerve palsies are larger than those found in VI nerve palsies.