Nerve Synkinesis Research Articles

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

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

Subjective and objective outcome measures in the treatment of facial nerve synkinesis with onabotulinumtoxinA (Botox).

To evaluate the Sunnybrook Facial Grading System (SFGS) and Facial Clinimetric Evaluation Scale (FaCE Scale) instrument outcome measures pre- and 30-day posttreatment of facial nerve synkinesis with botulinum toxin with attempts to correlate the 2 scales. An IRB approved retrospective review of 22 patients with facial nerve synkinesis where the surgeon completed the SFGS and the patient completed the FaCE prior to receiving onabotulinumtoxinA therapy, the SFGS, and FaCE scales were completed again 1 month later. Of the 22 patients, 9 complete datasets were analyzed. Mean patient age was 59.8; 8 (89%) women and 1 (11%) men. Overall SFGS composite score decreased from 57.6 ± 20.9 to 45.2 ± 13.5, (p = 0.001). SFGS subdomain synkinesis significantly improved (p < 0.001), while voluntary movement significantly decreased (p = 0.002). A difference in the resting symmetry was not statistically significant (p = 0.08). The FaCE scale composite score significantly improved from 40.9 ± 9.5 to 47.6 ± 11.9, (p = 0.03). FaCE subdomains facial comfort (p = 0.005) and social function (p = 0.009) significantly improved, while oral function, eye comfort, facial movement, and lacrimal control did not. The Δ pre/post-SFGS composite score did not correlate with the Δ pre/post-FaCE composite score (rs= -0.318). Subdomain analysis demonstrated significant negative correlation between Δ pre/post-SFGS synkinesis score and Δ pre/post-FaCE eye comfort score (rs = -0.826, p < 0.01). Significant improvement was seen in objectively reported synkinesis following botulinum toxin therapy. An improvement was noted in the overall subjective facial nerve functioning following therapy along with improvement in social functioning and facial comfort. A meaningful negative correlation was noted when comparing the SFGS "synkinesis" subdomain with the FaCE scale subdomain "eye comfort", implying improvement in eye comfort with control of synkinesis.

Congenital Oculomotor Nerve Synkinesis Associated Wwith Fetal Retinoid Syndrome

Isotretinoin (RA), used for the treatment of cystic acne, is a powerful teratogen, causing craniofacial dysmorphisms and neural tube defects. We present two patients with RA embryopathy and oculomotor nerve synkinesis. Retrospective review of patient records. Two patients presented with third nerve synkinesis and fetal RA exposure. Both had marked elevation of the upper eyelids on adduction such that the lid fissures alternately opened and closed on gaze from side to side. Both patients showed typical dysmorphisms of RA embryopathy. The first patient had complete agenesis of the cerebellar vermix and died at 2 years. The second patient had restricted extraocular muscles in one eye and was exotropic and hypotropic. Both patients demonstrated simultaneous innervation of the medial rectus and levator palpebrae muscles causing coincident lid elevation in adduction. This evidence of oculomotor nerve synkinesis is consistent with animal studies showing abnormalities in the formation of cranial nerve ganglia following fetal RA exposure. RA is a powerful teratogen. These patients provide additional clinical evidence of its influence on neural migration during early development.

Pathogenesis of facial nerve synkinesis in guinea pig

Problem: The facial nerve synkinesis is one of the common complaints after facial palsy. However, the precise mechanism of synkinesis is still unknown. In this study we tried to establish an animal model of synkinesis. Methods: Extratemporal portion of the facial nerve (group 1, n = 6) and the intratemporal portion (group 2, n = 6) were compressed by using a micro needle holder. After the compression, the grade of facial nerve injury was evaluated by electroneurography. The existence of synkinesis was judged by the presence of R1 in the orbicularis oris muscle by the electrophysiolgical blink reflex. For evaluating the misdirection of nerve fibers, double labeling was performed by injecting retrograde fluorescence tracer in the orbicularis oculi muscle and the orbicularis oris muscle, and then facial nucleus was investigated for the presence of the neurons with aberrant fluorescence. Results: In both groups, all animals showed the ENoG threshold under 10%. In group 1, none of animals developed synkinesis. On the other hand, in group 2, all animal developed synkinesis. Furthermore, disrupted neurons in the facial nucleus, representing the existence of misdirection, were observed in all animals of group 2. Conclusion: In this study we succeeded in making a synkinesis model only in group 2 and reported the existence of misdirection in these animals. Sunderland found that the facial nerve consisted of a single bundle in the intratemporal portion, even though it had a mulitifuniculated plexiform structure in the extratemporal portion. Because of this anatomical feature, when the facial nerve was injured in the intra- and extra-temporal portions, the misdirection may occur only in the intra-temporal portion. This is thought as a reason for the appearance of synkinesis only in group 2. Significance: It is important to know the pathogenesis of synkinesis for diagnosing and treating facial nerve disorders. Support: None reported.

Schwannoma of the greater superficial petrosal nerve

A case of an intracranial schwannoma originating from the greater superficial petrosal nerve with wide extension into the pterygopalatine fossa in a 20-year-old woman without neurofibromatosis is reported. The motor facial nerve including the geniculate ganglion was not affected. At presentation the patient had vertigo, progressive hearing loss, and mild facial nerve synkinesis without lacrimation deficit. The tumor was detected by CT and MRI. The tumor was completely removed with an intracranial, extradural middle fossa approach with complete preservation of the motor facial nerve function. To our knowledge, this is the first reported case of an isolated schwannoma of the greater superficial petrosal nerve without involvement of the motor facial nerve.

Neurinoma of the major petrosus nerve

Facial nerve schwannomas are rare benign tumors, when occurring, they are located most frequently in the distal fallopian canal and present as extracranial masses. The predominant symptom is a progressive facial nerve paralysis. We report a 20-year-old woman with an intracranial schwannoma originating from the greater superficial petrosal nerve that had wide extension into the pterygopalatine fossa. The motor facial nerve including the geniculate ganglion was not affected. The patient presented with vertigo, progressive hearing loss and mild facial nerve synkinesis but without a lacrimation deficit. The tumor was detected by computed tomography and magnetic resonance imaging. The schwannoma was completely removed using an intracranial, extradural middle fossa approach during which complete preservation of the motor facial nerve was possible. To our knowledge this is the first reported case of an isolated schwannoma of the greater superficial petrosal nerve without involvement of the motor facial nerve.

Patterns of III nerve synkinesis

PURPOSE Various patterns of synkinesis have been observed following both congenital and acquired III nerve palsies. Aberrant regeneration is the most widely accepted mechanism which explains this synkinesis. Two models of aberrant regeneration have been proposed, namely central collateral axon sprouting, and misdirection of regenerating neurones at the site of nerve injury. We have studied the clinical patterns of III nerve recovery and synkinesis following III nerve palsies and relate the findings to the proposed models of synkinesis. MATERIALS AND METHODS Twelve patients with acquired and two with early onset III nerve synkinesis were reviewed. The type, rate and pattern of recovery of III nerve palsy was established from case notes. Observations and measurements of ocular motility, pupil movements, eyelid position and intraocular pressure changes were performed on each patient. Signs of contralateral synkinetic movements were also sought. RESULTS Upper lid retraction on attempted down gaze and in adduction was the most frequent synkinetic movement recorded. Observation of pupil size revealed evidence of pupillary-extraocular muscle synkinesis in all gaze positions except abduction. Similarly, intraocular pressure changes and signs of globe retraction showed widespread extraocular muscle co-contraction. Synkinetic levator innervation of extraocular muscles [i.e., LPS to MR, IR, SR] was also observed, a finding not previously reported in III nerve palsy but predicted by our model of misdirection of regenerating neurones at the site of nerve injury. There was no evidence of contralateral aberrant innervation. CONCLUSION Evidence of III nerve synkinesis in patients with III nerve palsy is widespread and the patterns of synkinesis observed were broadly similar for all patients irrespective of the aetiology. Random aberrant III nerve regeneration at the site of nerve injury best explains the patterns of synkinesis observed. Central collateral axon sprouting does not seem to play a major part in the synkinetic movements observed in acquired III nerve lesions.

Primary Oculomotor Nerve Synkinesis Caused by an Extracavernous Intradural Aneurysm

Primary Oculomotor Nerve Synkinesis Caused by an Extracavernous Intradural Aneurysm

Primary Oculomotor Nerve Synkinesis Caused by an Extracavernous Intradural Aneurysm

Primary oculomotor nerve synkinesis is almost always caused by an intracavernous meningioma or aneurysm. We treated a patient who had signs of primary oculomotor nerve synkinesis from an unruptured extracavernous aneurysm located at the junction of the internal carotid artery and the posterior communicating artery. The aneurysm was successfully clipped, resulting in some improvement in ocular motility and alignment. Although most aneurysms affecting the subarachnoid portion of the oculomotor nerve cause an acute, painful oculomotor nerve paresis, such aneurysms may rarely produce painless primary oculomotor synkinesis and therefore should be considered in the differential diagnosis of this phenomenon.

Deglutition--trochlear synkinesis.

A 48-year-old woman had a history of diplopia induced by swallowing. During the initial volitional phase of deglutition, the left globe was seen to intort and move downward. To the best of our knowledge, this is the first report of this peculiar congenital cranial nerve synkinesis.