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Show Journal of Clinical Neuro- ophthalmology 10( 2): 111- 114, 1990. Acquired Trigemino- Abducens Synkinesis Scott K. Nelson, M. D., and Lanning B. Kline, M. D. © 1990 Raven Press, Ltd., New York Summary: A 26- year- old woman sustained closed head trauma following a motor vehicle accident. Her injuries included complete trigeminal and abducens nerve palsies. Eleven months later eye muscle surgery succeeded in making her orthophoric in primary gaze although her right abduction deficit persisted. Eighteen months after injury the patient was able to fully abduct her right eye with jaw thrust to the left. With abduction of the right eye there was associated globe retraction and narrowing of the palpebral fissure. This is the second reported case of trigemino- abducens synkinesis. Mechanisms to explain this phenomenon are discussed. Key Words: Aberrant regeneration- Abducens nerveSynkinesis- Trigeminal nerve- Trigemino- abducens synkinesis. From the Combined Program in Ophthalmology, Eye Foundation Hospital- University of Alabama School of Medicine, Birmingham, Alabama. Address correspondence and reprint requests to Dr. Lanning B. Kline, Suite 555, 1600 Seventh Avenue South, Birmingham, AL 35233, U. S. A. 111 Acquired oculomotor synkinesis is characterized by paradoxical movements of the muscles supplied by the third cranial nerve. The great majority of cases have a preceding oculomotor nerve palsy, but exceptions have been reported ( 1- 3). Additionally, case reports have described acquired synkineses between the oculomotor and abducens nerves ( 4,5) and between the trigeminal and abducens nerves ( 6). We report the second case of acquired trigemino- abducens synkinesis. CASE REPORT A 26- year- old woman sustained severe closed head trauma after being struck by a motor vehicle in June 1985. Examination showed the patient to be conscious but disoriented, with right facial palsy, right hemotympanum, and left tension pneumothorax. Visual acuity was light perception on the right and 20/ 25 on the left. There was complete right ophthalmoplegia with right ptosis, while eye movements on the left were full. The right pupil was 7 mm and nonreactive, the left pupil 4 mm and briskly reactive, and a right afferent pupillary defect was present. Fundi were normal. Facial tomograms and cranial computed tomography demonstrated fractures of the right temporal, parietal, frontal, and zygomatic bones with posterior displacement of the right pterygoid process of the sphenoid bone. Bilateral fractures of the maxillae and lateral orbital rims were also noted. Three weeks later there was partial recovery of right oculomotor nerve function. Visual acuity was 20/ 100 on the right and the right optic disc was pale. Decreased sensation over all three divisions of the right trigeminal nerve was present, as was weakness of the muscles of mastication supplied by the right mandibular nerve. By May 1986 the patient had complete recovery of right oculomotor nerve function, while abducens and facial nerve palsies persisted. Com- 112 S. K. NELSON AND L. B. KLINE FIG. 1. Abduction of the right eye is achieved with jaw thrust to the left, but not with jaw thrust to the right or voluntary opening of the mouth. plete right facial anesthesia remained, but there was return of motor function of the mandibular nerve. At this time the patient underwent a right Jensen procedure and an 8 mm recession of the right medial rectus muscle. Postoperatively, she was orthophoric in primary gaze, although a complete right abduction deficit persisted. In November 1987 ( 18 months following head injury) the patient reported the ability to abduct her right eye when she thrust her jaw to the left. Examination showed that she could not voluntarily abduct her right eye, but would achieve full abduction with left jaw thrust ( Fig. 1). During abduction there was retraction of the right eye and narrowing of the palpebral fissure ( Fig. 2). While ocular and eyelid movements and pupillary reactions showed no other signs of aberrant regeneration of the ocular motor nerves, there was evidence of anomalous reinnervation of the facial nerve ( Fig. 3). DISCUSSION Bielschowsky ( 7) first suggested misdirected peripheral nerve regeneration as an explanation for the observed synkinetic eye movements following some oculomotor nerve palsies. Only recently has this concept been challenged. In 1980, Lepore and Glaser ( 3) documented transient oculomotor synkinesis in a patient with ophthalmoplegic migraine. They also reported cases of " primary" aberrant regeneration- synkinetic eye movements occurring without preceding oculomotor nerve palsy ( 1,2). The traditional " hard wiring" concept of aberrant regeneration seemed incompatible with the findings they observed. Alternate mechanisms were proposed, including ephaptic transmission and central synaptic reorganization ( 8) ( Table). Aberrant regeneration involving other ocular motor cranial nerves is rare. Smith and Damast ( 4) rfJrnrtFd J01' 1: r,'( l retr'lCtion syndrome after sixth f'dt'r and Bienfang ( 5) de- J elm Ne- ura- uphtlwlmvl, \ ( 11. i 1'- 1'- 11/ FIG. 2. Eye position in primary gaze ( top) and attempted left and right gaze. With left jaw thrust. patient is able to fully abduct right eye ( bottom), with globe retraction and narrowing of the palpebral fissure. ACQUIRED TRiGEMINO- ABDUCENS SYNKINESIS FIG. 3. There is deepening of the right nasolabial fold when the patient closes her eyes ( right) compared to when they are open ( left). 113 scribed misdirection of right medial and right lateral rectus function after severe head trauma. One other case of acquired trigemino- abducens synkinesis has been reported. McGovern and coworkers ( 6) described a 25- year- old woman who sustained craniofacial trauma and 2 years later developed a synkinesis of involuntary abduction with attempted jaw closure. Using electromyography, these investigators demonstrated motor activity in the right lateral rectus muscle during contraction of the right masseter muscle. The authors felt these clinical findings could best be explained by the following pathway of peripheral nerve misdirection: Proprioceptive fibers from the lateral rectus muscle have been shown to travel with the abducens nerve and interconnect with the first division of the trigeminal nerve in the region of the posterior orbit or cavernous sinus ( 9). These proprioceptive fibers then run into the gasserian gan-glion, where they travel in close proximity to the motor root of the trigeminal nerve at the petrous apex ( 10). Trauma in the region of the petrous apex could result in trigeminal and abducens nerve palsies followed by misdirected regeneration of fibers from the motor root of the trigeminal nerve to the lateral rectus muscle ( Fig. 4). The patient described by McGovern et a1. exhibited globe retraction and palpebral fissure narrowing as seen in our patient. These findings may be due to lack of inhibition of the right medial rectus muscle during the abnormal synkinetic contraction of the right lateral rectus muscle ( 6). The misdirected fibers do not conform to the normal agonist- antagonist innervational pattern dictated by Sherrington's law. Our patient's observed findings cannot be adequately explained by the theory of central reorganization due to the spatial separation of the trigeminal and abducens nerve nuclei in the pons. Similarly, the anatomic separation of the abducens and TABLE. Proposed mechanisms of oculomotor synkinesis Theory Aberrant regeneration Ephaptic transmission Central synaptic reorganization Explanation Sprouting ofaxons from the proximal end of a severed or damaged nerve into inappropriate distal nerve sheath channels. Side- to- side interaxonal cross stimulation occurring when the Schwann cell- myelinendoneurial cell complex is damaged. Peripheral nerve injury induces retrograde changes that result in synaptic reorganization in the brainstem. Produces a synkinesis by unmasking previously encoded connections between subnuclei. Gasserian Ganglion Abducens n. ~ Ophthalmic n. Iff'?'~~ Maxillary n. / FIG. 4. Proposed pathway of trigemino- abducens aberrant regeneration. Motor trigeminal fibers regenerate aberrantly into the nerve sheaths of proprioceptive fibers of the ophthalmic nerve which travel to the abducens nerve. J Clin NeurD- ophthalmol, Vol. 10, No. 2, 1990 114 S. K. NELSON AND L. B. KLINE trigeminal nerves would argue against the concept of peripheral ephaptic transmission. We believe our case can best be explained by the process of peripheral nerve aberrant regeneration utilizing the anatomic pathway described above. REFERENCES 1. Schatz NI, Savino PI, Corbett JJ. Primary aberrant oculomotor regeneration: a sign of intracavemous meningioma. Arch Neurol 1977; 34: 29- 32. 2. Boghen D, Chartrand J- p, Laflamme P, et al. Primary aberrant third nerve regeneration. Ann NeuroI1979; 6: 415- 18. 3. Lepore FE, Glaser JS. Misdirection revisited- a critical appraisal of acquired oculomotor nerve synkinesis. Arch OphthalmoI1980; 98: 2206- 9. 4. Smith JL, Damast M. Acquired retraction syndrome after sixth nerve palsy. Br JOphthalmoI1973; 57: 110-- 14. 5. Packer AI, Bienfang DC. Aberrant regeneration involving the oculomotor and abducens nerves. Ophthalmologica 1984; 189: 80-- 5. 6. McGovern ST, Crompton JL, Ingham P. 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