Isolated Superior Divisional Oculomotor Nerve Palsy and Nystagmus Following Mild Trauma.

Traumatic isolated divisional oculomotor nerve palsy has not been reported following mild head injury. We present an interesting case of a 10-year-old male boy who presented with right-sided ptosis, upgaze palsy, and horizontal nystagmus following a mild head trauma. Magnetic resonance imaging showed right superior rectus muscle atrophy. After observing for 6 months, right inferior rectus recession was done. The abnormal head posture and diplopia got corrected, but nystagmus persisted, although with appreciably decreased amplitude. We here report a rare case of an isolated superior divisional oculomotor nerve palsy following mild head trauma. Nystagmus accompanying a divisional oculomotor nerve palsy has never been reported before, making this case more unique. A critical step-wise approach to the case with possible mechanisms are discussed.

INTRODUCTION

Traumatic isolated oculomotor nerve palsies are uncommon.[12] They are usually associated with severe head trauma and infrequently following a mild head injury. Mild trauma can result in divisional oculomotor nerve palsy in patients who have negative neuroimaging findings.

CASE REPORT

A 10-year-old boy presented with the complaints of drooping of the right upper lid associated with diplopia which worsened on up-gaze of 3 weeks. He suffered an injury to the right forehead region with a badminton racket preceding the onset of symptoms. There was no history of loss of consciousness, nasal bleed, or other neurological deficit following trauma. There was no history of fever, vaccination, or drug intake in the recent past. He had no other systemic comorbidity. There was no history of oscillopsia.

Visual acuity in both the eyes were 6/6 and N6. On examination, there was chin elevation with right-sided moderate ptosis, right frontalis overaction, and limitation of elevation in the right eye [Figure 1]. There was constant, small-amplitude horizontal jerk nystagmus of moderate frequency. There was no anisocoria. The pupillary reaction was normal both to light and accommodation. Orbital margins were intact, and there was no deficit in the infraorbital sensation. Thirty prism diopter of right hypotropia was present in primary gaze. Rest of the anterior and posterior segment was within normal limits.

Figure 1

Preoperative photograph showing chin elevation with right sided moderate ptosis, right frontalis over-action, and limitation of elevation in the right eye

General physical and systemic, including neurological examination was normal. Diplopia charting showed vertical diplopia in the primary gaze which increased on dextroelevation, suggestive of right superior rectus involvement. Forced duction test was negative, pointing toward nerve paresis. Levator palpebrae superior muscle action was 12 mm on the right side and 15 mm on the left side.

Magnetic resonance imaging showed a decrease in the bulk of right superior rectus muscle as compared to the left side suggestive of atrophy (a sign of lower motor neuron palsy) [Figure 2]. There was no evidence of damage to other extraocular muscles. No pathology was detected at the orbital apex region and bony orbital walls. The section at the cavernous sinus and midbrain level of the superior colliculus was normal. The paranasal sinuses were normal. Routine hematological and biochemical investigations were also normal.

Figure 2

Magnetic resonance imaging scan of orbits showing atrophy of the superior rectus-levator complex on the right side (red arrow)

During outpatient follow-up, the patient did not show any signs of recovery. After 6 months, a right inferior rectus recession of 5 mm was performed. The abnormal head posture and extra-ocular movements were improved [Figure 3]. Although the nystagmus persisted, its amplitude decreased appreciably.

Figure 3

Postoperative photograph showing improvement in head posture and elevation in the right eye

DISCUSSION

Traumatic isolated oculomotor nerve palsies, complete or incomplete, pupil involving or pupil sparing, are uncommon.[12] They are usually associated with severe head trauma and infrequently following a mild head injury. Till date, there are three case reports of partial oculomotor nerve palsy following mild head injury.[345] Interestingly, isolated divisional oculomotor nerve palsy following mild trauma has not been reported till date. Ours is a rare case of a superior divisional oculomotor nerve palsy following mild trauma. Even more unique about our case is the association of nystagmus, which has not been reported till date with oculomotor nerve palsy.

Although the anatomical division of the oculomotor nerve occurs in the anterior cavernous sinus, there exists a similar anatomical arrangement even at the level of fasciculus.[6] Thus, a divisional third nerve palsy may occur from pathologies at any location along the course of the oculomotor nerve from the fascicle to the orbit. There are several reports of divisional palsy in children following self-resolving viral neuritis, midbrain neurocysticercosis, cryptococcal meningitis, metastatic subarachnoid infiltration, erosive sinusitis, and orbital metastatic infiltration. Considering the age, history of trauma, clinical presentation and neuroimaging in the absence of red flag signs, further investigations seemed unnecessary in our case.

Solomons et al. and Memon and Paine reported an incidence of 1.2% and 1.1%, respectively, of isolated direct oculomotor nerve palsy in their large case series of the patient.[12] Interestingly, none of these cases was associated with the mild degree of trauma, unlike trochlear nerve palsy which can occur after apparently trivial head trauma. Minor head trauma in patients with occult intracranial mass lesion can precipitate oculomotor nerve palsy.[7] It seems highly unlikely in our case in the absence of neuroimaging and unremarkable clinical evaluation, although the possibility of an aneurysm (compressive or ischemic damage) cannot be ruled out entirely.[8]

The proposed mechanism in our case is the presumed avulsion and neuropraxic injury to the terminal nerve fibers of the superior division of the oculomotor nerve in orbit at the time of injury.[9] Closed head injury of severe degree can cause avulsion of nerve rootlets (resulting from differential movement between the brain stem and supratentorial structures) and neuropraxia and ischemic damage to the nerve anywhere along its path. Although possible, it seems unlike in our patient who sustained a mild head injury.

As the child was initially orthoptic and no history of oscillopsia, we assume that a manifest latent nystagmus due to the acquired palsy. Van Weerden and Houtman reported a case of manifest latent nystagmus of late onset in a 13-year-old girl due to the development of a hypertropia.[10] In patients with manifest latent nystagmus and strabismus, surgical alignment of the eyes can decrease the intensity of nystagmus and may also improve binocularity.

Prognosis of traumatic oculomotor palsy is variable, although full recovery is uncommon. Our patient required a strabismus surgery to improve the abnormal head posture and binocularity in primary gaze. Due to the involvement of a single muscle, the outcome was excellent.

CONCLUSION

Comprehensive regional neuro-anatomy knowledge, clinical skills, and critical approach is necessary when dealing with divisional oculomotor palsy patients. Mild trauma can also result in oculomotor nerve palsy in patients who have negative neuroimaging findings.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.