Isolated Fourth Cranial Nerve Paresis with Le Fort II Injury: Challenges to Diagnosis and Management

Introduction: Eye injury is an important consideration in every patient with maxillofacial trauma. Extraocular muscle involvement often results in ocular motility disorders and diplopia. The association between maxillofacial trauma without head injury and persistent cranial nerve IV deficit has not previously been reported in the oral and maxillofacial surgery or ophthalmology literature. The trochlear nerve innervates the superior oblique muscle of the eye.  Originating in the upper medial side of the orbit, the superior oblique muscle is responsible for intorsion, as well as depression and abduction of the globe. Palsy of the trochlear nerve manifests as binocular diplopia in all gazes. The affected globe demonstrates weakened abduction, as well as upward drift relative to the unaffected globe due to unopposed extraocular muscle activity. Because the depressor function of the superior oblique without input from the inferior rectus is most evident during globe adduction, this maneuver is used to test trochlear nerve function. This case study will review the ocular examination, findings, challenges to diagnoses, and treatment. 

Patient and Diagnosis:A forty-four year-old man presented to a regional trauma center after sustaining injury to the maxillofacial region. In addition to clinical and radiographic findings consistent with a classic LeFort II fracture, the patient acutely demonstrated binocular diplopia in all fields of view, including primary gaze. His ophthalmologic examination was otherwise within normal limits. Further examination with the Parks-Bielschowsky three-step and Maddox Rod test revealed persistent right trochlear nerve paresis.  

Management: Surgical intervention was postponed, as the patient’s diplopia on primary gaze was not explained by the minimally displaced orbital floor component of his fractures.  Interventions considered included open reduction and internal fixation, and delay of surgical intervention to correct malocclusion so as to allow for spontaneous resolution of the patient's superior oblique paresis.  After six weeks without resolution of the trochlear nerve paresis the patient underwent LeFort 1 osteotomy to correct his malocclusion.  His trochlear nerve paresis persisted following the osteotomy as anticipated. Subsequently, his diplopia was treated with a prism lense set to make indicated optical changes in vertical alignment.

Discussion: Acute post-traumatic paresis of the trochlear nerve is almost exclusively the result of closed head trauma rather than maxillofacial injury.  'Blurry' vision is most commonly experienced after such head trauma, with true diplopia resulting only in more severe cases. Isolated trochlear nerve paresis may result from a stretch or compression injury, as with increased intracranial pressure or tumor.  Nerve demyelinating conditions (e.g. multiple sclerosis) may also result in trochlear nerve dysfunction.  Persistent diplopia has significant effects on quality of life. Only 45% of patients with post-traumatic diplopia are able to perform their premorbid occupations. Rarely in any of these conditions is the trochlear nerve affected in isolation.  Even more uncommon is trochlear nerve paralysis in isolated maxillofacial trauma. During routine ophthalmologic examination with various directions of gaze, ocular movements may appear to be full despite weakness of the superior oblique muscle.  Isolated cranial nerve injury must be considered in the differential diagnosis of the maxillofacial trauma patient with diplopia.

References:

Brazis PW. Palsies of the trochlear nerve: diagnosis and localization – recent concepts. Mayo Clin Proc 68:501, 1993. 

Loba P, et al. Diplopia as a factor influencing occupational and social activities of people after orbital trauma. Medycyna Pracy 63(5): 541-546, 2012.