What is the pathophysiology of acquired trochlear nerve palsy (fourth nerve palsy)?

Updated: Oct 08, 2019
  • Author: Zafar A Sheik, MD, MD; Chief Editor: Andrew G Lee, MD  more...
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The long course of the trochlear nerve makes it especially susceptible to injury in association with severe head trauma. Contrecoup forces can compress the nerve against the rigid tentorium, which lies adjacent to the nerve for much of its course. Injury to nerve can occur anywhere along its course from midbrain to orbit. Lesions at the nucleus cause contralateral superior oblique palsy, since the nerve decussates at anterior medullary velum, caudal to inferior colliculus. Midbrain trauma can produce bilateral superior oblique palsy by contusive injury of decussation of nerves. Compression or ischemia at this site also can produce bilateral palsy.

See the image below.

Patient with traumatic bilateral superior oblique Patient with traumatic bilateral superior oblique palsy; note right hypertropia on right head tilt and left hypertropia on left head tilt.

One should suspect a lesion to the trochlear nucleus or fascicle when palsy is associated with a contralateral Horner syndrome or an ipsilateral relative afferent pupillary defect (RAPD; especially without concomitant visual loss [ie, tectal RAPD]). This is due to the close proximity of the sympathetic pathways in the dorsolateral tegmentum of the midbrain and the pretectal afferent pupillary fibers that run through the superior colliculus.

Tumors or aneurysms causing compressive injury in the subarachnoid space generally damage adjacent structures and produce associated neurologic signs. The same is true of lesions in area of cavernous sinus and orbital apex, which generally produce multiple cranial neuropathies. In rare cases, fourth nerve palsy may result from any cause of increased intracranial pressure such as pseudotumor cerebri or meningitis. Direct orbital injury can result in a clinical picture that resembles fourth nerve palsy, but superior oblique weakness in this setting most likely is due to direct damage to muscle or tendon.

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