By: Varsha Kumari
INTRODUCTION:
The trochlear nerve is the fourth cranial nerve (CN IV), that contains somatic efferent (motor) nerve fibers responsible for controlling eye movements. It is the smallest of all the cranial nerves, although it has the longest intracranial course making it more vulnerable to injury (Kim et al., 2023).
ANATOMY AND FUNCTION:
The trochlear nerve originates from the midbrain at the level of the inferior colliculus. It runs along the lateral wall of the cavernous sinus and enters the orbit via the superior orbital fissure to innervate the contralateral superior oblique muscle in the eye. It is the only cranial nerve that exits from the dorsal aspect of the brainstem and decussates to supply the muscle of the contralateral side controlling ocular movements. The primary action of superior oblique muscle function is intorsion (turn the eyeball inward), depression (especially in adduction) and abduction of the eye (Freddi, 2022; Kim et al., 2023).
TROCHLEAR NERVE PALSY:
Congenital:
The most common cause of an isolated fourth nerve palsy is congenital which is unilateral and characterized by eye deviation, diplopia and postural head abnormalities. This characteristic head tilt occurs towards the unaffected side to compensate for a lack of intorsion from the superior oblique muscle (Kim et al., 2023). Congenital trochlear nerve palsies generally caused by cranial dysinnervation syndrome, which in certain cases might include atrophy of the superior oblique muscle and hypoplasia or agenesis of the trochlear nerve (Trochlear Nerve Palsy – StatPearls – NCBI Bookshelf, n.d.).
Acquired:
Trauma is the most prevalent cause of fourth cranial nerve palsy. Traumatic trochlear nerve palsies are linked to automobile accidents and boxing because they result in rapid deceleration of the head (Kim et al., 2023). Other acquired causes include microvascular diseases (i.e. diabetes and hypertension) demyelinating disease, brainstem stroke or neoplasms, aneurysms, and cavernous sinus disease and some rare causes that have been reported include pseudotumor cerebri, meningioma, Lyme disease, and Guillain-Barre Syndrome, whereas trochlear nerve palsy resulting from moderate frontal or occiput head trauma is a frequent cause of bilateral trochlear nerve palsy (Morillon & Bremner, 2017; Trochlear Nerve Palsy – StatPearls – NCBI Bookshelf, n.d.). The presentation in acquired cases resembles that of congenital palsy. Patients may present with binocular vertical or oblique diplopia or blurry vision that deteriorates with contralateral gaze, ipsilateral head tilt, and down gaze. Patients may also experience difficulty with reading or walking down stairs (Tran & Thompson, 2021).
DIAGNOSIS:
Investigations that may help in diagnosing the etiology of a CN IV palsy include: Blood pressure, lipid panel, fasting blood glucose and hemoglobin A1c (Tran & Thompson, 2021). Most individuals who have isolated fourth nerve palsy do not require a comprehensive neurological assessment. The majority of cases are congenital, and an acquired origin may be ruled out by documenting long-standing head tilt and facial asymmetry. Neuroimaging (magnetic resonance imaging) is required in cases with acquired palsy since there is no correlation with head trauma or the existence of any related neurological abnormalities. Trochlear nerve palsy can occasionally be mistaken for disorders such as myasthenia gravis. Investigations should include nerve conduction studies, computed tomography of the chest to check for thymic mass, and anti-acetylcholine receptor antibody tests (Trochlear Nerve Palsy – StatPearls – NCBI Bookshelf, n.d.).
MANAGEMENT:
Addressing the underlying issue is the cornerstone of treatment after an etiology of CN IV palsy has been established. If microvascular ischemia is the cause of the CN IV palsy, the prognosis is good, and the nerve’s function usually recovers in about six months. Patching the patient’s eye is done to relieve symptomatic diplopia (Tran & Thompson, 2021). It could also be managed with the use of prism glasses. While waiting for a natural recovery, Botulinum toxin injections into the overacting inferior oblique muscle have been explored in cases of acute traumatic trochlear nerve palsy. In many situations, surgical correction is necessary; the pattern and degree of deviation determines the procedure of choice. The most commonly performed procedure is inferior oblique weakening with additional vertical and horizontal rectus surgery if required (Trochlear Nerve Palsy – StatPearls – NCBI Bookshelf, n.d.).
REFERENCES:
Freddi, T. de A. L. (2022). The Trochlear Nerve: Anatomy and Pathology. Seminars in Ultrasound, CT and MRI, 43(5), 400–402. https://doi.org/10.1053/J.SULT.2022.04.007
Kim, S. Y., Motlagh, M., & Naqvi, I. A. (2023). Neuroanatomy, Cranial Nerve 4 (Trochlear). StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK537244/
Morillon, P., & Bremner, F. (2017). Trochlear nerve palsy. British Journal of Hospital Medicine (London, England : 2005), 78(3), C38–C40. https://doi.org/10.12968/HMED.2017.78.3.C38
Tran, L., & Thompson, L. (2021). 3. Cranial nerve IV palsy (trochlear nerve). Disease-a-Month, 67(5), 101132. https://doi.org/10.1016/J.DISAMONTH.2021.101132
Trochlear Nerve Palsy – StatPearls – NCBI Bookshelf. (n.d.). Retrieved March 22, 2025, from https://www.ncbi.nlm.nih.gov/books/NBK565850/
