Eye Movements

Abstract

Eye movements are produced by six extraocular muscles for each eye, which are controlled by the third, fourth and sixth cranial nerves, their nuclei, and specialized populations of neurons in the medulla, pons, midbrain, cerebellum and cerebral hemispheres. Together, these neurons allow the eyes to move quickly together to an object of interest (saccades), follow a moving target (pursuit), maintain ocular alignment (conjugate gaze), and converge on a close target (vergence). Vestibular inputs allow vision to remain fixed on an object despite head movement, whereas their suppression helps the eyes and head follow a moving object together. A lesion in the pathways subserving eye movements leads to characteristic abnormalities that can often be localised upon careful clinical examination. Understanding the anatomy of these pathways and common diseases that affect them facilitates accurate diagnosis and appropriate treatment.

Key Concepts:

  • The third, fourth, and sixth cranial nerves are the final common pathway for all eye movements.

  • Binocular diplopia (that resolves with either eye covered) is the cardinal clinical symptom of misalignment of the eyes.

  • Saccades are fast conjugate eye movements that direct the eyes to a point of interest and originate with signals in the cortex.

  • Pursuits are slower conjugate eye movements that allow the eyes to follow a moving point of interest.

  • Abnormalities of conjugate horizontal eye movements may localise to the pons, where saccadic eye movements are controlled by neurons of the paramedian pontine reticular formation (PPRF) and maintained by neurons of the nucleus prepositus hypoglossus.

  • Abnormalities of conjugate vertical eye movements may localise to the midbrain, where saccadic eye movements are controlled by neurons of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and maintained by neurons of the interstitial nucleus of Cajal (inC).

  • Head and eye movements are coordinated by information from the semicircular canals and otolith organs and their specialized connections with the ocular motor nuclei.

  • The medial longitudinal fasciculus (MLF) is a highly myelinated fibre tract connecting the abducens nuclei and contralateral oculomotor nuclei, serving to facilitate rapid coordinated horizontal eye movements and maintain conjugate gaze.

  • Nystagmus (back and forth oscillations of the eyes) primarily results from abnormalities of the slow eye movement systems and gazeā€holding mechanisms.

Keywords: eye movements; diplopia; vision; gaze; saccade; pursuit; nystagmus; extraocular muscles

Figure 1.

The right superior oblique in varied positions of gaze. (a) With the eye in primary position, the insertion site is pulled toward the trochlea, resulting in a combination of intorsion, depression, and abduction. (b) When adducted, the superior oblique primarily depresses the eye. (c) When abducted, the superior oblique primarily intorts the eye.

Figure 2.

Cardinal Eye Positions of Gaze. The primary muscles active in each position are indicated below the associated eye. Abbreviations: First letter indicates right (R) or left (L), and the next two letters specify the muscle. SR, superior rectus; LR, lateral rectus; IR, inferior rectus; MR, medial rectus; IO, inferior oblique; SO, superior oblique. Note the superior and inferior rectus muscles contribute to vertical eye movements in all positions of gaze. Contributions from the oblique muscles are greatest in adduction.

Figure 3.

Ventral view of the brainstem showing some of the nuclei, pathways, and cranial nerves critical for horizontal eye movements. The ‘X’ over the left medial longitudinal fasciculus illustrates the site of a lesion that would cause a left internuclear ophthalmoplegia (INO).

Figure 4.

Sagittal view of the brainstem showing nuclei and pathways critical to vertical and horizontal saccades. Neurons participating in the initial saccade (burst neurons) are located in the PPRF and riMLF for horizontal and vertical saccades respectively. Neurons holding the eyes in their new position (integrators) are located in the NPH and medial vestibular nucleus for horizontal gaze and in the inC for vertical gaze. RiMLF, rostral interstitial nucleus of the medial longitudinal fasciculus; inC, interstitial nucleus of Cajal; PPRF, paramedian pontine reticular formation; NPH, nucleus propositus hypoglossus.

Figure 5.

Pathways involved in vertical nystagmus. Downbeat nystagmus can result from a relative excess of output from the anterior canals (purple), which can be a consequence of decreased cerebellar flocculus inhibitory output (dark red), or decreased posterior canal output (orange) (e.g. from a cervicomedullary lesion). The eyes drift up, leading to corrective downbeats. Upbeat nystagmus can result from disinhibition of the flocculus by a caudal medullary lesion, or from a lesion to the VTT, which transmits the upward vestibular signal and would cause downward drifting eyes with corrective upbeat nystagmus when lesioned. All structures and pathways listed are bilateral – note only pathways from one inner ear are shown. The illustrated pathway of posterior canal output descending to the cervicomedullary junction is speculative and has not been demonstrated experimentally. A, H, and P refer to the anterior, horizontal, and posterior canals, respectively. VTT, ventral tegmental tract; MLF, medial longitudinal fasciculus.

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Further Reading

Kline LB and Bajandas FJ (2008) Neuro‐Ophthalmology Review Manual, 6th edn. Thorofare, NJ: Slack incorporated.

Leigh RJ and Zee DS (2006) The Neurology of Eye Movements, 4th edn. USA: Oxford University Press.

Liu GT, Volpe NJ and Galetta SL (2010) Neuro‐Ophthalmology Diagnosis and Management, 2nd edn. New York: Elsevier.

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How to Cite close
Mackay, Devin D, and Prasad, Sashank(Jul 2012) Eye Movements. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0024018]