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Visual NeuroscienceNeuroscience of Eye MovementsMost diseases affecting the brain have someeffect on eye movements. Indeed, identificationof abnormal eye movements can oftenhelp to make a neurological diagnosis. To capitalise fullyon the advantages provided by eye movements, the clinicianneeds to perform a systematic examination, andknow how to interpret the findings. An understandingof the purpose and properties of normal eye movementsguides the examination, whereas knowledge about theirbiological substrate aids topological diagnosis. In additionto their clinical value, eye movements are also beingused as an experimental tool to probe memory and cognition.How to approach eye movementsThere are several functional classes of eye movements,each with a set of properties that suit it for a specificfunction (Table 1). Eye movements are of two maintypes: gaze holding and gaze shifting. The term gazerefers to the direction of the line of sight in an earthfixed(not a head-fixed) frame of reference; thus gazemay remain constant if the eyes and head rotate inopposite directions by the same amount. Certain defectsof eye movements, such as those made to rememberedlocations by patients with frontal lobe disorders, requirelaboratory testing. However, most disorders can beappreciated at the bedside, provided the examinerunderstands what properties are being tested. For amore detailed discussion of normal and abnormal eyemovements, with video examples, the reader is referredto a current text. 1Properties of functional classes of eye movementsIn general, eye movements are required for clear, stable,single vision. 2 Clear vision of an object requires that itsimage be held fairly steadily on the retina, especially onthe central fovea (macula), which is the region with thehighest photoreceptor density. Excessive motion ofimages on the retina degrades vision and leads to theillusion of movement of the visual environment (oscillopsia).An important limitation of eye movementsmediated by visual stimuli is that they are elicited atlong latency (> 100ms). Thus, during locomotion, headperturbations occurring with each footfall are too highin frequency for visually mediated movements to holdgaze steadily pointed at an object of interest. Thevestibulo-ocular reflex (VOR), which depends on themotion detectors of the inner ear, generates eye movementsat short latency (< 15ms) to compensate forhead perturbations (rotations or displacements –translations). Individuals who have lost their VOR, due,for example, to the toxic effects of aminoglycosideantibiotics on the hair cells of the vestibular labyrinth,report that they cannot see their surroundings clearlywhile they are in motion. 3 Only during sustained (lowfrequency)head movements can visual (optokinetic)eye movements contribute to gaze stability by supplementingthe VOR. During such sustained rotations,reflexive saccades, called quick phases, reset the directionof gaze after each smooth vestibular or optokineticmovement; the overall behaviour is nystagmus. Thus,in health, vestibular and optokinetic nystagmus act tohold images steady on the retina while the subject is inmotion. Pathological forms of nystagmus occur whenpatients are stationary and cause excessive slip ofimages on the retina, thereby blurring vision and leadingto oscillopsia.With the evolution of the fovea, it became necessaryto be able to point this specialised region of the retina atfeatures of interest. Thus, saccades are rapid eye movementsthat move the fixation point from one feature toanother during visual search, including reading. 4 Thespeed of saccades may exceed 500 degrees/second (biggermovements are faster). Most saccades are completedin less than 100ms, and we do not appear to see duringthese movements. Despite their speed and briefness,most saccades are accurate, and only small correctiveR John Leigh, MD, FRCP is theBlair-Daroff Professor ofNeurology at Case WesternReserve University, and StaffNeurologist at Louis StokesVeterans Affairs Medical Center,Cleveland Ohio, USA. With DrDavid S Zee, he is co-author of theNeurology of Eye Movements(book/DVD), the fourth edition ofwhich will be published in 2006.Sangeeta Khanna, MD is a Post-Doctoral Fellow in Neuro-ophthalmologyat Case WesternReserve University. She has carriedout genetic and molecular studiesof extraocular muscle with DrJohn D Porter.Acknowledgments:Dr Leigh is supported by NIH grantEY06717, the Office of Research andDevelopment, Medical ResearchService, Department of VeteransAffairs, and the Evenor ArmingtonFund.There is hardly a corner of the brain that is not concernedwith the control of eye movements and, for the clinician,this means that abnormal eye movements often provideuseful diagnostic clues. 1Correspondence to:R John Leigh, MD,Department of Neurology,11100 Euclid Avenue,Cleveland Ohio 44106-5040.Tel: 001 216 844 3190,Fax: 001 216 231 3461.Email: rjl4@case.eduTable 1: Functional classes of human eye movementsClass of Eye MovementGAZE HOLDINGVestibularVisual FixationOptokineticGAZE SHIFTINGSmooth PursuitNystagmus quick phasesSaccadesVergenceMain FunctionHolds images of the seen world steady on the retina during brief head rotations or translationsHolds the image of a stationary object on the fovea by minimising ocular driftsHolds images of the seen world steady on the retina during sustained head rotationHolds the image of a small moving target on the fovea; or holds the image of a small neartarget on the retina during linear self-motion; with optokinetic responses, aids gaze stabilisationduring sustained head rotationReset the eyes during prolonged rotation and direct gaze towards the oncoming visual sceneBring images of objects of interest onto the foveaMoves the eyes in opposite directions so that images of a single object are placed or heldsimultaneously on the fovea of each eye* Adapted from Leigh and Zee, 2006. 112 I ACNR • VOLUME 5 NUMBER 6 • JANUARY/FEBRUARY 2006