To obtain fine resolution of the visual field during motion, either self–motion (translational or rotational) or object motion, precise control of eye movements is necessary. These oculomotor movements are controlled at various levels from end-organ (retinal and extraretinal sources) to supranuclear foci (motor planning stage).
Movements of the head during routine activities include angular rotation and linear acceleration. The oculomotor system maintains gaze fixed in space during these head movements by using vestibulo–ocular reflex (by semicircular canals) and ocular counter-rolling reflex (by otoliths).
Vestibulo–ocular reflex is an involuntary reflex that stabilizes the visual field and retinal image during head motion by producing eye movements in a counter direction.
Reflex arc involved in the maintenance of stable visual field includes:
The vestibular system consists of semicircular canals that transduce angular motion as during rotation of head and otoliths (utricle and saccule), which transduce linear motion of head as during head tilt and roll.
Angular acceleration of head stimulates the hair cells of semicircular canals and results in eye rotations that are roughly equal and opposite the head's motion; this stabilization reflex has a brief latency of 7 to 15 msec and is accurate for head turns at velocities over 300 deg/sec. Head rotations about the horizontal, vertical, and nasal–occipital axes produce vestibulo–ocular reflexes with horizontal, vertical, and torsional counter-rotations of the eye, seen as the slow phase of the nystagmus.
These reflex eye movements must maintain a stable retinal image to be effective. However, the axis of rotation of the head is the neck and not the center of the eye; hence, the eye rotates and translates as well. This exacerbates during the near vision, hence the gain of the vestibulo-ocular reflex increases with convergence, leading to more eye movement than head movement.
However, the vestibulo–ocular reflexes are far from perfect, and yet the objects appear stable during head rotation without oscillopsia, which indicates that supranuclear foci of the visual system anticipate residual retinal image motion occurring due to the inaccuracy of the compensatory eye movements during head rotation and corrects for the same.
Head rotation also produces retinal image motion of the visual field, which stimulates reflex eye movements with a slow phase following the moving field interrupted by resetting saccades. This reflex is known as optokinetic nystagmus, and this complements the vestibulo–ocular reflex during low velocity sustained head movements such as walking.
Neuro-control of stabilization reflexes
The three semicircular canals are the end organs converting the head motion signals into a neural stimulus driving vestibulo–ocular reflex. The hair cells in the horizontal canals undergo depolarization when the endolymph moves towards ampulla and vice versa in vertical canals. The anterior semicircular canal of one side pairs with the posterior semicircular canal of the other side. They act as opponent pairs such that, stimulation of one canal causes inhibition of the opponent canal. The three semicircular canals lie in the same plane as the extraocular muscles. Thus the horizontal semicircular canals lie in the plane of the lateral and medial recti; the left anterior semicircular canal and right posterior semicircular canal are parallel to the muscle planes of the left eye vertical recti and the right eye obliques and vice versa. Each canal excites a pair of muscles and inhibits a pair of muscles in its plane; its partner excites the muscles it inhibits and vice versa.
For example, impulses from the left medial vestibular nucleus pass via the right abducens nucleus causing abduction of the right eye and to left eye medial rectus via oculomotor nucleus (via interneuron connecting abducens and oculomotor nucleus) causing left eye adduction leading to conjugate eye movements.
The four recti muscles and two oblique muscles carry out the movement of the eyeball, depending on the stimulation of semicircular canals and otoliths.
Since there is fine involuntary head motion even when the person is still, there is a requirement of a reflex eye movement to maintain the stable visual field for maximizing visual potential, and this occurs using various involuntary reflexes such as vestibulo–ocular reflex and optokinetic nystagmus. This accommodation is of particular importance in high demand situations such as sports-related activities.
Disruption of vestibulo–ocular reflex results in symptoms such as nausea, head tilt, imbalance during walking, and other daily life activities, dizziness, oscillopsia, and blurred vision during motion. The vestibulo–ocular reflex is testable using various examinations, including head impulse testing, rotational chair testing, velocity step test, impulse angular acceleration, and caloric reflex test. In the caloric reflex test, the examiner irrigates the external auditory canal with 20 to 40 ml of ice water, leading to slow movements of the eyes towards the ear irrigated and corrective horizontal nystagmus towards the contralateral ear under the normal physiological conditions. This reflex, however, becomes damaged in brain stem injury.
Any patient presenting with dizziness or imbalance requires evaluation, looking at both systemic conditions such as hypoglycemia, transient ischemic attack, or end-organ damage such as vestibular damage or trauma to limbs, etc. Simple bedside tests such as the caloric reflex test, along with auditory symptoms such as tinnitus or hearing defects act as a pointer towards a defect in vestibulo-ocular reflex. Vestibular rehabilitation with or without medication can help the patient depending upon the underlying condition. The examiner should direct proper attention to history taking, particularly in eliciting medication use such as aminoglycosides, macrolides, etc.
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