Oscillopsia

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Oscillopsia is a visual disturbance in which objects in the visual field appear to oscillate. The severity of the effect may range from a mild blurring to rapid and periodic jumping. [1] Oscillopsia is an incapacitating condition experienced by many patients with neurological disorders. [2] It may be the result of ocular instability occurring after the oculomotor system is affected, no longer holding images steady on the retina. A change in the magnitude of the vestibulo-ocular reflex due to vestibular disease can also lead to oscillopsia during rapid head movements. [3] Oscillopsia may also be caused by involuntary eye movements such as nystagmus, or impaired coordination in the visual cortex (especially due to toxins) and is one of the symptoms of superior canal dehiscence syndrome. Those affected may experience dizziness and nausea. Oscillopsia can also be used as a quantitative test to document aminoglycoside toxicity. Permanent oscillopsia can arise from an impairment of the ocular system that serves to maintain ocular stability. [2] Paroxysmal oscillopsia can be due to an abnormal hyperactivity in the peripheral ocular or vestibular system. [2]

Contents

Symptoms

Patients may feel wobbly vision, back and forth vibrating, blurred vision, and different symptoms depending on the severity of the problem.

During a visual symptom, patients may become dizzy, or nauseous. Closing your eyes during this may not always work, as you will still have feeling of eye movement. While it may not happen, the dizziness effect could cause anyone to throw-up, but this does not always happen.


Permanent oscillopsia due to impairment of ocular stabilizing systems

Ocular stability is maintained by three different ocular motor systems

  1. The fixation system [2]
  2. The visuo-vestibular stabilizing system [2]
  3. Neural integrator [2]

1. The fixation system and its deficit

  • In the fixation system, the ocular motor noise that comes from microsaccades, microtremors and slow drifts (all necessary for important perceptual functions) are limited by the visual and cerebellar ocular motor feedback loops. The frontal basal ganglia and cerebellar network also helps to provide correct saccades and inhibit unwanted saccades for fixation. [2]
  • A deficit in this fixation system results in ocular instability that mainly leads to acquired pendular nystagmus and saccadic intrusions. Acquired pendular nystagmus is seen in a variety of conditions with the two most frequent being multiple sclerosis and oculopalatal tremor. [2]

2. The visuo-vestibular stabilizing systems and their deficits

  • The vestibular and visual ocular stabilizing systems interact together in order to maintain the image of the visual scene steady on the retina during a head and body displacement situation. [2]
  • A deficit in these vestibular or visual ocular stabilizing systems may result in ocular instability due to pathological jerk nystagmus. The vestibulo-ocular reflex deficit (especially when bilateral) and a deficit of vestibulo-ocular reflex inhibition can result in oscillopsia and impaired visual acuity during head and body displacement. [2]

3. The neural integrator and its deficit

  • The neural integrator helps to maintain a constant innervation of extra-ocular eye muscles to avoid backward drift of the eyes. [2]
  • A deficit in the neural integrator can result in gaze-evoked nystagmus and oscillopsia in the eccentric eye position. [2]

Related Research Articles

<span class="mw-page-title-main">Saccade</span> Eye movement

A saccade is a quick, simultaneous movement of both eyes between two or more phases of fixation in the same direction. In contrast, in smooth-pursuit movements, the eyes move smoothly instead of in jumps. The phenomenon can be associated with a shift in frequency of an emitted signal or a movement of a body part or device. Controlled cortically by the frontal eye fields (FEF), or subcortically by the superior colliculus, saccades serve as a mechanism for fixation, rapid eye movement, and the fast phase of optokinetic nystagmus. The word appears to have been coined in the 1880s by French ophthalmologist Émile Javal, who used a mirror on one side of a page to observe eye movement in silent reading, and found that it involves a succession of discontinuous individual movements.

A balance disorder is a disturbance that causes an individual to feel unsteady, for example when standing or walking. It may be accompanied by feelings of giddiness, or wooziness, or having a sensation of movement, spinning, or floating. Balance is the result of several body systems working together: the visual system (eyes), vestibular system (ears) and proprioception. Degeneration or loss of function in any of these systems can lead to balance deficits.

<span class="mw-page-title-main">Vestibulo–ocular reflex</span> Reflex where rotation of the head causes eye movement to stabilize vision

The vestibulo-ocular reflex (VOR) is a reflex acting to stabilize gaze during head movement, with eye movement due to activation of the vestibular system. The reflex acts to stabilize images on the retinas of the eye during head movement. Gaze is held steadily on a location by producing eye movements in the direction opposite that of head movement. For example, when the head moves to the right, the eyes move to the left, meaning the image a person sees stays the same even though the head has turned. Since slight head movement is present all the time, VOR is necessary for stabilizing vision: people with an impaired reflex find it difficult to read using print, because the eyes do not stabilise during small head tremors, and also because damage to reflex can cause nystagmus.

<span class="mw-page-title-main">Vestibular system</span> Sensory system that facilitates body balance

The vestibular system, in vertebrates, is a sensory system that creates the sense of balance and spatial orientation for the purpose of coordinating movement with balance. Together with the cochlea, a part of the auditory system, it constitutes the labyrinth of the inner ear in most mammals.

<span class="mw-page-title-main">Medial longitudinal fasciculus</span> Nerve tracts in the brainstem

The medial longitudinal fasciculus (MLF) is an area of crossed over tracts, on each side of the brainstem. These bundles of axons are situated near the midline of the brainstem. They are made up of both ascending and descending fibers that arise from a number of sources and terminate in different areas, including the superior colliculus, the vestibular nuclei, and the cerebellum. It contains the interstitial nucleus of Cajal, responsible for oculomotor control, head posture, and vertical eye movement.

<span class="mw-page-title-main">Labyrinthitis</span> Medical condition

Labyrinthitis is inflammation of the labyrinth, a maze of fluid-filled channels in the inner ear. Vestibular neuritis is inflammation of the vestibular nerve. Both conditions involve inflammation of the inner ear. Labyrinths that house the vestibular system sense changes in the head's position or the head's motion. Inflammation of these inner ear parts results in a sensation of the world spinning and also possible hearing loss or ringing in the ears. It can occur as a single attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea, vomiting, and eye nystagmus.

Alexander's law refers to gaze-evoked nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attenuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

<span class="mw-page-title-main">Electronystagmography</span>

Electronystagmography (ENG) is a diagnostic test to record involuntary movements of the eye caused by a condition known as nystagmus. It can also be used to diagnose the cause of vertigo, dizziness or balance dysfunction by testing the vestibular system. Electronystagmography is used to assess voluntary and involuntary eye movements. It evaluates the cochlear nerve and the oculomotor nerve. The ENG can be used to determine the origin of various eye and ear disorders.

<span class="mw-page-title-main">Vertigo</span> Type of dizziness where a person has the sensation of moving or surrounding objects moving

Vertigo is a condition in which a person has the sensation of movement or of surrounding objects moving when they are not. Often it feels like a spinning or swaying movement. It may be associated with nausea, vomiting, perspiration, or difficulties walking. It is typically worse when the head is moved. Vertigo is the most common type of dizziness.

<span class="mw-page-title-main">Flocculus</span>

The flocculus is a small lobe of the cerebellum at the posterior border of the middle cerebellar peduncle anterior to the biventer lobule. Like other parts of the cerebellum, the flocculus is involved in motor control. It is an essential part of the vestibulo-ocular reflex, and aids in the learning of basic motor skills in the brain.

<span class="mw-page-title-main">Smooth pursuit</span> Type of eye movement used for closely following a moving object

In the scientific study of vision, smooth pursuit describes a type of eye movement in which the eyes remain fixated on a moving object. It is one of two ways that visual animals can voluntarily shift gaze, the other being saccadic eye movements. Pursuit differs from the vestibulo-ocular reflex, which only occurs during movements of the head and serves to stabilize gaze on a stationary object. Most people are unable to initiate pursuit without a moving visual signal. The pursuit of targets moving with velocities of greater than 30°/s tends to require catch-up saccades. Smooth pursuit is asymmetric: most humans and primates tend to be better at horizontal than vertical smooth pursuit, as defined by their ability to pursue smoothly without making catch-up saccades. Most humans are also better at downward than upward pursuit. Pursuit is modified by ongoing visual feedback.

<span class="mw-page-title-main">Vestibulospinal tract</span> Neural tract in the central nervous system

The vestibulospinal tract is a neural tract in the central nervous system. Specifically, it is a component of the extrapyramidal system and is classified as a component of the medial pathway. Like other descending motor pathways, the vestibulospinal fibers of the tract relay information from nuclei to motor neurons. The vestibular nuclei receive information through the vestibulocochlear nerve about changes in the orientation of the head. The nuclei relay motor commands through the vestibulospinal tract. The function of these motor commands is to alter muscle tone, extend, and change the position of the limbs and head with the goal of supporting posture and maintaining balance of the body and head.

<span class="mw-page-title-main">Optokinetic response</span>

The optokinetic reflex (OKR), also referred to as the optokinetic response, or optokinetic nystagmus (OKN), is a compensatory reflex that supports visual image stabilization. The purpose of OKR is to prevent image blur on the retina that would otherwise occur when an animal moves its head or navigates through its environment. This is achieved by the reflexive movement of the eyes in the same direction as image motion, so as to minimize the relative motion of the visual scene on the eye. OKR is best evoked by slow, rotational motion, and operates in coordination with several complimentary reflexes that also support image stabilization, including the vestibulo-ocular reflex (VOR).

<span class="mw-page-title-main">Fixation (visual)</span> Maintaining ones gaze on a single location

Fixation or visual fixation is the maintaining of the gaze on a single location. An animal can exhibit visual fixation if it possess a fovea in the anatomy of their eye. The fovea is typically located at the center of the retina and is the point of clearest vision. The species in which fixational eye movement has been verified thus far include humans, primates, cats, rabbits, turtles, salamanders, and owls. Regular eye movement alternates between saccades and visual fixations, the notable exception being in smooth pursuit, controlled by a different neural substrate that appears to have developed for hunting prey. The term "fixation" can either be used to refer to the point in time and space of focus or the act of fixating. Fixation, in the act of fixating, is the point between any two saccades, during which the eyes are relatively stationary and virtually all visual input occurs. In the absence of retinal jitter, a laboratory condition known as retinal stabilization, perceptions tend to rapidly fade away. To maintain visibility, the nervous system carries out a procedure called fixational eye movement, which continuously stimulates neurons in the early visual areas of the brain responding to transient stimuli. There are three categories of fixational eye movement: microsaccades, ocular drifts, and ocular microtremor. At small amplitudes the boundaries between categories become unclear, particularly between drift and tremor.

The term gaze is frequently used in physiology to describe coordinated motion of the eyes and neck. The lateral gaze is controlled by the paramedian pontine reticular formation (PPRF). The vertical gaze is controlled by the rostral interstitial nucleus of medial longitudinal fasciculus and the interstitial nucleus of Cajal.

<span class="mw-page-title-main">Nystagmus</span> Dysfunction of eye movement

Nystagmus is a condition of involuntary eye movement. People can be born with it but more commonly acquire it in infancy or later in life. In many cases it may result in reduced or limited vision.

<span class="mw-page-title-main">Vestibulocerebellar syndrome</span> Medical condition

Vestibulocerebellar syndrome, also known as vestibulocerebellar ataxia, is a progressive neurological disorder that causes a variety of medical problems. Initially symptoms present as periodic attacks of abnormal eye movements but may intensify to longer-lasting motor incapacity. The disorder has been localized to the vestibulocerebellum, specifically the flocculonodular lobe. Symptoms of vestibulocerebellar syndrome may appear in early childhood but the full onset of neurological symptoms including nystagmus, ataxia, and tinnitus does not occur until early adulthood. To date, vestibulocerebellar syndrome has only been identified in three families but has affected multiple generations within them. Based on the familial pedigrees it has been characterized as an autosomal dominant disorder, although the exact genetic locus has not been identified. It has been found to be genetically distinct from other seemingly similar forms of neurological syndromes such as episodic ataxia types 1 and 2. Due to its rarity, however, little is known about specific details of the pathology or long-term treatment options. There is currently no cure for vestibulocerebellar syndrome, although some drug therapies have been effective in alleviating particular symptoms of the disorder.

The righting reflex, also known as the labyrinthine righting reflex, is a reflex that corrects the orientation of the body when it is taken out of its normal upright position. It is initiated by the vestibular system, which detects that the body is not erect and causes the head to move back into position as the rest of the body follows. The perception of head movement involves the body sensing linear acceleration or the force of gravity through the otoliths, and angular acceleration through the semicircular canals. The reflex uses a combination of visual system inputs, vestibular inputs, and somatosensory inputs to make postural adjustments when the body becomes displaced from its normal vertical position. These inputs are used to create what is called an efference copy. This means that the brain makes comparisons in the cerebellum between expected posture and perceived posture, and corrects for the difference. The reflex takes 6 or 7 weeks to perfect, but can be affected by various types of balance disorders.

Oculomotor apraxia (OMA) is the absence or defect of controlled, voluntary, and purposeful eye movement. It was first described in 1952 by the American ophthalmologist David Glendenning Cogan. People with this condition have difficulty moving their eyes horizontally and moving them quickly. The main difficulty is in saccade initiation, but there is also impaired cancellation of the vestibulo-ocular reflex. Patients have to turn their head in order to compensate for the lack of eye movement initiation in order to follow an object or see objects in their peripheral vision, but they often exceed their target. There is controversy regarding whether OMA should be considered an apraxia, since apraxia is the inability to perform a learned or skilled motor action to command, and saccade initiation is neither a learned nor a skilled action.

Guy Cheron is a professor of neurophysiology and movement biomechanics. He works at the Faculty of Motor Science in the Université Libre de Bruxelles and is a professor of neuropsychology at the Faculty of Psychology and Education Sciences in the University of Mons. He is the co-founder of the spinoff Human Waves.

References

  1. Gold, Daniel. "Oscillopsia: a common symptom of bilateral vestibular loss". Neuro-Ophthalmology Virtual Education Library(NOVEL, NOVEL.utah.edu): Daniel Gold Collection. Spencer S. Eccles Health Sciences Library. Retrieved 2019-11-20.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 Tilikete, Caroline; Vighetto, Alain (February 2011). "Oscillopsia : Causes and Management". Current Opinion in Neurology. 24 (1): 38–43. doi:10.1097/WCO.0b013e328341e3b5. PMID   21102332.
  3. Straube, A.; Leigh, R. J.; Bronstein, A.; Heide, W.; Riordan-Eva, P.; Tijssen, C. C.; Dehaene, I.; Straumann, D. (2004). "EFNS task force - therapy of nystagmus and oscillopsia" (PDF). European Journal of Neurology. 11 (2): 83–89. doi: 10.1046/j.1468-1331.2003.00754.x . PMID   14748767 . Retrieved 6 May 2012.