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
involuntaryeye 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]
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
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]