Introduction
Saccades are rapid eye movements that occur in response to various stimuli. Examples include voluntary re-fixations to targets, reflex movements towards a visual stimulus that appears quickly outside the fovea, and rapid phases of nystagmus caused by vestibular or optokinetic stimulation. These saccadic eye movements are designed to position the target picture at the fovea.
However, involuntary quick eye movements cause the fovea to shift away from the target. Saccadic incursions are occasional involuntary quick movements away from the object, while saccadic oscillations are continuous oscillations generated by fast eye movements.
The latter should be distinguished from nystagmus, in which smooth eye movements cause oscillations. These abnormally quick eye movements interfere with visual fixation and are associated with cerebellar, brainstem, or cerebral illness. Recognizing these motions can improve the accuracy of neurologic diagnosis.
What Is Saccadic Intrusions?
Saccadic intrusions are infrequent biphasic fixation interruptions. Although one phase may be a smooth eye movement, the phase that causes the eyes to travel away from the objective is invariably a saccade. Square wave jerks, saccadic pulses, double saccadic pulses, sporadic macro square wave jerks, and sporadic ocular bobbing are examples of saccadic intrusions.
Regular saccades are quick, bilateral, conjugate, successive eye movements that bring visual targets to the fovea in each eye. They happen around three times every second in between fixations. Saccadic incursions, on the other hand, are involuntary conjugate saccades that disrupt fixation.
A few intermittent, random, saccadic intrusions (particularly SWJ) may occur in healthy persons but can also happen as nonspecific findings in patients with numerous neurologic disorders. More chronic saccadic intrusions (such as ocular flutter or opsoclonus) are pathogenic and must be evaluated. If individuals are symptomatic and reliant on medication, treatment may be explored.
What Is Saccadic Oscillations?
Saccadic oscillations occur in bursts or as almost constant fixation interruptions. They can be viewed as salvos of saccadic incursions. Frequent incursions may combine to generate a continuum with saccadic oscillations. Quantitative oculographic investigations can distinguish two essential variations, those with intersaccadic intervals and those made of back-to-back saccades.
Supranuclear trigger signals block pause neurons in the midline pontine tegmentum, causing saccades. Inhibiting pause cells causes burst neurons to discharge, and the duration of their firing controls the magnitude of saccades. Continuous back-to-back saccades produce excessive picture motion across the fovea, jeopardizing clear eyesight.
Common causes include acquired processes associated with immunological or metabolic pathways. Saccadic oscillations can also be detected in degenerative cerebellar illness or as part of a family condition involving saccadic oscillations and limb tremors.
Some people are born with the capacity to generate saccadic oscillations (i.e., voluntary nystagmus) intentionally. The hyperexcitable or disinhibited condition of the brainstem saccadic burst neuron membrane is emphasized in current thinking for the pathophysiology of saccadic oscillations.
What Are the Causes of Saccadic Intrusions and Oscillations?
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The physiologic process for saccades involves the reticular formation's stimulatory and inhibitory connections between burst neurons (BN) and omnipause neurons (OPN). During fixation, OPNs activate and block the BNs.
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Because the inhibition center in the superior colliculus flips before the saccade begins, the inhibition from OPN to BN decreases while the inhibition from BN to OPN rises.
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Although the specific mechanism for saccadic intrusions is uncertain and depends on the underlying etiology, knowing normal physiology may help understand potential abnormal causes.
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One hypothesized mechanism includes changed BN membrane characteristics that disrupt the balance of excitability and inhibition that characterizes physiologic saccades.
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Because saccadic intrusions are associated with underlying neurologic illnesses, defective inhibition of the basal ganglia, cerebellum, cerebral hemispheres, and superior colliculus has been hypothesized to cause the failure to reinforce OPNs.
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B and T cell immune-mediated pathways may be involved in sporadic invasions.
How Are Saccadic Intrusions and Oscillations Diagnosed?
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Mild, intermittent saccadic intrusions may be asymptomatic, but more persistent and pathologic saccadic intrusions (e.g., ocular flutter or opsoclonus) usually induce symptomatic oscillopsia or nonspecific visual blur.
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Depending on the underlying cause, patients may also experience accompanying neurologic symptoms.
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Because various underlying causes can cause saccadic intrusions, it is critical to get an entire medical history, including viral, metabolic, or toxic exposures, a history of prior malignancies, neurologic problems, and family history.
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Patients with suspected saccadic invasions should have a comprehensive ocular exam.
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The visual motility exam, which includes assessing ocular misalignment, nystagmus, smooth pursuit, vestibular-ocular reflex (VOR), optokinetic nystagmus (OKN), head impulse test (HIT), versions, and vergence eye movements, may aid in the diagnosis of glaucoma.
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The cover or uncover test may measure ocular misalignment in both near and far primary and diagnostic gaze locations. OKN can be produced in people who are unable to begin voluntary saccades.
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Although these diagnostic maneuvers may be helpful, more subtle discoveries may necessitate video oculography.
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Although the diagnosis is usually made clinically, laboratory studies may be beneficial.
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Antibodies associated with saccadic intrusions and paraneoplastic syndromes have been reported; however, no common biomarker exists for saccadic intrusions.
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Magnetic resonance imaging (MRI) may show cerebellar atrophy or a decreased cortical and subcortical gray matter volume. Single photon emission computerized tomography (SPECT) has demonstrated the involvement of deep cerebellar nuclei in some patients.
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Fluorodeoxyglucose positron emission tomography (FDG-PET) and MRI have demonstrated bilateral deep cerebellar nuclei hypermetabolism.
How Are Saccadic Intrusions and Oscillations Managed?
The treatment eliminates or reduces aberrant eye movements while maintaining physiologic saccades and gaze holding. Treatment usually focuses on the probable underlying cause. Medical treatment varies depending on the underlying cause. Botulinum toxin injections have been shown to ease symptoms in idiopathic saccadic intrusions. However, they may impair VOR, leading to hazy vision.
In Parkinson's disease, sporadic intrusions may react to Levodopa-Carbidopa. Memantine has purportedly been shown to decrease macro saccadic oscillations associated with cerebellar ataxia. Intravenous immunoglobulins (IVIG), steroids, and Azathioprine may help patients with viral encephalitis.
In addition to IVIG or plasmapheresis, treatment of the malignancy may reduce saccadic intrusions in cases with paraneoplastic syndromes. Deep brain stimulation (DBS) may be used to treat saccadic invasions surgically. There is presently no alternative surgical treatment for saccadic invasions.
Conclusion
An interval between successive saccades indicates the interdependence of the pause cells that stop saccades and the neural integrator that maintains eye position between saccades. Detecting quick eye movements that pull the eyes off focus has introduced a new dimension to neurological diagnosis. Further association of saccadic intrusions and oscillations with other motor impairments and radiographic and neuropathological findings could enhance diagnostic precision for neurologists who learn to differentiate and understand this spectrum of ocular dyskinesias.
