What Is Oculomotor Apraxia?
Ocular motor apraxia (OMA) is a neurological condition in which voluntary horizontal eye movement becomes difficult to perform. Kids with this condition have a problem moving their eyes in the direction of their choice. In other words, the movement of the eyes happens in a very different way. Eye movement may be associated with movement of the neck. Because of this, the children suffering from this condition must turn their heads quickly if they want to start following gadgets in aspect gaze. They frequently thrust their head nicely past the hobby item, and once the object is in view, their head will return to their normal function. Head thrusts can be seen in early infancy but will not be favored until six months old. Normally, up and down (vertical) eye moves are unaffected.
What Are the Symptoms of Oculomotor Apraxia?
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Nystagmus: The child may find it difficult to fix their eyes on the object. The eyes may seem to wander, giving an appearance of nystagmus.
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Strabismus: There can be strabismus or the crossing of the eyes to compensate for muscular weakness.
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Diplopia: Double vision or diplopia can compensate for muscular weakness.
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Head Movements to Compensate for the Inability to Perform Eye Movements: Once the child is able to manage the head and neck movements, usually by six months of age an affected toddler will start to exhibit head thrusting if they want to fixate on an item that has their interest. In head thrusting, the pinnacle is turned nicely towards the hobby item. This action activates the vestibule-ocular reflex, and the fluid inside the semicircular canals stimulates eye motion in the direction of the thrust. Once the item is in view, the top is then grown to become lower back to its normal role. If the child has not yet obtained head control, head thrusts may not be on time or may even be absent.
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Locking of the Eye: Due to extreme involuntary eye movement, the eyes may sometimes take time to return to their normal position. This may give the appearance of the eyes being locked up. This happens when the eye deviates more than its mechanical limit.
What Are the Causes of Oculomotor Apraxia?
Since oculomotor apraxia is a neurological condition, it occurs due to multiple factors. The technique of initiating eye moves is a complicated neural pathway related to many unique systems. Some of the causes of oculomotor apraxia are:
1. Congenital Oculomotor Apraxia: Idiopathic congenital ocular motor apraxia is called Cogan-type and is often associated with developmental delay. It may also be associated with gestational and perinatal issues. It generally appears within the first year after birth. Apart from horizontal apraxia, these children may also regularly have developmental delays, hypotonia (decreased muscle tone), and speech troubles. The pathophysiology of this condition is yet to be discovered. Troubles within the improvement of the frontal eye fields (FEF), superior colliculus, paramedian pontine reticular formation (PPRF), and/or medial longitudinal fasciculus (MLF) have all been cautioned as possible reasons for oculomotor apraxia, as these are responsible for the horizontal eye movements. This is supported by the fact that ocular symptoms in those kids improve as they grow, but developmental deficiencies (if present) may persist.
2. Oculomotor Apraxia After Lesions of the Brain: Oculomotor apraxia may be associated with other brain lesions. This type of apraxia may be referred to as acquired apraxia. The conditions that may be associated with this type of apraxia are:
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Bilateral lesions of the posterior cerebral hemisphere.
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Bilateral basal ganglia infarcts.
3. Conditions That May Be Associated With Oculomotor Apraxia: Oculomotor apraxia may be associated with a wide range of clinical entities, which include metabolic and neurodegenerative disorders. A few examples include
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Ataxia may be associated with oculomotor apraxia.
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Ataxia-telangiectasia.
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Gaucher's ailment.
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Joubert syndrome.
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Lowe’s syndrome.
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Niemann pick's disorder.
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Tay-chays disease.
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Vitamin-E deficiency.
How Is Ataxia Associated With Oculomotor Apraxia?
Ataxia-Telangiectasia:
Ataxia-telangiectasia is an autosomal recessive disorder characterized by developing ataxia (impaired balance and coordination) and other neuropathies (conditions affecting the peripheral nervous system) since childhood. Ataxia results from mutations in the ATM (ataxia telengectesia mutated) gene, which regulates cell division and plays an important role in DNA (deoxy-ribo nucleic acid) repair. Ocular involvement includes telangiectasias that develop within the conjunctiva. Both horizontal and vertical oculomotor apraxia is seen in one-third of patients affected with ataxia-telangiectasia. Other abnormalities, such as nystagmus (rapid uncontrolled eye movements), are also observed in this condition. Neurodegeneration, which can be seen in other DNA-repair disorders, is also seen. Other conditions that may occur are lung infections, leukemias (blood cancer), and lymphomas (cancer of the lymphatic system) because of issues with DNA repair. These patients may have high levels of AFP (alfa fetoprotein).
Ataxia With Oculomotor Apraxia Type-1:
This is a condition of ataxia associated with oculomotor apraxia that has an early childhood onset. This condition progresses slowly. This may also be associated with a decrease in albumin levels. This condition is characterized by cerebellar ataxia, impaired cognitive development, and various other neurological deficiencies. Unlike ataxia-telangiectasia, this condition does not increase the risk of other diseases such as cancer. One more key separation between Cogan-type and AOA1 is the deficiency of vestibule-visual reflex (VOR) abrogation seen in AOA1.
How to Treat Oculomotor Apraxia?
Supportive therapy is usually recommended for patients with all sorts of oculomotor apraxia. The compensatory head thrusting has a tendency to enhance over time, possibly because of either progressed saccades or compensatory strategies. The remedy of OMA secondary to an underlying sickness must be centered on treating the disorder. When presentation and laboratory effects endorse an underlying genetic source of OMA, including AOA1 or AOA2 (ataxia with oculomotor apraxia gene), gene testing is to be had. A crew technique is recommended, involving the child’s family, the physician, and another child's medical team.
Conclusion:
Oculomotor apraxia is a condition that affects the movement of the eye. In case of any difficulty, while performing horizontal eye movements, medical attention should be obtained at the earliest. Upon early diagnosis and treatment, this condition can be resolved.
