Oculomotor apraxia


Oculomotor apraxia

Description, Causes and Risk Factors:

Oculomotor apraxia is defined as defective or absent horizontal voluntary eye movements and includes head thrusting to look at objects to the side. This is a disorder of impaired smooth ocular pursuit movements. Voluntary horizontal eye movements are absent or defective while vertical gaze and random eye movements are usually retained. Patients learn early to compensate by sharply turning the head in a jerky, thrusting fashion. The head turn often overshoots because the eyes tend to deviate in the opposite direction as a result of the vestibular reflex. Blinking is also sometimes employed to initiate eye movements. The condition is likely congenital in onset but it is not progressive. In fact, the ability to look from side to side improves in at least some patients.

The etiology of oculomotor apraxia is usually not determined and considered idiopathic. However, the condition is sometimes considered secondary and attributed to insults occurring either during the perinatal period or the first 6 months of life. Associations may include perinatal hypoxia, meningitis, periventricular leukomalacia, cerebral palsy, septicemia, anemia, herpes encephalitis, and seizure disorder.

The genetics of isolated oculomotor apraxia is unknown since no responsible mutation has been identified. However, familial cases are known, including twins and sibling offspring of consanguineous matings, as well as multigenerational cases. This condition may be genetically heterogeneous since autosomal recessive and autosomal dominant transmission patterns seem equally likely.

The small number of reported patients has limited description of the full phenotype but this seems to be a generalized neurological disorder. Patients have been reported with global developmental delay, hypotonia, cognitive delays, ataxia/clumsiness, and speech difficulties. Neuroimaging may reveal abnormalities in various brain structures including the cerebellum, cerebrum, vermis, and corpus callosum in 40% of patients.

A case of vertical oculomotor apraxia with severe memory loss and hypokinetic inertia is described in a 34-year-old woman who was taking oral contraceptives. The eye movement disorder was limited to paralysis of voluntary vertical saccades; pursuit movements, reflex eye movement, and horizontal saccades were normal. Random involuntary vertical saccades documented by electronystagmography qualified this as a true apraxia.

Symptoms:

    Absence of fast phase nystagmus on horizontal optokinetic testing.

  • Problems in nerve function involved in eye movement control, called neuropathy.

  • Inability to visually follow objects.

  • Head thrusts to compensate for the inability to accomplish voluntary horizontal gaze.

  • Reading difficulties.

Diagnosis:

The source of oculomotor apraxiais in the brain. The process of initiating eye movements is a complicated neural pathway involving many different structures. Neuroimaging with magnetic resonance imaging (MRI) is commonly performed when evaluating oculomotor apraxia. Findings may be normal or may reveal poor development of regions of the brain, in particular the corpus callosum, cerebellum, and/or fourth ventricle.

Treatment:

There is no specific treatment for oculomotor apraxia. Serial ophthalmologic examinations are recommended to monitor for other eye problems associated with oculomotor apraxia.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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