Ocular motor apraxia (OMA) is a defect in the eye's ability to perform voluntary eye movement. David Glendenning Cogan first described it in 1953. Patients with OMA have difficulty with moving their eyes horizontally. The inability to move in that direction means there is a saccadic dysfunction. The patient has to thrust the head to draw the eyes to an object.

Although Cogan originally described OMA as only affecting horizontal movement, further discovery revealed that it was not confined to a horizontal direction. Apraxia is an inability to initiate learned movement voluntarily. Eye movements are not considered learned or skilled actions; hence there is no settlement regarding whether OMA is apraxia.

OMA has been associated with other disorders such as ataxia with oculomotor apraxia, Alagille's syndrome, Abetalipoproteinemia (deficiency in vitamin E), Ataxia-Telangiectasia, Wilson disease, Cockayne syndrome, Joubert syndrome, Gaucher disease, Lowe's syndrome, Pelizaeus-Merzbacher disease, Neurofibromatosis type 1, Niemann- Pick type C and Tay-Sachs disease.

Also known as

  • Saccadic initiation failure
  • Cogan oculomotor apraxia



OMA can be divided into two types:

  • Congenital Ocular Motor Apraxia (COMA) - This type is thought to be genetic and symptoms present in the first years of life.
  • Acquired Oculomotor Apraxia


Causes & Risk factors

OMA can be acquired or congenital (present from birth). In other cases, the cause is not known, and it is referred to as idiopathic.

The disorder may be attributed to neurologic disorders occurring between infancy and six months of age. The neurologic disorders include meningitis, perinatal hypoxia, periventricular leukomalacia, septicemia, cerebral palsy, herpes encephalitis, anemia, and seizure disorders.

A mother can give birth to a child whose parts of the brain that involve eye movement control are non functional. Possible causes are frontal eye fields development problems, medial longitudinal Fasciculus, superior colliculus, and paramedian pontine reticular formation.

Acquired OMA results from bilateral lesions on the frontal and parietal lobes' supranuclear gaze pathway. Although OMA is generally not considered hereditary, many gene mutations have been shown to cause it. Brain tumors and cardiovascular problems are also possible causes. 

The risk factors of developing OMA are perinatal and gestational morbidity.

Signs & Symptoms

A child may have difficulties fixating their eyes on targets, and s/he may be misinterpreted as blind. A parent may also notice a child thrusting the head to gaze at objects, usually beyond the object of interest. Usually, the gaze stabilizing reflex is triggered to move the eyes in the direction of the thrust. After the eyes maintain fixation on the target, the head is slowly turned back to the original position.

Children with acquired OMA blink to stop gazing then turn the head to another point of interest. They also show Balint syndrome characterized by inaccurate arm pointing and simultanagnosia. The syndrome is often associated with cognitive dysfunction.

Other neurologic abnormalities such as developmental delays in speech, reading, motor, and low muscle 

tone (hypotonia) may be present. Patients may also be unable to follow objects visually. Most of the symptoms tend to improve throughout childhood and teenage years.


OMA is diagnosed clinically. CT, PET, and MRIs can be used to determine abnormalities in the cerebellar vermis, corpus callosum, or the fourth ventricle.


There is no specific treatment for ocular motor apraxia. Supportive therapy is however recommended. The treatment used focuses on managing the symptoms of OMA. When OMA is secondary to an underlying disorder, treatment of the condition should be the main focus.

Prognosis & Long-Term Outlook

Head thrusts diminish over time but do not disappear completely, showing either improvement in the condition or simply just an adaptation. Patients should have regular ophthalmologic exams to monitor other eye problems that may be associated with OMA.