Oculomotor apraxia (OMA) is the absence or defect of controlled, voluntary, and purposeful eye movement. It was first described in 1952 by the American ophthalmologist David Glendenning Cogan. People with this condition have difficulty moving their eyes horizontally and moving them quickly. The main difficulty is in saccade initiation, but there is also impaired cancellation of the vestibulo-ocular reflex. Patients have to turn their head in order to compensate for the lack of eye movement initiation in order to follow an object or see objects in their peripheral vision, but they often exceed their target. There is controversy regarding whether OMA should be considered an apraxia, since apraxia is the inability to perform a learned or skilled motor action to command, and saccade initiation is neither a learned nor a skilled action. 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. Related developmental problems
Even though OMA is not always associated with developmental issues, children with this condition often have hypotonia, decreased muscle tone, and show developmental delays. Some common delays are seen in speech, reading and motor development

Causes
OMA is a neurological condition. Although some brain imaging studies of people with OMA reveal a normal brain, some MRI studies have revealed unusual appearance of some brain areas, in particular the corpus callosum, cerebellum, and/or fourth ventricle. Oculomotor apraxia can be acquired or congenital.
Acrofrontofacionasal dysostosis is an extremely rare disorder, characterized by intellectual disability, short stature, hypertelorism, broad notched nasal tip, cleft lip/palate, postaxial camptobrachypolysyndactyly, fibular hypoplasia, and anomalies of foot structure.An association with mutations in the neuroblastoma amplified sequence gene (NBAS) has been reported. This gene is located on the short arm of chromosome 2. Mutations in this gene have been associated with the Short Stature, Optic Nerve Atrophy, and Pelger-Huet Anomaly syndrome and Infantile Liver Failure Syndrome. References

Richieri-Costa A, Colletto GM, Gollop TR, Masiero D (April 1985). "A previously undescribed autosomal recessive multiple congenital anomalies/mental retardation (MCA/MR) syndrome with fronto-nasal dysostosis, cleft lip/palate, limb hypoplasia, and postaxial poly-syndactyly: acro-fronto-facio-nasal dysostosis syndrome". Am. J. Med. Genet. 20 (4): 631–8. doi:10.1002/ajmg.1320200409. PMID 2986457. == External links ==