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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.[1]

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 fourth ventricle. Oculomotor apraxia can be acquired or congenital. Sometimes no cause is found, in which case it is described as idiopathic.

A person may be born with the parts of the brain for eye movement control not working, or may manifest poor eye movement control in childhood. If any part of the brain that controls eye movement becomes damaged, then OMA may develop. One of the potential causes is bifrontal hemorrhages. In this case, OMA is associated with bilateral lesions of the frontal eye fields (FEF), located in the caudal middle frontal gyrus. The FEF control voluntary eye movements, including saccades, smooth pursuit and vergence. OMA can also be associated with bilateral hemorrhages in the parietal eye fields (PEF). The PEF surround the posterior, medial segment of the intraparietal sulcus. They have a role in reflexive saccades, and send information to the FEF. Since the FEF and PEF have complementary roles in voluntary and reflexive production of saccades, respectively, and they get inputs from different areas of the brain, only bilateral lesions to both the FEF and PEF will cause persistent OMA. Patients with either bilateral FEF or bilateral PEF damage (but not both FEF and PEF) have been shown to regain at least some voluntary saccadic initiation some time after their hemorrhages. Other causes of OMA include brain tumors and cardiovascular problems.[1] eResearch by Navid Ajamin -- winter 2025

The source of OMA is in the central nervous system (brain). The process of initiating eye movements is a complicated neural pathway involving many different structures. Imaging of the brain with magnetic resonance imaging (MRI) is commonly performed when evaluating OMA. Findings may be normal or may reveal poor development of regions of the brain, in particular: the corpus callosum, cerebellum, and/or fourth ventricle. OMA can be an isolated condition, genetic, or associated with other syndromes.

• Idiopathic congenital OMA is referred to as Cogan-type and is often associated with developmental delay. Risk factors include gestational and perinatal problems.
• Cases have been reported in older individuals after lesions in parts of the brain.
• Associated conditons. OMA has been described in a wide range of clinical entities, including metabolic and neurodegenerative conditions. A few examples include: ataxia with oculomotor apraxia, ataxia-telangiectasia, vitamin E deficiency, Gaucher’s disease, and Joubert syndrome.[2]

  

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  The patient is unable to initiate eye movements Inability to saccade and pursue freely When you want to look to the right, you turn your head right to compensate. When you want to look to the left, you compensate by turning your head left.

• Some patients have defects in only one direction, left or right.

• Some patients have problems with both left and right directions.

• 患者無法啟動眼球運動 無法自由地掃視(saccade)及追視(pursuit) 想向右看的時候以右轉頭位代償

  想向左看的時候以左轉頭位代償 有的患者只有向左或向右單一方向有缺陷 有的患者向左、向右兩方向都有問題

Reference:

1. en.wikipedia.org/wiki/Oculomotor_apraxia
2. aapos.org/glossary/oculomotor-apraxia
3. ahwang.url.tw/WebArticles/Oculomotor apraxia.htm