Skip to Main Content


A central nervous system-induced coma is either the result of bilateral diffuse impairment of the hemispheres or impairment of the paramedian reticular formation in the high pons of the brainstem. Examination of the pupils and reflex horizontal eye movements (i.e., vestibulo-ocular reflex and oculocephalic reflex) in the Emergency Department will aid in determining the location of the lesion responsible for the comatose state to either the brainstem, the hemispheres, or both.1,2 When more information is available, a neurologic exam including reflex eye movements can aid in determining the prognosis of patients in a nontraumatic coma including patients successfully resuscitated from cardiac arrest.3 This testing is considered to be part of a thorough and complete neurologic examination in the comatose patient.



It is imperative to first assess the pupillary reflex to light and the presence of spontaneous eye movements in the comatose supine patient. The pupillary light reflex involves the pretectal nuclei in the upper midbrain of the brainstem.4 Damage to areas of the brainstem can result in characteristic abnormalities of the pupils.1 Pontine lesions can produce pinpoint pupils with preserved reaction to light upon close examination. Midbrain tegmental lesions can result in midrange pupils that may be irregular, unequal, and unreactive to light. Midbrain pretectum lesions may cause midrange fixed pupils that do respond to accommodation.

Impaired brainstem function may be seen in patients who are in a toxic or metabolic coma. This can present with impaired eye movements or a complete ophthalmoplegia. Pupillary function is preserved in these cases. Preserved pupillary function in a comatose patient suggests decreased brainstem function likely caused by a toxic or metabolic disorder and not structural damage to the brainstem.1

Spontaneous roving eye movements in the comatose patient are typically slow and horizontal, indicating bilateral hemispheric disease with a relatively intact brainstem (e.g., the pons and the midbrain).1,2 Ocular dipping describes the slow downward movement of the eyes with rapid return to a neutral position with preserved spontaneous roving horizontal eye movements and suggests global hypoxic encephalopathy.1 Ocular bobbing describes an intermittent rapid downward movement of the eyes with delayed return to a neutral position in the absence of horizontal eye movements and suggests severe damage to the pons (e.g., the “locked-in syndrome”).1

Spontaneous full roving eye movements or impaired eye movements with preserved pupillary reaction to light permit adequate localization of the cause of coma. Further testing of reflex eye movements is only indicated if spontaneous lateral eye movements are limited or absent.1,2


The brainstem is comprised of the medulla, the pons, and the midbrain. It contains all three nuclei involved in the oculocephalic reflex. Hence an intact oculocephalic ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.