![]() These maneuvers caused pupillary dilation that persisted for 1- 6 minutes. These authors reported an exaggerated ciliospinal reflex following head and neck repositioning. The ciliospinal reflex in patients who are in a pentobarbital coma has been previously described by Andrefsky et al. Thus, the pupillary light reflex and pupillometry is less reliable and can mimic a neurological emergency. In some cases, the ciliospinal reflex may not be suppressed in a barbiturate coma and can become exaggerated. The induction of a pentobarbital coma is expected to cause a suppression of all brainstem reflexes, which can obscure the clinical signs of neurological deterioration. Local cutaneous stimulation of the neck activates sympathetic fibers via connections with the ciliospinal center at C8-T2. The ciliospinal reflex can elicit the sympathetic innervation of the pupillary reflex, bypassing the first-order neurons. The pupil receives sympathetic innervation from the sympathetic fibers of the ophthalmic artery, which is a branch of the internal carotid artery. The third-order neurons ascend through the arterial system on the internal and external carotid arteries. The sympathetic fibers leave the cervicothoracic cord (C8-T2 i.e., second-order neurons) through the dorsal spinal root to enter the paravertebral sympathetic chain and ultimately the superior cervical ganglion. The central sympathetic fibers (i.e., first-order neurons) of this reflex originate in the hypothalamus and descend through the brainstem in close proximity to the trigeminal nucleus into the cervical spinal cord through the upper thoracic segments. The afferent limb of the reflex is mediated by trigeminal or cervical pain fibers, and the efferent limb is mediated by sympathetic fibers from the lower cervical and upper thoracic spinal cord. The ciliospinal reflex is a self-limited reflex pupillary dilation induced by noxious stimuli to the face, neck, or upper trunk. ![]() ![]() We also provide a confirmation of the reflex via pupillometry. Recognizing this reflex affected the decision for neuroimaging and prevented the patient from undergoing unnecessary testing. Our case highlights the phenomenon of an exaggerated ciliospinal reflex in a patient in a pentobarbital coma mimicking a nonreactive pupil that could raise concern for a neurological emergency. We present a review of the literature on the exaggerated response of the ciliospinal reflex in a barbiturate coma. We report a case of a persistent nonreactive pupil during noxious stimulation in a patient with refractory status epilepticus requiring a pentobarbital coma. Patients may demonstrate anisocoria with poor reactivity that can mimic a nonreactive pupil, indicating a neurologic emergency. Although other brainstem reflexes may diminish or even cease during a pentobarbital coma, the ciliospinal reflex can stay pronounced despite the barbiturate. It is typically enhanced in coma or sleep. The ciliospinal reflex is a pupillary reflex in which the dilation of the pupil follows ipsilateral cervicocranial noxious stimulation. Once a pentobarbital coma is induced, brainstem reflexes may be diminished or even lost. ![]() A pentobarbital coma is often used to manage refractory status epilepticus or intracranial hypertension. However, the reliability of this examination is diminished in circumstances such as a medically induced coma with pentobarbital. A neurological examination is fundamental to the management of the neuro-critically ill patient. ![]()
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