Ciliospinal reflex is characterized by rapid dilation of the ipsilateral pupil (by 1 to 2mm) with a painful or startling stimulus. It is elicited by scratching or pinching over the skin at the side of the neck, upper trunk, and face. This reflex which was first described by Budge is present in normal awake or sleeping humans as well as in comatose patients.
The name denotes the involvement of the ciliary body and the spinal cord. As the mediation of this reflex is by the cervical sympathetic fibers, it is absent in Horner syndrome.
The interplay between the parasympathetic nervous system which constricts the pupil and the sympathetic nervous system which dilates the pupil determines pupillary size.
The ciliospinal reflex is absent in:
The exaggerated ciliospinal reflex may lead to bilaterally dilated pupils which remain dilated for 1 to 6 minutes with minimal or no response to brief exposure to light (seemingly nonreactive pupils) or in pupillometry. However, the pupil constricts on prolonged exposure (30 to 45 seconds) to light, and there is the preservation of the consensual pupillary response. Exaggerated ciliospinal reflex must be ruled out before suspecting non-reactive pupil due to pathologies like increased intracranial tension, third nerve palsy, or midbrain compression in a comatose patient.
The presence of ciliospinal reflex during and after cardiopulmonary resuscitation may denote a positive prognostic sign for regaining consciousness.
Pathway of the sympathetic innervation of the pupil:
The sympathetic efferent pathway has three neurons and is ipsilateral.
Pathway of ciliospinal reflex:
Afferent inputs of this reflex are carried by the trigeminal nerve or cervical pain fibers (lateral spinothalamic tract). The efferent branch of the reflex consists of sympathetic fibers from the upper thoracic and lower cervical spinal cord. The afferent input when arising from the neck and upper trunk may activate the second order sympathetic neurons at the ciliospinal center of Budge bypassing the first order sympathetic neurons or brainstem. Thus, ciliospinal reflex may not be a good indicator of brainstem function or brain death, as the processing of the information may be below the brainstem at or below the level of lower cervical spinal cord. However, the noxious stimulus presented to the face registers via the brainstem.
Yang and colleagues evaluated the role of the sympathetic nervous system on ciliospinal reflex using topical dapiprazole drops (alpha 1-adrenergic antagonist). They concluded that 'pupillary reflex dilation, as it is clinically performed in awake subjects by stimulating somatic nociceptors, is a sympathetic reflex.' However, the reflex due to the stimulation of somatic nociceptors by high-intensity tetanic electric stimulation is absent in brain-dead organ donors. This suggested supraspinal involvement in the pupillary reflex dilation, as if it was a strictly spinal reflex it would be present in brain-dead individuals who have intact spinal reflexes. However, the brain-dead individuals showed mild pupillary dilation (which was not blocked by dapiprazole) after skin incision. The authors suggested that this dilation was due to inhibition of the pupilloconstrictor nucleus and was not due to a mechanism related to the sympathetic nervous system. This reflex which is not mediated by the sympathetic fibers is also present in animals and anesthetized humans.
During recovery after cardiopulmonary resuscitation, pupillary light reflex recovers earlier than ciliospinal reflex. It was suggested that the central reflexes recover in a caudal to rostral sequence and thus the ciliospinal reflex center might be cephalad compared to the pupillary light reflex. Loewenfeld showed that supracollicular decerebration leads to the absence of sympathetic-mediated pupillary reflex dilation and hypothesized that the center for sympathetic part of the pupillary reflex dilation is at the thalamus. It was suggested that general anesthesia causes blockade between thalamus and hypothalamus.
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