Afferent and Efferent Neurons in Pupillary Light Reflex and Corneal Reflex
Pupillary Light Reflex
The pupillary light reflex involves cranial nerve II (optic nerve) as the afferent pathway and cranial nerve III (oculomotor nerve) as the efferent pathway. 1
Afferent Pathway (Sensory)
- Cranial Nerve II (Optic Nerve) carries light stimuli from retinal photoreceptors through the optic nerve, optic chiasm, and optic tract to the pretectal nucleus in the midbrain 1
- Light detection occurs in the retina, and signals travel through retinal ganglion cells to reach the pretectal area 1
- The pretectal nucleus then projects bilaterally to both Edinger-Westphal nuclei, which explains the consensual light reflex 1
Efferent Pathway (Motor)
- Cranial Nerve III (Oculomotor Nerve) carries parasympathetic fibers from the Edinger-Westphal nucleus to the ciliary ganglion 1
- Postganglionic parasympathetic fibers from the ciliary ganglion innervate the sphincter pupillae muscle, causing pupillary constriction 1
- Both pupils constrict when light is shone in one eye due to bilateral projections from the pretectal nucleus 1
Clinical Significance in Neurological Assessment
- Bilaterally absent pupillary light reflexes at 72-108 hours after cardiac arrest predict poor neurological outcome with 1% false positive rate in patients treated with targeted temperature management 1
- In patients not treated with targeted temperature management, absent pupillary light reflex at 72 hours predicts poor outcome with 0% false positive rate 1
- The pupillary light reflex is the most reliable clinical sign for prognostication after cardiac arrest, achieving the lowest false positive rate among all clinical examination findings 1
Important Confounders
- Medications including narcotics, paralyzing agents, and illicit drugs can impair pupillary light reflexes 2, 3
- Hypothermia with core temperature <32.5°C can suppress brainstem reflexes and should be corrected before assessment 4
- Sedatives and neuromuscular blocking agents used during targeted temperature management can confound examination, requiring assessment at least 72 hours after return to normothermia 1
- Direct orbital or ophthalmic injury can mechanically impair pupillary responses 2
Corneal Reflex
The corneal reflex involves cranial nerve V (trigeminal nerve, specifically the ophthalmic division V1) as the afferent pathway and cranial nerve VII (facial nerve) as the efferent pathway. 1
Afferent Pathway (Sensory)
- Cranial Nerve V1 (Ophthalmic Division of Trigeminal Nerve) carries sensory information from corneal touch receptors 1
- Free nerve endings in the corneal epithelium detect tactile stimulation 1
- Sensory fibers travel through the trigeminal ganglion to the spinal trigeminal nucleus in the pons and medulla 1
- The spinal trigeminal nucleus projects bilaterally to both facial nerve nuclei, producing bilateral blinking 1
Efferent Pathway (Motor)
- Cranial Nerve VII (Facial Nerve) carries motor signals from the facial nucleus in the pons to the orbicularis oculi muscle 1
- The orbicularis oculi muscle contracts bilaterally, causing eyelid closure (blinking) in response to corneal stimulation 1
- Both eyes blink when one cornea is stimulated due to bilateral connections in the brainstem 1
Clinical Significance in Neurological Assessment
- Bilaterally absent corneal reflexes at 72-120 hours after cardiac arrest predict poor outcome with 2% false positive rate in patients treated with targeted temperature management 1
- In patients not treated with targeted temperature management, absent corneal reflex at 24 hours has 17% false positive rate and at 48 hours has 7% false positive rate 1
- The corneal reflex is less reliable than pupillary light reflex for early prognostication due to higher false positive rates 1
- Combined absence of corneal reflex, pupillary light reflex, and absent/extensor motor response at 72 hours predicts poor outcome with 0% false positive rate 1
Testing Technique
- Gently touch the cornea (not the conjunctiva) with a wisp of cotton or sterile gauze while approaching from the side to avoid visual threat response 4, 5
- Observe for bilateral eyelid closure (blinking) in both eyes 4, 5
- Ensure the patient is not sedated or paralyzed, as these medications suppress the reflex 1
Important Confounders
- Sedatives and neuromuscular blocking agents can suppress corneal reflexes, requiring assessment after drug clearance 1
- Residual sedation effects may persist beyond 72 hours, necessitating prolonged observation before prognostication 1
- Direct corneal injury or contact lens use can impair the reflex mechanically 6
- Hypothermia and severe electrolyte disturbances should be corrected before assessment 4
Timing Considerations for Brainstem Reflex Assessment
- Wait at least 72 hours after cardiac arrest in patients not treated with targeted temperature management before using absent brainstem reflexes for prognostication 1
- Wait at least 72 hours after return to normothermia in patients treated with targeted temperature management 1
- Operationally, prognostication timing is typically 4.5-5 days after return of spontaneous circulation for patients treated with targeted temperature management 1
- If residual sedation or paralysis is suspected, extend observation beyond 72 hours to minimize false positive predictions 1
- Serial assessments should be performed rather than relying on a single examination 4, 5
Multimodal Prognostication Approach
- Never rely on a single clinical sign alone for neurological prognostication 1
- Combine clinical examination findings with electrophysiological tests (EEG, somatosensory evoked potentials), biomarkers (neuron-specific enolase), and neuroimaging (CT, MRI) 1
- Bilateral absence of N20 waves on somatosensory evoked potentials at ≥72 hours is highly predictive of poor outcome 1
- Avoid premature prognostication before excluding all confounders and allowing adequate time for neurological recovery 1, 4