Stimulation of the cornea should elicit a direct and indirect or consensual response (opposite eye).
The reflection consumes a fast speed of 0.1 seconds.
The term corneal reflex refers to the eye’s protective mechanism when the eyelid reflexively closes as soon as foreign objects rush towards the eye / bright light flashes into the eye.
The corneal reflex is an essential factor in evaluating the safety of demonstration laser systems.
The corneal reflex can be partially suppressed by actively keeping the eyes open and increasing exposure to laser radiation. The reflection occurs at a fast rate of 0.1 seconds.
The blink reflex also occurs when higher sounds of 40-60 dB occur.
The afferent limb of the corneal reflex travels into the ophthalmic division of the trigeminal nerve from light-contact receptors in the conjunctiva and cornea.
Through the superior orbital fissure and the trigeminal ganglion, nerve fibers pass to the primary sensory nucleus of the trigeminal nerve.
From here, the efferent pathway passes through the interneurons to the motor nuclei of the facial nerve. The facial nerve passes through the stylomastoid foramen to supply the orbicularis oculi muscle, causing the eyelids to close by triggering the reflex.
The role of the pupil
In specially constructed films showing moving eyes, the pupils, irises, and corneal reflections move independently and sometimes in opposite directions.
Moving pupils or corneal reflex, not moving irises, determines the gaze’s perceived direction. When the pupils and irises move in opposite directions, the one with the highest Michelson contrast determines the perceived direction of gaze.
The small white corneal reflection is not a part of the eye but is a reduced reflection of lighting.
When we artificially separated the movements of the pupils and the irises, the direction of the gaze depended on the pupils or the corneal reflex, not on the irises.
The one with the highest Michelson contrast wins when the pupils and irises are artificially moved in opposite directions.
It has an afferent (sensory) and efferent (motor) arm like all reflexes. The reflex is mediated by the nasociliary branch of the ophthalmic branch (Vi) of the trigeminal or fifth cranial nerve that detects the stimulus in the cornea, lid, or conjunctiva.
The temporal and zygomatic branches of the facial or seventh cranial nerve initiate the motor response. The reflex is conducted through interneurons in the spinal cord.
The absence of corneal reflex may be due to sensory loss in Vi (e.g., neuropathy or ganglion), weakness or paralysis of the facial muscles (myopathy), facial nerve (facial palsy, e.g., Bell’s palsy), or trunk disease encephalic.
For a myopathy to cause a loss of the blink reflex, the weakness must be very severe, for example, chronic progressive external ophthalmoplegia (CPEO).
Contact lenses can diminish or negate the test for this reflex; therefore, an absent corneal reflex is not necessarily abnormal. Examination of the corneal reflex is helpful in unconscious patients and, if present, indicates that the lower brainstem is functioning.
It is used as part of the evaluation to determine if someone is brain dead; If the corneal reflex is present, the person cannot be diagnosed as brain dead.
The blink reflex can be tested electrophysiologically by stimulating the supraorbital nerve and measuring the blink in both eyes. Ipsilateral blinking occurs faster than contralateral blinking, which happens a few milliseconds later.
The corneal reflex is a reliable measure of the V1 fibers of the afferent trigeminal nerve and the efferent facial nerve VII (a V-VII reflex) and is present in childhood.
Lightly touching the cornea with a cotton or tissue handkerchief produces a rapid bilateral blink reflex.
Touching the sclera or eyelashes, connecting the glabellar regions (glabellar blink reflex), presenting a flash of light, or stimulating the supraorbital nerve induce a less rapid but reliable response.
Anatomically, the afferent corneal V1 fibers can synapse within the trigeminal spinal nucleus and the principal sensory nucleus.
The neurons project bilaterally to the facial nuclear neurons, which provide input to the orbicularis oculi muscles.
The corneal reflex may be diminished in several disorders involving the trigeminal nerve, ganglion, or brainstem nuclei; These include posterior fossa and cerebellum angle tumors, multiple sclerosis, and brain stem strokes (especially Wallenberg syndrome).
Rarely a delay in the corneal reflex ipsilateral to a hemispheric lesion has been reported.
The reflex is mediated by:
- The nasociliary branch of the ophthalmic branch (V1) of the fifth cranial nerve (trigeminal nerve) detects the stimulus only in the cornea (afferent fiber).
- The temporal and zygomatic branches of the seventh cranial nerve (facial nerve) initiate the motor response (efferent fiber).
- The center (nucleus) is the bulge of the brainstem.
Examination of the corneal reflex is part of some neurological examinations, particularly when evaluating coma. Damage to the fifth cranial nerve’s ophthalmic branch (V1) produces an absent corneal reflex when the affected eye is stimulated.
When awake, the eyelids spread tear secretions over the corneal surface for 2 to 10 seconds (although this may vary individually). However, flickering does not just depend on dryness and irritation.
One brain area, the globe pallidum of the basal ganglia, contains a blinking center that controls blinking. However, external stimuli are still involved.
Blinking is related to the extraocular muscles. The blinking usually coincides with a change in gaze, which is believed to aid eye movement.
The trick of the trade: corneal reflex test
The corneal reflex test (blink test) examines the reflex pathway that involves cranial nerves V and VII. Classically, the provider lightly touches a cotton ball on the patient’s cornea. This foreign body sensation should cause the patient to blink reflexively.
This maneuver is always concerned about causing a corneal abrasion, especially if you are examining a very drowsy patient.
More substantial pressure is applied but still does not blink. Repeat the test, and now the patient finally blinks. That’s three times you just scraped the cornea.
An alternative approach
Apply drops of sterile saline solution to the eye. When a patient has a low Glasgow Coma Scale (GCS), they want to do a quick neurological exam.
Grab a pre-filled sterile saline syringe, usually used to flush intravenous lines, and squirt a few drops into the eye. Look for the patient to blink. This seems much safer and more definitive than a corneal reflex test.
Corneal reflex (CN V) and intermittent reflex (CN VII)
The corneal reflex is usually tested after the pupils, but the involved cranial nerves are out of order.
The afferent arc is mediated by the nasociliary branch of the ophthalmic branch (Vi) of the trigeminal or fifth cranial nerve, and the efferent arch is the seventh (facial) nerve.
Naturally, on the way to examining the eye, the intensivist usually needs to open the eyelids.
The corneal reflex (afferent sensory CN V) is tested with the blink reflex (efferent motor CN VII) to minimize repeated patient exposure to the stimulus instrument. The test procedure is the same for both tests.
The examiner will assess afferent motor and sensory responses by observing whether the patient senses the stimulus (sterile cotton swab or cotton swab) and at the same time blinks in response to gentle touch against the sclera of the cornea/eye.
The patient can look away from where the stimulus is applied to help avoid contact with the pupil and iris.
The afferent arm (the sensory component) is served by the trigeminal nerve (CN V), and the efferent arm is done by the facial nerve (CN VII).
Generally, this appears to be done in intensive care units by scratching the cornea with the corner of a piece of gauze; the cornea, rather than the sclera, should be analyzed.
When one eye is tested, both should blink. When the opposite eye does not blink, contralateral facial nerve palsy may be the cause.
When only the untested eye blinks, the seventh nerve palsy is ipsilateral. A sensory injury produces a negative corneal reflex (that is, neither blinks when the affected eye is analyzed).
Bell’s phenomenon or the “oculogyric reflex” is mentioned in the Diagnosis of Stupor and Coma. It is the closure of both eyelids and the elevation of both eyes of the profoundly unconscious patient and indicates that the entire path of reflection is intact.
Specifically, it involves the fifth, seventh, and third nerve nuclei. This reflex has a defensive role, moving the pupil under the lid in response to noxious corneal stimuli.
The mesencephalic reticular nucleus is responsible for integrating the eyelid and eye movements. Ergo, a midbrain injury can result in blinking without an upward trend of the eye.
Conversely, injury to the lower motor neuron of the seventh nerve (or damage to the nerve itself) can cause the eye to move upward without blinking.
Rare eyelid signs
Although generally neglected as a tedious inconvenience, the eyelids are a source of attractive clinical signs.
For example, Plum and Posner report that “the eyelids of a comatose patient gently and gradually close, a movement that cannot be duplicated by an awake individual simulating unconsciousness.”
The tone of the eyelids is remarkable: in the unconscious individual, the resting tone of the orbicularis oculi muscle keeps the eyes closed.
Therefore, failing to keep the eyelids closed in a coma or not closing them again after a forced opening may suggest weakness of the facial nerves. Plum and Posner list a whole series of eyelid signs and their pathophysiological correlations:
Ptosis: brain or hemispheric injury or Horner’s syndrome.
Lack of tone or inability to close the eye with open force: facial nerve palsy (NC VII).
Gentle and gradual eye closing: actual coma, instead of “pseudocoma.”
Strong resistance to eye-opening, “blepharospasm,” and rapid closure: often voluntary; the patient is not truly unconscious.