The light reflex is mediated by retinal photoreceptors and 4 neurons.
- The first neuron (sensory) connects each retina to both pretectal midbrain nuclei at the level of the superior colliculus. Impulses arising in the temporal retina are conducted by uncrossed fibers (ipsilateral optical path), which end in the ipsilateral and retinal core.
- The second neuron (intercalated) connects each pretext nucleus to both Edinger-Weslphal nuclei. A monocular light stimulus causes a bilateral symmetric constriction of the pupil. Damage to the intercalary neurons causes the dissociation of reactions to light and close distances in neurosyphilis and insalomas.
- The third neuron (preganglionic motor) connects the core of Edinger-Westphal with the ciliary node. Parasympathetic fibers go as part of the oculomotor nerve and, entering into its lower branch, reach the ciliary node.
- The fourth neuron (postganglionic motor) leaves the ciliary node and, passing through the short ciliary nerves, innervates the sphincter of the pupil. The ciliary node is located in the muscle cone, behind the eye. Different fibers pass through the ciliary node, but only the parasympathetic forms a synapse in it.
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The reflex to approximation (synkinesia, not the true reflex) is activated when looking from a distant object to a close one. Includes accommodation, convergence and miosis. Vision is not necessary for the reflex to approximation, and there are no clinical conditions in which the light reflex is present but the reflex to the approximation is absent. Despite the fact that the final paths for the approaching reflex and the light reflex are identical (ie, the oculomotor nerve, the ciliary node, the short ciliary nerves), the center of the approach reflex is not well understood. Two subnuclear influences are likely: the frontal and occipital lobes. The mid-brain center of the reflex to the approximation is probably located ventral than the pretectal nucleus, which is why compression lesions, such as pinealomas, preferentially affect the dorsal intercalated neurons of the light reflex, sparing the ventral fibers to the last.
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Sympathetic innervation of the pupils
Sympathetic innervation includes 3 neurons:
- The neuron of the first order (central) begins in the posterior hypothalamus and descends, uncrossed, along the brainstem until it terminates at the ciliiospinal center Budge in the lateral intermediate substance of the spinal cord between C8 and T2.
- The neuron of the second order (preganglionic) goes from the ciliospial center to the upper cervical node. On its way, it is closely related to the apical pleura, where it can be affected by bronchogenic carcinoma (Pancoasl tumor) or during surgery on the neck.
- A neuron of the third order (postganglionic) rises along the internal carotid artery before entering the cavernous synapse, where it connects to the ocular branch of the trigeminal nerve. Sympathetic fibers reach the ciliary body and the dilator of the pupil through the nasociliary nerve and the long ciliary nerves.
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Afferent pupillary defects
Absolute afferent pupillary defect
The absolute afferent pupillary defect (amarotic pupil) is caused by a complete lesion of the optic nerve and is characterized by the following:
- The eye on the affected side is blind. Both pupils are the same size. During light stimulation of the affected eye, neither pupil does not respond, but when stimulating a normal eye, both pupils react normally. The approximation reflex is normal for both eyes.
Relative afferent pupillary defect
A relative afferent pupillary defect (Marcus Gunn pupil) is caused by incomplete damage to the optic nerve or severe damage to the retina, but is not caused by dense cataracts. Clinical manifestations are similar to the amaurotic pupil, but lighter. Thus, the pupils react sluggishly to the stimulation of the patient's eye, and the normal one is alive. Distinctions of pupillary reactions of both eyes are emphasized by the test of “swinging the flashlight”, in which the light source is transferred from one eye to the other and back, sequentially stimulating each eye. First, stimulate the normal eye, causing the constriction of both pupils. When light is transferred to a sore eye, both pupils expand instead of narrowing. This paradoxical dilation of the pupils in response to illumination arises because the expansion caused by the rejection of light from the normal eye outweighs the narrowing caused by stimulation of the sore eye.
When afferent (sensory) lesions pupils have the same size. Anisocoria (unequal pupil size) is the result of a lesion of the efferent (motor) nerve, iris or pupil muscles.
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Dissociation of pupillary reflexes to light and short distances
The reflex to light is absent or dull, but the reaction to the approximation is normal.
Causes of pupillary reflex dissociation into light and short distances
- affection defect
- bitch Adie
- herpes zoster ophthalmicus
- aberrant regeneration n. Oculomotorius
- type 1 diabetes
- myotonic dystrophy
- dorsal middle cerebral syndrome Parinaud
- familial amyloidosis
- chronic alcoholism
- Moderate ptosis (usually 1–2 mm) as a result of Muller’s muscle weakness.
- Slight elevation of the lower eyelid due to weakness of the lower tarsal muscle.
- Mioz due to the unhindered action of the sphincter of the pupil, with the emergence of anisocoria, which increases in low light, as the pupil of Hörner does not expand, like a paired one.
- Normal reaction to light and approximation,
- Reduction of sweating is ipsilateral, but only if the lesion is lower than the upper cervical node, since the fibers that innervate the skin of the face go along the external cervical artery.
- Hypochromic heterochromia (iris of a different color — the pupil of Horner is lighter) is visible if the lesion is congenital or has existed for a long time.
- The pupil expands slowly.
- Less important symptoms: hyperactivity of accommodation, hypotonia of the eye and conjunctival hyperemia.
Pupil Argyll Robertson
Called neurosyphilis and is characterized by the following:
- The manifestations are usually bilateral, but asymmetrical.
- Pupils are small, irregularly shaped.
- Dissociation of reactions to light and approximation.
- Pupils are very difficult to expand.
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The pupil of Adie (tonic) is caused by postganglionic denervation of the sphincter of the pupil and the ciliary muscle, possibly due to a viral infection. Usually occurs in young and unilateral in 80% of cases.
- Evenly widened pupil.
- The reflex to light is absent or lethargic and is combined with wormlike movements of the edge of the pupil, visible in a slit lamp.
- On approaching the object, the pupil responds slowly, the subsequent expansion is also slow.
- Accommodation may show similar tonicity. So, after fixing on a close object, the time of refocusing on a distant object (relaxation of the ciliary muscle) is increased.
- After a long time, the pupil may become small (“little old Adie”).
Concomitant in some cases are the weakening of deep tendon reflexes (Holmes-Adie syndrome) and autonomic dysfunction.
Pharmacological tests. If mecholil 2.5% or pilocarpine 0.125% is instilled into both eyes, the normal pupil will not narrow, and the affected pupil will narrow due to denervation hypersensitivity. Some people with diabetes can also have this reaction, and in healthy people both pupils narrow very rarely.
Oculo-sympathetic paralysis (Horner's syndrome, Horner's)
Causes of Horner's Syndrome
Central (first order neuron)
- brain stem lesions (vascular, tumors, demyelination)
- alternating syndrome Wallenberg
- spinal tumors
Preganglionic (second order neuron)
- pancoast tumor
- carotid and aortic aneurysms and stratification
- neck diseases (glands, trauma, postoperative)
Postganglionic (third order neuron)
- cluster headaches (migraine neuralgia)
- bundle of internal carotid artery
- nasopharyngeal tumors
- otitis media
- cavernous sinus neoplasm
The diagnosis is confirmed with cocaine. Hydroxyamphetamia (paredria) is used to differentiate a preganglionic lesion from a postganglionic one. Epinephrine can be used to evaluate denervation hypersensitivity.
Cocaine 4% is instilled into both eyes.
- Result: the normal pupil expands, Horner's pupil does not.
- Explanation: Noralrenaline, isolated by postganglionic sympathetic endings, is re-captured, and its action ends. Cocaine blocks reuptake, so norepinephrine accumulates and causes pupil dilation. With Horner’s syndrome, norepinephrine will not be released, so cocaine does not work. Thus, cocaine confirms the diagnosis of Horner syndrome.
Hydroxyamphetamine 1% is instilled into both eyes.
- Result: in preganglionic lesions, both pupils will expand, while in postganglionic pupil Horner will not expand. (The test is performed the day after the effects of cocaine have passed.)
- Explanation: Hydroxyamphetamine increases the release of norepinephrine from postganglionic nerve endings. If this neuron is intact (a lesion of a neuron of the first or second order, as well as a normal eye), the NA will be released and the pupil will expand. With the defeat of the neuron of the third order (postganglionic) expansion can not be, because the neuron is destroyed.
Adrenaline 1: 1000 is instilled into both eyes.
- Result: in a preganglionic lesion, no pupil will expand, because adrenaline will quickly collapse with monoamyoxidase; with postganglionic lesion, Horner’s pupil will expand, and ptosis may temporarily decrease, since adrenaline does not collapse due to the lack of monoamine oxidase.
- Explanation: A muscle lacking motor innervation is more sensitive to the excitatory neurotransmitter released by the motor one. In Horner’s syndrome, the pupil dilator muscle also exhibits “denervational hypersensitivity” to adrenergic neurotransmitters, therefore adrenaline, even in low concentrations, causes a noticeable expansion of Horner’s pupil.
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