The light reflex is mediated by photoreceptors of the retina and 4 neurons.
- The first neuron (sensory) connects each retina with both prefectal nuclei of the midbrain at the level of the upper hills. Pulses arising in the temporal retina are carried out by uncrossed fibers (ipsilateral optical path), which terminate in the ipsilateral nuclear irradiator.
- The second neuron (intercalary) connects each prefectal nucleus to both Edinger-Weslphal nuclei. The monocular light stimulus causes a two-sided symmetrical narrowing of the pupil. Damage of intercalary neurons causes dissociation of reactions to light and close distances in neurosyphilis and yinsalomas.
- The third neuron (preganglionic motor) connects the nucleus of Edinger-Westphal with the ciliary knot. Parasympathetic fibers go in the oculomotor nerve and, entering its lower branch, reach the ciliary unit.
- The fourth neuron (postganglionic motor) leaves the ciliary unit and, passing in the short ciliary nerves, innervates the pupil sphincter. The ciliary knot is located in the muscle cone, behind the eye. In the ciliary unit, different fibers pass, but only parasympathetic ones form a synapse in it.
Reflex to approach
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 an approximation reflex, and there are no clinical conditions for which a light reflex is present, and there is no reflex to approximation. Despite the fact that the final paths for the reflex to the approximation and the light reflex are identical (ie, the oculomotor nerve, ciliary knot, short ciliary nerves), the center of the reflex to the approximation is not sufficiently studied. There are two supranuclear influences: frontal and occipital lobes. The median cerebral center of the reflex to the approximation is probably located ventrally than the preterital nucleus, which is why compression lesions, such as pinealomas, mainly affect the dorsal intercalary neurons of the light reflex, sparing the ventral fibers until the last.
Sympathetic innervation of pupils
Sympathetic innervation includes 3 neurons:
- The neuron of the first order (central) starts in the posterior hypothalamus and descends, uncrossed, along the brain stem to the end in the ciliospinal center of Budge in the lateral intermediate substance of the spinal cord between C8 and T2.
- The second-order neuron (preganglionic) comes from the ciliospial center to the upper cervical node. On its way it is closely connected with the apical pleura, where it can be affected by bronchogenic carcinoma (Pancoasl tumor) or in the operation on the neck.
- The third-order neuron (postganglionic) rises along the internal carotid artery until it enters the cavernous synapse, where it joins 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.
Afferent pupillary defects
Absolute afferent pupillary defect
Absolute afferent pupillary defect (amaurotic pupil) is caused by complete damage to the optic nerve and is characterized by the following:
- The eye on the side of the lesion is blind. Both pupils are the same size. With light stimulation of the affected eye, no pupil reacts, but with stimulation of the normal eye, both pupils react normally. The reflex to approximation is normal for both eyes.
Relative afferent pupillary defect
The relative afferent pupillary defect (the pupil of Marcus Gunn) is caused by an incomplete lesion of the optic nerve or a severe retinal lesion, but is not caused by dense cataracts. Clinical manifestations are similar to amaurotic pupils, but lighter. So, to stimulate the patient's eyes, the pupils react sluggishly, and the normal ones - vividly. Differences in the pupillary responses of both eyes are emphasized by the "swinging flashlight" test, 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 a narrowing of both pupils. When light is transferred to a sore eye, both pupils dilate instead of narrowing. This paradoxical dilatation of the pupils in response to the illumination appears because the enlargement caused by the removal of light from the normal eye outweighs the constriction caused by the stimulation of the diseased eye.
With afferent (sensory) lesions, the pupils are the same size. Anisocoria (unequal pupil size) is a consequence of afferent (motor) nerve, iris or pupillary muscle damage.
Dissociation of pupillary reflexes into light and close distances
The reflex to light is absent or sluggish, but the reaction to the approximation is normal.
Causes of dissociation of pupillary reflexes into light and close distances
- defect of afferentation
- pupil Adie
- herpes zoster ophthalmicus
- aberrant regeneration n. Oculomotorius
- type I diabetes
- myotonic dystrophy
- dorsal mediastinal syndrome Parinaud
- familial amyloidosis
- chronic alcoholism
- Moderate ptosis (usually 1-2 mm) as a result of muscle weakness of Muller.
- A slight uplift of the lower eyelid due to the weakness of the lower tarsal muscle.
- Miosis due to the unhindered action of the sphincter of the pupil, with the appearance of anisocoria, amplified in low light, since the pupil of the Hörner does not expand, like a pair.
- A normal reaction to light and approximation,
- Reducing sweating ipsilateral, only if the lesion is below the upper cervical node, since the fibers innervating the skin of the face go along the outer cervical artery.
- Hypochromic heterochromia (irises of different colors-the pupil of Horner lighter) is visible if the lesion is congenital or exists long ago.
- Pupil dilates slowly.
- Less important symptoms: hyperactivity of accommodation, eye hypotension and conjunctival hyperemia.
Pupil Argyll Robertson
Called neurosyphilis and is characterized by the following:
- Manifestations are usually bilateral, but asymmetric.
- Pupils are small, irregular in shape.
- Dissociation of reactions to light and approximation.
- Pupils are very difficult to expand.
The pupil of Adie
The Adie pupil (tonic) is caused by postganglionic denervation of the sphincter of the pupil and ciliary muscle, possibly due to a viral infection. Usually happens in young and one-sided in 80% of cases.
- Evenly dilated pupil.
- Reflex to light is absent or flaccid and is combined with vermicular movements of the pupil's edge, visible in the slit lamp.
- At the approach of the object, the pupil reacts slowly, the subsequent expansion is also slow.
- Accommodation can detect a similar tonicity. So, after fixing on a nearby object, the refocusing time to the distant object (relaxation of the ciliary muscle) is increased.
- After a long time, the pupil can 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 2,5% or pilocarpine 0,125% instillirovat in both eyes, normal pupil will not narrow, and affected - will be narrowed due to denervation hypersensitivity. Some people with diabetes can also have this reaction, and in healthy people, both pupils narrow very rarely.
Oculosympathetic paralysis (Horner syndrome, Horner)
Causes of Horner's Syndrome
Central (first-order neuron)
- lesions of the brain stem (vascular, tumors, demyelination)
- alternating syndrome Wallenberg
- spinal cord tumors
Preganglionic (second-order neuron)
- swelling of Pancoast
- carotid and aortic aneurysms and bundles
- neck diseases (glands, trauma, postoperative)
Postganglionic (third-order neuron)
- cluster headaches (migraine neuralgia)
- internal carotid artery dissection
- Nasopharyngeal tumors
- otitis media
- cavernous sinus neoplasm
The diagnosis is confirmed with the help of cocaine. Hydroxyamphetamines (paedraries) are used to differentiate preganglionic lesions from postganglionic lesions. Adrenaline can be used to assess denervation hypersensitivity.
Cocaine 4% is instillated into both eyes.
- Result: the normal pupil is dilated, the pupil of Horner is not.
- Explanation: Noralrenaline, isolated by postganglionic sympathetic endings, undergoes a reverse capture, and its action terminates. Cocaine blocks the reuptake, so norepinephrine accumulates and causes the pupil to dilate. In Horner's syndrome, noradrenaline will not be excreted, so cocaine does not work. Thus, cocaine confirms the diagnosis of Horner syndrome.
Hydroxyamphetamine 1% is instillated into both eyes.
- Result: with preganglionic lesions, both pupils will expand, whereas in the postganglionic lesion, the pupil of Horner will not expand. (The test is performed the day after the effects of cocaine have passed.)
- Explanation: Hydroxyamphetamine enhances the release of norepinephrine from postganglionic nerve endings. If this neuron is intact (the damage of a neuron of the first or second order, and also the normal eye), the HA will be allocated, and the pupil will expand. With the defeat of a neuron of the third order (postganglionic) expansion can not be, because the neuron is destroyed.
Adrenaline 1: 1000 is instillated into both eyes.
- Result: with preganglionic lesions, no pupil will expand, as adrenaline is rapidly destroyed by monoamine oxidase; with postganglionic lesion, the pupil of Horner will expand, and ptosis may temporarily decrease, since epinephrine is not destroyed due to the lack of monoamine oxidase.
- Explanation: a muscle devoid of motor innervation exhibits increased sensitivity to the exciting neurotransmitter isolated by the motor one. In Horner's syndrome, the pupillary dilating muscle also exhibits "denervation hypertension" to adrenergic neurotransmitters, so adrenaline even in small concentrations causes a noticeable dilatation of the Gorner pupil.