Horner's Syndrome

Symptoms appear on the side of the lesion, mainly on the face:

• ptosis (omission of the upper eyelid due to insufficient sympathetic innervation of the upper tarsal muscle ( musculus tarsalis superior ), or Müller muscle ^[3] ), "inverted ptosis" (a slight elevation of the lower eyelid);
• miosis (narrowing of the pupil),
• pathology of the pupil sphincter ( sphincter pupillae ) (this leads to a weak reaction of the pupil to light).
• enophthalmos (dropping of the eyeball ),
• dyshidrosis (perspiration disturbance) on the affected side of the face, a decrease in the severity of the ciliospinal reflex , injection (vasodilation) of the conjunctiva, and facial skin hyperemia on the side affected by the lesion.

In children, Horner's syndrome sometimes leads to heterochromia ^[4] (a different color of the iris in the eyes). This is due to the fact that the absence of sympathetic innervation prevents the melanin pigmentation of the melanocytes that are at the base (stroma) of the iris ( lat. Stroma iridis ).

The syndrome is named after the Swiss ophthalmologist Johann Friedrich Horner, who first described the syndrome in 1869. Previously, there were several cases of the description of symptoms, but Horner's description is used more often. In Great Britain and Italy, the name of Claude Bernard is also included in the name of the syndrome — Bernard – Horner syndrome, in France it is called Claude Bernard syndrome ^[5] .

Horner's syndrome is acquired as a result of a pathological process; a congenital or iatrogenic (as a result of medical intervention) pathway is also possible. Although most causes are relatively benign, Horner's syndrome may indicate a serious pathology in the neck or chest area (for example, a Pancost tumor (apex of the lung) or a thyroid-cervical venous dilation).

• Due to damage to or compression of the cervical or thoracic sympathetic chain on one side, resulting in symptoms on the ipsilateral (the same as the damage) side of the body.
• Lateral medullary syndrome
• Cluster headache
• Trauma - the base of the neck, usually a blunt injury, can be surgical.
• Inflammation of the middle ear .
• Tumors are most often a brochogenic carcinoma of the apex of the lung ( Pancost tumor ).
• Aortic aneurysm .
• Mediastinitis
• Neurofibromatosis type I.
• Goiter (thyroid hyperplasia).
• Stratification of the aortic aneurysm .
• Thyroid carcinoma .
• Multiple Sclerosis
• Stellate ganglion traction due to extra cervical rib
• Paralysis Degerin-Klumpke .
• Cavernous sinus thrombosis .
• Sympatectomy (transection of the sympathetic nerve of the neck).
• Syringomyelia .
• Nerve block, for example, cervical plexus block, stellate ganglion block.
• As a complication of Bulau drainage .

Horner's syndrome occurs due to a lack of sympathetic innervation . The site of damage to the sympathetic paths is on the ipsilateral side of the symptoms. The following are examples of conditions causing clinical manifestations of Horner's syndrome:

• The defeat of the first neuron (the section of the path between the hypothalamus and the cervical ciliospinal center is called the first neuron (although it is probably interrupted by several synapses in the bridge and midbrain )): central lesions, including the hypothalamic spinal path (for example, dissection of the cervical spinal cord).
• Damage to the second neuron (the section from the ciliospinal center to the upper cervical node is called the second neuron (that is, preganglionic fibers)): preganglionic lesions (for example, compression of the sympathetic pathway by a tumor of the apex of the lung).
• The defeat of the third neuron (the section from the upper node to the muscle that dilates the pupil is called the third neuron (these are postganglionic fibers)): postganglionic lesions at the level of the internal carotid artery (for example, a cavernous sinus tumor).

When determining the presence and severity of Horner's syndrome, three tests are used:

1. Test with a drop of cocaine (obsolete) - eye cocaine drops block the reuptake of norepinephrine , which leads to the expansion of the pupil. Due to the lack of norepinephrine in the synaptic cleft, the pupil will not expand with Horner's syndrome. Recently, a method has been introduced which is more reliable and which has no difficulty in obtaining cocaine. It is based on the use of apraclonidine in both eyes (sympathomimetic, α2-adrenergic agonist), which leads to the appearance of mydriasis on the side of the lesion with Horner's syndrome.
2. Test with oxamphetamine (paredrin). This test helps determine the cause of myosis. If the third neuron (the last of the three neurons in the neural pathway, which ultimately discharges norepinephrine into the synaptic cleft) is intact, then amphetamine causes the neurotransmitter vesicle to empty, thus releasing norepinephrine into the synaptic cleft, which leads to the appearance of persistent mydriza on the affected side. If the aforementioned third neuron is damaged, then amphetamine will have no effect, and the pupil will remain narrowed. however, there is no test to differentiate damage to the first and second neurons.
3. Test to determine the delay in pupil expansion.

It is important to distinguish ptosis caused by Horner's syndrome from ptosis caused by damage to the oculomotor nerve . In the first case, ptosis is combined with a narrowed pupil (due to insufficient sympathetic innervation of the eye), in the second case, ptosis is combined with an enlarged pupil (due to insufficient innervation of the pupil sphincter). In real clinical work, these two different ptoses are fairly easy to distinguish. In addition to the dilated pupil, in case of damage to the oculomotor nerve, ptosis is more severe, sometimes completely covering the entire eye. Ptosis in Horner's syndrome will be moderate or barely noticeable.

If, upon detection of anisocoria (a difference in the size of the pupils), the examiner doubts which of the pupils is dilated and which is narrowed relative to the norm, then in the presence of ptosis, the pupil located on the same eye as ptosis will be pathological.

Anisocoria

Pete Syndrome - Reverse Horner Syndrome

• Richard S. Snell, Horner's syndrome