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Horner’s syndrome is a clinical syndrome caused by damage to the sympathetic nervous system. It is also known by the names Bernard-Horner syndrome or oculosympathetic palsy.
Signs found in all patients on affected side of face include ptosis (drooping upper eyelid from loss of sympathetic innervation to the Müller or superior tarsal muscle [1]), upside-down ptosis (slight elevation of the lower lid), and miosis (constricted pupil) and dilation lag. Enophthalmos (the impression that the eye is sunk in) and anhidrosis (decreased sweating) on the affected side of the face, loss of ciliospinal reflex and blood shot conjunctiva may occur depending on the site of lesion. Also flushing of the face is common on the affected side of the face due to dilation of blood vessels under the skin.
In children Horner’s syndrome sometimes leads to a difference in eye color between the two eyes (heterochromia).[2] This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.
It is named after Johann Friedrich Horner, the Swiss ophthalmologist who first described the syndrome in 1869.[3][4] Several others had previously described cases, but “Horner’s syndrome” is most prevalent. In France and Italy, Claude Bernard is also eponymised with the condition (“Claude Bernard-Horner syndrome”).
Horner’s syndrome is acquired as a result of pathology but may also be congenital (inborn) or iatrogenic (caused by medical treatment). Although most causes are relatively benign, Horner’s syndrome may reflect serious pathology in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).
Horner’s syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner’s syndrome:
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