• Clinical science

Horner syndrome (Oculosympathetic paresis)

Abstract

Horner syndrome (HS) is a neurological disorder characterized by a symptom triad of miosis (an abnormally small pupil), partial ptosis (drooping of the upper eyelid), and facial anhidrosis (absence of sweating). This condition results from lesions that interrupt the sympathetic nervous supply to the head, eye, and neck. Most cases of HS are idiopathic, but conditions such as brainstem stroke, carotid dissection, and neoplasm are occasionally identified as the cause of HS. Because of the wide array of possible causes, diagnosis of the underlying disorder frequently poses a challenge and requires a systematic approach. Once the lesion has been identified, treatment should be tailored to the specific cause.

Pathophysiology

Type Anatomical trajectory Typical lesion

Central

Hypothalamus (first neuron) brainstem, cervical, and thoracic spinal cord → ciliospinal center (C8–T2)

Preganglionic

Ciliospinal center (second neuron) → pulmonary apex → stellate ganglionsuperior cervical ganglion

Postganglionic

Superior cervical ganglion (third neuron) → internal carotid artery and ophthalmic nerveiris dilator muscle

References:[1][2]

Clinical features

  • Triad of Horner syndrome
    • Ipsilateral miosis
    • Partial ptosis
    • Anhidrosis or reduced sweating on the face and arm, depending on the location of the lesion
  • (Apparent) enophthalmos
  • Atrophy of arm and hand muscles
  • Facial flushing due to vasodilatation
  • Heterochromia seen only in children under 2 years of age. Iris pigmentation is not completed until the age of 2 years and is subject to sympathetic control during development.

References:[1][2]