Hornersyndrom

Horner syndrome, also known as oculosympathetic palsy, is a neurological condition caused by disruption of the sympathetic nerve pathways that supply the eye and facial structures. The classic clinical features are ptosis (drooping of the eyelid), miosis (constricted pupil), and anhidrosis (reduced sweating) on the affected side. Affected individuals may also appear to have a sunken eye (enophthalmos) and slight facial flushing; anisocoria is typically more evident in dim light.

Anatomy and causes: Horner syndrome results from a disruption in the three-neuron sympathetic chain that reaches the eye. The first-order neuron runs from the hypothalamus to the ciliospinal center in the spinal cord (C8–T2). The second-order, preganglionic neuron travels to the superior cervical ganglion, and the third-order, postganglionic neuron reaches the eye via the internal carotid plexus and to facial sweat glands. Lesions can be central (brainstem or spinal cord), preganglionic (apical lung tumors such as Pancoast, trauma, cervical rib), or postganglionic (carotid artery dissection, cavernous sinus disease). Congenital Horner syndrome can occur in newborns.

Diagnosis and evaluation: Diagnosis is clinical but refined by pharmacologic testing and imaging. In suspected Horner syndrome, pharmacologic tests such as apraclonidine or cocaine tests help confirm a Horner pupil and localize the lesion; hydroxyamphetamine testing can distinguish preganglionic from postganglionic lesions. Imaging (MRI/MRA of the brain, neck, and chest) is used to identify causes such as tumors, vascular disorders, or trauma; carotid Doppler may be indicated to assess dissection.

Management and prognosis: Treatment targets the underlying cause. Congenital Horner syndrome may require observation. Secondary cases require management of the underlying pathology (tumors, vascular injury, trauma). Ocular symptoms like ptosis can be addressed surgically or with assistive devices if needed. The prognosis depends on the cause and its reversibility.