Although most causes are relatively benign, Horners syndrome may reflect serious disease in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).Causes can be divided according to the presence and location of anhidrosis:
Central (anhidrosis of face, arm and trunk)
Syringomyelia
Multiple sclerosis
Encephalitis
Brain tumors
Lateral medullary syndrome
Preganglionic (anhidrosis of face)
Cervical rib traction on stellate ganglion
Thyroid carcinoma
Thyroidectomy
Goiter
Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung
Klumpke paralysis
Trauma - base of neck, usually blunt trauma, sometimes surgery. As a complication of tube thoracostomy
Thoracic aortic aneurysm
Postganglionic (no anhidrosis)
Cluster headache - combination termed Hortons headache
An episode of Horners syndrome may occur during a migraine attack and be relieved afterwards
Carotid artery dissection/carotid artery aneurysm/trauma
Cavernous sinus thrombosis
Middle ear infection
Sympathectomy
Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

Pathophysiology
Horner 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 Horners syndrome:
First-order neuron disorder: Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord). Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor) that releases acetylcholine. Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection) that releases norepinephrine.
It has since been marketed under more than 100 trade names, from Amepromat through Quivet to Zirpon.A December 1955 study of 101 patients at the Mississippi State Hospital in Whitfield, Rankin County, Mississippi, found meprobamate useful in the alleviation of "mental symptoms": 3% of patients made a complete recovery, 29% were greatly improved, 50% were somewhat better, while 18% realized little change. Self-destructive patients became cooperative and calmer, and experienced a resumption of logical thinking. In 50% of the cases, relaxation brought about more favorable sleep habits. Following the trial, hydrotherapy and all types of shock treatment were subsequently halted. Meprobamate was found to help in the treatment of alcoholics by 1956. By 1957, over 36 million prescriptions had been filled for meprobamate in the US alone, a billion pills had been manufactured, and it accounted for fully a third of all prescriptions written. Berger, clinical director of Wallace Laboratories, described it as a relaxant of the central nervous system, whereas other tranquilizers suppressed it. A University of Michigan study found that meprobamate affected driving skills. Though patients reported being able to relax more easily, meprobamate did not completely alleviate their tense feelings. The disclosures came at a special scientific meeting at the Barbizon Plaza Hotel in New York City, at which Aldous Huxley addressed an evening session.