What is the primary mechanism behind the symptoms of Horner's syndrome?

Horner's syndrome is characterized by a specific set of symptoms that arise from a disruption in the sympathetic nervous system pathway to the eye. The primary mechanism involves the impairment or interruption of the sympathetic fibers that innervate the eye and surrounding structures. This disruption can occur at various points along the sympathetic pathway, which begins in the hypothalamus, travels down to the spinal cord, and then ascends back up to the level of the eye.

The hallmark signs of Horner's syndrome include ptosis (drooping of the upper eyelid), miosis (constricted pupil), and anhydrosis (lack of sweating) on the affected side of the face. These symptoms result directly from the loss of sympathetic innervation, which results in the unopposed action of parasympathetic fibers, particularly affecting pupil size and eyelid elevation.

While nerve damage or its variations could potentially be involved in the development of Horner's syndrome, the essence of the condition is rooted in the disruption of the entire sympathetic pathway. Vascular disruptions could theoretically impact the nerves as well, but they are not the primary cause of Horner's symptoms as understood in clinical practice. Damage to the optic nerve would not lead to the signs associated with Horner's syndrome