A patient has been diagnosed with Horner’s syndrome, a disorder that is due to damage of sympathetic nerves that travel to the eye. It occurs unilaterally and results in extreme pupil constriction and reduced sweating on the affected side. The young resident who diagnosed the condition is an autonomics freak and is eager to determine if it is the pre-ganglionic nerve or the post-ganglionic nerve that is damaged. For his determination, he injects acetylcholine, which caused sweating on the affected side, but he sees no change in pupil size. He then injects norepinephrine and the pupil dilates, but no sweating occurs.

Question: Is the pre-synaptic or the post-synaptic neuron damaged? Explain your rationale in detail (in other words, detail how you came to your conclusion). You're going to have to really think on this one. It's not something you can look up in the text. You will need to use what you have learned about the autonomic nervous system and some critical thinking to arrive at the answer.

Horner's Syndrome riddle: Ach is the neurotransmitter at all ANS preganglionic fibers, including SNS. The pt has decreased sweating and pupil constriction, indicating blockage of SNS transmission. When the MD gave ACh it induced sweating, but not pupil dilation. This is because the sweat glands are an exception in normal SNS transmission, as the postganglionic fibers utilize ACh as their neurotransmitters. Other SNS pathways utilize NE as their neurotransmitter. So ACh acted directly on the sweat gland to produce sweating, but could not stimulate the typical postsynaptic neurons to release NE. When the MD gave NE he saw pupil dilation, but not sweating, indicating the NE worked directly at the iris to produce pupil dilation. This indicaates the problem was with the postsganglionic neuron. If the preganglionic neuron were the problem injecting ACh would have solved both problems.