Horner’s syndrome develops when the sympathetic pathway of the cervical spine, emanating from the hypothalamus to the eye, is affected. It manifests itself in the area of the eyes with damage to the muscle tissue joints of the body and the eyeballs. The disease was discovered by Dr. Horner, but several other physicians investigated before him and described the disease. As a result, the disease was named after him, but in some countries, it is also called Bernard Horner’s syndrome or Claude Horner’s syndrome (Poeck, 1985).
There are three main symptoms: enophthalmos – retraction of the eyeball; miosis – a decrease in the pupil, which is considered abnormal; ptosis – drooping of the upper eyelid of the affected eye. However, these are not all the symptoms that can characterize this disease; there are much more of them, and among them is anhidrosis – sweating is disturbed in the area of the affected nerve.
Acetylcholine is known as the primary neurotransmitter of pre-ganglionic nerves. Hence, the injection of acetylcholine naturally results in the sweating of the person. On the other hand, norepinephrine, or noradrenaline, is a hormone and neurotransmitter responsible for our response in dangerous situations and the dilation of the pupil. If we inject a healthy person with norepinephrine, their pupil will naturally dilate. Hence, the reaction of the young resident’s body to the injection of norepinephrine was natural, meaning that post-ganglionic nerves are not damaged. However, the injection of acetylcholine prevented the reduced sweating on the affected side, indicating the damage to pre-ganglionic nerves. Therefore, it can be concluded that pre-ganglionic nerves are damaged since they were not able to provide the body with enough acetylcholine to cause sweating.
Poeck, K. (1985). Horner’s Syndrome. Diagnostic Decisions in Neurology, 66–69. Web.