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Neurology Networks tries to offer broad exposure to various topics that may be presented on the veterinary neurology board exam.

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Horners

*First order neurons (UMN) originate in the hypothalamus and travel through the tectotegmental system of the brainstem, along the lateral funiculus (lateral tectotegmental spinal tract) of the spinal cord to the lateral grey column at the level of the T1-3 spinal cord segments before synapsing in the paravertebral sympathetic ganglia (rami communicans and sympathetic chain ganglia).

*The second order neurons (preganglionic) will leave the sympathetic chain ganglia and travel through the thorax, mediastinum, and thoracic inlet to travel up the neck with the vagosympathetic trunk.  The neurons will pass through the cervicothoracic and middle cervical ganglia to synapse in the cranial cervical ganglion that is near (usually just caudal to) the middle ear cavity (or guttural pouch in horses).

*The third order neurons (postganglionic) will then pass across the middle ear cavity, enter the skull through the tympano-occipital fissure and follow the ophthalmic branch of CN V.  The fibers will then exit through the orbital fissure to the long ciliary nerves and act on the ciliary body muscle and periorbital muscles.  The sympathetic fibers course near the carotid sinus before exiting the skull - this path from entry to the skull to the ciliary ganglion is ill-defined.

 

Horners syndrome develops when part of this autonomic pathway is damaged.  The clinical results are ipsilateral miosis, ptosis, enophthalmus in most animals.  This can include sweating of the cranial third of the neck and face in horses, anhydrosis of the head and neck in humans, and vasodilation with warm ear in ruminants.

Loss of ciliospinal reflex can also be seen in humans - equivocal in domestic animals.  In this reflex, a slight ipsilateral pupil dilation is noted when a painful stimulus is applied to that side of the face, neck, and upper trunk.

 

Parfour du petit syndrome occurs when part of this pathway is stimulated and the clinical results are essentially the opposite of that seen in Horners.  This is mydriasis, eyelid retraction, exophthalmus, and hyperhydrosis.  This is sometimes seen due to nerve irritation before disease progression causes destruction and then Horners signs.

 

Veterinary Neuroanatomy and Clinical Neurology, 3rd edition.  De Lahunta, Glass.  Saunders Elsevier 2009: pp 173-174

**Cartoon courtesy of Neuropetvet