Johann Friedrich Horner originally described the Horner syndrome (HS) in humans in 1869 (van der Wiel HL. 2002). HS is caused by a disruption in the oculosympathetic circuit between the hypothalamus and the orbit (Amonoo-Kuofi HS, 1999). The characteristic trio of ipsilateral eyelid ptosis, miosis, and face anhidrosis is what distinguishes HS. There are numerous causes of HS, but herniated cervical disc (HCD) is a fairly rare one.

The oculosympathetic circuit starts with a first-order neuron in the hypothalamus’s posterior lateral aspect and extends down the spinal cord from C8 to T2. A second-order (preganglionic) neuron exits the spinal cord via the ventral roots and enters the paravertebral sympathetic chain from the intermediolateral grey material of the spinal cord at level C8-T2 (Budge-Waller’s Cilionospinal Centre). The preganglionic pathway crosses the apex of the lung and ascends through the cervical sympathetic chain to the superior cervical ganglion. The superior cervical ganglion’s third-order (postganglionic) neuron, located at C2-C3, posterior to the carotid sheath and anterior to the longus colli muscle, travels through the carotid plexus into the skull, where it connects with the ophthalmic nerve and enters the orbit. HS may arise as a result of an injury anywhere along the route (Amonoo-Kuofi HS. 1999; Lee JH, et al. 2007; Reede DL, et al. 2008).

A HS can be classified as central (first-order neuron), preganglionic (second-order neuron), or postganglionic (third-order neuron) based on the location of the interrupted oculosympathetic pathway.

Central HS can be caused by brain stem ischemia, brain tumours, demyelinating disorders, syringomyelia, or transverse myelitis (Amonoo-Kuofi HS, 1999; Kerrison JB et al., 2000). Central HS is rarely seen in isolation. First-order neuron fibres pass in Budge’s centre, directly lateral to the dorsal grey matter, and synapse in the spinal cord grey matter (Reede DL et al. 2008).

Preganglionic HS can be caused by a thoracic or neck tumour, spinal cord trauma, herniated disc at C8-T1, iatrogenic sympathetic pathway disruption (e.g., radical neck dissection, selective nerve root block, carotid angiography, stenting, or endarterectomy), spontaneous carotid dissection, and aortic aneurysm, as well as malignant conditions that affect normal sympathetic innervations (Kaplowitz K, and Lee AG. 2011; Lee JH, et al. 2007; Miura J, et al. 2003; Montgomery DM, and Brower RS. 1992; Reede DL, et al. 2008; Russell JH, et al. 2009; Walton KA, and Buono LM. 2003; Zhao CQ, et al. 2007). Tumours or trauma are the most common causes of the preganglionic type.

Postganglionic HS can be caused by vascular headaches, a tumour or aneurysm in the cavernous sinus, a nasopharyngeal tumour, or trauma accompanying a basal skull fracture. The most common causes include carotid artery dissection and cluster headaches. However, most postganglionic lesions are idiopathic. Anhidrosis is rarely apparent, and in the postganglionic subtype, it is nearly absent (Amonoo-Kuofi HS. 1999; Reede DL, et al. 2008).

HCD is a prevalent cause of spinal cord compression; however, HS linked with HCD has only been recorded in a few studies. Only two cases of herniated thoracic disc at T1-2 were the aetiology of HS (Gelch MM. 1978; Lloyd TV, et al. 1980). Cervical herniated disc-related HS were extremely rare; I have found just two cases documented in the literature (Lee JH, et al., 2007; Russell JH, et al., 2009; Ma H, et al., 2012). Spinal cord compression is associated with cervical disc herniation at C4-C5 or C5-C6 levels, which causes an insult to the sympathetic system and may be a cause of HS (Lee JH, et al., 2007; Russell JH, et al., 2009; Ma H, et al., 2012). The HCD may directly compress the spinal cord, causing an injury to the sympathetic pathway’s first-order neuron at C4–C5. Patients with HCD frequently have neck pain, cervical radiculopathy, myelopathy, or a combination of these symptoms. However, if individuals have no cervical symptoms at all, this uncommon presentation might lead to a delayed or inaccurate diagnosis in a variety of directions. For example, because the patient had no cervical symptoms at first, the doctor suspected a brain stroke.

MR imaging is the most reliable investigative technique and should be used as the first diagnostic tool for HS associated with HCD. Early diagnosis and surgical decompression are required for therapy, since severe cord compression will result in additional neurological impairments. 

 References

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