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SYMPATHETIC ROUTE TO HORNER’S SYNDROME: SIGNS
AND DIAGNOSIS
Categories : Vets
Date : April 11, 2011
Elena Scarpante and Victoria Doyle discuss a common condition in cats and dogs, using MRI
scans to highlight lesions and softtissue infl ammation consistent with its cause
Summary
Horner’s syndrome (HS) is a common neurological syndrome that occurs due to the loss of
sympathetic innervation to the eye. The clinical signs include miosis, ptosis of the upper eyelid,
decreased tone in the lower eyelid, protrusion of the third eyelid and enophthalmos. Horner’s
syndrome can be classified as first order, second order (preganglionic) or third order
(postganglionic) according to the anatomical location of the lesion. Localisation of the lesion
requires information from the clinical, neurological and ophthalmic examinations to be used in
conjunction with pharmacologic testing. Based on this information, further diagnostic tests can be
performed to identify the underlying cause.
Key words
cat, dog, Horner’s syndrome, idiopathic, sympathetic, innervation to the eye
HORNER’S syndrome (HS) is a common neurological condition seen in both cats and dogs.
It occurs due to lesions affecting the sympathetic supply to the eye.
The aims of this article are to describe:
• the anatomy of the sympathetic supply to the eye;
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• the clinical signs associated with Horner’s syndrome;
• the common differential diagnoses for this condition; and
• the further diagnostic tests that are indicated.
Anatomy
The pathway that provides the sympathetic innervation to the eye consists of three neurons. The
cell bodies of the first order neurons are located in the hypothalamus and rostral midbrain. The
axons pass caudally through the brainstem and in the lateral part of the cervical spinal cord
(tectotegmental spinal tract) to reach the first three thoracic spinal cord segments (T1-3). Here, the
first order neurons synapse on the cell bodies of the second order neurons (preganglionic neurons)
located in the intermediolateral grey column of the spinal cord.
The second order neurons exit the spinal canal through the intervertebral foramina together with
the ventral nerve root arising from the first three thoracic spinal cord segments (T1-3). The axons of
the second order neurons leave the spinal nerve as the ramus communicans and join the thoracic
sympathetic trunk.
The thoracic sympathetic trunk courses inside the thorax ventrolateral to the vertebral bodies and
runs cranially along the neck, associated with the vagus nerve forming the vagosympathetic trunk
within the carotid sheath. The axons of the second order neurons travel rostrally to the cranial
cervical ganglion, which is located ventromedially to the tympanic bulla.
At the level of the cranial cervical ganglion the axons of the second order neurons synapse on the
cell bodies of the third order neurons (postganglionic neurons). From the cranial cervical ganglion,
the postganglionic neurons project through the ventral part of the tympanic bulla and enter the
cranial cavity through the tympano-occipital fissure together with the carotid artery and
glossopharyngeal nerve (CN IX).
Within the cranial cavity the axons travel rostrally adjacent to the middle cranial fossa. The
postganglionic fibres then exit the cranial cavity through the orbital fissure with the ophthalmic
branch of the trigeminal nerve to innervate the smooth muscle of the eyelids (including third eyelid),
orbit and iris dilator muscles. The sympathetic innervation also supplies the smooth muscles of the
).
blood vessels to the head (Figure 1
Clinical signs
The loss of sympathetic innervation of the eye causes a combination of clinical signs, which are
collectively referred to as HS. They include ipsilateral miosis, ptosis of the upper eyelid, decreased
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tone in the lower eyelid, protrusion of the third eyelid and enophthalmos (Figures 2 and 3).
No visual deficits are directly associated to damage along the sympathetic pathway to the eye, but
vision might be obscured in a case of bilateral HS, due to the prominent third eyelid protrusion.
Partial HS can also be seen. This usually consists of only the presence of miosis (Figure 4) and is
most commonly observed with lateralised cervical lesions in dogs. On clinical examination the
anisocoria is more pronounced when examined in a darkened room. Enophthalmos can be best
appreciated by viewing the patient from above.
In dogs the protrusion of the third eyelid occurs passively as a consequence of enophthalmos,
whereas in the cat the third eyelid has a small amount of smooth muscle, which is innervated by
the sympathetic supply to the eye. Therefore, in cats with HS the third eyelid protrusion is partly
due to the loss of innervation to the smooth muscle of the third eyelid preventing it from being
retracted, as well as the presence of enophthalmos.
In addition to the signs related to the eye and the orbital smooth muscle, the paralysis of the
sympathetic supply to the head causes a peripheral vasodilation that may be shown by increased
warmth and hyperaemia of the pinna, as well as congestion of the scleral vessels and nasal
mucosa ipsilaterally. A fundic exam may show congested retinal blood vessels. Reduced sweating
(anhidrosis), usually on the ipsilateral nostril, is also possible. However, these signs are not
commonly detected in small animals.
The sympathetic supply to the eye is a very long pathway and damage anywhere along its route
can cause HS.
HS is classified as first, second and third order. Damage to the sympathetic supply to the eye due
to a lesion anywhere between the hypothalamus and the T1-3 spinal cord segments can cause
damage to the first order neuron (Figures 5 and 6). Damage to the sympathetic supply from the cell
bodies in the intermediate grey matter of T1-3 spinal cord segments to the tympanic bulla will
cause a second order (preganglionic) HS (Figures 7 and 8). Damage to the sympathetic supply
anywhere between the tympanic bulla and the eye will cause a third order (postganglionic) HS
(Figures 9 and 10).
Differential diagnoses for the first, second and third order HS and the associated clinical signs are
listed in Table 1.
Diagnosis
A full history, clinical, ophthalmological and neurological examinations are required in any patient
presenting with HS. Pharmacological testing using topical one per cent phenylephrine may be used
to aid the classification of the HS (first, second or third).
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After topical administration of one per cent phenylephrine (sympathomimetic) to both eyes
simultaneously, the time for the mydriasis to occur is recorded (Table 2). The phenylephrine test is
based on the principle of denervation hypersensitivity, which takes approximately two weeks to
develop. According to this phenomenon, the smooth muscles increase their sensitivity to
neurotransmitters (norepinephrine) following denervation. The shorter the time for the pupil to
dilate, the closer the lesion is to the iris. The test is not 100 per cent reliable and should be
interpreted in light of the other clinical signs.
Based on the history, clinical, ophthalmological and neurological findings and result of the
pharmacological test further investigations can be planned (Table 3).
Treatment and prognosis of the most common causes of HS
The prognosis is closely related to the underlying disease process (Table 1).
Conclusion
The sympathetic supply to the eye is extremely long and, therefore, lesions at many different
anatomical locations from a variety of pathologies can cause HS. Consequently, it is important to
interpret the results of clinical, neurological and pharmacological tests to localise the lesion before
embarking on the diagnostic investigation. In this way an accurate diagnosis can be made and any
required treatment can be instituted expediently.
• The authors would like to thank Alberta de Stefani for her support and supervision.
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