I’m now officially back at uni after a lovely 5 weeks of lamb-filled Easter fun. It’s been back to a harsh reality for me as exams are looming and we’re still being taught new and complicated things to add to the stress! We’re currently studying the innervation of the head, and one illness commonly presented to vets due to complications in these nerves is Horner’s syndrome.
Horner’s syndrome occurs due to lack of sympathetic innervation to the orbit (eye socket). Sympathetic nerves are autonomic, meaning they control things that happen without us thinking about them. Some examples are digestion, blood pressure regulation and heart rate. The sympathetic branch is responsible for the ‘fight or flight’ response, so is involved in raising the heart rate, increasing bronchiole diameter, slowing digestion, dilating the pupil and increasing blood flow to the muscles needed for running away. Its opposing nerves are the parasympathetic nerves, responsible for the body’s ‘rest and digest’ mode. These nerve fibres slow the heart rate, increase salivation and digestion, decrease bronchiole diameter and increase blood flow to the digestive system. These two autonomic nerve divisions basically counteract each other’s effects, meaning our body is forever in balance with the two opposing inputs. Horner’s syndrome occurs when this balance goes wrong and the sympathetic input to the eye is taken away.
Horner’s syndrome only occurs on the side of the face with the affected nerve fibres, so is most commonly only seen on one side of the face. When sympathetic input is lost from the eye, four main symptoms occur:
1) Miosis – constriction of the affected pupil. This is because the parasympathetic fibres that want the pupil to be constricted are now uninhibited, as the sympathetic input that would normally dilate the pupil has gone.
2) Enopthalmus – this is sinking of the eyeball in to the socket, as there is loss of sympathetic innervation to orbital smooth muscles responsible for protruding the eye.
3) Protrusion of the third eyelid (also known as the nictitating membrane) – in dogs this usually occurs as a passive effect of the previous enopthalmus. In cats the protrusion can be a combination of enopthalmus and loss of third eyelid retraction, as cats have strands of smooth muscle that extend to their third eyelids that are no longer innervated.
4) Ptosis – drooping of the upper eyelid. This is due to lack of innervation to the smooth muscle attached to a facial muscle known as the levator palpebrae superiosis responsible for raising the upper eyelid.
It can be difficult to confirm Horner’s syndrome at first, as symptoms such as anisocoria (unequal pupil size) can arise from a range of illnesses. Here are a few ways to help diagnose it without the need for expensive and invasive tests:
1) Is the animal blind? Horner’s syndrome will not interfere with vision, although protrusion of the third eyelid might. Try a few tests to check the dog can see and follow objects around the room. If the third eyelid is obstructing vision tests, wait until it retracts.
2) Does the smaller pupil dilate in the dark? This test is very commonly used to diagnose Horner’s syndrome. In an animal with Horner’s syndrome the smaller pupil will not dilate substantially in the dark. It simply can’t as the surrounding muscles do not have the sympathetic innervation to do so. The normal, larger pupil will, however, dilate.
3) Does the larger pupil constrict in the light? With Horner’s syndrome it should do so, as it is a normal functioning pupil.
4) Does the pupil react to a drop of 4-10% cocaine eyedrops? In theory cocaine should cause a healthy pupil to dilate as it inhibits the re-uptake of the sympathetic neurotransmitter (noradrenaline) at the synapses. This means that the neurotransmitter continues to innervate the pupil more than usual, leading to it getting larger. In Horner’s syndrome, the sympathetic nerves are disrupted so no noradrenaline is released. This means cocaine drops have no effect on the pupil as there’s no neurotransmitter to begin with.
Horner’s syndrome is classified according to where the lesion causing the damage has occurred. Sympathetic innervation to the head and eye consists of first, second and third order neurons. The first order neurons originate in the brain and travel down the spinal tract to the thoracic 1-3 region. The second order neurons exit the spinal cord at the same T1-3 region, with some fibres closely associated to the nerves innervating the forelimb. This can mean that lesions affecting the forelimb can also result in Horner’s syndrome. These nerves synapse at the cranial cervical ganglion, which lies close to the tissue of the ear, meaning ear disease can also lead to Horner’s syndrome if it affects these sympathetic nerves. From here, third order neurons travel through the middle ear and brain before finally reaching the eye. Lesions of the cranium can cause the syndrome, but these come hand in hand with other obvious neurological problems.
I read an interesting article about the use of pharmacological testing to predict the site of the lesion causing Horner’s syndrome, locating the nerve damage as first order, second order (also known as pre-ganglionic) or third order (post-ganglionic). It suggested that as the synapse of the parasympathetic nerve hadn’t been used in a while, degradative enzymes at the synapse are lost, leaving the receptors at the synapse hypersensitive to agonists (like neurotransmitters). By adding a drop of an agonist (commonly 1% phenylephrine) and waiting for the pupil to dilate, it is suggested that you can make a good estimate as to where the lesion is. If the dilation occurs in less than 20 minutes it’s likely to be a third order nerve affected. 20-45 minutes is second order and 45-90 suggests first order (or no sympatheic de-nervation… time to rediagnose!).
There are a huge number of lesions that can lead to Horner’s syndrome affecting any of the three types of neuron. They can range from a spinal trauma to an ear disease. With first order Horner’s syndrome the cause is often unknown. This is the most common cause and is known as idiopathic Horner’s syndrome. It often has a sudden onset and can affect one or both eyes. It is particularly prevalent in golden retrievers. There’s no treatment however the disorder may resolve itself spontaneously, which can take as long as 8 months. It has no major effect on the animal’s life and is mostly a cosmetic problem. If it is affecting both eyes and the third eyelids are obscuring eyesight, drops of phenylephrine can be administered and the effects can last up to 18 hours.
So there’s an example of a disorder caused by nerve damage. It’s making my head spin imagining one day being presented with an animal showing neurological signs and having to distinguish which nerves are affected through thorough examinations. Us vets are as good as Sherlock.. right?
