Horner’s Syndrome Flashcards
Horner’s syndrome refers to a classic triad of …
Horner’s syndrome refers to a classic triad of miosis, ptosis and anhidrosis.
Horner’s syndrome is a classic medical condition that is characterised by a unilateral triad of:
Miosis: small pupil
Ptosis: drooping eyelid
Anhidrosis: lack of sweat
Horner’s syndrome is due to a lesion anywhere along the sympathetic pathway, also known as the oculosympathetic pathway. This pathway is important for pupillary dilatation. As such, Horner’s is also known as oculosympathetic paresis
Horner’s syndrome is due to a lesion anywhere along the sympathetic pathway, also known as the oculosympathetic pathway. This pathway is important for pupillary dilatation. As such, Horner’s is also known as oculosympathetic paresis.
First order horners
Caused by a lesion anywhere between the brainstem and cervicothoracic spinal cord. Lesions of the central nervous system are usually present with other neurological features.
Stroke (e.g. lateral medullary syndrome): most common cause of first-order lesion. Other features of lateral medullary syndrome include vertigo, nystagmus, ataxia (ipsilateral), pain and temperature loss (contralateral body, ipsilateral face), nausea/vomiting, dysphagia, and hiccups.
Space-occupying lesion
Multiple sclerosis
Syringomyelia (fluid-filled cyst spinal cord)
Cervical cord trauma
The classic cause of Horner’s syndrome affecting the second-order neuron is a … tumour. This refers to a tumour in the apex of the lung.
The classic cause of Horner’s syndrome affecting the second-order neuron is a pancoast tumour. This refers to a tumour in the apex of the lung.
Up to 60% of carotid artery … will have an isolated, ipsilateral Horner’s syndrome on presentation.
Up to 60% of carotid artery dissection will have an isolated, ipsilateral Horner’s syndrome on presentation.
Miosis in horners syndrome
The degree of anisocoria, which describes unequal pupils, is more marked in the dark. The pupil will also dilate slower following removal of a light source compared to the other eye.
Ptosis in horners syndrome
Ptosis is usually minimal (<2 mm), which reflects the minimal contribution of Müller’s muscle to lid elevation.
The degree of anhidrosis, which describes a lack of sweating, is dependent on the neuron affected.
Horners syndrome
First order: affecting the ipsilateral body
Second order: affecting the ipsilateral face. However, usually mild and only affecting the forehead.
Third order: absent
Brainstem signs: diplopia, vertigo, ataxia, focal weakness
Spinal cord signs: bilateral or ipsilateral weakness, sensory level, bowel and bladder impairment
Axillary or lung apex involvement: arm pain and/or hand weakness
Isolated Horner’s: concerning for … dissection
Brainstem signs: diplopia, vertigo, ataxia, focal weakness
Spinal cord signs: bilateral or ipsilateral weakness, sensory level, bowel and bladder impairment
Axillary or lung apex involvement: arm pain and/or hand weakness
Isolated Horner’s: concerning for carotid dissection
In patients presenting with an acute Horner’s syndrome, it is pertinent to exclude a … …dissection with a CT angiography due to the high risk of subsequent stroke. Those with brainstem features or symptoms localising to the cavernous sinus (e.g. multiple cranial nerve palsies - III, IV, V1, VI) warrant further investigation with MRI. An MRI spine is usually needed for suspected spinal cord lesions and a CT chest should be undertaken in suspected … tumour.
In patients presenting with an acute Horner’s syndrome, it is pertinent to exclude a carotid artery dissection with a CT angiography due to the high risk of subsequent stroke. Those with brainstem features or symptoms localising to the cavernous sinus (e.g. multiple cranial nerve palsies - III, IV, V1, VI) warrant further investigation with MRI. An MRI spine is usually needed for suspected spinal cord lesions and a CT chest should be undertaken in suspected pancoast tumour.
Confirmation
Horner’s syndrome is usually determined based on clinical assessment. However, in subtle cases, cocaine or apraclonidine drops can be used to confirm the diagnosis.
Cocaine drops: blocks reuptake of noradrenaline at the nerve synapse. Leads to activation of the pupillary dilator and subsequent dilatation. Has no effect in eyes with impaired sympathetic innervation. Degree of anisocoria is measured after 1 hour.
Apraclonidine: alpha agonist with weak action on alpha-1-receptors and strong action on alpha-2-receptors. Activation of alpha-1 causes pupil dilatation and alpha-2 causes pupil constriction. If administered to a ‘normal pupil’ it will constrict slightly due to the stronger alpha-2 action. If administered to a ‘Horner’s pupil’ it will dilate due to alpha-1 receptor denervation supersensitivity (i.e. it’s more sensitive to the drug affects due to a period of not being stimulated).
Localisation of horners
Hydroxyamphetamine
Hydroxyamphetamine eye drops are used to help localise the lesion to the first, second or third order neuron. Hydroxyamphetamine stimulates release of stored noradrenaline from post-ganglionic neurons. This enables it to differentiate between first or second order lesions and third order lesions.
After administration, a ‘normal pupil’, first-order lesion or second-order lesion will all result in pupillary dilatation. There is no effect on the pupil in third order lesions. Thus, it is useful for diagnosis of a post-ganglionic (i.e. third order) lesion.
The treatment of Horner’s syndrome is directed towards the underlying cause.
It is most important to remember that an acute, painful Horner’s syndrome is a neurological emergency that requires urgent assessment for a carotid dissection. These patients need urgent neuroimaging and discussion with a hyperacute stroke unit (HASU). If clinical features of stroke are already present they usually require urgent transfer to the hyperacute stroke unit.
If dissection has led to stroke, these patients may be suitable for thrombolysis or mechanical therapies if they meet eligibility criteria. This should be decided by a stroke specialist in a stroke centre. In the absence of acute stroke, patients may be treated with anti-platelets or anticoagulation depending on the vessels involved (e.g. intracranial versus extracranial).
