11/29/2023 0 Comments Acute unilateral miotic pupilPtosis is usually minimal (<2 mm), which reflects the minimal contribution of Müller's muscle to lid elevation. The pupil will also dilate slower following removal of a light source compared to the other eye. The degree of anisocoria, which describes unequal pupils, is more marked in the dark. Remember, a variety of other neurological features may be present depending on the cause. The degree of anhidrosis depends on which neuron has been affected. Miosis and ptosis are universal to all causes of Horner’s syndrome. Horner’s syndrome causes a classic triad of ipsilateral miosis, ptosis and anhidrosis. Up to 60% of carotid artery dissection will have an isolated, ipsilateral Horner’s syndrome on presentation. The should be suspected in any patient presenting with an acute, painful Horner’s syndrome. The most concerning cause of Horner’s secondary to a third-order neuron lesion is carotid artery dissection. 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. Syringomyelia (fluid-filled cyst spinal cord).Other features of lateral medullary syndrome include vertigo, nystagmus, ataxia (ipsilateral), pain and temperature loss (contralateral body, ipsilateral face), nausea/vomiting, dysphagia, and hiccups. lateral medullary syndrome): most common cause of first-order lesion. Lesions of the central nervous system are usually present with other neurological features. First orderĬaused by a lesion anywhere between the brainstem and cervicothoracic spinal cord. The aetiology of Horner’s syndrome can be divided by the order of neuron affected. Horner’s syndrome develops due to a lesion anywhere along the oculosympathetic pathway. This is why ptosis is a phenomenon of Horner’s. This muscle contributes a small proportion to upper eye lid elevation and lower lid retraction. The post-ganglionic sympathetic fibres also innervates a small muscle known as ‘Müller's muscle’. They join the ophthalmic portion of the trigeminal nerve at the cavernous sinus and subsequently pass to the pupillary dilator via ciliary nerves. Its fibres pass within the adventitia of the internal carotid artery. Here they travel upwards over the apex of the lung to the superior cervical ganglion. Its fibres exit the spinal cord via the dorsal roots and enter the sympathetic chain. This area of the spinal cord is known as the ciliospinal centre of Budge. Fibres travel from the hypothalamus to the spinal cord (C8-T2). Horner’s syndrome can develop due to a lesion anywhere along this pathway. Knowledge of the neuroanatomy of the oculosympathetic pathway is important because it helps us determine the possible aetiology. The oculosympathetic pathway is composed of three neurons: first, second and third order.
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