Horner syndrome is caused by interruption of the sympathetic nerves to an eye due from any cause. Horner syndrome refers to the combination of a constricted pupil, drooping eyelid, and loss of sweating around the affected eye. Disorders outside the brain that affect the sympathetic nervous system include tumors and injuries that involve the neck or upper part of the chest. Brain disorders that can affect these pathways include strokes, brain hemorrhage (spontaneous or due to head injury), and, less commonly, certain tumors or infections. Thus, people with nervous system disorders that affect the pupil often also have a drooping eyelid, double vision, and/or visibly misaligned eyes. These pathways carry nerve impulses to the pupil and to the muscles that control the eye and eyelid. Pupils should be round, equally sized and equally reactive to light, but often they are not- it is important to be able to differentiate between the pupils that are of concern with those that are normal for you. This system works automatically (autonomously), without a person’s conscious. Your pupils and pupil reactions are an important part of the eye examination. Stroke 1998 29: 2646-8.Nervous system disorders that cause unequal pupils are those that affect the 3rd cranial nerve or certain parts of the sympathetic or parasympathetic nervous system (the autonomic nervous system Overview of the Autonomic Nervous System The autonomic nervous system regulates certain body processes, such as blood pressure and the rate of breathing. Stroke patterns of Internal Carotid Artery Dissection in 40 patients. It is necessary to seek neurological advice and/or make urgent hospital referral for further investigations if this is suspected. ICAD is an important diagnosis to consider in patients presenting with Horner's syndrome. Treatment is usually with heparin and then warfarin, or antiplatelet therapy. Most ischaemic events arise within seven days of the dissection, although it can be a few months. Neck pain can also be a clinical feature in many of these patients. It is a recognised cause of ischaemic stroke in young people. This is thought to be from hyperextension, rotation or full flexion of the neck. ICAD can occur spontaneously or from minor trauma, such as from coughing or weightlifting. MRI is now the gold standard for looking at carotid arteries. This has previously been underdiagnosed due to lack of accurate imaging techniques. It is thought that dissection causes inflammation, which stretches (or damages) the pericarotid sympathetic area. In recent years, ICAD has been identified as an important cause of Horner's syndrome. The clinical signs depend on the location of the lesion on the sympathetic pathway. Horner's syndrome includes ptosis of the upper and lower eyelids, ipsilateral constricted pupil and/or ipsilateral anhidrosis (loss of sweating). In the absence of any other neurological signs, it was likely that Mr S had now presented with a long-standing left small pupil, which had led to an impression of a dilated right pupil. Mr S was reassured though kept under close review, and advised to report any further problems. A follow-up MRI scan had been carried out six months later and revealed a normal internal carotid artery. There had been no evidence of microemboli at the time and he had therefore been treated conservatively with aspirin for anticoagulation. Medical history revealed that Mr S had an internal carotid artery dissection (ICAD)while in the Caribbean. However, they were both reactive to light and accommodation, although the left pupil was slow to dilate in darkness. His pupils were unequal in size, the right being more dilated. There was no deficiency of eye movements or evidence of ptosis. His visual acuity was normal when corrected by his spectacles and his fields were intact. His BP was 130/76mm Hg with a regular pulse of 76bpm. On clinical examination he was well with no motor weakness or sensory deficits. He was a long-term smoker of about 10 cigarettes a day. He was not hypertensive and his current medications included a statin and aspirin. He felt that the left side of his forehead had never been 'quite the same' since the TIA. He had been living in the Caribbean at the time and remembered that a CT scan of his brain had been normal, though an MRI scan of his neck had shown some slight abnormality. This had concerned her as he had presented with left-sided facial weakness and unequal pupils three years earlier following a transient ischaemic attack (TIA). Mr S was a 52-year-old man who reported that his wife had noticed his right pupil was more dilated than the left.
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