The CT angiogram also revealed aneurismal dilatation (20 × 11 mm) and stenosis of the first part of the right subclavian artery (Fig. Aneurysmal dilation and stenosis were also evident at the right proximal subclavian artery (Fig. Blood supply to the right middle cerebral artery was maintained via the anterior communicating and the posterior communicating arteries. Following this we performed a cerebral digital subtraction angiogram, which showed total occlusion of the right ICA from its origin (Fig. Multiple focal T2 and FLAIR hyper intensities with partially restricted diffusion, suggestive of acute infarcts, were also seen in the right parietal lobe (Fig. This was compressing the right cavernous sinus. The thrombosed lumen was of intermediate signal intensity in T1, T2 and Fluid-attenuated inversion recovery (FLAIR) images and did not enhance with contrast. Dissection of the right ICA was noted in the cavernous sinus, with a false lumen of 1.5 × 1 cm, which was thrombosed (Fig. MRI done on day 23 showed significantly narrowed right ICA. (Fig.1) 1) done on day 4 revealed generalized caliber reduction of right ICA. Cerebrospinal fluid analysis, performed on day 2 to exclude a subarachnoid heamorrhage, was normal with absent cells, normal protein level and did not reveal xanthochromia. Noncontract CT brain was done soon after the admission and was normal. She did not have features of Ehlers–Danlos syndrome, Marfan syndrome or manifestations of connective tissue disorder. Rest of the cardiovascular, respiratory and abdominal examination was normal. She had bruit over right subclavian and carotid arteries. Blood pressure on the right arm was 90/ 60 mmHg and on the left arm it was 120/ 80 mmHg. Brachial pulse was decreased on the right side compared to left side. Upper limbs and lower limbs were neurologically normal and she did not have any cerebellar signs. She did not have scalp tenderness or tenderness over the superficial temporal artery. Other cranial nerves including sensory component of the trigeminal nerve were normal. Left eye was normal with full eye movements and light reflexes. Vision and fundoscopic examination was normal. Direct and consensual light reflexes were absent on the same side. On examination she had complete ptosis, ophthalmoplegia and a fixed dilated pupil (5 mm) on the right side. She did not have a history of diabetes, hypertension, dyslipidemia or any connective tissue disorder. The headache and vomiting lasted for one day, but the ptosis and ophthalmoplegia persisted. At the same time she developed right-sided complete ptosis and ophthlamoplegia. This is the first case report of Takayasu arteritis presenting as complete ophthalmoplegia due to ICA dissection.Ī 38-year-old Sri Lankan female presented with sudden onset severe right side headache and vomiting. ICA dissection in Takayasu arteritis is very rare and complete ophthalmoplegia due to ICA dissection is also rare. She also had stenosis and aneurysmal dilatation of right subclavian artery and Takayasu arteritis was diagnosed subsequently. On imaging dissection and dilatation was evident in the right ICA from the origin up to the cavernous segment. Here we describe a middle aged female who presented with sudden onset complete ptosis, complete ophthalmoplegia and fixed dilated pupil on the right side. Common causes for internal carotid artery (ICA) dissection include trauma, Ehlers–Danlos syndrome, Fibromuscular dysplasia, Marfan syndrome, cystic medial necrosis, autosomal dominant polycystic kidney disease and homocystinuria. In addition, dissection and aneurysmal dilatation of carotid arteries can cause neurological manifestations due compression of adjacent nerves and their feeding vessels resulting in pain, Horner syndrome and cranial neuropathies. Neurological sequelae of intracranial arterial dissection result from cerebral ischemia due to thromboembolism and hypo perfusion. Subclavian artery involvement is common and involvement of the carotid and vertebral arteries causes neurological symptoms such as headache, visual disturbance, strokes, transient ischemic attacks and seizures.Īrterial dissection is due to separation of the layers of an arterial wall resulting in a false lumen, where blood seeps into the vessel wall. As the disease progresses the active inflammation of large vessels leads to dilation, narrowing and occlusion of the arteries. Females are affected more and the age of onset is usually between 10 and 40 years. Takayasu arteritis is a rare, chronic large vessel vasculitis involving the aorta and its primary branches.
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