A 75-year-old man presented with an acute left hemiparesis. His past history included chronic atrial fibrillation (AF) for which he had received warfarin for 5 years. Fourteen days prior to the onset of his symptoms he had an orchidectomy for prostatic carcinoma, for which warfarin had been discontinued. He remained well until this presentation when he was found to be orientated with a mild upper-motor-neurone seventh cranial nerve palsy. He had symmetrical upper and lower limb signs with weakness on his left side (graded 4/5). He had no bulbar dysfunction, Horner’s syndrome (oculosympathetic palsy), or any sensory or cerebellar deficits. He was in AF with a controlled ventricular response and there were no arterial bruits. Investigations included computed tomography brain scan, which revealed a large, old, left frontal infarct and a subacute lacunar infarct at the right internal capsule genu. Controlled AF was confirmed on a 12-lead electrocardiogram. Transthoracic echocardiography identified an enlarged left atrium but no evidence of cardiac thrombus. Duplex carotid ultrasound demonstrated high resistance, low velocity flow in the right internal carotid artery consistent with a long tight stenosis, as is seen in a carotid artery dissection. Carotid angiography (Figs 1 and 2) confirmed an extensive right internal carotid artery dissection with the typical ‘string sign’ appearance (Fig. 2). An intimal flap, which is demonstrated in <10% of dissected carotid arteries,1 was not detected. During the subsequent 48 h, the patient’s condition stabilized with persisting 4/5 left-sided weakness. He was anticoagulated with i.v. heparin followed by oral warfarin and has almost regained premorbid level of neurological functioning following a short period of rehabilitation. Carotid artery dissection is uncommon, with an annual incidence of 2.5–3/100 000 population.2 It is typically seen in young and middle-aged patients, with a distinct peak in the fifth decade.3 Apart from his relatively advanced age, our patient’s presentation was atypical because of the lack of neck or craniofacial pain, which is the presenting symptom in the majority of cases and precedes neurological signs by a median of 4 days.4 Without prompt recognition and treatment, dissection lesions cause symptoms of cerebral ischaemia due to low flow or embolism, which can occur minutes, hours or even days prior to a devastating stroke. The reported mortality associated with dissection is <5%.4 The risk of recurrent dissection in a previously unaffected artery is approximately 2% during the first month, decreasing to <1% per year beyond this period.3 Dissections rarely recur in the same artery. Following carotid dissection, prognosis is favourable, with 75% of patients regaining premorbid functional capacity.