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Answers on p 451.
Q1: What does the carotid arteriogram show?
The digital subtraction arteriogram reveals dissection of the left internal carotid artery. The lateral (fig 1) and oblique (fig 2) views are shown (see p 431). The middle third of the internal carotid artery shows marked narrowing giving it a rat-tail appearance (arrows). This extends to the petrous segment, beyond which the vessel is normal.
Q2: What is the best way to manage this patient?
The patient was immediately started on intravenous heparin therapy, with the target activated partial thromboplastin time set at 2–2.5 times normal. His was admitted to the intensive care unit for monitoring and to ensure hypotension and hypertension were promptly controlled. His anticoagulation continued for six months with warfarin. With physiotherapy, his deficit largely resolved in the ensuing six months.
Q3: What is the differential diagnosis of acute neurological deficit after trauma?
There are many ways for sorting out the various causes of acute neurological dysfunction after trauma. The acronym HEADACHE may help when timely diagnoses are needed (see box 1).
Box 1: HEADACHE
Elevated intracranial pressure
Air or fat embolism
Diffuse axonal injury
Alcohol and drugs, metabolic causes (diabetes, thyroid, etc)
Hypoperfusion and hypoxia
In this case, the patient likely suffered an acute embolic event, causing hypoperfusion.
When stroke occurs in a young adult, one must consider cervicocerebral (carotid and vertebral) artery dissection. The cause is usually traumatic: sports, instrumentation, penetrating injuries, cervical manipulation, etc. However, even minor activities such as brushing teeth, coughing, and intercourse have resulted in dissection.1 Post-traumatic dissection involves a longitudinal intimal tear with intramural bleeding. A large clot obstructs the vascular lumen and can lead to thrombosis and distal embolism. Atherosclerosis and vascular pathology predispose to dissections.
The extracranial internal carotid artery is the most frequently reported site of cervicocerebral dissection.1 The vessel is tethered as it enters the foramen lacerum and can be injured along its entire relatively unprotected course.2 Carotid dissections sometimes result in cerebral ischaemia owing to haemodynamic compromise from stenosis, but more often to embolism of thrombotic fragments.3 Disruption of the endothelial surface exposes thrombogenic elements to the blood.
The diagnosis of cervical carotid dissection is based on clinical picture (head and neck pain, cerebral ischaemia, cranial nerve compression, and subarachnoid haemorrhage) and arteriographic findings.1 2 Normal brain computed tomography in an acutely hemiplegic person who has had recent cervicocerebral trauma (our patient had a concussion and left humeral fracture) should prompt the diagnosis of an arterial dissection.1 Stroke occurs in 56% of cases of blunt internal and common carotid traumatic injury.4 The deficits, usually from an embolic event, occur after a lucid interval usually of several hours to a few days after the insult (∼1 hour in our case).2 Dissection usually begins >2 cm distal to the carotid bifurcation and extends rostrally, terminating before entry of the artery into the petrous bone (as was seen in this case), where mechanical support limits further dissection. Irregular narrowing of the artery is the most frequent arteriographic finding, resulting in a “wavy ribbon” appearance, or a “string sign” if severe.2 A tapered occlusion beginning distal to the carotid sinus is less specific, but occurs in about 20% of cases.2 Intimal flaps may be seen near the proximal margin of the dissection. An extraluminal pouch (dissecting aneurysm) may be visualised distally, usually near the base of the skull.2
Cervicocranial arterial dissections can result from even minor trauma; it is an uncommon cause of acute ischaemic stroke, except among young adults.
Extracranial carotid dissection is the commonest type of cervicocranial dissection.
Normal computed tomography of the brain in an acutely hemiplegic person after trauma should raise the possibility of cervicocranial arterial dissection.
In the absence of haemorrhage, most carotid dissections with ischaemia can be treated with 3–6 months of anticoagulants; antiplatelet therapy is given in dissection with no ischaemia.
Long term prognosis tends to be favourable in dissections without subarachnoid haemorrhage.
The acute prognosis of patients who have arterial dissections not complicated by strokes is good.1 The acute prognosis of ischaemic stroke is less favourable and reflects the extent of the infarction and is not specific to the arterial process.1 Bogousslavsky et alwrote that of 30 patients with strokes secondary to dissections, seven died, and 12 made good recoveries.5 Patients with intracranial dissections have a poorer prognosis than those with extracranial lesions, in part because the dissections may be complicated by subarachnoid haemorrhage.1 The danger of early and late recurrent stroke is not high for those without severe underlying atherosclerosis or vascular pathology. Overall, regression or resolution of the stenotic arterial lesion is the rule.
Since most cerebral injury probably results from thromboembolic complications of the dissection,3 patients with acute ischaemic events and without subarachnoid haemorrhage (as in extracranial carotid dissection) are given intravenous heparin, followed by oral anticoagulants. Therapy is continued until repeat vessel imaging at three months, and beyond if necessary, shows good resolution.2 Long term antiplatelet therapy may be needed for those with persistent lumen irregularities. Patients without ischaemic symptoms may be given antiplatelet therapy for 6–12 months from the outset. Surgical intervention may be contemplated in select cases.
Traumatic dissection of the extracranial internal carotid artery.
Answers on p 451.