The initial event of dissection of a cervico-cephalic artery is disruption of the intima and internal elastic lamina of the arterial wall, either by trauma or haemodynamic stress. Pulsatile arterial flow extends this tear longitudinally further into the media, even to subadventitial layer. It may become a blind pouch filled with thrombus, or communicate with true lumen of the involved artery becoming a pseudoaneurysm or creating a second channel, false lumen. The dissected space can expand outwards causing local symptoms and signs by increasing vessel diameter or inwards causing thromboembolic events by narrowing arterial lumen. Pseudoaneurysms in the intradural space often rupture, resulting serious subarachnoid haemorrhage.
Dissections of cervicocephalic arteries are classified by their etiology as traumatic, spontaneous and iatrogenic. Spontaneous dissections are often related to repeated minor traumas or underlying vasculopathy, such as hypertention, hypercholesterolemia, fibromuscular dysplasia, Ehlers-Danlos syndrome, Cystic medial degeneration, Marfan’s disease, etc.
Clinical presentations are primarily depending on its location and depth of dissection. The first symptom is often sudden neck pain or headache in varying degree. Majority of dissections do not progress beyond local pain, therefore, they are undetected medically. When an intramural haematoma or a pseudoaneurysm become larger, it progress to cause more serious local mass effects as well as secondary neurological events. Horner’s syndrome or cranial nerve deficits may develop following a latent period of a few hours to a few days. Expansion of arterial wall toward the true lumen leads to partial or total occlusion of involved artery which results in thromboembolism. Ischemic strokes of dissections are more likely due to embolic events rather than haemodynamic origin. When an intradural artery is involved, especially Ml segment of MCA or vertebrobasilar artery, occlusion of origins of perforators by dissection may induce infarcts in the basal ganglia or brain stem respectively.
The pseudoaneurysm from dissection in the intradural space is highly vulnerable since they are covered only by a thin layer of fibrous tissue or clots. Untreated intradural dissecting aneurysms have a high incidence of subsequent rupture even if haemorrhage is not the initial presentation.
Treatment
Treatment strategy is different by its location of dissection; intradural vs extradural. When dissection is diagnosed without any acute neurological events for extradural ICA or VA, the recommended treatment is heparin for a week and followed by warfarin for 3 -6 months to prevent a thromboembolic complication. Local mass effects such as Horner’s syndrome or cranial nerve palsies are often resolved without intervention.
Endovascular treatment is indicated when a neurological event, stroke or haemorrhage, occurs in acute stage or mass effects persist in spite of proper medical treatment. Permanent occlusion of the involved artery with or without EC-IC bypass surgery was the standard treatment before era of stenting. It is still applicable when dissection is extensive and multiple aneurysms are present. When dissection is localized, stenting across the tear (with coil placement if an aneurysm is present) will succeed to heal dissections.
For intradural dissections, urgent treatment is necessary when an pseudoaneurysm is present, even if SAH did not occur. Endovascular occlusion of involved artery with balloons or coils is preferable treatment. Surgical clipping is often impossible, therefore, wrapping of the aneurysm or proximal occlusion of parent artery is the only choice when these lesions are approached surgically.