ISCHEMIC STROKE / CLASSIFICATION AND ETIOLOGY

Arterial dissection

Created 05/05/2023, last revision 24/05/2023

Definition and pathophysiology

arterial dissection is characterized by a tear in the inner layer of the arterial wall
blood enters the tear and separates the wall layers – a false lumen is formed in addition to the true lumen
the false lumen is often thrombosed and leads to stenosis or occlusion of the artery (in the case of occlusion, the diagnosis of dissection is more difficult).
thrombus growth and/or arterio-arterial embolization may occur (more common in extracranial arteries)
dissecting aneurysm may also develop
rupture through the adventitia leads to bleeding (SAH in intracranial lesion)

dissection mainly affects younger and middle-aged people
- cause of ∼ 5% of strokes in the age group < 45 years
- it is rarely the cause of stroke in the older population
- incidence is increasing due to better diagnostics
carotid arteries are most commonly affected (∼ 80%; typically, the lesion is located below the skull base), and vertebral arteries are involved in ∼ 20% (level C1-2 – atlas loop)
- more than one vessel is affected in ∼ 25% of cases
intracranial dissection is relatively rare
dissection poses the highest risk of stroke in the first 14 days (absolute increase in risk is ~1.25%, decreasing to 0.18% in weeks 3-4) [Morris, 2017]

spontaneous x traumatic (trauma, the C-spine manipulation)
- in both cases, the arterial wall or some of its layers is presumed to be defective
abrupt hyperextension/rotation of the head causes tension of the carotid artery over the transverse processes of C2, C3 or the lateral process of the atlas with subsequent tearing of the intima, or, conversely, the carotid artery is wedged between the mandible and C1 after extensive and rapid flexion
similarly, the vertebral artery is usually bruised over the edges of the transverse foramina or the atlas arch
if spontaneous dissection is suspected, renal artery imaging (in addition to cerebral artery imaging) is recommended to exclude FMD

Some conditions associated with arterial dissection
Fibromuscular dysplasia (FMD) Syphilitic angiopathy Proliferative inflammation in some forms of arteritis Moya-moya Connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome)

Carotid dissection

unilateral neck, head, or orbital pain
Horner’s syndrome (caused by damage to the adventitial sympathetic plexus)
Harlequin sign (hyperhidrosis and flush of the contralateral half of the face during physical exertion) [Drexler, 2014]
lesion of cranial nerves IX-XII (compressed by the dissecting aneurysm) [Kasravi, 2010]
- may imitatate brainstem lesion
stroke symptoms in ~ 2/3 of cases
pulsatile tinnitus may occur (DDx of CCF or dural fistula)
symptoms of carotid dissection vary from asymptomatic carotid occlusion to extensive territorial stroke

Vertebral artery dissection

ipsilateral neck pain
a combination of extra- and intracranial involvement is common
symptoms depend on the extent of dissection (are basilar artery or spinal arteries involved?) and the status of the collaterals
- dissection without concomitant distal embolization may remain asymptomatic if the contralateral VA is fully functional
- spinal cord ischemia may occur with occlusion or hypoperfusion of spinal arteries

Aortic arch dissection → see separate chapter

can itself be a source of emboli or lead to steno-occlusive involvement of the arch branches (most commonly ACC and ICA)
presents with:
- severe sudden chest pain that propagates between the shoulder blades (initially suspected to be a coronary event)
- hypotension; sometimes with transient loss of consciousness
- asymmetrical or very weak pulse in the neck and upper limbs
- cardiac tamponade may occur ⇒ urgent surgery is indicated

intracranial dissections are rare in the absence of systemic connective tissue disease
predominantly occurring in the vertebrobasilar territory and the supraclinoid portion of the ICA
headache typically occurs at the onset, almost always followed by the development of a neurological deficit
- in extracranial dissections, the development of a neurological deficit is gradual, often occurring several days after the initial headache; asymptomatic lesions are not uncommon
the main mechanism is hemodynamic failure behind the occlusion or stenosis (including occlusion of perforators); fluctuation of deficit (hemodynamically induced) is common
- distal embolization predominates in extracranial dissections
intracranial dissection may also lead to subarachnoid hemorrhage (in the absence of lamina externa)
diagnosis is difficult; angiographic findings are often nonspecific (occlusion, stenosis); typical features (string sign, double lumen) can usually not be seen
intracranial dissection may be confused with vasculitis
- ICA involvement may be suggestive of giant cell arteritis, which predominantly affects the petrous and cavernous segments
intracranial dissection usually has a worse prognosis than extracranial dissection (decreased potential for collateral circulation)

Content available only for logged-in subscribers (registration will be available soon)

treatment strategy for dissection-related stroke must be individualized
treatment options include:
- thrombolysis
- endovascular treatment
- anticoagulant/antiplatelet therapy (SAPT or DAPT)

Content available only for logged-in subscribers (registration will be available soon)

standard treatment of vascular risk factors (especially maintaining normal blood pressure)
oral contraception is not recommended
avoid statins unless otherwise indicated