Arterial dissection refers to the formation of a tear in the intima layer of the vessel and blood enters and tracks along the media layer of the artery ( Fig. 1) .
Cervical arterial dissection (CAD) may affect ICA and/or VA. CAD is a common cause of ischemic stroke in young and middle-aged people although it is rare in the overall population.
Even dissection could be located in the all segments of ICA and VA extracranial segments are more likely affected especially the cervical part of the ICA (distal to the carotid bulb),
the pars transversaria segment (V2) and the atlas loop segment (V3) of VA ( Fig. 2) . Almost 20% of CAD involves two or more vessels ( Fig. 3 ).
The cause of a CAD could be traumatic,
spontaneous or underlying arteriopathy:
- Approximately 60% of cervical artery dissections are spontaneous.
Spontaneous dissection is considered as a result of inconsequential trauma such as coughing,
sneezing,
vomiting,
sports,
and cervical manipulation.
These minor traumas do not follow by dissection in normal subjects generally,
whereas dissection is triggered in susceptible individuals with an underlying arteriopathy.
- Underlying arteriopathy could be Fibromuscular dysplasia,
Ehlers- Danlos syndrome type IV,
Marfan syndrome,
autosomal dominant polycystic kidney disease,
and osteogenesis imperfecta type I.
If there is an underlying vasculopathy,
commonly dissection involves more than one artery.
Hypertension,
diabetes mellitus,
hyperlipidemia,
and smoking are also risk factors for CAD dissection.
- Traumatic dissection occurs with serious blunt head and neck trauma and affects vertebral artery more frequently than carotid artery.
Pathophysiology; the wall of ICA and VA artery contains 3 layers (intima,
media,
and adventitia).
Dissection of ICA and VA occurs when there is a tear in the intima followed by penetration of blood into the media,
forming as an intramural hematoma.
The lumen lined by intima is termed as ‘true lumen’ and the media layer that contains intramural hematoma is called the ‘false lumen’.
The true lumen is usually under pressure of the intramural hematoma which also causes enlargement of the external diameter of the artery ( Fig. 1 ). If there is also a tear at the adventitia,
it can lead vessel rupture with subarachnoid hemorrhage.
The clinical manifestations of CAD dissection vary between the range from minor head-neck pain to severe neurologic morbidity and mortality.
The early symptom is generally headache for both ICA and VA dissection.
Considering ICA if the dissection causes critical stenosis or occlusion patients come with ischemia in the carotid territory.
Whereas dissections without severe stenosis at the ICA causes symptoms such as localized pain,
pulsatile tinnitus,
Horner syndrome,
and cranial nerve palsy. Patients with vertebral artery dissection may show posterior circulation or spinal cord ischemia and cervical root disorder.
The aim of treatment is to prevent thromboembolic complications.
The nature of most extracranial CAD is benign.
Most of the stenosis resolve ( Fig. 4 ).
Anticoagulant medication is the most selected therapy at the cervical segment ICA and VA dissections.
However,
because of the risk of subarachnoid hemorrhage,
it is less preferred at the intracranial dissections.
Surgical or endovascular intervention could be a choice in patients who remain symptomatic and have dissecting aneurysms.
Reoccurrence of dissection at the different segments of arteries may be presented at any time especially after 4-6 weeks later from the onset.