carotid dissection

1. Cervico-cephalic artery
dissection
(CeAD)
DR MUDASIR MUSHTAQ SHAH

2. • A 35-year-old man presents to the emergency department accompanied by his wife.
• He was fishing the previous day and when he yanked the fishing rod he had neck pain
associated with dizziness, he went home took acetaminophen, and slept.
• The next morning his wife noticed he was confused and was complaining of neck pain.
• His blood pressure is 130/86 mmHg, pulse 88/min regular, and temperature 36.6 °C.
• Neurological examination reveals
 difficulty in forming complete sentences, naming and comprehending complex
commands
left Horner syndrome, and
normal motor or sensory exam..

3. • Labs show
hemoglobin 14.4 mg/dl platelets 2.2 lac/dl,
total leucocytes 8600/microL creatinine 0.8 mg/dl,
LDL 77 mg/dl, Hba1c 4.9 % ,
prothrombin time 12 seconds, aPTT 22 seconds and
homocysteine 11.5 micromoles/L.
• CT brain revealed a small area of hypo density in the left frontal region, adjacent to Sylvian fissure -
likely an acute infarct.
• MRI brain with angiography

6. • Diagnosis :
Left internal Carotid artery dissection with ischemic stroke
• Management:
Started on dual antiplatelets Aspirin/Clopidogrel
Speech and Language therapy
• Follow-up after 3 months
Modified Rankin Score (mRS): 0-1

7. BEFORE AFTER 3 MONTHS

8. AT PRESENTATION AFTER 3 MONTHS

9. Cervico-cephalic artery dissections (CeAD)
• Cervico-cephalic artery dissection is defined by a tear and hematoma in the wall of a
cervical or intracranial artery.
• uncommon entities of stroke in general
• relatively common causes of acute ischemic stroke in young and middle-aged groups,
accounting for up to 25% of such cases
• incidence is estimated to be 2.6–3/ 100,000

10. Pathophysiology
• The arterial wall includes 3 layers; from the lumen outwardly in order;
1. tunica intima (also known as the endothelium)
2. tunica media (muscular layer)
3. tunica adventitia

11. • A tear in the tunica intima of the vessel wall is the most common triggering event in the
pathophysiology of CeADs
• Immediately after the initial tear, blood dissects into the space immediately under the tunica intima
(false lumen or pseudolumen), which causes an intramural hematoma
• In some cases, CeAD can be triggered by a primary intramural hematoma, without an intimal tear

12. • Once formed, intramural hematomas can become enlarged due to bleeding in the vasovasorum of
tunica media
• The downstream effect of this intramural hematoma depends on its location. If subintimal, the
hematoma often leads to arterial stenosis and/or occlusion. If subadventitial, it often leads to the
formation of a pseudoaneurysm, often called a dissecting pseudoaneurysm.
• The effects of CeADs are often related to mass effect, arterial stenosis, and distal thromboembolism

14. Common types of Cervico-cephalic dissection
• Internal carotid artery dissection
• extracranial dissections
• intracranial dissections
• Vertebral artery dissections
• extracranial dissections
• intracranial dissections
 Carotid dissections are 3 times more common
 Extracranial dissection are more common than intracranial dissection accounting for 90-95%
of cases.

16. Risk factors
• Trauma
• Collagen Vascular Disorders
• Familial predisposition
• Recent Infections
• Anatomic variation/aberrations
• Vascular Risk Factors

17. TRAUMA
• prior trauma is identified in only up to 40% of cases
• Most traumatic events (up to 90%) are mild or trivial insults
• Cervical chiropractic neck manipulations, heavy lifting, sport associated injuries, and whiplash are
the most common etiologies
• Other etiologies like childbirth, coughing, sneezing, vomiting, practicing yoga or vigorous exercise
have been implicated
• Of the major traumatic events leading to CeADs, half are due to motor vehicle accidents, followed
by assault, falls, and hanging .

18. Collagen Vascular Disorders
Collagen vascular disorders that meet diagnostic and genetic criteria account for less than 1–5% of
spontaneous CeADs
1. Fibromuscular dysplasia (FMD) 1%-3%
2. vascular Ehlers-Danlos syndrome (EDS IV, COL3A1 gene). 0.5%–2.0%
3. Marfan syndrome (MFS, FBN1 gene) 0.6%–0.9%
4. pseudoxanthoma elasticum (PXE, ABCC6 gene)
5. osteogenesis imperfecta, and
6. Loeys-Dietz syndrome

19. • a workup for Collagen vascular disorders like Marfan, Ehlers- Danlos type IV, and Loeys-Dietz
should be considered with features such as
1. hyperflexible joints,
2. disproportionately long arms and fingers,
3. pectus carinatum or excavatum,
4. hyperelastic skin,
5. scoliosis,
6. clubfoot,
7. bifid uvula, or cleft palate.

20. Anatomical variation
• An elongated styloid process is not uncommon, incidence ranging from 4% to 28%.
• this anatomic anomaly can cause irritation and compression of the maxillio-vertebral recess, which
contains the internal carotid arteries, internal jugular vein, and cranial nerves (Eagle syndrome)
• elongated styloid processes causes dissection due to direct mechanical injury

22. Vascular and Other Risk Factors
• hypertension,
• smoking
• elevated homocysteine levels
• oral contraceptive use,
• pregnancy, especially in the postpartum period
• Migraine without aura , One-fifth to one-third of CeAD patients were found to have comorbid
migraine. A previous systematic review and meta-analysis reported that migraine is associated with
a twofold increased risk of CeAD.

23. Clinical features
• The most common SYMPTOMS related to CeAD are
1. headache and neck pain,
2. TIA/ischemic stroke
3. partial Horner’s syndrome
4. Pulsatile Tinnitus
5. Cranial Neuropathies
6. Cervical Radiculopathy/Myelopathy
7. Subarachnoid hemorrhage

24. Headache and Neck Pain
• Headache or neck pain are amongst the most common symptoms after CeAD (65–95% of cases)
• Headache associated with CeAD is typically severe. Migraine-like headache is common, though
cluster headache and thunderclap headache have also been reported.
• Typically, carotid dissections present pain in the ipsilateral temporal area and vertebral dissections
in the ipsilateral occipital area.

26. TIA/Ischemic Stroke
• More than half of the cases with CeAD experience TIA or ischemic stroke
• Depending on the site of CeAD and location of the affected vessel, patients with CAD can present
with sudden focal neurologic deficits, such as
unilateral weakness,
speech impairment,
facial droop,
vision loss or double vision,
balance issues,
or a combination of these symptoms.

27. Horner’s Syndrome
• third most common symptom of CeAD
• One-fourth of patients with CeAD present with partial Horner’s syndrome (miosis, ptosis, and but
not anhidrosis)
• Post-ganglionic third-order oculosympathetic nerve fibers are located in the carotid sheath adjacent
to the internal carotid and can be compressed by enlarging vessel wall secondary to intramural
hematoma or a dissecting pseudoaneurysm
• Horner’s syndrome can also occur after a brainstem stroke secondary to vertebral artery dissection.

28. Pulsatile Tinnitus
• 8% of patients with CeAD reported pulsatile tinnitus, which is more often associated with carotid
dissections.
• This could be related to the fact that the petrous segment of the internal carotid artery is located
near the tympanic cavity.
• Interestingly, patients who experience pulsatile tinnitus tend to have a more favorable clinical course
and experience ischemic stroke less commonly.

29. Cranial Neuropathies
• Cranial neuropathies typically occur with carotid artery dissections and
• 12% of spontaneous carotid dissections can have isolated or multiple cranial nerve palsies.
• Cranial nerves mostly affected are IX, X, XI, XII.
• The hypoglossal nerve is the most commonly involved nerve palsy
• Patients can also experience cranial nerve III, IV, V, VI palsies.

31. Cervical Radiculopathy/Myelopathy
• Can rarely occur secondary to vertebral artery dissection.
• Compressive cervical radiculopathy, most commonly at C5-C6 level
• myelopathy secondary to compression or spinal cord ischemic stroke

32. How to Diagnose?
• The American Heart Association (AHA) recommends computerized tomography angiography (CTA)
or magnetic resonance imaging (MRI) with fat suppression with MRA as the first-line non-invasive
imaging techniques for CeAD
• compared to MRA, CTA
1) has a better spatial resolution (potentially better at visualizing dissections in a small- caliber
vertebral artery),
2) can be acquired faster,
3) is more readily available in most healthcare settings, and
4) is superior at diagnosing pseudoaneurysms and intimal flaps.
• Compared to DSA, the gold standard, sensitivity, and specificity for diagnosing CeAD ranges
between 65% and 100%.

33. • MRA with MRI fat suppression is superior to CTA at identifying small intramural hematomas and
provides better vessel wall resolution.
• MRI also sensitive for detection of ischemic strokes.
• Classically, dissections on MRA appear as a region of crescentic hyperintensity on T1 fat-saturated
images, representing the intramural hematoma. This can be seen without or with associated luminal
narrowing and enlargement of the vessel wall diameter.

34. A 40-year-old woman with right ICA dissection. Vessel wall hematoma
(white arrow) is nicely demonstrated as high signal on axial T1 fat sat
sequence (A and C), while luminal narrowing is better appreciated on
corresponding axial CTA slices (B and D)

35. • Digital subtraction angiography (DSA) is the gold standard for diagnosis when in doubt or when an
intervention such as stenting is planned
• Classic signs of dissection in DSA are
1) flame-shaped “contrast tapering off”
2) intimal flaps
3) dissecting aneurysm or pseudoaneurysm

36. Abrupt change in diameter of the internal carotid artery with a long string-like
narrowing (string sign)

37. Long carotid-artery dissection with regions of narrowing
and aneurysmal pouches. (string and pearl sign)

38. Vertebral angiogram-lateral view. A long vertebral artery dissection showing regions of irregular narrowing (top arrows
and an aneurysmal pouch (lower arrow)

39. 3D Reconstructed Angiogram showing dissecting aneurym of distal Cervical ICA

40. • Ultrasound is readily available but has limited value in the diagnosis of carotid artery dissection, as
it is provides better visualize of the mid-cervical carotid segments.
• One benefit of duplex over MR/CT-based imaging is that the flow dynamics can be assessed.
• On duplex imaging, CeADs may be recognized by the finding of a double lumen or hyperechoic
intramural hematoma

41. Management
• As with other ischemic strokes, the management of stroke due to CeAD has two components:
1. acute treatment and
2. secondary stroke prevention

42. Acute treatment
• Many studies have investigated and established the safety and efficacy of thrombolytics in
hyperacute ischemic stroke and CeAD.
• In patients with symptomatic CeAD with acute ischemic stroke within 4.5 hours of onset, it is
recommended to give intravenous thrombolysis with alteplase by American Heart Association
(AHA) as well as by European Stroke Organisation (ESO), if the standard inclusion / exclusion
criteria are met.
• In acute ischemic stroke patients with large vessel occlusion Mechanical thrombectomy is
recommended by AHA and ESO
• For the cases with occlusive CeAD and intracranial LVO (tandem occlusion), emergent stenting of
the internal carotid artery is safe and leads to more successful reperfusion.

43. Secondary stroke prevention
• Antithrombotic therapy either antiplatelet or anticoagulant
• Based on evidence from two phase 2 RCTs that have shown no difference between the benefits
and risks of anticoagulants versus antiplatelets in the acute phase of symptomatic CeAD
• Both AHA/ESO recommend that clinicians can prescribe either option

45. • Anticoagulation is preferred if :
1. there is intraluminal thrombus and significant luminal narrowing,
2. recurrent TIA/strokes.
• Anticoagulation should be avoided if :
1. patients with large ischemic stroke,
2. there is intracranial extension of dissection

46. Indications for Endovascular therapy
• patients with recurrent symptoms despite medical therapy,
• patients with hemodynamic hypoperfusion (involvement of multiple vessels or poor collateral
vessels),
• patients with expanding or symptomatic pseudoaneurysm.

47. 56-year-old man with left ICA dissection. Left image shows tapering of the proximal ICA (white arrow) with no distal
flow. Patient had poor collateral flow and hypoplastic Anterior Communicating Artery, he was taken for carotid
stenting with subsequent placement of a balloon-expandable coronary stent in the petrous segment and self-
expandable stents in the cervical segment of the ICA

48. 45-year-old women with recurrent embolic infarcts from a left vertebral artery dissection. Successful coil
embolization of the V3 segment of the left vertebral artery (left image). Normal flow is demonstrated in the
posterior circulation with preservation of the left PICA (white arrow).

49. Long-Term Outcomes
Spontaneous Healing of the Vessel
• One-fourth of cervical carotid dissections and half of the vertebral artery dissections present with
occlusion
• Radiologically, most patients demonstrate “remodeling” and complete healing is seen in most of
cases, more commonly in the carotid arteries.
• Similarly, after complete occlusion of the carotid artery, the rate of complete recanalization is 16% at
one month, 50% at three months, and 80% at 6 and 12 months

50. Dissecting Pseudoaneurysm Formation
• dissecting pseudoaneurysms are seen in 19% of carotid dissection and 11% of vertebral
dissections.
• > 80 % aneurysms resolve spontaneously.

51. Clinical Outcome
• Good recovery (mRS 0–2) is achieved in 75–92% of CeAD cases.
• Mortality in CeAD is estimated to be low <5%.
• With the healing of carotid dissection, partial Horner’s syndrome usually improves.
• Typically, pulsatile tinnitus resolves approximately 2–3 months after the initial injury.
• compressive symptomatology like cranial neuropathy or cervical radiculopathy usually improves and
resolves over a few months with the resolution of intramural hematoma.

53. THANKYOU