Vertebral and carotid artery DISSECTION

1. CERVICOCEREBRAL ARTERIAL
DISSECTIONS (CAD)
Dr Ummer

2. OUTLINE:
 Introduction
 Epidemiology
 Classification
 Etiology
 Pathophysiology
 Clinical manifestation
 Diagnostic
 Treatment
 Prognosis
 Summary

3. INTRODUCTION
 Important cause of stroke in younger patients
 Carotid and vertebral artery dissections

4. EPIDEMIOLOGY
 35-50 y.o (peak 50)
 20 % of strokes in age < 45
 Incidence: 2,6 per 100.000 per year
 Maybe asymtomatic

5. CLASSIFICATION
 Internal carotid artery dissection
 – extracranial dissections
 – intracranial dissections
 Vertebral artery dissections
 – extracranial dissections
 – intracranial dissections

6. CLASSIFICATION
 Carotid dissections 3 times more common than vertebral
dissections.
 Extracranial segment dissection more common than
intracranial segment because more mobile and is also
prone to damage by bony structures such as the
vertebrae and styloid processes.
 The site predilection for dissection is quite different from
that of atherosclerosis affecting the cervical arteries.
 Dissection involves the pharyngeal and distal parts of
the internal carotid artery, whereas atherosclerosis
usually affects the origin and the carotid bulb.
 Similarly, dissections affect distal parts of the
extracranial vertebral artery, whereas atherosclerosis
tends to involve the proximal segments

7. Schema of interaction of genetic and environmental factors in the pathogenesis of
cervicocerebral dissections.
B Thanvi et al. Postgrad Med J 2005;81:383-388

8. PATHOPHYSIOLOGY
Local thrombus formation promotes by luminal
stenosis and the release of thrombogenic factors by
the intimal damage.
Cerebral ischaemia:
(1) a narrowed lumen with the consequent
haemadynamic failure (borderzone infract) or,
(2) embolisation from local thrombus (more common),
or both

9. CLINICAL MANIFESTATION OF CAROTID
DISSECTIONS
 Constant and non-throbbing
head and neck pain
ipsilateral in frontal /
frontoparietal area
 Partial Horner’s syndrome
without anhidrosis (fibers of
sweat function travel along
ECA)
 Pulsatile tinnitus
 Ipsilateral cranial nerve
palsies especially lower
ones
 TIA
 Amaurosis fugax,
 Hemiplegia,
 Dysphasia, etc.
LOCAL EFFECTS
CEREBRAL & RETINAL
ISCHAEMIA

10. INTRACRANIAL CAROTID SYSTEM DISSECTIONS
 Lack of spesific angiographic features
 Younger age ( 2nd – 3rd decade)
 Associated with large stroke (75% mortality rate)
 Subarachnoid haemorrhage (SAH) can result from
intracranial dissections, because of the extension of
an intramural haematoma through the adventitia.
 Can cause aneurysmal dilatations of the arteries
that may behave as space occupying lesions
compressing adjacent cranial nerves or the brain
 Surgical interventions are more often needed.

11. CT Angiogram showing dissection of right ICA
with stenosis 2 cm distal to bifurcation

12. VERTEBRAL DISSECTIONS
 Neck trauma may clearly precede an extracranial
vertebral dissection.
 The vertebral artery is most mobile and thus most
vulnerable to mechanical injury at C1 to C2 as it
leaves the transverse foramen of the axis vertebra
and suddenly turns to enter the intracranial cavity.
 F is 2,5 times than M (extracranial);
M>F (intracranial)

13. Spontaneuos dissection of left vertebral artery in a young patient

14. Spinal cord ischemia in young patient due to right vertebral
artery dissection

15. VERTEBRAL DISSECTIONS
 Severe neck pain
 Dizziness,
 Vertigo,
 Double vision,
 Ataxia,
 Dysarthria
 Wallenberg Syndrome
 Cerebellar infarction
 SAH
 Brainstem infarction
 Aneurysm presenting
as SOL
Extracranial Intracranial

16. DIAGNOSIS
 Doppler ultrasound
 CTA
 MRI/MRA
 DSA

17. DOPPLER ULTRASOUND
 Non-invasive, inexpensive, readily available
 90 % sensitivity
 High resistance flow pattern in the distal arteries
 Intramural haematoma or double lumen and intimal
flap are rarely found
 TCD for intracranial dissections
 Limitation: Technical difficulties
- Scanning in distal ICA.
- Detecting emboli.
- A lower sensitivity with dissections that cause low
grade stenoses.

18. MRI/MRA & CTA
 Intramural haematomas can be shown as
hyperdense signals on T1 weighted imaging and
characteristically have a crescent shape adjacent to
the lumen.
 MR scans can also show a luminal stenosis or an
occlusion.
 Sensitivity of MRI/MRA is highest two days after
dissections.
 MR imaging can also be used for follow up
monitoring of the dissections.
 CTA: high sensitivity

19. DSA
 Invasive
 Risk of stroke: 0,5 – 1 %
 “string sign”—a long segment of narrowed lumen
 The pathognomonic features of dissection, such as
an intimal flap or a double lumen, are found in less
than 10% of cases.
 The artery may show sudden tapering because of
occlusion of the lumen.
 Aneurysmal dilatation are also found in some
cases.

20. TREATMENT
 Medical: anticoagulation (heparin followed by
warfarin)  continued with antiplatelet
 Surgical / endovascular treatment:
- SAH
- Aneurysmal dilatation
- Failed after 6 months medical therapy
- persistence of high grade stenosis

21. PROGNOSIS
 Extracranial CADs generally carry a good prognosis.
 A literature review reports 50% of cases having no
neurological deficit, 21% mild deficits only, and 25% moderate
to severe deficits, the remaining 4% having died.
 The neurological outcome was dependent on the lesion
localisation and the presence of good collaterals.
 Intracranial dissections are usually associated with severe
neurological deficits or subarachnoid bleed and carry a poor
prognosis.
 The recurrence rate for CAD is usually low. Higher recurrence
rates have been noted in the immediate post-dissection period
and CAD associated with familial disorders of connective
tissue.
 There is no evidence to suggest that anticoagulation or
antiplatelet therapy prevents recurrence of CAD.

22.  Thank You