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Dissections..intra and extracranila.pptx
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- 2. OUTLINE: Introduction Epidemiology Classification Etiology Pathophysiology Clinical manifestation Diagnostic Treatment Prognosis Summary
- 3. INTRODUCTION Important causeof 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 carotidartery dissection – extracranial dissections – intracranial dissections Vertebral artery dissections – extracranial dissections – intracranial dissections
- 6. CLASSIFICATION Carotid dissections3 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 interactionof 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 formationpromotes 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 OFCAROTID 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 SYSTEMDISSECTIONS 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 showingdissection of right ICA with stenosis 2 cm distal to bifurcation
- 12. VERTEBRAL DISSECTIONS Necktrauma 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 ofleft vertebral artery in a young patient
- 14. Spinal cord ischemiain young patient due to right vertebral artery dissection
- 15. VERTEBRAL DISSECTIONS Severeneck 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 Riskof 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 CADsgenerally 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.
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