Vertebral and carotid artery dissection: Difference between revisions

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==Background==
==Background==
*Primarily categorized as Spontaneous vs. Traumatic
*Primarily categorized as Spontaneous vs. Traumatic/mechanical
*Most frequent cause of [[CVA]] in young and middle-aged patients (median age - 40yrs)
*Most frequent cause of [[CVA]] in young and middle-aged patients (median age - 40yrs)
*Symptoms may be transient or persistent
*History pearls
*Consider in trauma patient who has neurologic deficits despite normal head CT
**Symptoms may be transient or persistent
*Consider in patient with CVA + [[neck pain]]
**Consider in trauma patient who has neurologic deficits despite normal head CT
**Consider in patient with CVA + [[neck pain]]
*Pathophysiology: Dissection of arterial vessel wall results in false lumen formation, leading to lumen stenosis and exposure of platelet aggregation factors ---> local thrombus formation ---> possible thromboembolism to intracranial vessels
**Less commonly, dissection of thinner intracranial arteries may lead to SAH through vessel rupture


[[File:Carotid_dissection.jpg|thumb|CTA brain showing filling defect in the right carotid artery (circled)]]
[[File:Carotid_dissection.jpg|thumb|CTA brain showing filling defect in the right carotid artery (circled)]]
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===Risk Factors===
===Risk Factors===
*[[Neck trauma]] (often minor)
*Any mechanical event involving neck; symptoms typically occur 2-3 days after event
**Symptoms typically occur 2-3 days after event
**[[Neck trauma]] (often minor)
*Cervical manipulation
**Cervical manipulation
*Coughing
**Coughing/sneezing, vigorous exercise, weightlifting, intercourse, etc
*[[Connective tissue disease]]
*[[Connective tissue disease]]
*History of [[migraine]]<ref>De Giuli V et al. Association Between Migraine and Cervical Artery Dissection: The Italian Project on Stroke in Young Adults. JAMA Neurol. Published online March 6, 2017. doi:10.1001/jamaneurol.2016.5704</ref>
*History of [[migraine]]<ref>De Giuli V et al. Association Between Migraine and Cervical Artery Dissection: The Italian Project on Stroke in Young Adults. JAMA Neurol. Published online March 6, 2017. doi:10.1001/jamaneurol.2016.5704</ref>
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**Pain can precede other symptoms by hours-days (median 4d)
**Pain can precede other symptoms by hours-days (median 4d)
**Headache most commonly is frontotemporal; severity may mimic SAH or preexisting migraine
**Headache most commonly is frontotemporal; severity may mimic SAH or preexisting migraine
*[[Cranial nerve palsies]]
*Vision loss
*Partial [[Horner syndrome]] (miosis and ptosis) in 50% of cases
*Partial [[Horner syndrome]] (miosis and ptosis) in 50% of cases
*[[Cranial nerve palsies]]
*Symptoms of [[Stroke]], [[Transient ischemic attack]]


===Vertebral Artery Dissection===
===Vertebral Artery Dissection===
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**Headache is typically occipital
**Headache is typically occipital
*Unilateral facial [[paresthesia]]
*Unilateral facial [[paresthesia]]
*[[Dizziness]]
*[[Dizziness]] or [[Vertigo]]
*[[Vertigo]]
*[[Nausea/vomiting]]
*[[Nausea/vomiting]]
*[[Diplopia]] and other visual disturbances
*[[Diplopia]], [[nystagmus]], and other visual disturbances
*[[Ataxia]]
*[[Ataxia]]
*[[Lateral Medullary Syndrome]] seen in up to 20% of cases of VAD<ref>Lee MJ, Park YG, Kim SJ, Lee JJ, Bang OY, Kim JS. Characteristics of stroke mechanisms in patients with medullary infarction. Eur J Neurol. 2012;19(11):1433-1439.</ref><ref>Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(Pt 8):1864-1872.</ref>
*[[Lateral Medullary Syndrome]] seen in up to 20% of cases of VAD<ref>Lee MJ, Park YG, Kim SJ, Lee JJ, Bang OY, Kim JS. Characteristics of stroke mechanisms in patients with medullary infarction. Eur J Neurol. 2012;19(11):1433-1439.</ref><ref>Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(Pt 8):1864-1872.</ref>
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==Evaluation==
==Evaluation==
*Consider noncontrast CTH to assess for concomitant SAH
*Denver screening criteria is one way to evaluate for blunt cerebrovascular injury (BCVI)
*Denver screening criteria is one way to evaluate for blunt cerebrovascular injury (BCVI)
*If positive findings on screening → obtain CTA or MRA (CTA has been shown to be equivalent to MRA)
**If positive findings on screening → obtain CTA or MRA (CTA has been shown to be equivalent to MRA)<ref>Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 2009 Oct;193(4):1167-74. doi: 10.2214/AJR.08.1688. PMID: 19770343.</ref>


{{Denver Screening Criteria}}
{{Denver Screening Criteria}}
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==Management==
==Management==
*'''[[Anticoagulation]] (prevents clot propagation along dissecting lumen) followed by vascular repair is the generally accepted treatment.'''<ref>Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011;42:2515–2520.</ref>
*'''[[Anticoagulation]] (prevents clot propagation along dissecting lumen) followed by vascular repair is the generally accepted treatment.'''<ref>Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011;42:2515–2520.</ref>
*Obtain emergent vascular surgery consult for possible endovascular intervention
*Obtain emergent vascular surgery or neuro-interventionalist consult for possible endovascular intervention, including mechanical thrombectomy and/or angioplasty or stenting of dissected artery


===[[tPA]]===
===[[tPA]]===
*Do not give if dissection enters the skull (ie Intracranial)
*Do not give if dissection enters the skull (ie Intracranial), due to risk of SAH or ICH
*Do not give if aorta is involved
*Do not give if aorta is involved; may worsen dissection
*Otherwise, give according to same guidelines as for ischemic CVA (see [[CVA (tPA)]])
*Otherwise, give according to same guidelines as for ischemic CVA (see [[CVA (tPA)]])
**In a limited meta-analysis, thrombolytics appear equally efficacious in patients presenting with ischemic stroke due to cervical artery dissection vs ischemic stroke from other causes<ref>Zinkstok SM, Vergouwen MD, Engelter ST, Lyrer PA, Bonati LH, Arnold M, Mattle HP, Fischer U, Sarikaya H, Baumgartner RW, Georgiadis D, Odier C, Michel P, Putaala J, Griebe M, Wahlgren N, Ahmed N, van Geloven N, de Haan RJ, Nederkoorn PJ. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011 Sep;42(9):2515-20. doi: 10.1161/STROKEAHA.111.617282. Epub 2011 Jul 28. PMID: 21799165.</ref>


===[[Antiplatelet]] vs [[Anticoagulation]] Therapy===
===[[Antiplatelet]] vs [[Anticoagulation]] Therapy===
''Very controversial with poor data''
''Very controversial with poor data''
*[[Heparin]]: If dissection causes neuro deficits and is EXTRACRANIAL
*Specific anticoagulation vs antiplatelet therapy is listed below based on expert consensus and theoretical risks
*[[Aspirin]]: If dissection is INTRACRANIAL
**[[Heparin]]: If dissection causes neuro deficits and is EXTRACRANIAL<ref>Vasc Med. 2011 Feb;16(1):35-77. doi: 10.1177/1358863X11399328. Erratum in: Vasc Med. 2011 Aug;16(4):317. PMID: 21471149.</ref>
*Aspirin: If dissection is extracranial but no neuro deficit, for prevention of thromboembolic event
**[[Aspirin]]: If dissection is INTRACRANIAL<ref>Debette S, Mazighi M, Bijlenga P, Pezzini A, Koga M, Bersano A, Kõrv J, Haemmerli J, Canavero I, Tekiela P, Miwa K, J Seiffge D, Schilling S, Lal A, Arnold M, Markus HS, Engelter ST, Majersik JJ. ESO guideline for the management of extracranial and intracranial artery dissection. Eur Stroke J. 2021 Sep;6(3):XXXIX-LXXXVIII. doi: 10.1177/23969873211046475. Epub 2021 Oct 13. Erratum in: Eur Stroke J. 2023 Mar;8(1):399. PMID: 34746432; PMCID: PMC8564160.</ref>
***Anticoagulants are avoided due to the weaker medial walls of intracranial vessels that have a higher theoretical risk for bleeding
**Aspirin: If dissection is extracranial but no neuro deficit, for prevention of thromboembolic event
**In a small RCT study, there is no significant difference between antiplatelets vs anticoagulation in preventing subsequent stroke/death due to carotid/vertebral dissection<ref>CADISS trial investigators; Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr;14(4):361-7. doi: 10.1016/S1474-4422(15)70018-9. Epub 2015 Feb 12. Erratum in: Lancet Neurol. 2015 Jun;14(6):566. PMID: 25684164.</ref>
*If tPA was given, wait 24hr before starting antiplatelet therapy
*If tPA was given, wait 24hr before starting antiplatelet therapy
*Do not give if NIHSS score ≥ 15 (risk of hemorrhagic transformation)
*Do not give if NIHSS score ≥ 15 (risk of hemorrhagic transformation)

Revision as of 05:21, 7 December 2023

Background

  • Primarily categorized as Spontaneous vs. Traumatic/mechanical
  • Most frequent cause of CVA in young and middle-aged patients (median age - 40yrs)
  • History pearls
    • Symptoms may be transient or persistent
    • Consider in trauma patient who has neurologic deficits despite normal head CT
    • Consider in patient with CVA + neck pain
  • Pathophysiology: Dissection of arterial vessel wall results in false lumen formation, leading to lumen stenosis and exposure of platelet aggregation factors ---> local thrombus formation ---> possible thromboembolism to intracranial vessels
    • Less commonly, dissection of thinner intracranial arteries may lead to SAH through vessel rupture
CTA brain showing filling defect in the right carotid artery (circled)

Anatomy

  • Vertebral artery comes off the subclavian and runs upward through the formina in the transverses processes of C6 to C2.

Risk Factors

  • Any mechanical event involving neck; symptoms typically occur 2-3 days after event
    • Neck trauma (often minor)
    • Cervical manipulation
    • Coughing/sneezing, vigorous exercise, weightlifting, intercourse, etc
  • Connective tissue disease
  • History of migraine[1]

Clinical Features

Internal Carotid Dissection

Vertebral Artery Dissection

Differential Diagnosis

Neck Trauma

Evaluation

  • Consider noncontrast CTH to assess for concomitant SAH
  • Denver screening criteria is one way to evaluate for blunt cerebrovascular injury (BCVI)
    • If positive findings on screening → obtain CTA or MRA (CTA has been shown to be equivalent to MRA)[4]

Denver screening criteria for blunt cerebrovascular injury

The Denver Screening Criteria are divided into risk factors and signs and symptoms

Signs and Symptoms

  • Arterial hemorrhage
  • Cervical bruit
  • Expanding neck hematoma
  • Focal neurologic deficit
  • Neuro exam inconsistent with head CT
  • Stroke on head CT

Stroke Syndromes

Anterior Circulation

  • Blood supply via internal carotid system
  • Includes ACA and MCA

Internal Carotid Artery

  • Tonic gaze deviation towards lesion
  • Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
  • Spatial or visual neglect (non-dominant lesion)

Anterior Cerebral Artery (ACA)

Signs and Symptoms:

  • Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
  • Urinary and bowel incontinence
  • Left sided lesion: akinetic mutism, transcortical motor aphasia
  • Right sided lesion: Confusion, motor hemineglect
  • Presence of primitive grasp and suck reflexes
  • May manifest gait apraxia

Middle Cerebral Artery (MCA)

Patient with stroke (forehead sparing).

Signs and Symptoms:

  • Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
  • Motor deficits found more commonly in face and upper extremity than lower extremity
  • Dominant hemisphere involved: aphasia
    • Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and does not understand verbal communication
    • Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
  • Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
  • Contralateral homonymous hemianopsia
  • Gaze preference toward side of infarct
  • Agnosia (inability to recognize previously known subjects)

Posterior circulation

Signs and Symptoms:

Basilar artery

Signs and Symptoms:

  • Quadriplegia, coma, locked-in syndrome
  • "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
    • Millard-Gubler syndrome (ventral pontine syndrome) -- ipsilateral CN VI and VII palsy with contralateral hemiplegia of extremities
  • Sparing of vertical eye movements (CN III exits brainstem just above lesion)
    • Thus, may also have miosis b/l
  • One and a half syndrome (seen in a variety of brainstem infarctions)
    • "Half" - INO (internuclear ophthalmoplegia) in one direction
    • "One" - inability for conjugate gaze in other direction
    • Convergence and vertical EOM intact
  • Medial inferior pontine syndrome (paramedian basilar artery branch)
    • Ipsilateral conjugate gaze towards lesion (PPRF), nystagmus (CN VIII), ataxia, diplopia on lateral gaze (CN VI)
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial midpontine syndrome (paramedian midbasilar artery branch)
    • Ipsilateral ataxia
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial superior pontine syndrome (paramedian upper basilar artery branches)
    • Ipsilateral ataxia, INO, myoclonus of pharynx/vocal cords/face
    • Contralateral face/arm/leg paralysis and decreased proprioception

Superior Cerebellar Artery (SCA)

Posterior Cerebral Artery (PCA)

Signs and Symptoms:

  • Common after CPR, as occipital cortex is a watershed area
  • Unilateral headache (most common presenting complaint)
  • Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
  • Visual agnosia - can't recognize objects
  • Possible macular sparing if MCA unaffected
  • Motor function is typically minimally affected
  • Lateral midbrain syndrome (penetrating arteries from PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral hemiataxia, tremor, hyperkinesis (red nucleus)
  • Medial midbrain syndrome (upper basilar and proximal PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral paralysis of face, arm, leg (corticospinal)

Anterior Inferior Cerebellar Artery (AICA)

Posterior Inferior Cerebellar Artery (PICA)

Signs and Symptoms:

  • Lateral medullary/Wallenberg syndrome
  • Ipsilateral cerebellar signs, ipsilateral loss of pain/temperature of face, ipsilateral Horner syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
  • Contralateral loss of pain/temp over body
  • Also caused by vertebral artery occlusion (most cases)

Internal Capsule and Lacunar Infarcts

  • May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[7]
    • Pure c/l motor - posterior limb of internal capsule infarct
    • Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
  • C/l motor plus sensory if large enough
  • Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[8]:
    • Gaze preference
    • Visual field defects
    • Aphasia (dominant lesion, MCA)
    • Spatial neglect (non-dominant lesion)
  • Others
    • Ipsilateral ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
    • Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct

Anterior Spinal Artery (ASA)

Superior ASA

  • Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
  • Contralateral arm/leg weakness and proprioception/vibration
  • Tongue deviation towards lesion

Inferior ASA

  • ASA syndrome
  • Watershed area of hypoperfusion in T4-T8
  • Bilateral pain/temp loss in trunk and extremities (spinothalamic)
  • Bilateral weakness in trunk and extremities (corticospinal)
  • Preservation of dorsal columns

Risk Factors

  • Midface Fractures (Le Fort II or III)
  • Basilar Skull Fracture with carotid canal involvement
  • Diffuse axonal injury with GCS<6
  • Cervical spine fracture
  • Hanging with anoxic brain injury
  • Seat belt abrasion or other soft tissue injury of the anterior neck resulting in significant swelling or altered mental status
    • Isolated seatbelt sign without other neurologic symptoms has not been identified as a risk factor[9][10][11]
Algorithm for evaluation of BCVI with high risk criteria based on Memphis and Denver Screening Criteria

Management

  • Anticoagulation (prevents clot propagation along dissecting lumen) followed by vascular repair is the generally accepted treatment.[12]
  • Obtain emergent vascular surgery or neuro-interventionalist consult for possible endovascular intervention, including mechanical thrombectomy and/or angioplasty or stenting of dissected artery

tPA

  • Do not give if dissection enters the skull (ie Intracranial), due to risk of SAH or ICH
  • Do not give if aorta is involved; may worsen dissection
  • Otherwise, give according to same guidelines as for ischemic CVA (see CVA (tPA))
    • In a limited meta-analysis, thrombolytics appear equally efficacious in patients presenting with ischemic stroke due to cervical artery dissection vs ischemic stroke from other causes[13]

Antiplatelet vs Anticoagulation Therapy

Very controversial with poor data

  • Specific anticoagulation vs antiplatelet therapy is listed below based on expert consensus and theoretical risks
    • Heparin: If dissection causes neuro deficits and is EXTRACRANIAL[14]
    • Aspirin: If dissection is INTRACRANIAL[15]
      • Anticoagulants are avoided due to the weaker medial walls of intracranial vessels that have a higher theoretical risk for bleeding
    • Aspirin: If dissection is extracranial but no neuro deficit, for prevention of thromboembolic event
    • In a small RCT study, there is no significant difference between antiplatelets vs anticoagulation in preventing subsequent stroke/death due to carotid/vertebral dissection[16]
  • If tPA was given, wait 24hr before starting antiplatelet therapy
  • Do not give if NIHSS score ≥ 15 (risk of hemorrhagic transformation)

Complications

  • CVA
    • Risk of stroke or recurrent stroke is highest in the first 24hr after dissection
  • SAH (if dissection extends intracranially)

See Also

References

  1. ↑ De Giuli V et al. Association Between Migraine and Cervical Artery Dissection: The Italian Project on Stroke in Young Adults. JAMA Neurol. Published online March 6, 2017. doi:10.1001/jamaneurol.2016.5704
  2. ↑ Lee MJ, Park YG, Kim SJ, Lee JJ, Bang OY, Kim JS. Characteristics of stroke mechanisms in patients with medullary infarction. Eur J Neurol. 2012;19(11):1433-1439.
  3. ↑ Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(Pt 8):1864-1872.
  4. ↑ Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 2009 Oct;193(4):1167-74. doi: 10.2214/AJR.08.1688. PMID: 19770343.
  5. ↑ Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  6. ↑ Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
  7. ↑ Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  8. ↑ Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  9. ↑ DiPerna CA, Rowe VL, Terramani TT, et al. Clinical importance of the “seat belt sign” in blunt trauma to the neck. Am Surg. 2002;68:441–445
  10. ↑ Rozycki GS, Tremblay L, Feliciano DV, et al. A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs. J Trauma. 2002;52:618–623; discussion 623–624
  11. ↑ Sherbaf FG, Chen B, Pomeranz T, et al. Value of emergent neurovascular imaging for “Seat belt injury”: A multi-institutional study. American Journal of Neuroradiology. 2021;42(4):743-748
  12. ↑ Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011;42:2515–2520.
  13. ↑ Zinkstok SM, Vergouwen MD, Engelter ST, Lyrer PA, Bonati LH, Arnold M, Mattle HP, Fischer U, Sarikaya H, Baumgartner RW, Georgiadis D, Odier C, Michel P, Putaala J, Griebe M, Wahlgren N, Ahmed N, van Geloven N, de Haan RJ, Nederkoorn PJ. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011 Sep;42(9):2515-20. doi: 10.1161/STROKEAHA.111.617282. Epub 2011 Jul 28. PMID: 21799165.
  14. ↑ Vasc Med. 2011 Feb;16(1):35-77. doi: 10.1177/1358863X11399328. Erratum in: Vasc Med. 2011 Aug;16(4):317. PMID: 21471149.
  15. ↑ Debette S, Mazighi M, Bijlenga P, Pezzini A, Koga M, Bersano A, Kõrv J, Haemmerli J, Canavero I, Tekiela P, Miwa K, J Seiffge D, Schilling S, Lal A, Arnold M, Markus HS, Engelter ST, Majersik JJ. ESO guideline for the management of extracranial and intracranial artery dissection. Eur Stroke J. 2021 Sep;6(3):XXXIX-LXXXVIII. doi: 10.1177/23969873211046475. Epub 2021 Oct 13. Erratum in: Eur Stroke J. 2023 Mar;8(1):399. PMID: 34746432; PMCID: PMC8564160.
  16. ↑ CADISS trial investigators; Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr;14(4):361-7. doi: 10.1016/S1474-4422(15)70018-9. Epub 2015 Feb 12. Erratum in: Lancet Neurol. 2015 Jun;14(6):566. PMID: 25684164.
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