Vertebral and carotid artery dissection: Difference between revisions
No edit summary
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*Consider in trauma patient who has neurologic deficits despite normal head CT
*Consider in trauma patient who has neurologic deficits despite normal head CT
*Consider in patient with CVA + neck pain
*Consider in patient with CVA + neck pain
[[File:Carotid_dissection.jpg|thumb|CTA brain showing filling defect in the right carotid artery (circled)]]


===Risk Factors===
===Risk Factors===
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==Evaluation==
==Evaluation==
*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)
{{Denver Screening Criteria}}
{{Denver Screening Criteria}}
====If Denver Criteria positive, CTA or MRA====
 
*CTA has been shows to be equivalent to MRA
[[File:BCVI-Algorithm.png|thumb|Algorithm for evaluation of BCVI with high risk criteria based on Memphis and Denver Screening Criteria]]
<gallery>
File:Carotid_dissection.jpg|CTA brain showing filling defect in the right carotid artery (circled)
</gallery>


==Management==
==Management==
Anti-coagulation followed by vascular repair is the generally accepted treatment. Anti-coagulation prevents clot propagation along the dissecting lumen<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>
*'''Anti-coagulation (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
 
===tPA===
===tPA===
*Do not give if dissection enters the skull (ie Intracranial)
*Do not give if dissection enters the skull (ie Intracranial)
*Do not give if aorta is involved
*Do not give if aorta is involved
*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)]])
===Antiplatelet vs Anticoagulation Therapy===
===Antiplatelet vs Anticoagulation Therapy===
''Very controversial with poor data''
''Very controversial with poor data''
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*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)
===Endovascular Therapy===
*Emergent consultation with vascular surgery.
*tPA use does not exclude patients from endovascular therapy


==Complications==
==Complications==

Revision as of 17:37, 28 June 2017

Background

  • Most frequent cause of CVA in young and middle-aged patients (median age - 40yrs)
  • 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
CTA brain showing filling defect in the right carotid artery (circled)

Risk Factors

Clinical Features

Internal Carotid Dissection

  • Unilateral headache, face pain, anterior neck pain
    • Pain can precede other symptoms by hours-days (median 4d)
    • Headache most commonly is frontotemporal; severity may mimic SAH or preexisting migraine
  • Partial Horner syndrome (miosis and ptosis) in 50% of cases
  • Cranial nerve palsies

Vertebral Artery Dissection

  • Posterior neck pain, headache
    • May be unilateral or bilateral
    • Headache is typically occipital
  • Unilateral facial paresthesia
  • Dizziness
  • Vertigo
  • Nausea/vomiting
  • Diplopia and other visual disturbances
  • Ataxia
  • Lateral Medullary Syndrome seen in up to 20% of cases of VAD[2][3]

Differential Diagnosis

Neck Trauma

Evaluation

  • 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)

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)[6]
    • 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[7]:
    • 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[8][9][10]
Algorithm for evaluation of BCVI with high risk criteria based on Memphis and Denver Screening Criteria

Management

  • Anti-coagulation (prevents clot propagation along dissecting lumen) followed by vascular repair is the generally accepted treatment.[11]
  • Obtain emergent vascular surgery consult for possible endovascular intervention

tPA

  • Do not give if dissection enters the skull (ie Intracranial)
  • Do not give if aorta is involved
  • Otherwise, give according to same guidelines as for ischemic CVA (see CVA (tPA))

Antiplatelet vs Anticoagulation Therapy

Very controversial with poor data

  • Heparin: If dissection causes neuro deficits and is EXTRACRANIAL
  • Aspirin: If dissection is INTRACRANIAL
  • Aspirin: If dissection is extracranial but no neuro deficit, for prevention of thrombo-embolic event
  • 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. ↑ Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  5. ↑ 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.
  6. ↑ Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  7. ↑ Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  8. ↑ 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
  9. ↑ 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
  10. ↑ 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
  11. ↑ 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.
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