We have a very bizarre case of a 23 year old woman, with a history of hypertension, presenting as a stroke alert. She has dysarthria and focal right-sided deficits, and she required intubation for airway protection. She has no prior stroke or clotting history, no illicit drug use (other than marijuana), and no significant family history. CT of the head was unremarkable, but CTA revealed a… vertebral artery dissection! We later learned that the patient was in the middle of getting a massage when the stroke occurred!

That’s right, this is a case of cervical artery (more specifically the vertebral artery) dissection secondary to traumatic massage!

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Stroke typically is due to atherosclerotic disease in most cases, but if you need a case that occurred in a young patient, and you’ve ruled out everything else that would present similar, consider the following:

Stroke in young patients 

• Coagulopathy
  • APLS (one of the most common)
  • DIC
  • HIT
  • Hypercoagulable/hyperviscosity states
• Vascular
  • Vasculitis
    • Primary: Takayasu, GCS, Kawasaki, PAN, ANCA
    • Secondary: TB, HIV, syphilis, fungi, SLE
  • Dissection (most common in young patients)
  • Trauma
  • Structural malformation i.e. AVM, aneurysms
  • Cerebral venous sinus thrombosis
• Metabolic
  • CADASIL
  • MELAS
  • Fabry’s disease
  • Homocysteinuria
• Drugs
  • Cocaine
  • Meth
• Cardiac
  • Congenital defects
  • PFO/ASD leading to paraoxysmal stroke
  • Arrhythmias
  • Endocarditis
  • Rheumatic valve disease

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Vertebral artery dissection: 

Epidemiology

• Can occur at any age and usually infrequent, but vertebral arterial dissection in general is a common cause of stroke in the young.
• Carotid artery dissection is much more common than vertebral.
• Incidence: 1-1.5 per 100,000.
• Spontaneous dissections of the carotid and vertebral artery account for ~ 2% of ischemia strokes but in young and middle age patients, they can account up to 10-25%.
• Peak incidence at 5^th decade of life, occurs earlier in F > M
• Most of these patients likely have underlying connective tissue pathology leading to weakening of artery structural integrity but this is a theory.

Pathophysiology

• False lumen expansion leading to cerebral ischemia from hypoperfusion or thromboembolism, also can cause neurological sx from compression of adjacent nerves/vessels leading to CN involvement, Horner syndrome, pain, etc.
• Main mechanism, as revealed by angiography studies, point toward a thromboembolic mechanism from the dissection leading to stroke.
• Hemorrhage due to rupture, expanding hematoma can also lead to focal neurological signs.

Risk Factors

• Connective tissue disorders (i.e. Ehlers Danlos, Marfans, ADPKD, osteogenesis imperfecta, subclinical/unnamed)
• Yoga
• Migraine
• Coughing
• Painting a ceiling
• Vomiting
• Sneezing
• Sudden neck movement
• Trauma
• Chiropractic manipulation, estimated 1 in 20000 spinal manipulations lead to a stroke.

Presentation

• Most cases have a precipitating event
• Intracranial dissection
  • 50% of cases result in subarachnoid hemorrhage
• Extracranial dissection
  • Associated with trauma, vertebral artery is most mobile and vulnerable to mechanical injury at C1 to C2 as it leaves the transverse foramen of the axis vertebra and enters the intracranial space.
  • Severe neck pain, dizziness, vertigo, double vision, ataxis, dysarthria are common symptoms.
  • Lateral medullary and cerebellar infarctions are common
  • Typical: Local pain, HA, ipsilateral Horners, CN palsies, hemiparesis typically ipsilateral
  • Exam: Hematoma, vascular bruit (1/3 in carotid dissections, usually absent on vertebral), Horner’s syndrome, neck tenderness

Diagnosis

• Catheter angiography used to be the gold standard, nowadays moving toward…
• MRA
• CTA

Management

• Anticoagulation for at least 3-6 months to prevent thromboembolic complications unless there is hemorrhagic transformation of the infarct, an intracranial aneurysm, or intracranial extension.
  • Most ischemic damage is actually due to thromboembolic effect, not hypoperfusion.
• Surgical: May be required for SAH/intracranial VAD or if the defect fails to heal on its own
  • Endovascular stenting used for extracranial carotid or vertebral artery dissection when medical mgx fails, anticoag or thromboiysis does not exclude subsequent endovascular therapy but ideally endovascular intervention should be done within 6 hours.
• Thrombolytics: Consider in extracranial dissection, contraindicated in intracranial dissections or aorta involvement.

Prognosis

• Extracranial VAD: Generally has good prognosis, estimated 50% of patients will recover with no neurological deficit and 25% with moderate to severe deficits.
• Intracranial VAD: Prognosis is generally pretty poor.

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Take Home Points:

• Cervical (Carotid more common than vertebral) artery dissection is a common cause of strokes among young patients.
• Chiropractic manipulation, even massages, are risk factors for cervical artery dissection!
• A good portion of patients with cervical artery dissection might have underlying, sometimes subclinical, connective tissue abnormalities.