Emergent Acute Stroke Intervention with Primary Stenting

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A matched defect (decreased in CBV, CBF, and prolonged MTT) was observed in the anterior 1/3 of the left frontal lobe, with preservation within the remaining territories suggesting potential opportunity to salvage significant brain tissue. His cerebrovascular anatomy was particularly challenging in that his bilateral ACA, and left MCA circulations were isolated from direct collaterals, absent right A1 and left posterior communicating collaterals from the circle of Willis.

We performed emergent acute stroke intervention with primary stenting of the carotid dissection. Because of the length of his dissection and tortuosity of his vessel, a second overlapping stent was required to overcome a “kink” and completely revascularize his intracranial circulation safely (Figure 2. A, B, and C).

He made a dramatic initial clinical recovery regaining consciousness, alertness, smiling, following simple commands with persistent expressive aphasia and right sided hemiplegia on discharge. After 6 weeks of acute and subacute rehabilitation, he continued to regain function, walking with a 4 point cane, and beginning to develop expressive language.

Over the course of the next 2 years, continued surveillance imaging demonstrated wide patency and durability of the stent (Figure 3. A, B, 8/26/2020 Customize Your Email https://em-ui.constantcontact.com/em-ui/em/page/em-ui/email#edit/activity/4fe0294a-cae6-4679-982a-5c894f45973f 2/10 and C). With diligent physical and occupational therapy, as well as a regimen of hyperbaric oxygen therapy to encourage neuroplasticity, he continued to achieve functional improvement, ambulatory independence, and near complete language function (slight hesitancy in fluidity and word-finding). He has returned to work.

Figure 1. CT Brain Perfusion demonstrates active ischemia of the left MCA and bilateral ACA isolated circulations with matched defect in the anterior 1/3 of the left frontal lobe suggesting evolving infarct.

Figure 2. A) Initial AP angiogram confirms high grade long segment dissection of the left ICA

Figure 2. B) following placement of first stent with residual kink and vasospasm

Figure 2. C) after second overlapping stent, complete revascularization is achieved.

Figure 3. A) AP angiogram demonstrates wide patency at 8 months

Figure 3. B and C) CTA at 20 months confirms long-term durability and wide patency

KEY LEARNING POINTS:

  1. Acute stroke can occur in any age group and from a variety of cerebrovascular conditions including embolic events, intracranial vascular disease (atherosclerotic, inflammatory), or extracranial dissections.
  2. Emergent evaluation by a team of experts including advanced imaging should be considered up to 24-36 hours from the event to determine eligibility and safety for potentially life-saving interventions.
  3. Emergent stenting of the carotid arteries with rapid loading doses of antiplatelet medications can be safe and effective in quickly restoring blood flow and saving critically eloquent brain tissue.
  4. Diligent and committed PT, OT, and adjunctive strategies can often contribute to an exceptional functional outcome, especially in younger patients with a greater capacity for neuroplasticity.

REFERENCES:

  1. Chaloupka, J.C., Weigele, J.B., Mangla, S. et al. Cerebrovascular angioplasty and stenting for the Prevention of stroke. Curr Neurol Neurosci Rep 1, 39–53 (2001).
  2. Jovin, T. G., Gupta, R., Uchino, K., Jungreis, C. A., Wechsler, L. R., Hammer, M. D., Tayal, A., & Horowitz, M. B. (2005). Emergent stenting of extracranial internal carotid artery occlusion in acute stroke has a high revascularization rate. Stroke, 36(11), 2426–2430.

CATEGORY: ENDOVASCULAR // EMERGENT ACUTE STROKE INTERVENTION WITH PRIMARY STENTING

Emergent Acute Stroke Intervention with Primary Stenting

A 42-year-old man presented with acute onset of right hemiplegia and global aphasia with an initial NIHSS of 21.

Emergent CTA and CTP evaluation demonstrated near-complete occlusion of the left cervical internal carotid artery with severe hypoperfusion in the left hemisphere (ACA and MCA) and right anterior cerebral territory (ACA) (Fig 1).

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