J Neurocrit Care.  2022 Jun;15(1):69-75. 10.18700/jnc.210036.

Recanalization of the middle cerebral artery after prolonged induced hypertensive therapy to rescue early neurologic deterioration: a case report

• Na HK
• Kim T
• Yum JY
• Park W
• Kim J
• Kim S
• Kim JH
• Seo KD

• KMID: 2532004
• DOI: http://doi.org/10.18700/jnc.210036

Abstract

Background
Although decades have passed since the introduction of pharmacologically induced hypertensive therapy (PIHT) against early neurologic deterioration (END) in acute ischemic stroke, the optimal duration of PIHT remains elusive.
Case Report
A 70-year-old man developed right hemiplegia and aphasia 25 hours before arrival. Computed tomography angiography (CTA) revealed acute infarction in the left middle cerebral artery (MCA) territory and occlusion of the left internal carotid artery. He experienced END 36 hours after admission, and CTA revealed a newly developed proximal MCA occlusion. PIHT was initiated to augment cerebral perfusion. As his neurologic symptoms were highly dependent on blood pressure, PIHT was inevitably sustained for over 3 weeks. Follow-up CTA revealed recanalization of the MCA.
Conclusion
Although further investigation is required to expedite the future clinical application, prolonged PIHT may serve as a viable collateral-enhancing treatment for a certain subset of patients with END without alternative treatment options.

Keyword

Ischemic stroke; Clinical deterioration; Phenylephrine; Middle cerebral artery

Figure

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  Fig. 1. Brain perfusion computed tomography angiography (CTA) and magnetic resonance imaging at admission. (A) Brain CTA revealed collateral flow via the anterior communicating artery to the middle cerebral artery (MCA) and (B) left proximal internal carotid artery occlusion with calcification (arrow, spearhead shape). (C) Perfusion mismatch was confirmed by the RAPID software (iSchemaView, Menlo Park, CA, USA) (cerebral blood flow [CBF] <30%, volume: 23 mL; Tmax >6.0 seconds, volume: 101 mL). (D) Brain MRI revealed increased signals on the diffusion-weighted imaging sequence in the left MCA superior division territory (red circles) and (E) on the fluid-attenuated inversion recovery sequence at the same lesion.

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  Fig. 2. Brain perfusion computed tomography angiography (CTA) and magnetic resonance imaging after early neurologic deterioration. (A) Brain CTA revealed left proximal middle cerebral artery occlusion and (B) changes in the shape of the internal carotid artery occlusion (arrow, stump shape). (C) Perfusion mismatch identified using the RAPID software (iSchemaView, Menlo Park, CA, USA) was further expanded (cerebral blood flow [CBF] <30%, volume: 26 mL; Tmax >6.0 seconds, volume: 145 mL). (D) Diffusion-weighted imaging showed a newly developed acute lesion in the basal ganglia and corona radiata.

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  Fig. 3. Follow-up brain perfusion computed tomography angiography (CTA) and magnetic resonance imaging (MRI) were performed on day 24 after early neurologic deterioration. (A) Brain CTA showed spontaneous recanalization of the left middle cerebral artery and (B) no interval change of the internal carotid artery occlusion. (C) Perfusion mismatch was no longer observed. (D, E) No new lesions were identified on diffusion-weighted imaging or fluid-attenuated inversion recovery. CBF, cerebral blood flow.

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