Cerebral infarct - left MCA M1 & fetal PCA P2 occlusion

Case contributed by Arkadi Tadevosyan


Presented to the emergency department with altered consciousness, right-sided hemiplegia, gaze palsy facial droop, sensorimotor aphasia and swallowing dysfunction. NIHSS 22. The patient was found alone at home, and last seen well time was 12 hours ago by a family member. In medical history, the patient had atrial fibrillation, high blood pressure, and cardiac insufficiency. Blood pressure - 210/117 BPM - 97 SPO2 - 90 %

Patient Data

Age: 60 years
Gender: Male

Loss of grey-white matter differentiation on the left lower temporal lobe (ASPECTS 9).

Hyperdense left MCA sign.

No hemorrhage is identified.

Right-sided chronic infarction of the superior cerebellum.

The left posterior cerebral artery has a fetal origin. The left MCA M1 segment is occluded. Also present is a left PCA P2 segment occlusion.

On the left temporooccipital lobe

  • CBF (cerebral blood flow) is significantly reduced

  • CBV (cerebral blood volume) is reduced compatible with the ischemic core

  • MTT (mean transit time) - in the temporal lobe is significantly increased, and TTD (time to drain) is almost doubled characteristic of ischemic penumbra

Perfusion analysis - left hemisphere temporal lobe ischemic penumbra with significant large core (large mismatch, PRR = 9.6 %).

The study is suboptimal due to the lack of contrast washout and phase match.

However, the quality of perfusion examination was lacking due to low cardiac output. Therefore MRI was suggested.

30 min later after initial CT


Large diffusion restriction area in the left caudate body, lentiform nucleus and temporooccipital lobe. In the same area, subtle high FLAIR signal intensity is also already visible.

A large area of hypodensity in the left caudate body, lentiform nucleus & temporooccipital lobe, with associated mass effect and 12 mm contralateral midline shift.

Case Discussion

CT perfusion study was deemed to be unreliable due to the patient's atrial fibrillation and low cardiac output, therefore MRI was suggested for better evaluation of salvageable brain volume. It nonetheless accurately predicted the area of infarction.

MRI confirmed a large volume of infarction core with diffusion restriction and FLAIR signal change, which indicates no potential salvageable brain tissue. And therefore there was no indication for reperfusion therapy.

The vascular anatomy of this case is important as the clot ascended in the internal carotid artery but also occluded the posterior cerebral artery due to a fetal origin.

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