An 87-year old man with hypertension, diabetes, and renal failure was admitted with aphasia and right-sided weakness (Motor Research Council grade 2 in both arm and leg). The neurological symptoms were fluctuating upon admission. Previously, the patient was under regular medication with an angiotensin receptor blocker and metformin. Five days before the visit, the patient experienced severe diarrhea for 3 days without fever. The initial blood pressure was 90/60 mmHg and the heart rate was 102 beats/min. Serologic analysis revealed elevated blood urea nitrogen (31 mg/dL) and creatinine (1.64 mg/dL) levels. SWI revealed PVS without an acute lesion, with left carotid artery occlusion and decreased perfusion of the left hemisphere (Fig. 1A-D).

Induced hypertension treatment was administered with continuous intravenous phenylephrine infusion (1.6 mg/h). After 1 hour, the blood pressure had risen to 160/80 mmHg and the neurological deficits had fully recovered. Four hours later, the PVS had dynamically decreased as indicated by follow-up SWI (Fig. 1E). Furthermore, surgical bypass surgery was not considered due to the patient’s age, and blood pressure medications were discontinued, aiming to maintain a systolic blood pressure above 140 mmHg. No further worsening of neurological deficits was detected for 3 months after the event.

The PVS was developed due to the increased concentration of deoxyhemoglobin inside the vein where the oxygen extraction ratio was increased. Therefore, the PVS was thought to represent the ischemic penumbra. The PVS predicted infarct growth, early neurological deterioration, and poor outcome.^1,2 However, there is a lack of data showing how the PVS present on SWI may change dynamically.

Induced hypertension increases perfusion. The treatment is effective and feasible for those who may not receive reperfusion treatment. Several studies have reported promising results of the treatment.^3,4 In our patient with ICA occlusion, induced hypertension was effective. The treatment effect was not only reflected in the neurological improvement, but also objectively in the dynamic change in the PVS in the short-term follow-up analysis performed within a few hours.

The perfusion status is usually determined using computed tomography or magnetic resonance perfusion imaging.⁵ However, a considerable amount of the contrast agent is required in both studies. Using contrast repeatedly within a day may have a potential adverse effect on the renal function and should be avoided for patients with poor renal function.⁶ However, a contrast agent is not required in SWI; the scan time is relatively short, and the PVS changes dynamically according to the perfusion status after a few hours. Therefore, our case findings suggest that the PVS may be potentially beneficial for evaluating the perfusion status, especially after treatment inducing increased perfusion to the cerebral hemisphere, especially in patients with poor renal function.