Hyperperfusion Injury in Infarct

MRI Brain FLAIR and Diffusion images show right temporo parietal restricted diffusion with focal cytotoxic odema, seems to be a sub acute infarct. Area of involvement corresponds to right MCA cortical branches territory. No significant mass effect as there is no marked mid line shift or any internal herniations.

Gyriform low signal intensity in the corresponding region on T2*GRE attributed to hemosiderin staining as a part of hyperperfusion in the region of infarct.

Hyperperfusion injury in infarct or Reperfusion Syndrome 

- An abnormal focal major increase in cerebral blood flow above the metabolic demands of the infracted tissue.
- Characterized by a triad of ipsilateral headache, contralateral neurological deficits, and seizure clinically.
- Known to occur as a complication of revascularisation therapy with overdose of thrombolytics or procedure like carotid endarterectomy, intracranial stenting.  Even in absence of revascularization therapy, hemorrhagic transformation is a common and natural consequence of infarction.
- The overall prognosis in an infarct following hemorrhagic transformation worsens with increase in morbidity.
- Damage to the blood-brain barrier an important factor in reperfusion injury, occurs secondary to inflammatory response, including cytokine release and leukocyte adhesion.
- The higher lytic doses in revascularization therapy are associated with higher chances of hemorrhage risk, but whether lower doses can achieve adequate benefit with less risk is not known. Delayed revascularization likely increases risk. The goal of revascularization should not be just to open the occluded vessels but to open them quickly, prognosis is better and the incidence of intra cranial hemorrhage is decreased with early attempted revascularisation.
- Prevention of other precipitating factors like hypertension is equally important during revascularisation.
- Chances of reperfusion injury increases in elderly patients.