Introduction: Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but serious, complication following revascularization. Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue. Quantitatively, hyperperfusion is a 100% or greater increase in CBF compared with baseline. This definition also extends to rapid restoration of normal perfusion pressure, for example, with thrombolytic therapy for acute ischemic stroke. Reperfusion syndrome can occur as a complication of carotid endarterectomy (CEA), intracranial stenting, and even bland cerebral infarction. The prognosis following hemorrhagic transformation is poor. Mortality in such cases is 36-63%, and 80%of survivors have significant morbidity. Case Report A 78-year-old male hypertensive, diabetic, and known coronary artery disease patient came to emergency department with complain of weakness in left upper limb since 4 hours which was progressively improving without slurring of speech, leg weakness, palpitation, or loss of consciousness. On arrival patient was conscious and oriented with normal vital parameters and normal blood glucose level. On examination patient was having left upper limb power 4/5. Other than that neurological and systemic examination was normal. Patient was undergone basic blood test and Magnetic Resonance Imaging of brain which was suggestive of small acute infarct in right high fronto-parietal region. Patient was treated with dual antiplatelets and supportive measures. On carotid doppler patient was found to have 90% obstruction of internal carotid artery on right side and 60% on left side. Patient was opted for digital subtracted angiography and angioplasty of right internal carotid artery. After the successful completion of procedure patient became progressively drowsy and developed left upper limb and lower limb dense hemiplegia.To rule out intracranial hemorrhage immediately computed tomography of brain was performed and which was suggestive of hyperdense fingerlike projection were noted in sulci all over right side of brain. Differential diagnosis of subarachnoid hemorrhage and hyperperfusion syndrome was suspected. Subsequent computed tomography of brain was suggestive of no hyperdence projections after 24 hours conforming the hyperperfusion syndrome. Patient was treated conservatively and improved in 15 days and discharge home with left hemiparesis. Disscussion: An abrupt increase in cerebral blood flow following revascularization has been identified as the direct physiological cause of hyperperfusion syndrome. Several factors including advanced age, underlying leukoaraiosis, and post-procedural high blood pressure have been associated with this condition .Two interlinked and synergistic mechanisms may lead to development of syndrome; impaired cerebral autoregulation and postoperatively elevated systemic blood pressure . If not treated properly, it can result in severe brain oedema, intracerebral hemorrhage, or death. Treatment strategies are directed towards regulation of blood pressure and limitation of rises in cerebral perfusion.