Cerebral hypoxia refers to reduced oxygen supply to the brain.
Cerebral anoxia refers to complete lack of oxygen to the brain.
Hypoxic Ischemic Encephalopathy (HIE) is a condition result when the entire brain is deprived of an adequate oxygen supply, but the deprivation isn't total. HIE is often seen in the neonate as a part of birth asphyxia, but it can occur in all age groups and often seen as a complication of cardiac arrest.
Cerebral hypoxic – ischemic brain damage can be grouped as follow.
Global cerebral hypoxia (Diffuse Hypoxic ischemic brain damage): Brain damage resulting from low oxygen levels in the blood.
Cerebral ischemia or infarction: Focal when particular vascular territory is involved, as a result of thrombotic or embolic event. Global when a complete stoppage of blood flow to the brain occurs.
Brain is most sensitive organ to oxygen deprivation, Hypoxic – ischemic brain damage follows a typical pattern on CT or MR Imaginng depending upon the selective vulnerability of different areas of brain.
On CT; Diffuse cerebral odema, loss of the normal cortical gray white matter differentiation, blurring of the insular ribbon are the best known signs of global hypoxia. In severe cases, reversal of the gray -white matter densities with relatively increased density of the thalami, brainstem and cerebellum so called “reversal sign on CT” and is associated with bad prognosis. Some time these findings may be subtle and difficult to recognize .
On left side CT of a 7 day old with history of perinatal asphyxia, shows diffuse low attenuating supratentorial brain parenchyma with relatively hyperdense Cerebellum - "CT Reversal sign" of Global hypoxia.
MRI is much more superior over CT in these regard, in that diffusion-weighted imaging (DWI) is most sensitive and specific sequence, earliest to pick up the ischemic changes.
On MR, the involved area shows abnormal bright signal on diffusion described as restricted diffusion results from cytotoxic odema in response to ischemia.
Different patterns seen in Diffuse Hypoxic brain damage are as follow
1.
Cortical involvement :
2.
Deep grey nuclei involvement.
3.
Border zone involvement.
Cortical involvement:
Cortical grey matter is involved result in cortical laminar necrosis, occurs because of the selective vulnerability of cortical layers 3, 4, and 5 to anoxia and ischemia. The selective vulnerability of gray matter may be due to higher metabolic demand and higher concentration of excitatory amino acids receptors that are released after the anoxic ischemic event, precipitating the excitotoxicity. In addition to neurons Glial cells are also damaged. The area of involvement show thin band of high signal in the region of cortical grey matter on DW images. Sometimes hyper intense signal observed on T1 is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent Meth Hb from haemorrhage.
In a patient with cardiac arrest, cortical abnormalities are associated with poor outcome.
In very severe cases of cortical necrosis can be visualized on CT scan, as a gyriform high attenuation.
A 35yo female brought unconscious to casualty with low pulse and blood pressure. On admission MRI Diffusion shows bilateral cerebral cortical involvement with involvement of bilateral basal ganglia and thalami.
Cortical laminar necrosis seen as high signal intensity confined to cortical grey matter.
Basal Ganglia Involvement:
Changes in the deep gray nuclei are seen in most cases of anoxic-ischemic brain damage.
Involvement is usually bilateral and often symmetrical, seen in isolation or in association with cortical involvement.
Thalami, lenticular nuclei, and caudate nuclei involved in various combinations even in same patient the distribution of lesions may change over period of time.
Border zone involvement:
Border zone infarcts are seen along the Watershed between major cortical branches or between cortical and deep perforator branches of intra cranial vessels.
Between cortical branches of ACA , MCA and PCA called cortical border zone and between cortical branches and deep branches called internal border zone.
I would like to add that watershed infarcts are not typically seen in conjunction with laminar necrosis as hypoxic ischemic damage is seen in both of these but mechanism of injury is different. It is hypothesized that watershed infarcts occur in cases of severe hypo perfusion without anoxia as happens when they are caused by carotid occlusion, systemic hypotension or severe blood loss; whereas laminar necrosis results from Global hypoxic or anoxic injury where cerebral perfusion is often normal.
A 60 yo male brought unconscious to casualty with possible cardiac event. On admission MRI Diffusion show bilateral fronto parietal and parieto occipital cortical restricted diffusion. Similar restricted diffusion in caudate nuclei. Area of involvement corresponds to cortical as well as internal border zone infarcts.
Imaging wise : Bilateral border infarcts.
Vulnerable Cortical Areas:
Perirolandic and Occipital Cortex are often involved to a greater extent than other cortical areas.
The medial occipital cortex is most commonly affected after anoxic-ischemic brain injury.
The intense baseline metabolic demand of these regions explains their selective vulnerability.
Although it is commonly held that the hippocampi in the mesial temporal lobes are the cortical areas most susceptible to anoxia, evidence of damage to these structures on imaging is seen much less commonly seen after cardiac arrest than the lesions in the medial occipital lobes and perirolandic regions.
A 14yo with delayed milestones showing bilateral peri rolandic cortical and occipital cortical Gliosis suggestive of Perinatal Hypoxic Ischemic injury. 
