These infarct follow the vascular territory of paramedian pontine perforators and are confined to midline.

Stasis is Demonstrated in a Carotid Web, which produces a risk for thromboembolic events. 

A carotid web may contribute to recurrent ischemic stroke in patients with no other determined stroke mechanism. Intimal variant fibromuscular dysplasia (also shown here) is the pathologic diagnosis in most cases. The prevalence of carotid web is low, while the optimal management strategy remains unknown. See Paper 

Hypoxic-ischemic brain injury is a diagnostic term that encompasses a complex constellation of pathophysiological and molecular injuries to the brain induced by hypoxia, ischemia, cytotoxicity, or combinations of these conditions.

Typical causes includes cardiac arrest, respiratory arrest, drowning, hanging, and other forms of incomplete suffocation or carbon monoxide and other poisonous gas exposures and/or severely diminished blood supply. 

The diffuse abnormality might be difficult to detect and history is key to suspecting the bilateral and symmetric pattern. 

Diffuse loss of grey/white differentiation with presence of pseudo-subarachnoid sign, diffuse edema and loss of sulci, and tonsillar herniation through foramen magnum in keeping with diffuse hypoxic ischemic injury.

Cortical laminar necrosis is the death of cells in the cortex of the brain in a band-like pattern, with a relative preservation of cells immediately adjacent to the meninges.

The difference can be seen as a consequence of the neurons within the cortex being far more metabolically active than glial cells or adjacent white matter.

It is a finding that can be seen in late subacute to chronic stroke.

A watershed stroke or watershed infarct is defined as a brain ischemia that is localized to the vulnerable border zones between the tissues supplied by the anterior, posterior and middle cerebral arteries. The actual blood stream blockage/restriction site can be located far away from the infarcts.

Severe reduction of perfusion secondary to severe left carotid stenosis was responsible in this case. 

Striatocapsular infarcts involve the striatum (ie the caudate nucleus and putamen), without involvement of the cortex secondary to either a complete or partial proximal MCA occlusion limiting flow to the lenticulostriate arteries.

Classically patients exhibit both cortical (e.g. aphasia, sensory neglect or extinction, apraxia) and subcortical (e.g. upper limb hemiparesis, dysarthria) neurological signs.

 

Tmax (red) and CBV (blue) demonstrate very increased time of transit of blood, and very low blood volume in the exact same areas. This is no perfusion mismatch here and all the brain tissue has been infarcted with no pneumbra present to save.

Susceptibility sequences SWI demonstrate diffuse hemorrhagic change within an area of previous Infarct. With corresponding diffusion DWI restriction in the right panel.