PCA Territory loss of Grey White - Look out For

PCA territory infarct can be subtle on non-contrast CT of the head. Make sure you look in this vascular territory and strutinize the grey white differentiation in all vascular territories, including the PCA and the ACA. 

Calcified Carotid Plaque - Source of Emboli

Calcified carotid plaques can serve as an embolic source in acute stroke. Although considered more stable than atheromateous plaque, their rupture could lead to vascular occlusion. Given their calcified nature, they are refractory to IV thrombolysis and their retrieval using interventional techniques is more challenging. Given their solid nature, it would not incorporate as a traditional cloth would within the stent retriever and can get be pushed against the intimal wall as the stent opens. 

Cortical Laminar Necrosis

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.

Watershed Infarct Secondary to Severe Carotid Stenosis

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 infarct

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.

Matched Perfusion - No Ischemic Penumbra Present on CTP

 

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.

The Hyperdense MCA Sign - Essential Finding

The increased density of the MCA or any other intracranial vessel should be treated with suspicion for presence of thrombus. Comparison with other vessels, dural venous sinuses, history of previous contrast from another radiologic study, or delayed contrast excretion post previous administration could be consideration. Unilateral and asymmetric hyperdensity in any vessel of any size can be suggestive of presence of acute cloth and should be further investigated with a CT Angiogram CTA. 

Calcified Emboli - Imaging Sign

Look for small calcific emboli with the vessels. These could be acute or chronic but are suggestive of proximal embolic source, such as a ruptured calcified plaque. 

Carotid Web

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 

Diffuse Hypoxic Injury

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 Hypoxic Ischemic Injury

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.

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ICA Occlusion - Look at the skull base for