Pontine infarct

Case contributed by Caleb Siocha
Diagnosis certain

Presentation

Left sided weakness right facial weakness.

Patient Data

Age: 40 years
Gender: Female
ct

The basilar artery appears hyperdense (basilar dot sign) suggestive of acute thrombosis. Streak artefact in the posterior fossa makes assessment of the pons difficult although the right side appears hypodense potentially representing an infarct.

mri

Complete occlusion of the whole extent of the basilar artery with partial occlusion of the intracranial segments of both vertebral arteries.

Resultant acute ischemic infarction of the right hemipons is seen as a well-marginated area of diffusion restriction and T2/FLAIR isointense signal.

On T2/FLAIR and DWI sequences, a smaller hyperintense region in the left paramedian pons is also noted, suggestive of infarction.

Case Discussion

Pontine infarcts are typically caused by the interruption of blood flow to the area, resulting in the death of brain cells due to oxygen and nutrient deprivation. The most common cause of a pontine infarct is the occlusion often due to a blood clot. A paramedian pontine infarct is an ischemic stroke that occurs in the brainstem, specifically in the pons near the midline.

Diffusion-weighted imaging (DWI) is highly sensitive in detecting acute infarcts. In pontine infarcts, and like infarcts in other areas, the affected region appears hyperintense due to restricted diffusion of water molecules. This restriction is caused by cellular swelling and loss of membrane integrity. The corresponding apparent diffusion coefficient map shows decreased signal intensity in the infarcted area.

Fluid-attenuated inversion recovery sequences (FLAIR) suppress the signal from cerebrospinal fluid, enhancing the visibility of pathological changes. In pontine infarcts, images typically reveal hyperintensity in the affected region due to edema, making the infarct more conspicuous.

It is important to note that the appearance of pontine infarcts on MRI can evolve over time. In the acute stage, there may be a combination of cytotoxic and vasogenic edema. As the infarct progresses, the hyperintensity on T1-weighted images decreases, while the hypointensity on T2-weighted images may persist or increase due to ongoing vasogenic edema.

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