Intracranial infections - 1 - General principles

Intracranial infections are a common consideration in neuroradiology. Patients often present with altered mental status, often with a fever or systemic symptoms. The radiologist needs to know how to proceed in those instances, both in terms of what types of imaging to perform and how imaging findings might relate to the systemic findings.
This lecture is the first in a series of 5 about intracranial infection and covers general principles behind imaging the patient with suspected intracranial infection. The subsequent 4 videos cover additional more specific considerations.
The two main imaging techniques used in imaging intracranial infection are CT and MRI. CT is a rapid screening test which can detect edema, hemorrhage, midline shift, and prominent masses. It is available in the vast majority of hospitals (at least in the US, but also many abroad), and doesn't require much compliance from the patient. It also requires no screening for metallic implants and other MRI considerations.
MRI is much better at evaluating intracranial infection however. Key sequences include DWI, FLAIR, T2, and T1 postcontrast. DWI is ideal for seeing pus and infarct. FLAIR is ideal for imaging edema. T2 can give you some unique clues, as a few diseases such as lymphoma, tuberculosis, and abscess can be T2 dark. Many infections also cause breakdown of the blood brain barrier, which shows up as enhancement on postcontrast MRI.
Lumbar puncture and echocardiogram are the two main systemic tests which may help you determine if an intracranial infection is present. LP directly assesses for infections agents and inflammatory cells in the CSF, while echocardiogram indirectly assesses for bacterial endocarditis, which can spread to the CSF through emboli.
The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in neuroradiology or may see patients with CNS infections.
Check out this video and additional content on www.learnneuror...

[@neuronone]

Caution regarding need to use generic not trade names. Thank you for an outstanding series!

[@LearnNeuroradiology]

Yeah, that's a good point, although unfortunately here many patients don't know the generic names. Probably best to be familiar with both.

[@ashrafshafei7220]

Thanks alot for these great lectures.... they are very interesting....

[@LearnNeuroradiology]

Glad you like them!

[@caiyu538]

Revisit and thumb up.

[@hanyelbanna3673]

Wonderful work Go on Thanks

[@LearnNeuroradiology]

Thank you! Cheers!

[@jatinderkumar5864]

Thank you for wonderful series , as always. What was the final diagnosis in the case shown in this lecture..was it toxoplasmosis or ? Multiple pyogenic abscesses. Thanks

[@LearnNeuroradiology]

Sorry, that wasn't clear. The case shown throughout the lecture is multiple abscesses. The clue is the diffusion imaging (1:55). Toxoplasmosis usually doesn't have that internal restricted diffusion like that.

[@jatinderkumar5864]

@@LearnNeuroradiology ok. Thanks a lot

[@drklopotes3591]

Calcium hyperintense on nonenhanced T1WI? Isn't it hypointense?thank you

[@LearnNeuroradiology]

Calcium has complex behaviors on MRI. Hydrated calcium, or calcium in the presence of water, tends to cause the region to be T1 hyperintense. Dense calcium, like bone or dystrophic calcification, will be dark on all sequences because it lacks free water to create signal. Check out this reference: pubs.rsna.org/doi/10.1148/radiology.179.1.1848714

[@drklopotes3591]

@@LearnNeuroradiology thanks! I've looked it up. It makes sense now! Outstanding work!