Meningitis can be caused by a diverse array of infectious agents. Acute forms can be distinguished into lymphocytic (usually viral) and pyogenic (mainly bacterial). Chronic forms (tubercular or granulomatous) can also occur. Bacterial infections can result in high mortality rates and cause significant permanent neurological damage in survivors. The pathogen responsible for the infection may vary depending as shown in Table 1.

Table 1: Causes of meningitis

There are four common routes through which infectious agents can enter the central nervous system:

- Haematogenous spread from a distant systemic infection (most common);

- Direct geographical spread from sinusitis, orbital cellulitis, otitis media or mastoiditis;

- Penetrating injuries and skull fractures, particularly at the base of the skull;

- Spread of infection along the peripheral nervous system.

Regarding symptoms, adults present with fever (≥ 38.5°C) and headache, followed by signs of meningeal irritation (nuchal rigidity) and/or endocranial hypertension (vomiting). Infants present with fever, lethargy, poor feeding and irritability. N.meningitidis can cause a purpuric rash, while Meningococcal or H. Influenzae can lead to the development of Diffuse Intravascular Coagulopathy.

Once suspicion has been established based on clinical-anamnestic and blood laboratory data (as shown in Table  2), the best diagnostic clue for detecting meningitis is the CSF analysis by lumbar puncture (“gold standard”).

Table 2: CSF analysis

Imaging is not a highly sensitive or specific method for detecting meningitis. Although CT is often used as a screening tool for headaches and suspected meningitis, MR is the method of choice for studying infectious-inflammatory pathology and often allows early diagnosis, an indispensable element for effective therapy.

MR protocol included T1-weighted (T1W), T2-weighted (T2W), T2-FLuid Attenuated Inversion Recovery (FLAIR), Diffusion-weighted Imaging (DWI), Contrast-Enhanced T1-Weighted e Contrast-Enhanced T2-FLAIR-Weighted Images. Advanced MRI techniques such as magnetic transfer sequence, diffusion tensor imaging (DTI), MR spectroscopy, and perfusion imaging have significantly contributed to the evaluation of meningitis complications.

Typical patterns of extra-axial meningeal enhancement (pachymeningeal or leptomeningeal) are more frequent with pyogenic meningitis. The pachymeningeal enhancement is also known as dura-arachnoid enhancement due to the attachment of the normal, thin arachnoid membrane to the inner surface of the dura mater. On the other hand, enhancement on the brain's surface is referred to as pial or pia-arachnoid enhancement, commonly known as leptomeningeal enhancement. This enhancement typically has a gyriform or serpentine appearance. It follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. Combined dura-arachnoid and pia-arachnoid enhancement may coexist (Fig. 1).

Fig 1: Pattern of meningeal enhancement

The use of post-contrast FLAIR sequences is important because they have greater sensitivity and specificity than T1W images in detecting these patterns (Fig. 2, 3, 4).

Fig 2: Leptomeningeal enhancement

Fig 3: Leptomeningeal enhancement

Fig 4: Leptomeningeal enhancement

CT FINDINGS:

NECT

• Normal in the early disease process
• Mild enlargement of the ventricular system and subarachnoid space with diffuse cerebral swelling
• Blurred ventricular margins that indicate acute obstructive hydrocephalus
• Obliteration of the cisterns
• Hyperdensity in basal cisterns or Sylvian fissures related to inflammatory debris (D.D. subarachnoid hemorrhage)

Bone CT: Sinusitis and otomastoiditis

CECT

• Enhancement of the inflammatory exudate in sulci and cisterns

MR FINDINGS:

• Purulent exudates are isointense with the underlying brain on T1WI and isointense with CSF on T2WI
• Hyperintensity in the subarachnoid cisterns and superficial sulci on FLAIR

In cases of acute meningitis, meningeal enhancement is typically found over the cerebral convexity. However, in cases of chronic meningitis, enhancement is more commonly observed in the basal cisterns. Abnormal enhancement may still be visible in chronic meningitis even years after the initial infection. In some cases, en plaque dural thickening and popcorn-like dural calcification can be observed around the basilar cistern. Sequelae of chronic meningitis include ischemic changes and atrophy, which can be striking in some cases.