1) MENINGITIS

• Most do not show any remarkable findings. In any case, MRI is more sensitive. When present, the most common is leptomeningeal enhancement (Fig. 1), which ought to be distinguished from pachymeningeal enhancement (Fig. 2). There are some others (Fig. 3):
  • presence of purulent exudate in the subarachnoid space.
  • signs of expansivity.
  • a slight dilatation of the ventricular system.
  • acute sinusitis, otitis media, mastoiditis and/or petrositis.
•  Complications of acute meningitis:

  • Acute hydrocephalus: may be communicating, as described above, or non communicating (Fig. 4). 

  • Empyemas: can be subdural or epidural. On CT, they are usually hypodense collections with thickening and contrast enhancement of the external meningeal sheats, and generate important expansivity. The purulent contents typically show marked restricted diffusion restriction (Fig. 4). 
  • Hygromas: typically frontoparietal. Can also be epidural or subdural. Unlike empyemas, they do not show diffusion restriction (Fig. 6), since they are sterile collections, and usually transient.
  • Cranial nerve involvement: every cranial nerve may potentially be affected. The most frequent one is the VIII nerve (Fig. 6). 
  • Venous infarctions: caused by thrombosis of the venous sinuses/ cortical veins (Fig. 5)
  • Arterial infarctions: the inflammatory exudate in the CSF bathes the arterial vessels, leading to multifocal stenosis. It most frequently affects perforating arteries (Fig 5). 
  • Ventriculitis: it is the infection of the ventricular system. Most of the time arises due to rupture of an abscess (Fig. 9), but can also originate post-surgically. Can be fatal. 
  • Spread of infection to the parenchyma: cerebritis and brain abscess (Fig. 6).

2) BRAIN ABSCESS. 

Bacterial abscesses.

Findings are time-dependent.

1. Starts as a cerebritis; an ischemic/necrotic area of inflammatory infiltrate where the immune response is developing (Fig. 7).
2. As the infectious process matures, a capsule forms surrounding a central cavity filled with pus (Fig. 8).
   • The cavity with pus is hypointense on T1 and hyperintense on T2. In pyogenic abscesses, it clearly restricts on diffusion (Fig). However, metastases may occasionally exhibit restriction on the cavity (Fig. 11).
   • The capsule in pyogenic abscesses usually exhibits a "layered" appearance on T2 (Fig. 8) and shows contrast enhancement, which is thickest at its cortical margin (the most vascularized). On SWI, the double ring sign can be observed (Fig. 8).  
   • In perfusion studies, the wall of the abscess decreased cerebral blood volume values (Fig. 8).
   • Spectroscopy revels an elevation of succinate at 2.4 ppm (Fig. ), although it is very variable.

A characteristic feature of pyogenic abscesses is their typical progressive growth towards the ventricle (Fig. 9).

Abscesses may also occur in the spinal cord. Their radiological appearances are equivalent to those in the brain (Fig. 10). 

Tuberculomas/Tuberculous granulomas (Fig. 12). 

• They do not usually restrict on diffusion (although it may occur).
• The cavity is usually hypointense on T2 (as fungal and parasitic abscesses) (Fig. 13). 
• They usually present as meningoencephalitis, with multiple abscesses.
• They do not usually associate large areas of peripheral edema.

Fungal abscesses (Fig. 14).

• The cavity typically presents hypointense contents on both T1 and T2/FLAIR sequences. 
• Characteristically, they are non restricting lesions on diffusion.
• They may or may not show peripheral contrast enhancement. When they do, it is generally thin and uniform.
• On spectroscopy, they typically show a marked peak of acetate and succinate at 1.9 and 2.4 ppm.

3. HERPETIC ENCEPHALITIS

Most frequent cause of sparadic encephalitis.  May be associated with meningitis, myelitis or a variable combination of these (meningoencephalitis, encephalomyelitis, etc). 

Its a a very marked typical distribution: BILATERAL and ASYMMETRICAL, affecting:

• Temporal lobes, especially the temporal poles and mesial regions.
• Insular cortex.
• Frontobasal regions (in both the interhemispheric and lateral regions).
• Cingulate cortex.
• Finally, it affects the remainder of the parenchyma of the temporal and frontal lobes, and occasionally, can affect the parietal lobes.
• Typically spares basal ganglia.

It is represented as cortical hypodensities on CT scans, and giral thickening hyperintense on T2/FLAI,  with cortical diffusion restriction. Also hyperperfusion. 

The absence of contrast enhancement is a key imaging feature. However, it can be present in the subacute recurrent type (Fig. 16).

Radiologically, the differential diagnosis encompasses (Fig. 17):

• Autoimmune encephalitis (limbic encephalitis). 
• Gliomas of the temporal pole and insula. 
• Seizure related cortical changes.
• Middle cerebral artery (MCA) infarction.

4. OTHER TYPES OF ENCEPHALITIS

• Rhomboencephalitis (Fig. 18).
  • Distribution: posterior aspect of the brainstem, surrounding the fourth ventricle. It may involve the dentate nuclei, the midbrain, the deep supratentorial nuclei, and may be associated with myelitis. 
  • Contast enhancement is uncommon. 
  • They rarely show diffusion restriction; it is an indicator of the severity of the condition.
  • Complications: hydrocephalus due to obstruction of the IV ventricle; more frequent due to Listeria.
• Acute cerebellitis (Fig. 19).
  • Findings: Cortical edematous changes in both cerebellar hemispheres, fairly symmetric.
  • May associate diffusion restriction and even leptomeningeal enhancement.
  • Possible complications: obstructive hydrocephalus, tonsillar herniation, cerebellar atrophy... In very severe cases, brainstem compression.
• Encephalitis with bithalamic involvement (Fig. 20).
• Neurosyphilis (Fig. 21). 

5. PARASITIC INFECTIONS (Fig. 22).

In our environment, usually seen in travelers, except toxoplasmosis, which may also appear in immunosuppressed patients. 

• Neurocisticercosis. 
  • The parasite has several evolutionary stages:
    • If the cystic lesion does not show contrast enhancement, the larva is alive.
    • If the periphery of the cystic lesion does show contrast enhancement, the larva is dead. 
    • If it shows calcifications, the lesion is old, and is considered cured.
  • Typically, the disease is extraaxial seated. The inflammatory reaction that seeks to isolate the lesion makes it appear intraaxial.
  • Sometimes there is a mural enhancing nodule on the inside, corresponding to the scolex.
• Toxoplasmosis: will be explained later. 
• Hydatidosis
  • More frequent in children.
  • Usually presents with cysts in other locations (liver, lung...).
  • Typically appears as a single rounded thin-walled lesion, generally affecting the supratentorial parenchyma. Intracystic daughter vesicles are often identified.

6. INFECTIONS IN IMMUNOSUPRESSED PATIENTS

Some of the following frequently affect HIV/AIDS patients. However, can also happen in oncologic/hematologic patients, transplant recipients and patients under immune treatments.

• Toxoplasmosis (Figs. 22 and 23). 
  • Localization: GGBB, thalami and at the cortico-subcortical junction.
  • Appearances: large perilesional vasogenic edema, and eccentric ring contrast enhancement. In CT perfusion, they show hypoperfusion (a key feature for the differential diagnosis with lymphoma). In chronic phase, when cured, they calcify. They usually do NOT restrict on diffusion.

• Cryptococosis (Fig. 24).
  • Frequently seen in HIV/AIDS patients and transplant recipients.
  • Localization: gelatinous pseudocysts, formed by extension of purulent exudate from the basal cisterns to the basal ganglia through perivascular spaces.
• Progressive multifocal leukoencephalopathy (Fig. 25).
  • Lesions are typically bilateral and parieto-occipital, involving juxtacortical white matter, with volume loss, without mass effect. Tend to by bilateral but asymmetric. 
  • These lesions do not show contrast enhancement (except in the PML-IRIS syndrome; Fig. 26). 
  • They are markedly T1 hypointense. In DWI, there is a restricting "advancing front" in the periphery.
• HIV encephalitis (Fig. 25).
  • Progressive parenchymal atrophy, with hypodense lesions on CT, located in the frontal, occipital and periventricular white matter, without mass effect. They respect the juxtacortical white matter.
  • No contrast enhancement.

• Nocardia (Fig.27).
• Aspergilosis and Mucormicosis (Fig. 28).

7) PRION-TRANSMITTED DISEASES (Creutzfeldt-Jakob).

• Presents with a rapidly progressive and fatal dementia.
• Appearances: Hyperintensities in T2 and FLAIR as well as diffusion restriction in the caudates, putamina, thalami and cortex (Fig. 28). The disease is usually bilateral, but asymmetric. And typically, there is usually sparing of the primary motor and sensory cortex. 
• In the variant form of the disease, a characteristic radiological sign known as the hockey stick sign appears, a characteristic T2 hyperintensity in the pulvinars of both thalami (Fig. 29).