Neuroimaging of meningitis

The author: Professor Yasser Metwally


June 17, 2009 —  Although hydrocephalus may be seen in all types of meningitis, the demonstration of inflammatory exudate in the nonventricular cerebrospinal fluid (CSF) spaces, especially at the base of the brain, usually depends on the type of offending organism present. In viral and bacterial meningitis, no abnormality may be demonstrated in the basal nonventricular CSF spaces. However, in granulomatous and fungal infections, exudate may be demonstrated in these spaces. This exudate can be hypo-, iso-, or hyperdense relative to the cerebral tissue and may show a variable degree of contrast enhancement.

Whereas 42 gm of iodine usually suffices for contrast CT scan, 70 to 80 gm may be needed in the adult to demonstrate abnormal enhancement by the meningeal exudate. In meningocerebritis, the entire brain is diffusely swollen by edema, and there may be generalized abnormal “gyral” enhancement. Complications of meningitis are discussed below.

Basal adhesion due to tuberculous brain infection    

Figure 1.  Basal adhesion due to tuberculous brain infection

 Enhancement of the basal cisterns due to basal adhesions in a case of tuberculous meningitis,notice the associated hydrocephalus  Enhancement of the basal cisterns due to basal adhesions in a case of tuberculous meningitis,notice the associated hydrocephalus

Figure 2.  Enhancement of the basal cisterns due to basal adhesions in a case of tuberculous meningitis,notice the associated hydrocephalus


  • Subdural effusion

Subdural effusion appears as a low-density area over the surface of the cerebra hemispheres and seems to occur commonly in influenzal meningitis. The pathogenesis is not clear, but the presence of high albumin to gamma globulin ratio in the subdural effusion, compared with that in the serum, suggests that the effusion forms by passage of fluid through irritated or damaged blood vessels (increased capillary permeability). This concept seems to be further borne out by the passage into subdural effusion of the human serum albumin injected intravenously, indicating that subdural effusion is derived from plasma.

CT scan pre,postcontrast showing a case of subdural effusion CT scan pre,postcontrast showing a case of subdural effusion

Figure 3.  CT scan pre,postcontrast showing a case of subdural effusion

  • Subdural empyema

Subdural empyema probably represents infected subdural effusion. Compared with subdural effusion, in which development of a subdural membrane is possible but rare, the membrane is the hallmark of subdural empyema. Subdural empyema occasionally may be isodense with the brain . If it is not of a significant size or it is bilateral but small, then it might be “missed” on the plain CT scan. It is, however, possible to at least suspect significant isodense subdural empyema on the plain CT scan by compression and elongation of the lateral ventricles, poor or nonvisualization of the cortical sulci, and medial displacement of the white matter digitations (“white matter buckling”). It is, therefore, advisable to perform a high-dose contrast CT scan (60 to 80 gm of iodine) in all cases of suspected subdural empyema because its early recognition should initiate its prompt surgical evacuation. In exceptional cases in which diagnosis of subdural empyema cannot be made with confidence on the basis of CT findings alone, angiography may be performed. Hypertrophy of meningeal branches strongly favors the presence of subdural empyema under such circumstances.

CT Scan pre,postcontrast showing a case of subdural empyema CT Scan pre,postcontrast showing a case of subdural empyema

Figure 4. CT Scan pre,postcontrast showing a case of subdural empyema

MRI T1 precontrast showing a case of subdural effusion    

Figure 5. MRI T1 precontrast showing a case of subdural effusion


Subdural and epidural empyemas are collections of purulent material most commonly caused by anaerobic streptococci, staphylococci and Gram-negative enterics. These subdural and epidural infections are uncommon, accounting for only 20-33% of all intracranial infections. Empyemas can result from the complications of meningitis or from haematogenous spread from a distant focus. Other causes include direct implantation through surgery or trauma. In adults, the most common cause is sinusitis or mastoiditis. In infants, a meningitis which induces an effusion is commonly the cause

Extraaxial empyemas usually develop 1-2 weeks following sinusitis or mastoiditis by retrograde thrombophlebitis of the transdiploic veins. The thrombophlebitis progresses to an irreversible thrombosis of the dural sinuses and venous structures leading to secondary parenchymal infection and infarction. The high morbidity and mortality rate (25-50%) along with the clinical and radiologic findings are related more to the response of the cerebral vasculature and brain to the inflammatory response and less to the mass effect of the extraaxial collection. Prompt surgical treatment is a requirement since systemically administered antibiotics do not penetrate the subdural space in therapeutic amounts. Aggressive surgical therapy is also important in limiting the amount of neurological deficits.

Postoperative and posttraumatic empyemas, in contrast to otorhinologically induced empyemas, occur months to years after the initial incident with few or minimal signs and symptoms. The benign course is due to formation of a limiting membrane from the previous surgery or trauma which acts as a barrier protecting the underlying CNS structures.

Because of the fulminant nature of extraaxial empyemas, prompt recognition is a necessity. MR imaging is superior to CT for demonstrating these lesions by enabling more sensitive detection, more accurate localization and more complete delineation of the disease.Superficial lesions are particularly easier to detect due to the absence of bony artifacts with MR imaging . Magnetic resonance imaging also allows the differentiation between benign and purulent effusions, because on both the Tl- and the T2-weighted images, a higher signal intensity will be seen with empyemas.

Posttraumatic empyemas are hypointense on both the Tl- and the T2-weighted images when compared to most chronic subdural haematomas. Also, MR imaging is more specific in differentiating subdural from epidural empyemas. A hypointense medial rim is seen in epidural collections, but not in subdural effusions. Improvement in prognosis can be expected with the use of MR imaging because of early and accurate diagnosis as well as the ability to monitor therapy.

  • Arteritis

Arteritis is more commonly seen in granulomatous meningitis (for example, tuberculosis or coccidioidomycosis) than in various types of purulent meningitides .Of course, arteritis as such cannot be visualized on the CT scan. Its indirect evidence is provided by the sequelae of arteritis (infarction). The infarcted brain appears as a hypodense area that may show a variable degree of irregular type of contrast enhancement.

Massive right hemispherical infarction secondary to tuberculous meningitis   


Figure 6. Massive right hemispherical infarction secondary to tuberculous meningitis

The presence of exudate over the brain surface can lead to venous or sinus thrombosis. The thrombosed cortical veins appear as linear areas of increased density that are traceable to the venous dural sinuses, usually the superior sagittal sinus. The superior sagittal sinus thrombosis appears as a triangular area of increased density on the plain CT scan, more often posteriorly. If the straight and transverse sinuses are also thrombosed, one sees increased density on the plain CT scan along their expected course as well. Besides direct visualization of the thrombosed veins or dural venous sinuses, the sequelae of venous or sinus thrombosis can be recognized as such. These are localized or generalized cerebral edema and infarction, which is usually hemorrhagic. This hemorrhagic type of infarction is usually seen in the superomedial part of the hemispheres, close to the superior sagittal sinus

The arteritis and venous or dural sinus thrombosis and the ischemic injury suffered by the brain can result in gliotic or porencephalic lesions that appear as low-density areas. The generalized ischemic insult suffered by the brain appears as corticocerebral atrophy (ventricular and nonventricular CSF space enlargement). It should be recognized that in all cases, enlargement of the ventricles and of the nonventricular CSF spaces does not necessarily mean that the patient has had corticocerebral atrophy. A similar appearance can be seen in some patients with impaired CSF absorption at the surface. In such cases, the CSF becomes dammed up in sulci and cisterns . Slight enlargement of the head circumference, sutural separation or fontanelle bulge, and clinical evidence of increased intracranial pressure should be considered as evidence against the diagnosis of corticocerebral atrophy. Impaired CSF absorption can be studied either by metrizamide CT scanning or radionuclide cisternography. Prolonged ventricular penetration and delayed appearance of metrizamiae or radionuclide at the brain surface should indicate impaired CSF absorption. Except for assessment of CSF dynamics, the role of RN scan in evaluation of meningitis is clinically insignificant. Similarly, angiography should rarely be necessary in the clinical management of these patients. However, angiography might be done to confirm the diagnosis of arteritis, venous or dural venous sinus thrombosis, and moyamoya disease or occlusion of the arteries at the skull base with appearance

  • Ependymitis (ventriculitis)

Ependymitis is not an infrequent complication of meningitis. On the CT scan, the acute stage of ependymitis manifests as contrast enhancement along the ventricular borders; in the chronic stage, the ventricular wall becomes irregular. Adhesions within the ventricular wall can lead to multiple and cystic cavities mimicking findings of multiple and cystic encephalomalacia.


  1. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publication, version 10.2a April 2009 [Click to have a look at the home page]

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