Meningitis and Ventriculitis

CHAPTER 40 Meningitis and Ventriculitis


Bacterial meningitis is an infectious inflammatory infiltration of the leptomeninges caused by bacteria. It can also be referred to as pyogenic meningitis and leptomeningitis.


In the United States, bacterial meningitis is predominantly a disease of adults.13 The most common (50%) cause of adult meningitis is Streptococcus pneumoniae. Other common causative organisms include Neisseria meningitidis and Haemophilus influenzae. Gram-negative bacillary meningitis shows an increased incidence in patients who have undergone neurosurgical procedures.3 Successful vaccination against H. influenzae type B has markedly reduced the incidence of this infection in infants and children, leaving group B streptococci as the most common cause of bacterial meningitis and sepsis in the neonate. Group B streptococci are also an infrequent cause of meningitis in adults, especially in patients with diabetes mellitus, liver disease, prior stroke, breast cancer, and human immunodeficiency virus (HIV) infection.2 Citrobacter is a distinct group of gram-negative bacilli that belong to the Enterobacteriaceae family. Citrobacter meningitis is frequent in neonates and young children but highly unusual in adults.



Fluid-attenuated inversion recovery (FLAIR) MR sequences appear to be the most sensitive technique for detecting meningeal diseases (Fig. 40-2). High signal in the subarachnoid space reflects high protein concentration in the CSF.57 Contrast-enhanced T1-weighted (T1W) images typically show leptomeningeal enhancement (Fig. 40-3).

Neuroimaging detects the complications of meningitis, which include hydrocephalus, ventriculitis, empyema, venous sinus thrombosis, and infarctions.

Communicating hydrocephalus is a common complication, because the inflammatory debris may impede the flow and reabsorption of CSF.8 The ventricles become distended. Transependymal “migration” of CSF appears as high signal intensity areas surrounding the portions of the ventricles that abut white matter. Pyogenic ventriculitis manifests as periventricular high signal on FLAIR MRI, ependymal enhancement, ventricular debris, and fluid-fluid levels within the ventricles.9 Subdural effusions are typically sterile in meningitis; only 2% will form subdural empyemas. Venous thrombosis appears as high signal intensity within the venous sinuses on spin-echo sequences and absence of high signal within the sinuses on gradient-echo sequences. Such thromboses can lead to venous infarctions that do not conform to well-defined arterial territories and often manifest concurrent hemorrhage. Venous infarctions typically show high signal on T2-weighted (T2W) and FLAIR images as well as high signal on diffusion-weighted imaging (DWI) with low apparent diffusion coefficient (ADC). They are usually located cortically/subcortically close to the vertex and the thrombosed superior sagittal sinus. Occlusions or stenosis of the arteries may be detected on magnetic resonance angiography (MRA). Arterial infarctions have typical MR features and follow the expected arterial distributions (see Fig. 40-2).


Empyema is a collection of purulent material confined within the epidural or subdural space and can also be known as subdural empyema, epidural empyema, epidural abscess, or sinogenic intracranial empyema.


Purulent subdural effusions occur most frequently in the second decade of life with a male-to-female ratio of 3 : 1.10 The most common pathogens are Streptococcus milleri, other streptococci, enterococci, and gram-negative bacilli. Most subdural empyemas develop as complications of sinusitis, then otitis media. In one study, 6% of patients with otitis media had a subdural or epidural empyema.11 Infratentorial empyema is an uncommon form of intracranial suppuration and is usually secondary to a neglected otogenic infection.12 Only 41 cases of infratentorial empyema were described in the literature from 1966 through 2006.12


Epidural empyemas tend to remain localized within the extradural space. Subdural empyemas commonly spread diffusely over the convexities and throughout the subdural space, because no anatomic constraints limit their spread.10 Subdural empyema usually occurs in association with otorhinologic infection as a result of direct spread of infection or retrograde thrombophlebitis via bridging emissary veins. Because the bridging veins are valveless, thrombophlebitis can easily pass retrograde into the cavernous sinus and other dural venous sinuses. In the acute phase, a thin unencapsulated layer of pus covers the cerebral hemisphere. Retrograde thrombophlebitis produces early involvement of the cortex.




Subdural empyema is usually crescentic, whereas epidural empyema is always lentiform. The pus within the subdural/epidural empyema is hypointense relative to the brain on T1W and hyperintense on T2W images. FLAIR MRI helps to distinguish infected effusions (high signal) from sterile hygromas (low signal) (Fig. 40-4A). The dura mater shows characteristically low signal on both T1W and T2W images, so identification of the low signal dura will help to distinguish a subdural empyema from an epidural empyema on both T1W and T2W imaging. On DWI, purulent subdural collections will show high signal due to restricted diffusion (Fig. 40-5D).15 Epidural empyemas may show high, low, or inhomogeneous signal on DWI. The difference in pressure and other factors between the subdural and epidural spaces, as well as the content of empyemas, may be the causes of differences in the activity of pleomorphic leukocytes.



Cerebritis is a purulent nonencapsulated parenchymal infection of the brain.

Jan 22, 2016 | Posted by in NEUROLOGICAL IMAGING | Comments Off on Meningitis and Ventriculitis
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