Acute Meningitis

NeuroLearn NeuroHelp Bacteria @ Neonatal meningitis

Background    Neuroimaging    Gross Pathology    Histopathology & Immunohistochemistry

Differential Diagnosis    Reference

BACKGROUND AND CLINICAL INFORMATION: Head

NEUROIMAGING: Head

GROSS PATHOLOGY: Head

Edema: Bacterial meningitis are frequently associated with prominent edema.

On autopsy:

• When death occurs within 24 hours there is no pus in the meninges, but the meninges are deeply congested, so much so as to sometimes suggest subarachnoid hemorrhage.

• Survival for 2 days or longer allows the migration of leucocytes, when the entire brain, vertex and base can be enveloped by pus, creamy, yellow or green depending on the responsible organism.

• If the patient dies at a stage intermediate between the hyperacute phase and fully developed purulent meingitis, pus is visible only as cloudiness in the basal cisternae and as thin creamy lines alongside cortical meningeal veins; even then it is not always easy to make the diagnosis of meningitis on microscopic grounds and microscopy should always be performed to confirm or refute such a diagnosis.

Ventricles: Although the brain is edematous, yet ehn it is sectined the ventricles may already be slightly enlarged rather than compressed. The ventricular CSF is purulent, particulary in fatal cases.                                                                  

Cochlea may ossify after meningitis.  

HISTOPATHOLOGY AND IMMUNOHISTOCHEMISTRY: Head

Inflammation is limited to the leptomeninges and the subarachnoird space. By definition, there is no parenchymal involvement. However, in previously damaged areas where leptomengeal-parenchymal adhesion is seen, the inflammation will extend into the parenchyma and cause a cerebritis. This is frequently seen in recurrent meningitis.

Polymorphs dominant the infiltration at the beginning (24 hours). Lymphocyes and a few plasma cells appear after 2-3 days and the polymorphs became less numerous. In contrast, the underlying cortex is remarkably minimally or not at all involved by the inflammatory infiltrates. Leptomengeal-parenchymal adhesion is frequently seen when the inflammation is over.

However, the cortex is edematous as shown by large erineuronal spaces. Small foci of cortical necrosis resulted from vascular thrombosis are also frequently seen.

Many vessels will develop obliterative enarteritis that eventually become obliterated/thrombosed and cause thrombolic infarction.

DIFFERENTIAL DIAGNOSIS: Head