Meningitis

Classically acute and chronic meningitis are distinguished. In the case of acute meningitis CSF testing leads to further classification into pyogenic (mostly bacterial) meningitis characterized by a suppurative reaction resulting in marked pleocytosis, hyperproteinaemia and hypoglicorrachia; and lymphocytic (or aseptic) (usually viral) meningitis characterized by a mild and mostly mononuclear pleocytosis, and a normal titre of glucose.

Clinically acute meningitis (pyogenic or aseptic) is characterized by rapid (over a few hours to a few days) onset of high fever, headache, photophobia, stiff neck and altered mental state ranging from simple irritability to confusion, obtundation and coma. Vomiting may occur, especially as a consequence of raised intracranial pressure.

Evaluation of the disease in neonates and infants may be more challenging and evidence of raised intracranial pressure visible through the open fontanelle plays an important role in reaching a diagnosis.

Chronic meningitis ( the prototype of which is tuberculous meningitis) runs its course over weeks, months or years. The clinical findings may be similar to those of acute meningitis but the onset is gradual, fever less prominent or even absent and most commonly patients present with chronic debility, often associated to focal neurological signs or seizures.

Acute pyogenic meningitis

Acute pyogenic meningitis is the most common form of meningitis. It represents a clinical emergency and it still has a high mortality rate (10-30%). Its incidence is estimated at around 4.6-10 per 100,000 people per year in developed countries. All ages may be affected but about 70% of cases occur in children under 5 years of age. There is no predilection for immunocompromised hosts. Bacteria may reach the leptomeninges and produce a meningitis by the haematogenous route (most frequently), by the contigous route and by direct (either traumatic or iatrogenic) inoculation. For haematogenous meningitis aetiological agents vary according to age, Neisseria meningitidis, Haemophilus influenzae and Streptococcus pneumoniae being the most common agents in children and adults and Gram-negative rods (Escherichia coli, Citrobacter, etc.) and group B streptococci being the principle pathogens in neonates. Staphylococci and streptococci are most common aetiological agents in meningitis, spreading from a contiguous infectious focus (e.g. otomastoiditis, sinusitis).

Pathologically, acute bacterial leptomeningitis results in congestion and hyperaemia of the pia-arachnoid and distention of the subarachnoid space by an exudate containing polymorphonuclear neutrophils.

A wide spectrum of complications may develop in the following days or weeks. Arterial and (most commonly) venous infarction may result from spasm and/or thrombosis of blood vessels exposed to the inflammatory exudate. Cerebritis or abscesses in the subpial cortex and adjacent white matter may result from parenchymal infectious seeding which is facilitated in infarcted areas. Hydrocephalus, more frequently in children than in adults, is produced as a result of obstructed CSF pathways (noncommunicating hydrocephalus) or of disorders of CSF resorption (communicating hydrocephalus). Aseptic or septic subdural collections may develop (typically bilateral frontoparietal collection are seen in association with hemophilus influenzae meningitis in children) and may become infected (empyema). Ventriculitis may occasionally result from infection of the ependymal lining.
 
Lymphocytic (aseptic) meningitis

Lymphocytic (aseptic) meningitis is less frequent. Viruses most commonly spread by the haematogenous route. An aetiological factor may be found in up to 70% of cases but laboratory search of virus DNA and RNA by proteinase chain reaction (PCR) is likely to increase diagnostic accuracy. In the immunocompetent patients the most common aetiological agents are enteroviruses (especially coxsackieviruses and echoviruses) and secondarily herpes simplex viruses (HSV) and mumps viruses. In the immunocompromised population the most frequent aetiological agents include human immunodeficiency virus (HIV) and the herpes viruses, especially cytomegalovirus (CMV) and occasionally herpes simplex viruses type 1 and 2 (HSV-1 and HSV-2).
 
Aseptic viral meningitis

Aseptic viral meningitis in the immunocompetent child or adult is conversely a much more benign and self-limiting process unless it is associated with concurrent encephalitis.
 
Imaging

In uncomplicated meningitis the imaging findings may be unremarkable. Meningeal enhancement may be absent, especially in viral meningitis and bacterial meningitis of children. When it is present it must be remembered that it may rarely result as a direct consequence of lumbar puncture, probably mediated by a transitory CSF hypotension. In severe bacterial meningitis it is nevertheless usually present and is associated with distention of the subarachnoid space with widening of the interhemispheric fissure by the inflammatory exudate. On CT this distention is seen as an obliteration of CSF due to the increased density of the exudate. On MR it is quite well visible as it is associated with a slight signal increase of both T1- and T2-weighted images this being related to the high proteinaceus content of the exudate.
In complicated meningitis neuroradiological examinations play a fundamental diagnostic role.

MR is the examination of choice in the assessment of parenchymal lesions due to its superior sensitivity (Fig. 1). Parenchymal foci of involvement are visible as T2 hyperintensities and they may represent arterial or venous infarcts or cerebritis. The presence or absence of conformity to a distinct vascular distribution, and the presence of venous T1 hyperintensities representing thrombosis (to be searched for in particular in the veins near the sagittal sinus) are features that assist in the differentiation of these entities. Sometimes differentiation of cerebritis from infarction may only become apparent with time as cerebritis typically evolves into a well formed abscess.

Hydrocephalus and its sequela transependymal migration are equally well demonstrated on CT and MR but identification of an eventual site of obstruction benefits from the multiplanarity of MR. Postcontrast imaging enables differential diagnosis between ependymitis associated with enhancement of the ependymal lining and simple transependymal migration.

Subdural effusions and empyemas are also well documented on both CT and MR imaging studies. Differentiation between the two entities is possible on MR on the basis of signal intensities (subdural effusion presents a CSF-like signal, whereas empyema shows hyperintensities on both T1 and T2 weighted images). Additionally empyema shows an enhancing membrane and it is usually associated with foci of parenchymal involvement.In complicated meningitis neuroradiological examinations play a fundamental diagnostic role.

GS

FS