Bacterial meningitis 

is the most common serious infection of the central

nervous system. Infection of the subarachnoid space leads to cerebrospinal
fluid (CSF) inflammation, meningeal irritation, and the clinical triad of
headache, fever, and meningismus. Approximately 10,000 cases of bacterial
meningitis occur each year in the United States, whereas other parts of the
world have substantially higher incidences. 72 Even when treated with highly
effective antibiotics, the disease is fatal in 5% to 40% of the patients and
causes neurologic sequelae in up to 30% of the survivors.5, 28
Neurologic sequelae from bacterial meningitis can be grouped into three
categories: (1) hearing impairment, which is most commonly the result of
direct invasion of the inner ear by the subarachnoid space inflammation;
(2) obstructive hydrocephalus; and (3) damage to the brain parenchyma,
leading to neurologic sequelae such as focal sensory-motor deficits, mental
retardation, and seizure disorders.5, 28
Over the last 3 decades, it has become clear that the multiplication of bacteria
within the central nervous system (CNS) compartment triggers a host
response with an overshooting progression of inflammation. Some of the
inflammatory and neurotoxic mediators involved in the processes leading to
neuronal injury during meningitis have been identified in recent
years.81, 84 As a result, the therapeutic approach to bacterial meningitis has
widened from eradicating the bacterial pathogen with antibiotics to
attenuation of the detrimental effects of host defenses. Corticosteroids
represent an example of the therapeutic strategies aimed at modulating and
decreasing inflammation in bacterial meningitis. 46 This article reviews current
concepts of the pathophysiology of the disease with an emphasis on possible
therapeutic strategies to prevent brain damage.