Bacterial meningitis is clinically characterized by stiff neck, headache, fever, photophobia, malaise, vomiting, alteration of consciousness, seizures, confusion, irritability, and, rarely, acute psychosis. Cerebrospinal fluid (CSF) usually reveals an elevated white blood cell count of more than 1000 white blood cells/^l, consisting of more than 60% polymorphonuclear leukocytes, an elevated total protein content and a decreased CSF/serum glucose ratio. A CSF white blood cell count of less than 1000 cells/^l may be found early in the disease, in partially treated bacterial meningitis, in overwhelming bacterial meningeal infection ('apurulent bacterial meningitis') and in immunosuppressed and leukopenic patients.
With the introduction of antimicrobial agents into clinical practice, the mortality rates of bacterial meningitis were markedly reduced. The mortality rates of meningitis due to Haemophilus influenzae type b are less than 7% and those of meningitis due to Neisseria meningitidis are 6-14%. With the advent of third-generation cephalosporins, the mortality of Gram-negative bacillary meningitis has decreased from 40-80% to 10-20%. However, despite further progress in antimicrobial therapy and improvements in intensive care medicine, the mortality rate of meningitis due to Streptococcus pneumoniae, the organism most often responsible for bacterial meningitis in adults, has remained relatively unchanged during the last decades and is still unacceptably high (approximately 20%). Neurologic and neuropsycho-logic sequelae resulting from bacterial meningitis are found overall in 10-30% of patients. Cerebral and systemic complications arising during the acute phase of the disease are responsible for both the mortality and the long-term sequelae caused by bacterial meningitis. The major acute complications involving the central nervous system include cerebrovascular insults, brain edema, and hydro-cephalus. Cerebrovascular involvement, of both arteries (arteriitis, vasospasm) and veins (septic sinus venous thrombosis), may lead to infarction with severe irreversible cerebral damage and an increase of intracranial pressure due to cytotoxic edema. In addition to edema, increased intracranial blood volume due to disturbed cerebrovascular autoregulation or to septic venous sinus thrombosis may lead to life-threatening elevation of intracranial pressure with the risk of herniation. There is a risk of cortical necrosis when cerebral perfusion pressure (defined as the difference between systemic mean arterial blood pressure and intracranial pressure) decreases as a result of increased intracranial pressure and systemic hypotension. Interstitial edema may occur owing to transependymal movement of CSF from the ventricular system into the surrounding brain parenchyma as a consequence of obstructive hydrocephalus. Systemic complications of bacterial meningitis include sepsis, including septic shock, disseminated intravascular coagulation, adult respiratory distress syndrome, and inappropriate secretion of antidiuretic hormone (ADH).
Recently, high-resolution MRI was used to demonstrate inner ear involvement in adults with bacterial meningitis.1 The structures most frequently involved were the cochlear nerve, the first cochlear turn, the vestibulum and the semicircular canals. There was a significant correlation between clinical and MRI findings: all patients with cochlear enhancement were deaf (hearing loss, > 90 dB), whereas none of the patients with normal MRI findings had hearing loss of more than 90 dB. This study shows that high-resolution MRI can visualize involvement of vestibulocochlear structures in bacterial meningitis, in both cooperative and consciously impaired patients. These findings suggest a correlation between abnormalities on MRI and the extent of cochlear dysfunction.
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