It has been stated that relatively few adult patients who recover from meningococcal meningitis show residual neurologic defects, whereas such defects are encountered in at least 25 percent of children with H. influenzae meningitis and up to 30 percent of child and adult patients with pneumococcal meningitis. Kastenbauer and Pfister, reporting on adults with pneumococcal meningitis, have emphasized that the mortality remains quite high and that cerebral venous or arterial thrombosis occurred in almost a third of cases, as discussed further on. They also had two patients with an associated myelitis. We have seen several instances of upper cervical cord and lower medullary infarction in bacterial meningitis; quadriparesis and respiratory failure were the result of compression from descent of the cerebellar tonsils (Ropper and Kanis). As already discussed, the role of lumbar puncture in promoting this complication of cerebellar herniation has not been clarified.
Among infants who survive H. influenzae meningitis, Ferry and coworkers, in a prospective study of 50 cases, found that about half were normal, whereas 9 percent had behavioral problems and about 30 percent had neurologic deficits (seizures or impairment of hearing, language, mentation, and motor function). In a report of a series of 185 children recovering from bacterial meningitis, Pomeroy and associates found that 69 were not normal neurologically at the end of a month; however, at the end of a year, only 18 were left with a hearing deficit, 13 with late seizures, and 8 with multiple deficits. The presence of a persistent neurologic deficit was the only independent predictor of later seizures. Dodge and colleagues in past decades found that 31 percent of children with pneumococcal meningitis were left with persistent sensorineural hearing loss; for meningococcal and H. influenzae meningitis, the figures were 10.5 and 6 percent, respectively. These events are seemingly less frequent now, specifically in developed countries, but still reflect the seriousness of these sequealae in less advantaged regions of the world.
Cranial nerve palsies other than deafness, if they occur, tend to disappear after a few weeks or months. Deafness in these infections is a result of suppurative cochlear destruction or, less often now, of the ototoxic effects of aminoglycoside antibiotics. Bacteria reach the cochlea mainly via the cochlear aqueduct, which connects the subarachnoid space to the scala tympani. This occurs quite early in the course of infection, hearing loss being evident within a day of onset of the meningitis; in about half or most of such cases, the acute deafness resolves. Hydrocephalus is an infrequent complication that may become manifest months after treatment and then requires shunting if gait or mentation is affected. It may be difficult to determine on clinical grounds whether a residual state of imbalance is the result of hydrocephalus or of eighth nerve damage. The acute complications of bacterial meningitis, the intermediate and late neurologic sequelae, and the pathologic basis of these effects are summarized in Table 31-1.