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Table 32-1 Pathologic-clinical correlations in acute, subacute, and chronic meningeal reactions I In acute meningeal in ammation: A Pure pia-arachnoiditis: headache, stiff neck, Kernig and Brudzinski signs These signs depend on the activation of protective re exes that shorten the spine and immobilize it Extension of the neck and exion of the hips and knees reduce stretch on in amed spinal structures; resistance to forward exion of the neck (Brudzinski sign) and extension of the legs (Kernig sign) involves maneuvers that oppose these protective exor re exes B Subpial encephalopathy: confusion, stupor, coma, and convulsions are related to this lesion The tissue beneath the pia is not penetrated by bacteria; hence the change is probably toxic (eg, cytokines) Cerebral infarction due to cortical vein thrombosis may underlie these symptoms in some cases C In ammatory or vascular involvement of cranial nerve roots: ocular palsies, facial weakness, and deafness are the main clinical signs Note: Deafness may also be due to middle ear infection, to extension of meningeal infection to the inner ear, or to toxic effects of antimicrobial agents D Thrombosis of meningeal veins: focal seizures, focal cerebral defects such as hemiparesis, aphasia (rarely prominent), may appear on the third or fourth day after the onset of meningeal infection, but more often after the rst week There may be spinal cord infarction E Ependymitis, choroidal plexitis: it is doubtful if there are any recognizable clinical effects aside from those of the associated meningitis and hydrocephalus F Cerebellar or cerebral hemisphere herniation: due to swelling (as in B), causing upper cervical cord compression with quadriplegia or signs of midbrain third nerve compression II In more subacute and chronic forms of meningitis: A Tension hydrocephalus, due at rst to purulent exudate around the base of the brain, later to meningeal brosis, and rarely to aqueductal stenosis In adults, there are variable degrees of impairment of consciousness, decorticate postures (arms exed, legs extended), grasp and suck re exes, and sphincteric incontinence CSF pressure may at rst be elevated; as the ventricles enlarge and the choroid plexuses are compressed, it may fall to within limits of normal (normal-pressure hydrocephalus) In infants and young children, the main signs are enlarging head, frontal bossing, inability to look upward (eyes turn down and lids retract on effort to look up sunset sign); in mildest form, there are only psychomotor retardation, unsteadiness of gait, and incontinence B Subdural effusion: impaired alertness, refusal to eat, vomiting, immobility, bulging fontanels, and persistence of fever despite clearing of CSF In infants, the effusion causes an exaggerated transillumination If fever is present but CSF pressure is normal, and if one-sided cerebral signs are clearly in evidence, thrombophlebitis with infarction of underlying brain is the leading possibility C Extensive venous or arterial infarction: unilateral or bilateral hemiplegia, decorticate or decerebrate rigidity, cortical blindness, stupor or coma with or without seizures III Late effects or sequelae: A Meningeal brosis around optic nerves or around spinal cord and roots: blindness and optic atrophy, spastic paraparesis with sensory loss in the lower segments of the body (opticochiasmatic arachnoiditis and meningomyelitis, respectively) B Chronic meningoencephalitis with hydrocephalus: dementia, stupor or coma, and paralysis (eg, general paralysis of the insane) If lumbosacral posterior roots are chronically damaged, a tabetic syndrome results C Persistent hydrocephalus in the child: blindness, arrest of all mental activity, bilateral spastic hemiplegia.

Summary

enhance their ability to cause infection; this is particularly true of the meningococcus (see Rosenstein et al) Avenues other than the bloodstream by which bacteria can gain access to the meninges include congenital neuroectodermal defects; craniotomy sites; diseases of the middle ear and paranasal sinuses, particularly perilymphatic stulas; skull fractures; and, in cases of recurrent infection, dural tears from remote minor or major trauma Occasionally a brain abscess may rupture into the subarachnoid space or ventricles, thus infecting the meninges The isolation of anaerobic streptococci, Bacteroides, Actinomyces, or a mixture of micro-organisms from the CSF should suggest the possibility of a brain abscess with an associated meningitis

Adults and Children The early clinical effects of acute bacterial meningitis are fever, severe headache, and stiffness of the neck (resistance to passive movement on forward bending), sometimes

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with generalized convulsions and a disorder of consciousness (ie, drowsiness, confusion, stupor, and coma) Flexion at the hip and knee in response to forward exion of the neck (Brudzinski sign) and inability to completely extend the legs (Kernig sign) have the same signi cance as stiff neck but are less consistently elicitable Basically, all of these signs are part of a exor protective re ex (one of the nocifensive responses in Fulton s terms) Stiffness of the neck that is part of paratonic or extrapyramidal rigidity should not be mistaken for that of meningeal irritation The former is more or less equal in all directions of movement, in distinction to that of meningitis, which is present only or predominantly on forward exion Whether it is stiffness in the initial few degrees of exion of the neck or in the subsequent part of the movement that is more speci c for meningitis has been debated; our experience has been that the latter is more sensitive but also proves to be mistaken for other disorders; therefore the rst may be more speci c for meningitis Diagnosis of meningitis may be dif cult when the initial manifestations consist only of fever and headache, when stiffness

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