Central nervous system disorders

III./4.3.: Histopatology of meningitis

III./4.3.1.: General characteristics

Due to a cell destructive feature bacterial propagation in the subarachnoideal space leads to the accumulation of citokines and inflammatory mediators. Endothelial destruction makes it possible for activated leukocytes to move through the endothelial gaps to the subarachnoideal space. Vessel permeability is increasing, which causes an interstitial cerebral oedema. Typical pathological findings of inflammations in the central nervous system include perivenous infiltration: leukocytes infiltrate perivenous and arteriolal gaps and the walls of venous sinuses, resulting in small vessel thrombosis. The inflammatory exudate can be millimetre-wide on the meninges, in the cysterns, sulci, near the venous sinuses, and around the brain stem and spinal cord. Rarely a subdural empyema occurs.

III./4.3.2.: The development of purulent meningitis

The development of purulent meningitis can be divided into stages:

• 1) Inflammation of the leptomeninges with fever and nuchal rigidity. Nausea and vomiting occur in the preliminary phase.

• 2) Pus accumulates in the basal cysterns and on the convexity, which hinders liquor circulation; causing occlusive and non-resorptive hydrocephalus and increased intracranial pressure. The effusion can damage the cranial nerves running in the cysterns (VI., VII., VIII.). Vasculitises result in cortical ischemic foci.

• 3) Pathogens reach the parenchyma via the Virchow-Robin space and a meningoencephalitis can develop. Cerebral oedema following the inflammation is one of the components of increased intracranial tension; the brain stem can herniate. An altered level of consciousness after vomiting is an unfavourable prognostic sign.

• 4) Purulent meningitis in the infancy and childhood often are not accompanied by such dramatic symptoms as in adulthood. Apathy with elevated body temperature can raise our suspicion; other typical symptoms are crying and refusing food. Vomiting and bulging fontanelles are symptoms of a fully developed meningitis.

III./4.3.3.: Etiology of meningitis

• 1) Hematogenic infection. The infection is transmitted via droplet contact or direct physical contact with the patient. After upper respiratory tract and pulmonary infections bacteria reach the meninges with the circulation. The source of infection can also be a bacterial endocarditis of osteomyelitis, from where Meningo/Pneumo/Strepto/Staphlyococcus can disseminate. Purulent brochiectasias or the nasopharynx are common sources of pneumococcal meningitis.

• 2) Direct transmission. Pathogens of sinusitises and mastoiditis can spread to the subarachnoideal space through the bony structure of the middle ear via the diploic veins and the liquor. Pneumococci and meningococci as the most frequent pathogens infect the dura mater first then the inflammation spreads over the pia mater reaching the cerebral and spinal subarachnoideal space.

• 3) Secunder meningitis. Can occur after head traumas when the liquor space opens up due to a fracture of the base of the skull and bacteria from the paranasal sinuses reach the intracranial space. Frequent pathogens include Pneumococci, Staphylococci and Haemophilus influenzae.