Porth's Essentials of Pathophysiology, 4e

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Nervous System

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caused by Streptococcus pneumoniae (pneumococcus) or Neisseria meningitidis (meningococcus), except in neonates, who are more commonly infected by group B streptococci. The development of effective vaccines against Haemophilus influenzae and S. pneumoniae has resulted in a profound decline in bacterial men- ingitis among children in the United States. 44 Among adults, however, the incidence of meningitis has not changed. Epidemics of meningococcal meningitis occur in settings such as colleges and the military, where young people reside in close contact with each other. Other pathogens in adults are gram-negative bacilli and Listeria monocytogenes. The very young and the very old are at highest risk for pneumococcal meningi- tis. Risk factors associated with contracting meningitis include head trauma with basilar skull fractures, otitis media, sinusitis or mastoiditis, neurosurgery, dermal sinus tracts, systemic sepsis, or immunocompromise. In the pathophysiologic process of bacterial meningi- tis, the microorganisms replicate and undergo lysis in the CSF, releasing endotoxins and cell wall fragments that cause inflammation, characterized by a cloudy, purulent exudate (Fig. 37-17). Thrombophlebitis of the bridging veins and dural sinuses or obliteration of arterioles by inflammation may develop, causing vascular congestion and infarction in the surrounding tissues. Ultimately, the meninges thicken and adhesions form. These adhesions may impinge on the cranial nerves, giving rise to cranial nerve palsies, or may impair the outflow of CSF, causing hydrocephalus. The most common symptoms of acute bacterial men- ingitis are sudden onset of headache, fever, and stiffness of the neck (nuchal rigidity), sometimes accompanied

SUMMARY CONCEPTS (continued)

Infections Infections of the brain may be classified according to the structure involved—meninges (meningitis) or parenchy- mal brain tissue (encephalitis). They also may be classi- fied by the type of invading organism: bacterial, viral, or other. In general, pathogens enter the CNS from the bloodstream or by direct invasion through a skull frac- ture, or, rarely, by contamination during surgery or lum- bar puncture. Local extension from an adjacent structure (e.g., infected sinus, tooth, middle ear) may also occur. Meningitis Meningitis is an inflammation of the pia mater, the arachnoid, and the CSF-filled subarachnoid space. Inflammation spreads rapidly because of CSF circulation around the brain and spinal cord. The inflammation usu- ally is caused by an infection, but chemical meningitis can occur. There are two types of acute infectious men- ingitis: acute purulent meningitis (usually bacterial) and acute lymphocytic (usually viral) meningitis. 1 Factors responsible for the severity of meningitis include viru- lence of the pathogen, host factors, brain edema, and the presence of permanent neurologic sequelae. Acute Bacterial Meningitis Acute bacterial meningitis, which has a high potential for morbidity and mortality, is an inflammatory pro- cess of the leptomeninges and CSF within the subarach- noid space. 1,4,42,43 Most cases of bacterial meningitis are ■■ A hemorrhagic stroke is caused by the spontaneous rupture of an intracerebral vessel with bleeding into the brain.The most common predisposing factors are advancing age and hypertension. ■■ A subarachnoid hemorrhage involves bleeding into the subarachnoid space. Most subarachnoid hemorrhages are the result of a ruptured cerebral aneurysm or arteriovenous malformations. ■■ Arteriovenous malformations are congenital abnormal communications between arterial and venous channels that result from failure in the development of the capillary network in the embryonic brain.The vessels in the arteriovenous malformations may enlarge to form a space- occupying lesion, become weak and predispose to bleeding or divert blood away from other parts of the brain.

FIGURE 37-17. Purlent meningitis. A creamy exudate opacifies the leptomeninges in bacterial bacterial meningitis.The superficial veins are engorged and may develop thrombosis and the arteries on the surface of the brain may also develop thrombosis leading to infarcts. (From Fuller GN, BouldinTW. The nervous system. In: Rubin R, Strayer DS, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams & Wilkins; 2012:1318.)