Central Nervous System Infections
The cerebrum, cerebellum, brainstem, spinal cord, and their covering membranes(meninges) constitute the central nervous system (CNS). Because of the unique anatomic and physiologic features of the CNS, infections of this site can represent special chal-lenges to the microbiologist and clinician. The CNS is encased in a rigid, bony vault, and it is highly vulnerable to the effects of inflammation and edema: its critical life-regulatory functions and the metabolic requirements to sustain these functions can also be easily dis-rupted by infection, with resultant local acidosis, hypoxia, and destruction of nerve cells. Thus, the effects of increased pressure, biochemical abnormalities, and tissue necrosis can be profound and sometimes irreversible. One specialized defense mechanism of the CNS is the blood–brain barrier, which serves to minimize passage of infectious agents and potentially toxic metabolites into the cerebrospinal fluid (CSF) and tissues, as well as to regulate the rate of transport of plasma proteins, glucose, and electrolytes. When CNS infection develops, however, this barrier also poses difficulties in control; some antimi-crobial agents and host immune factors, such as immunoglobulins and complement, do not pass as readily from the blood to the site of infection as they do to other tissues.
Within the brain are the ventricles, which are cavities in which CSF is actively pro-duced, primarily by specialized structures called the choroid plexuses. The CSF fills the lateral ventricles in each half of the brain, circulates into a central third ventricle, and then passes through the cerebral aqueduct to emerge through foramina at the brainstem. From cisterns at the base of the brain, the CSF circulates in the subarachnoid space over the en-tire CNS, including the spinal cord, to supply nutrients and serve as a hydraulic cushion for these tissues. It is reabsorbed primarily by the major venous system in the meninges. Obstruction of the normal flow of CSF in either the internal (ventricular) or external (sub-arachnoid) systems can result in increased intracranial pressure, because production of CSF by the choroid plexuses will continue within the ventricles. Such impairment of flow or normal reabsorption can occur as a result of inflammation or subsequent fibrosis, lead-ing to dilatation of the ventricles, compression of brain tissue, and a condition known as hydrocephalus.
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