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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