Chapter 22 The Central Nervous System
Gliosis is the most common reaction of the CNS to injury. It presents in the form of hypertrophy and hyperplasia of fibrillary astrocytes, some of which acquire abundant cytoplasm and transform into so called gemistocytes. Cytoplasmic extensions of these astrocytes form a dense meshwork of “glial fibrils,” which results in the formation of the so-called glial scar. Glial scars differ from scars in other organs in that they are devoid of collagen.
Microglia cells are bone-marrow-derived macrophages that accumulate at the site of CNS injury, forming glial nodules. Activated microglial cells show nuclear elongation resulting in rod cells. Microglia cells take part in phagocytosis of dying neurons, a process known as neuronophagia.
Herniations (Fig. 22-1) occur as a result of increased intracranial volume. Most often, they accompany space-occupying lesions, such as tumors, hematomas, or abscesses, but they may also be caused by trauma. The displacement of parts of the brain is morphologically most evident at three herniation sites:
Epidural hemorrhage results from bone fractures at the base of the skull that tear the middle meningeal artery. Arterial bleeding leads to the formation of a hematoma in the virtual space between the inner aspect of the cranial bones and the dura mater. Hematoma that forms under arterial pressure grows progressively, and without proper surgical intervention, it is invariably fatal within several hours after injury.
Subdural hemorrhage stems from traumatically severed “bridging veins” that connect superficial cerebral veins and the dural venous sinuses. This venous bleeding may stop on its own as soon as the pressure outside the veins exceeds the pressure inside the vascular lumen. However, as the blood clots and the external pressure on the bridging veins decreases, bleeding may resume even after minor cranial trauma. Subdural hematomas are typically found following repeated traumatic head injuries, as in:
Arteriovenous malformations (AVMs) result from defective formation of capillaries in a normal part of the brain. The arterial blood thus enters directly into the veins, usually by way of arteriovenous anastomoses that form at the defective site. Typical AVMs consist of tortuous arteries and veins that form cortical–subcortical networks of “wormlike” arteriovenous shunts embedded in hemosiderin–laden glial tissue. AVMs have a high blood flow, often pulsate, and may be a source of mixed parenchymal/subarachnoidal bleeding and seizures.
17 List the most important causes of nontraumatic intracerebral hemorrhage (i.e., hemorrhagic strokes)
The infection can be caused by a variety of microorganisms. Streptococcus pneumoniae has become the most common cause because immunization has eliminated many other causes such as Hemophilus influenzae. In neonates it is most commonly caused by Escherichia coli and group B streptococci. Among children and young adults, an important cause is Neisseria meningitidis (meningococcus), which may cause miniepidemics among army recruits or in student camps. Gram-negative bacteria (E. coli, Klebsiella, and Enterobacter) cause meningitis in immunosuppressed people following brain trauma or brain surgery.
Acute meningitis caused by bacteria resistant to treatment may become chronic, but even in this circumstance, the exudate remains purulent. This prolonged purulent meningitis must be distinguished clinically and for treatment purposes from chronic meningitis caused by pathogens that typically cause chronic diseases. Such chronic meningitis typically has an insidious onset and may last weeks or months. Chronic meningitis may be a feature of:
The pathologic findings in various forms of chronic meningitis vary depending on the causative pathogen. The infection is usually more circumscribed than in acute meningitis and may be localized to parts of the brain. For example, tuberculous meningitis typically involves the basal cisterns and the lateral sulci that contain gelatinous whitish gray material. Histologically, these lesions contain caseating granulomas. In secondary and tertiary syphilis, the meninges show focal irregular thickening. These changes are most prominent around the spinal cord but may be seen over the convexity of the brain or over the cerebellum. Histologically, thickened meninges contain infiltrates of lymphocytes and plasma cells, typically arranged around the meningeal blood vessels. Tertiary syphilis may also present in the form of a granulomatous inflammation (gumma of syphilis).
Viral meningitis (also known as aseptic meningitis) may occur as part of a systemic viral disease (e.g., varicella, mumps, and measles), or it may be limited to the CNS. The latter may be sporadic (e.g., herpes virus infection) or epidemic (e.g., arboviruses transmitted by arthropods such as eastern or western equine encephalitis), and is often associated with encephalitis (i.e, meningoencephalitis).
Tabes dorsalis (Fig. 22-2) is a manifestation of tertiary syphilis involving the lumbar spinal cord. Syphilitic meningitis leads to fibrosis, compressing the posterior nerve roots. In normal circumstances, these afferent nerves, originating from the spinal ganglia, form the posterior columns in the spinal cord, and transmit proprioceptive and sensory impulses. Wallerian degeneration that results from the injury of axons entering the spinal cord results in posterior columns. Clinically, these patients experience loss of vibration and proprioception, which affects their gait. Joint degeneration resulting in deformities (Charcot joints) is commonly found.