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involvement. Wallerian degeneration does not result from vacuolar myelopathy. The degree of
gliosis does not correlate with the severity or duration of disease.[770] This myelopathy is not
characteristic of pediatric cases, but decreased corticospinal tract axons and myelin does occur in
children.[771] T2-weighted MRI scans of the cord show bilateral, symmetrical regions of high
signal intensity in the posterior columns, especially in the gracile tracts.[772] Opportunistic
infections of the spinal cord are uncommon.

OPPORTUNISTIC INFECTIONS AND NEOPLASMS.-- Toxoplasmosis, malignant
lymphomas, cryptococcosis, and cytomegalovirus are the most commonly identified
opportunistic infections and neoplasms in the CNS in patients with AIDS (Table 5).[417]
Clinical use of Indium-111 WBC scintigraphy may aid in the detection of CNS inflammatory
changes before either computerized tomography (CT) or magnetic resonance imaging (MRI)
show structural changes.[657] A syndrome of inappropriate antidiuretic hormone (SIADH) may
occur with central nervous system lesions.[773]

CYTOMEGALOVIRUS (CMV).—The prevalence of CMV in AIDS patients at autopsy
has been declining from use of prophylaxis and therapy for CMV lesions outside the CNS, so
that about 10% of cases show evidence of CMV.[758] There are no specific clinical findings
seen with CMV in the brain. Nonspecific findings of disorientation, confusion, cognitive
dysfunction, focal neurologic deficits, and impaired memory may be present, but these findings
are similar to those of HIV dementia. Half of AIDS patients with CMV involving the CNS have
no neurologic problems. There is usually widespread dissemination of CMV when the CNS is
involved, though isolated CMV infection of the CNS is also possible. Concomitant CMV
retinitis may provide a clue to diagnosis. The abrupt onset of mental status changes, along with
radiologic findings of hydrocephalus and periventricular or meningeal enhancement, may also
suggest CMV meningoencephalitis.[746, 774]
Examination of cerebrospinal fluid (CSF) may reveal increased protein and a mild
lymphocytic pleocytosis. Cells with inclusions are generally not seen in the CSF. There is a
poor correlation between the appearance and degree of neurologic problems and the pathologic
findings with CMV infection of brain. The most common pattern of involvement is an
encephalitis, which tends to be progressive with advancement in the course of AIDS. Grossly,
there are no specific lesions to be seen.[774]
Radiographic studies of CMV infection in the CNS are nonspecific and in many cases do
not reveal any abnormality. Radiographic imaging with CT may show diffuse white matter
hypodensities, ependymal enhancement, and focal ring enhancing or nodular-enhancing lesions.
MR imaging is more sensitive for detection of lesions of CMV infection and may include
findings of increased signal with T2 weighting, particularly in periventricular regions. Necrotic
ventriculitis may cause periventricular subependymal enhancement around the lateral ventricles,
septum pellucidum, corpus callosum, and fornices, or demyelination may result in diffuse white
matter abnormalities. Additional MR imaging findings can include ring- or nodular-enhancing
lesions after gadolinium administration, or ependymal enhancement. Spinal cord and spinal
nerve root involvement leads to diffuse enhancement of the cord parenchyma, nerve roots and
meninges with contrast-enhanced MRI.[738,759]
Microscopically, CMV can be the cause for a meningoencephalomyelitis. The most
common locations for lesions are brainstem (pons or medulla most often), periventricular, basal
ganglia, cerebrum (with cortex and white matter equally involved) and cerebellum. Lesions may