Page 184 - AIDSBK23C

Page 184

Patients VSV vasculitis tend to present with deep, subcortical ischemic stroke and
vasculopathy affecting large and small arteries. Cerebrospinal fluid analysis shows pleocytosis
and high protein with normal glucose. VZV can affect small arteries in the CNS, accounting for
small subcortical strokes. Necrotizing vasculitis affecting small arteries such as vasa vasorum
can be associated with VZV infection with subsequent affection of large size arteries due to
ischemia and disruption of the vessel wall.[786]

MYCOBACTERIOSIS.-- Mycobacterial infections of the CNS in patients with AIDS are
uncommon. The diagnosis may be made by culture of cerebrospinal fluid or by acid fast staining
of tissue obtained by biopsy or autopsy. Lesions seen with CNS tuberculosis include: small
tuberculomas, abscesses, communicating hydrocephalus, and infarction. Most patients will have
concomitant pulmonary tuberculosis. Radiographic findings include supratentorial lesions at the
corticomedullary junction, meningeal enhancement, and target lesions with tuberculoma
characterized by ring-enhancement around a central area of enhancement or calcification, as seen
with CT or MR imaging. Tuberculous meningitis produces an exudate most prominent in basal
cisterns, which obscures the basal cisterns on unenhanced CT images, while diffuse enhancement
of these areas is seen with contrast-enhanced CT imaging. MR imaging is more sensitive for
detection of nodular enhancement of leptomeninges. Meningeal tuberculosis can be complicated
by obstructive hydrocephalus.[752,759]
Meningeal tuberculosis may manifest clinically with headache, vomiting, meningeal
signs, focal deficits, vision loss, cranial nerve palsies (typically the abducens), and raised
intracranial pressure. HIV-infected persons with tuberculous meningitis with higher CD4 cell
counts tend to have these findings but when the CD4 lymphocyte count is low then the
presentation can be subtle and atypical. Cerebral vascular involvement leads to inflammation
with vasospasm, thrombosis, and infarction of internal capsule, basal ganglia, and thalamus.
Tuberculous radiculomyelopathy is manifested as subacute paraparesis.[787]
M. tuberculosis reaching the brain hematogenously crosses the blood–brain barrier,
infects microglial cells, and leads to formation of small granulomas in the meninges and adjacent
brain parenchyma that may remain dormant for months to years. Tuberculous meningitis
develops when a caseating granuloma ruptures into the subarachnoid space with an intense
immune response and exudate formation. Tuberculous exudates may be less pronounced in
associate with HIV infection with diminished numbers of lymphocytes, epithelioid macrophages,
and Langhans giant cells but more numerous acid-fast bacilli. Diagnosis is made by finding M.
tuberculosis bacilli in the cerebrospinal fluid. The lipoarabinomannan antigen-detection test in
serum or cerebrospinal fluid is a rapid assay to assist in diagnosis.[787]
Mycobacterium avium complex (MAC) in the CNS is uncommon and is usually an
incidental finding at autopsy in patients who had disseminated MAC. No gross pathologic
findings are typically present, but histologically there can be small foci containing lymphocytes
and macrophages in a predominantly perivascular location. Clinical findings may suggest a
meningitis and/or encephalitis.[788]
Tuberculous brain abscess may produce intracerebral masses in patients with HIV
infection. Anergy is likely to cause a false negative tuberculin skin test. However, most patients
will have a prior history of extra-cerebral tuberculosis with chest radiographic abnormalities.
The CD4 lymphocyte count may be above 200/µL. Cerebral CT imaging will usually
demonstrate more than one intracranial mass lesion.[789] Tuberculous abscesses are usually
multiloculated; they are indistinguishable from pyogenic abscesses.[759]