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CNS penetration.
C. Myelopathy
1. HIV-related spinal cord involvement is uncommon. It presents as
spastic paraparesis with bowel and bladder dysfunction, gait ataxia,
and variable sensory loss, usually in the context of advanced
immunodeficiency.
2. Diagnosis must exclude cord-compression lesions (eg, lymphoma,
epidural abscess), vitamin B12 deficiency, and other viral infections
(eg, human T-cell lymphotropic virus type I, varicella-zoster virus,
cytomegalovirus).
3. Myelopathy may respond to highly active antiretroviral therapy. Addi
tional treatment should be directed at ameliorating symptoms.
D. Distal symmetric polyneuropathy
1. Distal sensory polyneuropathy may develop as a consequence of HIV
infection, but it is more commonly associated with use of antiretroviral
agents, specifically zalcitabine (HIVID), didanosine (Videx), and
stavudine (Zerit).It tends to occur with advanced infection. Symptoms
typically consists of distal paresthesias, with burning sensations and
numbness of fingertips and toes, that progress proximally.
2. Physical examination reveals diminished ankle reflexes and
decreased sensation to pinprick, light touch, and vibration. Nerve
conduction tests demonstrating axonal neuropathy can confirm the
diagnosis. The possibility of vitamin B12 deficiency should be
Neurologic Manifestations of HIV Infection 47
excluded.
3. Management consists of dose reduction or discontinuation of any
potentially offending agents. Symptomatic treatment with tricyclic
antidepressants, anticonvulsants (eg, carbamazepine, gabapentin
[Neurontin]), lidocaine 30% cream, and narcotic analgesics may be
effective.
II. Infectious processes
A. Cerebral toxoplasmosis
1. Cerebral toxoplasmosis occurs as a consequence of reactivation,
developing in about 2% to 10% of patients with HIV infection and prior
toxoplasma infection (identified by positive IgG titers). Most cases
occur when the CD4+ T-lymphocyte count is less than 100 cells/µL.
2. Clinical manifestations include headache, confusion, fever, focal
neurologic deficits, and seizures. CT and MRI reveal lesions with ring
enhancement. Lesions are often multiple with associated mass effect
involving the frontal and parietal lobes and basal ganglia.
Characteristic CT or MRI findings and positive serologic results are
indications for empirical therapy. Definitive diagnosis is by brain
biopsy.
3. Treatment regimens consisting of sulfadiazine or of clindamycin
(Cleocin) plus pyrimethamine (Daraprim) for 6 weeks have been
equally effective. Clinical improvement is usually seen in 10 to 14
days. Lifetime suppressive therapy is recommended.
4. Patients at risk for toxoplasmosis (CD4+ count less than 100 cells/µL
and positive serology) should be offered primary prophylaxis with
trimethoprim-sulfamethoxazole (Bactrim, Septra) or dapsone plus
pyrimethamine.
B. Cryptococcal meningitis
1. Cryptococcus neoformans can cause fungal meningitis in the
presence of HIV infection, usually in patients with a CD4+ count less
than 100 cells/µL. The organism disseminates widely, with predilection
for the CNS.
2. Headache and fever are the most common presenting symptoms;
others include nausea and vomiting, photophobia, blurred vision, stiff
neck, skin lesions, altered mentation, and seizures.
3. CSF culture confirms the diagnosis. India ink preparations of CSF and
cryptococcal antigen testing of serum and CSF are usually positive.
Blood cultures are positive in only about one fourth of cases.
Neuroimaging may reveal cryptococcomas, hydrocephalus, and
cerebral edema. The mortality rate of cryptococcal meningitis is 10%
to 20%.
4. Antifungal treatment regimens include either amphotericin B
(Fungizone) and flucytosine (Ancobon) or amphotericin B alone for 2
weeks, followed by daily fluconazole (Diflucan).
5. Elevated intracranial pressure should be aggressively managed with
CSF drainage by lumbar puncture, ventriculoperitoneal shunting, and
acetazolamide (Diamox). Long-term suppression with fluconazole is
recommended to avoid recurrence.
C. Progressive multifocal leukoencephalopathy
1. Reactivation of latent JC virus results in progressive multifocal
leukoencephalopathy. This condition usually occurs when CD4+
counts are less than 100 cells/µL. Clinical features are subacute in
onset and include limb weakness, impairment of cognitive function,
48 Neurologic Manifestations of HIV Infection
gait disturbance, incoordination, speech and visual disturbances,
headache, and seizures.
2. CT typically shows hypodense white-matter lesions, usually
parietooccipital, with no enhancement or mass effect. MRI may more
clearly show lesions.
3. A positive CSF polymerase chain reaction for JC virus is diagnostic;
however, a negative result cannot exclude the diagnosis. The
prognosis of progressive multifocal leukoencephalopathy is poor.
Remission with potent antiretroviral therapy may occur.
D. CMV encephalitis
1. In patients with a CD4+ T-lymphocyte count less than 100 cells/µL,
CMV disease develops within 2 years in 21.4%. The usual
presentation consists of retinitis and esophagitis, with or without
colitis; pneumonitis, hepatitis, encephalitis, and polyradiculopathy also
may occur.
2. Clinical features of encephalitis include rapidly progressive confusion,
delirium, apathy, and focal neurologic deficits. CT may reveal diffuse
low-attenuation areas. MRI reveals high signal intensity lesions on T2
weighted images. Periventricular enhancement and edema are
characteristic. CSF yields nonspecific findings.
3. Polyradiculopathy
manifests
as
lower
extremity
weakness,
paresthesias, and bladder and bowel dysfunction. Saddle pain and
urinary retention are common. Elevated protein level and
polymorphonuclear pleocytosis are noted on CSF analysis. Detection
of CMV DNA on CSF polymerase chain reaction testing is diagnostic.
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