A severe multifocal neuropathy caused by cytomegalovirus (CMV-MN) can
occur in the late stage of human immunodeficiency virus (HIV) infectio
n. In a retrospective study, we identified 15 consecutive HIV-positive
patients with a diagnosis of CMV-MN based on (1) markedly asymmetric
neuropathy, (2) fewer than 100 CD4(+) cells per mm(3), (3) exclusion o
f other causes of neuropathy, and (4) characteristic CMV cytopathic ch
anges on neuromuscular biopsy (2 patients), positive CSF culture for C
MV (2 patients), or clinical improvement on anti-CMV therapy given for
concurrent extraneurologic CMV disease (8 patients) or neuropathy (3
patients). All patients were men and had severe immunosuppression (mea
n CD4(+) cell count, 18 per mm(3)). The initial symptoms were numbness
and painful paresthesias showing a patchy, multifocal distribution. A
fter a mean of 11 weeks (range, 1 to 10 months), the patients develope
d moderate or severe sensorimotor asymmetric neuropathy. Extraneurolog
ic CMV infection occurred in 10 patients before diagnosis. Electrophys
iologic studies showed axonal neuropathy and CMV DNA was present in CS
F by the polymerase chain reaction (PCR) technique in 90% of patients
tested. Fourteen patients showed a marked improvement I to 4 weeks aft
er starting ganciclovir or foscarnet therapy. During follow-up on main
tenance therapy (13 patients), the neuropathy relapsed in three patien
ts and probable or confirmed CMV encephalitis occurred in five. Twelve
patients died during follow-up, at a mean interval of 9.5 months afte
r their first symptoms. These results extend the clinical spectrum of
CMV-MN and show that PCR detection of CMV DNA in CSF may be a useful d
iagnostic marker.