93
NEUROIMAGING
Neuroimaging in the Brain
in HIV-1–Infected Patients
a,
Majda M. Thurnher, MD *, M. Judith Donovan Post,
- HIV-associated central nervous system
abnormalities
- Opportunistic infections
Viral infections
Bacterial infections
As the HIVAIDS epidemic approaches the 20th
anniversary of the first mysterious reports of people
with the syndrome, researchers and clinicians con-
tinue to grapple with the complexities of the virus.
An estimated 36 million people worldwide are cur-
rently living with HIV, and some 20 million people
have already died. If the number of new infections
continues at the current rate, even the most devas-
tating impact that can be anticipated from current
levels of infection may seem minor compared
with that of the future.
HIV enters the central nervous system (CNS)
early in the course of infection, and the virus resides
primarily at the cellular level in microglia and mac-
rophages. Cerebrospinal fluid (CSF) analysis has
demonstrated that HIV can enter the CNS soon
after exposure, even before antibodies are detect-
able in the blood. HIV has been detected in the
brain as early as 15 days after accidental intravenous
inoculation [1]. More than a decade ago, it became
clear that the neuron dysfunction or death that un-
derlies the clinical symptoms of HIV CNS disease
could not result from direct infections of neurons.
The mechanism of HIV-related brain injury remains
a
Section of Neuroradiology, Department of Radiology, Medical University of Vienna, Waehringer Guertel
18–20, 1090 Vienna, Austria
b
Section of Neuroradiology, Department of Radiology, University of Miami L. Miller School of Medicine,
1611 NW 12th Avenue, Miami, FL 33136, USA
* Corresponding author.
E-mail address: majda.thurnher@meduniwien.ac.at (M.M. Thurnher).
1052-5149/08/$ – see front matter ª 2008 Elsevier Inc. All rights reserved.
neuroimaging.theclinics.com
CLINICS
OF NORTH AMERICA
Neuroimag Clin N Am 18 (2008) 93–117
b
MD
Fungal infections
Parasitic infections
- Neoplastic lesions
Lymphoma
- References
poorly understood, however. The predominant
pathogenesis is believed to involve the combined
influence of HIV infection and the activation of im-
mune-competent cells and their subsequent release
of toxins, which leads to neuronal and astrocytic
dysfunction [2].
The brain may be affected by a variety of
abnormalities in association with HIV infection.
Knowledge of these abnormalities and their charac-
teristic imaging features is important to neuroradi-
ologists for the detection, diagnosis, and initiation
of appropriate treatment. Nowadays, patients who
have AIDS form a considerable part of routine neu-
roradiologic work. The imaging modalities com-
monly used in patients who have HIV or AIDS are
CT and MR imaging. In addition, nuclear medicine
techniques, such as single-photon emission com-
puted tomography (SPECT) and positron emission
tomography (PET), are helpful. The spectrum of
CNS abnormalities can be divided into three
main categories: (1) HIV-associated lesions, (2) op-
portunistic infections, and (3) neoplasms.
This review attempts to describe the
imaging findings associated with brain disorders
doi:10.1016/j.nic.2007.12.013
94 Thurnher & Donovan Post

in HIV-seropositive patients and the rationales for

integrating neuroradiologic techniques.

HIV-associated central nervous system

abnormalities
Like all viruses, HIV is a parasite that replicates
within the living cells of the host. HIV infection of
the CNS produces a range of cognitive, motor, and
behavioral abnormalities [3–6]. The syndrome ob-
served after infection with HIV has been designated
as HIV-associated dementia (HAD) [2]. The preva-
lence of HAD was estimated in the early 1990s to
be as high as 20% to 30% in those patients who
have advanced HIV disease and low CD4 cell counts.
HAD is now probably the most common cause of
dementia worldwide among people aged 40 years
or younger. With the advent of potent combination
antiretroviral therapy (highly active antiretroviral
therapy [HAART]), the incidence of HAD has de-
creased to as low as 10.5% [7]. Although the inci-
dence of HAD seems to be declining, the
prevalence of milder yet debilitating neuropsycho-
logic impairments may increase as individuals
infected with HIV live longer. These findings support
the hypothesis that HAART does not provide com-
plete protection from the development of HAD.
The histopathologic marker of the HIV-infected
brain is the presence of multinucleated giant cells
(MGCs). Two neuropathologic correlates of cere-
bral infection by HIV include multinucleated giant
cell encephalitis (MGCE) and progressive diffuse
leukoencephalopathy (PDL) [8,9]. MGCE and
PDL may be end points, with a morphologic spec-
trum of HIV-induced changes in between.
The most common reported imaging finding is
cerebral atrophy (Fig. 1). The predominant pattern
of atrophy may be central (ventricular dilatation),
peripheral (sulcal dilatation), or mixed (central
and peripheral) [10–16]. Levy and colleagues [14]
reported in their early CT study of 200 patients
who had AIDS that 37.5% of the patients presented
with cerebral atrophy. Serial CT studies have dem-
onstrated progression of the atrophy over time in
patients who have HAD. Jacobsen and colleagues
[17] reported cortical atrophy in one third of 400
patients who had AIDS with neurologic manifesta-
tions. Studies with symptomatic patients showed
cortical atrophy in 85% of patients, which suggests
that cortical atrophy may be relatively specific to pa-
tients who have neuropsychologic impairment. Ayl-
ward and colleagues [18] found an association
between HAD and specific gray matter volume re-
duction in the basal ganglia and posterior cortex
and with generalized volume reduction of white
matter. The total CSF volumes were significantly
greater for HIV-positive patients who had HAD
Fig. 1. HIV leukoencephalopathy in an HIV-positive
patient presenting with dementia. Precontrast axial
CT scan shows bilateral hypodensity of the white
matter with dilatation of the ventricular system.
than for HIV-positive patients who did not have
dementia.
White matter lesions are the second most com-
mon MR imaging finding in patients who have
HAD (Fig. 2). The average frequency of white mat-
ter lesions in patients who have AIDS is 78%, with
a range of 43% to 100% [11]. A review of the MR
imaging scans of 365 patients who had AIDS
revealed signal abnormalities in the white matter
in 31% of patients [19], with four patterns
observed: diffuse, patchy, focal, and punctate.
The white matter lesions demonstrate high signal
on T2-weighted MR imaging sequences and usu-
ally are isointense or minimally hypointense on
T1-weighted MR imaging sequences. Enhancement
and mass effect are not present. Two distinct MR
imaging patterns on T2-weighted imaging were
observed, which allows a distinction between the
two types of HAD: (1) diffuse, bilateral, and sym-
metric high signal intensity involvement of the
white matter (butterfly-like; see Fig. 1) and (2)
bilateral, scattering, high signal intensity lesions
in the white and gray matter (patchy, see Fig. 2)
[19]. The appearance of MR imaging scans most
likely reflects an increase in water content and
the leakage of serum proteins resulting from
altered vascular permeability, possibly related to
the presence of circulating cytokines. Prospective
studies with long-term follow-up comparing
 Neuroimaging in the Brain in HIV-1–Infected Patients 95

Fig. 2. HIV leukoencephalopathy. (A–C) Fluid-attenuated inversion recovery (FLAIR) (repetition time [TR]/echo
time [TE]/time after inversion pulse [TI] 5 10,000/130/2100 milliseconds) axial MR imaging scan shows high signal
intensity abnormalities without mass effect in the white matter bilaterally. Note sparing of the subcortical fibers
and dilatation of the ventricles, indicating associated atrophy. The lesions are isointense to hypointense on T1-
weighted MR imaging and show no enhancement on postcontrast images (not shown).

asymptomatic with symptomatic patients have
shown that the percentage of white matter abnor-
malities significantly increases with disease pro-
gression [20–22].
Although MR imaging is the most sensitive im-
aging modality for depicting the effects of HIV in
the brain, it is nevertheless not sensitive enough
to show early pathologic involvement. Several in-
vestigators have claimed that neuroimaging studies
are relatively insensitive in the detection of early
changes in the brain attributable to HIV infection.
Compared with the postmortem studies, MR imag-
ing underestimated the presence of HIV-related
lesions in the brain [23]. Fluid-attenuated inver-
sion recovery (FLAIR) techniques have been shown
to improve conspicuity of the lesions in the peri-
ventricular and subcortical locations significantly
[24].
96 Thurnher & Donovan Post
The data from recent studies suggest that proton
(1H) magnetic resonance spectroscopy (MRS)
could potentially be more sensitive in detecting
early CNS involvement by HIV than MR imaging
[25–37]. Results of recent studies have shown that
the metabolite pattern in patients who have HAD
indicates decreased N-acetylaspartate (NAA) and el-
evated choline (Cho) and myoinositol (MI) levels
that are not observed in healthy subjects (Fig. 3)
(lower NAA/creatine [Cr] ratio, increased Cho/Cr
ratio, and increased MI/Cr ratio) [25–34,37]. The
findings indicate that diffuse brain involvement in
AIDS can be marked not only by a loss of neurons,
as indicated by increased NAA levels, but by
increased MI levels. Chang and colleagues [27] re-
cently reported an increased Cho/Cr ratio in the
frontal white matter and in the basal ganglia and
an elevated MI/Cr ratio and MI concentrations in
the basal ganglia.
Perfusion MR imaging can also detect abnormal-
ities that correlate with disease severity in HAD
(Fig. 4). Chang and colleagues [27] evaluated the
regional cerebral blood flow (rCBF) in 19 patients
who had early stages of HAD and correlated the
results with 15 healthy seronegative subjects. The
Fig. 3. MRS in a symptomatic HIV-positive patient. The
findings of MR imaging were normal. The proton
spectrum (point-resolved spectroscopy [PRESS]; echo
time [TE] 5 23 milliseconds, repetition time [TR] 5
6365 milliseconds) from the voxel outlined from the
frontal white matter shows slightly decreased NAA
and increased MI, which are findings that are consis-
tent with the early stage of HIV encephalitis. Cr,
creatine.
patients who had HAD had a statistically significant
decrease of rCBF bilaterally in the inferior lateral
frontal cortices and an increase in the posterior in-
ferior parietal white matter. Because pMR imaging
is faster and safer than nuclear medicine tech-
niques, these investigators suggested that pMR im-
aging can be used to monitor rCBF changes in
patients who have HIV initially and during therapy.
Diffusion tensor imaging (DTI) is another prom-
ising MR imaging technique with the possibility to
measure tissue anisotropy, thus providing details
on tissue microstructure [38,39]. Calculating the
diffusion constant and anisotropy in the subcortical
white matter and corpus callosum in patients who
had HIV, Filippi and colleagues [40] recently found
abnormalities despite normal-appearing white mat-
ter on conventional MR imaging. Patients who had
advanced HIV disease (high viral load) had the
highest diffusion constant elevations and largest an-
isotropy decreases. The diffusion changes observed
in the study of Filippi and colleagues [40] may be
a result of activation of inflammatory pathways in
HIV infection of the brain. In another study with
60 HIV-positive patients, a statistically significant
decrease of fractional anisotrpy (FA) was found in
the genu of the corpus callosum in patients who
had HIV compared with controls. FA was reduced
in the frontal white matter and hippocampi in pa-
tients who had HIV compared with controls. Differ-
ences were not statistically significant, however [41].
In addition, DTI did not correlate well with virologic
and immunologic parameters in that particular
study. It seems that FA and apparent diffusion coef-
ficient (ADC) measurements are not sufficient in
identifying patients who have early HIV infection.
An increased knowledge of the pathogenesis of
HIV, the development of sensitive measurements
for such viral parameters as viral load determi-
nations, and the availability of new classes of anti-
retroviral drugs have profoundly improved the
therapeutic management of HIV infection [42–44].
The results of several recent studies [45–48] suggest
that MR imaging and MRS may help in the clinical
management of patients who have HAD and are
receiving potent antiretroviral therapy and can be
used to characterize changes attributable to HAART.
A combination of antiretroviral drugs in patients
who have HAD may result in stabilization or even re-
gression of white matter signal intensity abnormali-
ties observed on MR imaging (Fig. 5) [47,48]. The
progression of white matter lesions on initial fol-
low-up studies should not be mistaken for therapy
failure, because the progression of MR imaging find-
ings is likely the result of postinflammatory reac-
tions attributable to immune reconstitutive effects
after the initiation of HAART [46,48]. Some other
observations could also be important in
 Neuroimaging in the Brain in HIV-1–Infected Patients 97

Fig. 4. Perfusion MR imaging in a patient who had AIDS with AIDS-dementia complex. Perfusion MR imaging
(T2*echo planar imaging [EPI] time-to-peak [std.TTP]) demonstrates delayed std.TTP in the white matter
bilaterally, indicating disturbance of the periventricular microcirculation. Axial FLAIR MR imaging showed no
abnormality (not shown).

understanding the discrepancies between the evolu-
tion of MR imaging findings and cognitive function
in patients who have HAD and are receiving HAART.
The progression of cerebral atrophy was observed in
all patients who had HAD and underwent HAART in
one study, suggesting that despite potent therapy, the
neuronal damage seems to progress without clinical
manifestations [48].
Opportunistic infections
Viral infections
Cytomegalovirus
Cytomegalovirus (CMV) is a member of the herpes-
virus family; in adults, the infection is a result of the
reactivation of a latent infection, most commonly
presenting as mild infection mimicking mononu-
cleosis. In immunocompromised patients, CMV
can produce a variety of clinical syndromes. CMV
infections have been described with increasing fre-
quency in patients who have AIDS [49,50]. Five dis-
tinct neurologic syndromes attributable to the CMV
infection have been described: retinitis, myelitis
or polyradiculopathy, diffuse micronodular en-
cephalitis, ventriculoencephalitis, and mononeuri-
tis multiplex.
Diffuse micronodular encephalitis resembles HIV
encephalitis histologically. Small microglial nodules
and inclusion-bearing cytomegalic cells are widely
distributed in the cortex, basal ganglia, brain stem,
and cerebellum. In an autopsy series of 30 cases of
CMV encephalitis, 76% of the patients had micro-
glial nodules containing inclusion-bearing cells
and 24% had CMV inclusions outside the nodules
[49]. A distinct clinical syndrome of dementia asso-
ciated with CMV has been described and compared
with HAD [51]. Those two dementia syndromes dif-
fer in clinical presentation, course, associated elec-
trolyte disturbances, and imaging findings. The
most common imaging findings in patients who
have CMV encephalitis are cortical atrophy, periven-
tricular enhancement, and diffuse white matter ab-
normalities [52,53]. Generalized atrophy is the
most commonly reported CT abnormality, but it is
a nonspecific finding seen frequently in patients
who have AIDS [53]. Periventricular enhancement
is also not diagnostic, but it has been described in
cases of lymphoma, toxoplasmosis, and other infec-
tions. White matter disease occurs as a result of in-
flammation of the subependymal region and
spread of the infection to the adjacent astrocytes of
the white matter with infectious demyelination
[54,55]. In six patients who had pathologically
98 Thurnher & Donovan Post

Fig. 5. HIV encephalitis is being treated with HAART. (A) Axial FLAIR-turbo spin echo (TSE) (repetition time [TR]/
echo time [TE]/time after inversion pulse [TI] 5 7385/130/2100 milliseconds) MR imaging shows bilateral, sym-
metric, high signal intensity abnormalities in the periventricular white matter and white matter of the centrum
semiovale. Additional widening of the sulci and ventricle is present. The patient had a high viral load level in
plasma and in the CSF and a low CD41 T-lymphocyte count. Results of the neuropsychologic examination
were consistent with subcortical dementia. The diagnosis of HIV leukoencephalopathy was made, and combina-
tion antiretroviral therapy was started. (B) Nine months after the initiation of therapy, follow-up FLAIR TSE (TR/
TE/TI 5 7385/130/2100 milliseconds) MR imaging shows progression of the white matter signal intensity abnor-
malities. (C) At 18 months after the initiation of HAART, follow-up MR imaging shows interval decrease of the
white matter signal intensity abnormalities. (D) At 26 months after the initiation of the therapy, follow-up MR
imaging shows regression of the white matter disease (not seen), and stabilization is seen after 33 months.

confirmed CMV infection of the CNS, Hassine and
colleagues [52] found atrophy in three cases, sube-
pendymal nodular lesions without enhancement
in two cases, and ventriculitis in one case.
Patients who have ventriculoencephalitis have
a more acute onset, with death usually occurring
quickly. Autopsy reveals periventriculitis, ependy-
mal and subependymal necrosis, and associated in-
clusion-bearing CMV cells [56,57].
Rarely, cerebral mass lesions attributable to CMV
could be observed in patients who had AIDS. In
one study, two cases of cerebral mass lesions attrib-
utable to CMV were described [58]. In both cases,
a large contrast-enhancing mass was seen in the
frontal lobe with surrounding edema. Both patients
described in the study died despite treatment. CMV
should be considered in the differential diagnosis
of mass lesions in patients who have AIDS with se-
vere immune deficiency.
CMV infection can also be present as choroid
plexitis. In one reported case, a contrast-enhanced
CT scan showed marked enhancement of the
slightly enlarged right plexus. MR imaging con-
firmed the findings and the absence of enhance-
ment of ependyma [59]. Infections of the choroid
plexus are not common; nevertheless, CMV should
be included in the causes of choroid plexitis in pa-
tients who have AIDS.
Infection of the CNS is difficult to diagnose while
the patient is alive because CMV is difficult to
 Neuroimaging in the Brain in HIV-1–Infected Patients 99

culture from CSF. The recent development of the Bacterial infections

polymerase chain reaction technique has allowed
isolation of CMV based on the presence of DNA
within the CSF [60]. The discrimination between
HIV and CMV-associated CNS disease is often diffi-
cult using clinical and imaging findings. MRS could
be potentially useful in such cases. In one study,
MRS was used to distinguish HIV encephalitis
from CMV encephalitis [61]. These findings suggest
that a larger Cho signal and a smaller NAA signal
could be inferred within the white matter abnor-
malities attributable to HIV encephalitis or enceph-
alopathy compared with CMV encephalitis.
Mycobacteria
The increased incidence of tuberculosis in devel-
oped countries is clearly related to the increase in
AIDS. At present, approximately 30% of patients
who have tuberculosis are HIV-positive; conversely,
5% to 9% of patients who have AIDS develop tuber-
culosis [62]. Currently, AIDS is considered the main
risk factor for the development of tuberculosis [63].
It is known that clinical manifestations, manage-
ment, and epidemiology are altered in patients
who have AIDS [64]. HIV-positive patients may
develop active tuberculosis by two different

Fig. 6. Tuberculous osteomyelitis and meningitis in a patient who had AIDS. (A) Coronal short tau inversion re-
covery (STIR) turbo spin echo (TSE) (repetition time [TR]/echo time [TE]/time after inversion pulse [TI] 5 2500/15/
140 milliseconds) MR imaging shows signal abnormalities in the bony calvarium and scalp of the right frontal
region. (B) Contrast-enhanced T1-weighted spin echo (SE) (TR/TE 5 695/15 milliseconds) MR imaging demon-
strates intense enhancement of the scalp, bone, and fusiform epidural lesion. A biopsy of the lesion revealed
tuberculous osteomyelitis in an HIV-positive patient with simultaneously present pulmonary tuberculosis. (C)
Six months later, axial FLAIR TSE (TR/TE/TI 5 11,000/120/2800 milliseconds) MR imaging shows extensive high sig-
nal intensity abnormalities in the pons, in the subarachnoid space, around the forth ventricle, and in the cere-
bellum. (D, E) Contrast-enhanced T1-weighted turbo field echo (TFE) (TR/TE/flip angle 5 20 milliseconds/1.9
milliseconds/35 ) MR imaging in axial and coronal planes shows marked meningeal and parenchymal enhance-
ment consistent with extensive tuberculous meningitis.
100 Thurnher & Donovan Post
mechanisms: reactivation of a latent infection or
rapid progression of a newly acquired infection
[63,64]. Another important fact is that tuberculosis
may appear in the early stages of immunodefi-
ciency. The most striking clinical feature is the
extremely high frequency of extrapulmonary
involvement.
Approximately 10% of all patients who have
AIDS with tuberculosis present with CNS disease
[65,66].
Basically, tuberculous infection of the CNS re-
sults in tuberculous meningitis, which is char-
acterized by a thick gelatinous exudate with
a predilection for the meninges covering the base
of the brain. Meningeal enhancement on enhanced
CT and MR imaging in the basal cisterns and over
the convexity of the brain could be seen in approx-
imately 36% to 61% of the cases (Fig. 6) [67–70].
Involvement of the vessels that course through
the subarachnoid space by the tuberculous inflam-
mation results in narrowing, and occlusions of the
vessels and subsequent infarctions, which are usu-
ally located in the middle cerebral artery territory
and small perforating arteries supplying the basal
ganglia [71]. Diffusion-weighted MR imaging is
helpful in detecting early infarcts, and magnetic res-
onance angiography (MRA) has been reported to be
useful in showing the tuberculosis-induced vascular
pathologic changes [71]. Communicating-type hy-
drocephalus is the most common complication in
meningeal tuberculosis [72].
Villoria and colleagues [69] reported hydroceph-
alus in 51% of patients in their series of 35 patients
who had AIDS-related CNS tuberculosis.
Parenchymal forms of the tuberculous infection
include tuberculomas, tuberculous abscesses,
and focal tuberculous cerebritis. In the AIDS popu-
lation, parenchymal involvement is not often seen.
Tuberculous granulomas (tuberculomas) result
from hematogenous spread of infection or from ex-
tension of meningitis into the parenchyma. Tuber-
culomas may be solitary or multiple and can be
located anywhere in the brain but are predomi-
nantly found in the supratentorial compartment
[69]. The radiologic features of tuberculomas de-
pend on the maturity of the lesion. On CT, mature
granulomas are ring-enhancing lesions. The ‘‘target
sign’’ was first described as a pathognomonic fea-
ture for CNS tuberculoma [73], representing central
calcification or punctate enhancement surrounded
by a zone of hypodensity and a rim of enhance-
ment. Later reports have shown that the target
sign on CT could also be caused by other lesions,
such as toxoplasmosis, lymphoma, or brain abscess
[74]. The tuberculomas appear isointense with a hy-
perintense ring on T1-weighted MR imaging and
have a variable signal on long echo time (TE) im-
ages. Some tuberculomas are hypointense on T2-
weighted images. The possible explanation for the
low signal of tuberculomas on T2-weighted images
is the presence of paramagnetic free radicals pro-
duced by macrophage activity. Other tuberculomas
have high signal on long TE images because of
central liquefactive necrosis [75]. Kim and col-
leagues [76] compared MR imaging findings with
pathologic features in tuberculomas and found
that the outer enhancing portion consisted of a layer
of collagenous fibers and that inflammatory
Fig. 7. Dilated Virchow-
Robin spaces in cerebral
cryptococcosis (autopsy
proved). (A, B) Axial T1-
weighted spin echo (SE)
(repetition time [TR]/TE 5
700/19 milliseconds) and
coronal T2-weighted (TR/
TE 5 2500/90 milliseconds)
MR imaging demonstrates
small cystic-like lesions bi-
laterally in the basal gan-
glia, representing dilated
perivascular spaces filled
with fungi. On enhanced
T1-weighted MR imaging,
no enhancement was ob-
served (not shown).
 Neuroimaging in the Brain in HIV-1–Infected Patients 101

infiltrates showed on MR imaging as a hypointense weighted MR imaging. Typically, tuberculous

ring on T2-weighted images; central caseation ne-
crosis was recognized as isointense or hypointense
on all pulse sequences. Healed tuberculomas do
not enhance but may calcify.
Tuberculous abscess is a true pyogenic lesion
that demonstrates a typical imaging appearance
of pyogenic abscesses: hyperintense on T2-
weighted MR imaging and hypointense on T1-
abscesses are multiloculated, are larger than tuber-
culomas, and show ring-like enhancement [77,78].
Differentiation of tuberculous abscess from pyo-
genic abscess is important for patient manage-
ment. A recent study has shown that with MRS
combined with MR imaging, it might be possible
to distinguish those two entities [79,80]. In that
study, all pyogenic brain abscesses had lipid and

Fig. 8. Cryptococcosis in an HIV-positive patient. (A) Axial FLAIR turbo spin echo (TSE) (repetition time [TR]/TE/time
after inversion pulse [TI] 5 11,000/120/2800 milliseconds) MR imaging of the brain shows bilateral high signal in-
tensity abnormalities in the temporal and occipital cortex (also note high signal in the cingulate gyrus). A low signal
intensity lesion is demonstrated on the right side with a hyperintense rim. The lesion has low signal on T1-weighted
MR imaging (B) and shows no enhancement on postcontrast T1-weighted MR imaging (C). The cortex is inhomoge-
neously enhancing (C). Note the small round lesions in the left basal ganglia representing dilated perivascular
spaces. MR imaging findings were consistent with meningoencephalitis, and the diagnosis was confirmed at au-
topsy. (D) Cystic-like lesions are observed on axial T1-weighted MR imaging in the dentate nucleus. Small CSF iso-
intense nonenhancing lesions in the basal ganglia and dentate nucleus represent dilated Virchow-Robin spaces.
The larger nonenhancing lesion in the right basal ganglia represents a gelatinous pseudocyst.
102 Thurnher & Donovan Post

lactate peaks and amino acid peaks. Patients who
had tuberculous abscesses had only lipid and lac-
tate levels. The magnetization transfer (MT) ratio
from the wall of the pyogenic abscess was signifi-
cantly higher than that from the tuberculous ab-
scess wall. In another series of 28 tuberculomas,
lipid peaks were seen in 86% of the tuberculomas
[81]. Large resonances of fatty acids at 1.3 ppm and
0.9 ppm, which are assigned to a methylene group,
and terminal methyl groups of fatty acids de-
scribed in tuberculomas are attributable to the
high lipid content of caseous material [80].
Focal tuberculous cerebritis is a rare form of tu-
berculosis characterized by intense gyral enhance-
ment on CT scans [82]. Calvarial tuberculosis is
another rare manifestation of extrapulmonary tu-
berculosis. The presence of lytic lesions of the skull
in a young individual in an endemic area should
raise the suspicion of tuberculosis. Patankar and
colleagues [83] have described CT findings in five
cases of tuberculosis of the calvarium. A case of
proved calvarial tuberculosis in a young patient
who had AIDS from the author’s institution is
shown in Fig. 6.

Fig. 9. Cerebral aspergillosis in an HIV-positive patient. (A) Axial FLAIR turbo spin echo (TSE) (repetition time
[TR]/TE/time after inversion pulse [TI] 5 11,000/120/2800 milliseconds) MR imaging shows multiple small corti-
cally located lesions in the both hemispheres. (B) On coronal T2-weighted TSE (TR/TE 5 2500/130 milliseconds)
MR imaging, low signal of the lesions with high signal perifocal edema is demonstrated. (C) The lesions have low
signal on a T1-weighted turbo field echo (TFE) (TR/TE/flip angle 5 10 milliseconds/3.4 milliseconds/10 ) MR im-
aging sequence. (D) On postcontrast T1-weighted TFE (TR/TE/flip angle 5 10 milliseconds/3.4 milliseconds/10 )
MR imaging, nodular and ring-like enhancement could be observed.
 Neuroimaging in the Brain in HIV-1–Infected Patients 103

Fungal infections multiple organisms and capsular material. CT scans

Cryptococcosis
CNS infection caused by the saprophytic yeast-like
fungus Cryptococcus neoformans is the most common
form of fungal infection in patients who have AIDS.
The infection is the result of a newly acquired infec-
tion with hematogenous dissemination of the in-
fection from the lung to the CNS. Approximately
5% to 10% of patients who have AIDS develop
CNS cryptococcosis. Cryptococcal meningitis is
the most common manifestation, wherein the sub-
arachnoid spaces are thickened and filled with
rarely show meningeal enhancement, whereas en-
hanced T1-weighted MR imaging may demonstrate
meningeal disease, but this is the exception rather
than the rule [84,85]. In a case of prominent men-
ingeal enhancement on MR imaging, causes other
than cryptococcosis should be considered first.
From the subarachnoid space, cryptococcus ex-
tends along the Virchow-Robin perivascular spaces
into the basal ganglia, thalami, midbrain, and cere-
bellum. The Virchow-Robin spaces become dilated,
without involvement of the brain parenchyma. On

Fig. 10. Cerebral toxoplasmosis responding to therapy. (A) Axial T2-weighted turbo spin echo (TSE) (repetition
time [TR]/TE 5 2500/130 milliseconds) MR imaging shows a hyperintense lesion in the left basal ganglia region.
(B) Postcontrast T1-weighted turbo field echo (TFE) (TR/TE/flip angle 5 10 milliseconds/3.4 milliseconds/10 ) MR
imaging demonstrates peripheral enhancement of the necrotic lesion surrounded by edema. One year after
antitoxoplasmosis therapy, follow-up MR imaging examination reveals only a linear hyperintense abnormality
without mass effect (C) and without enhancement (D), representing residual gliosis.
104 Thurnher & Donovan Post

MR imaging, widened perivascular spaces are recog-
nized as multiple, bilateral, and small round- or
oval-shaped lesions usually located in the basal
ganglia, which show high signal on T2-weighted
MR imaging and have signal slightly higher than
the CSF on T1-weighted MR imaging (Figs. 7 and
8). The reason for the signal intensity characteristics
is the mucoid content produced by fungi. Perivas-
cular spaces are anatomically outside the brain, an
inflammatory response is absent, there is no inva-
sion of the brain parenchyma, and contrast en-
hancement is therefore always absent.
With disease progression, dilated perivascular
spaces become confluent and cystic lesions develop
called ‘‘gelatinous pseudocysts’’ or ‘‘soap bubbles’’
(see Fig. 8). Those lesions do not have a capsule
and contain mucinous material and fungal organ-
isms. Dentate nuclei are shown to be frequently in-
volved [86]. On MR imaging, the appearance does
not differ from the dilated Virchow-Robin spaces,
because mucinous material shortens the T1 relaxa-
tion time and the lesions appear isointense to the
cortex. Enhancement and mass effect are also
absent.
Cryptococcoma is the only parenchymal form of
the cryptococcal CNS infection. The lesions result
from the direct invasion of the brain by the fungus,
with the development of a granulomatous reaction.
On CT, cryptococcomas are hypodense with high
signal on T2-weighted MR imaging and low signal
on T1-weighted MR imaging. On enhanced imag-
ing, the lesions usually demonstrate a ring-like or

Fig. 11. Cerebral toxoplasmosis in a 30-year-old HIV-positive patient. (A) Low signal intensity lesion is shown in
the left basal ganglia region on axial FLAIR MR imaging. Note the perifocal edema and compression of the left
ventricle. (B) Lesion is hypointense on coronal T2-weighted MR imaging. An additional lesion is present in the
right temporal lobe. (C) On diffusion-weighted MR imaging (trace), low signal was observed, indicating in-
creased diffusivity. (D) Peripheral enhancement of the acute toxoplasma lesion is present after gadolinium in-
jection on postcontrast T1-weighted MR imaging.
 Neuroimaging in the Brain in HIV-1–Infected Patients 105

nodular enhancement and cannot be distinguished cryptococcoma showed signal higher than that of
from granulomas of other origin. Recently, imaging the CSF and a mosaic pattern on diffusion-weighted
findings with FLAIR and DWI of an intracerebral images was observed, reflecting the inorganic struc-
granuloma were described [87]. On FLAIR images, ture of the lesion.

Fig. 12. Cerebral toxoplasmosis. (A) Low signal intensity lesion with high signal intensity edema located in the
right cerebellum is shown on axial FLAIR turbo spin echo (TSE) (repetition time [TR]/TE/time after inversion pulse
[TI] 5 11,000/140/2800 milliseconds) MR imaging. (B) Lesion shows ring enhancement after gadolinium injection
on T1-weighted turbo field echo (TFE) (TR/TE/flip angle 5 20 milliseconds/1.8 milliseconds/35 ) MR imaging. (C)
Proton magnetic resonance spectrum acquired from a lesion demonstrates a large lipid or lactate peak, de-
creased NAA, and an increased Cho peak. The MR imaging findings and magnetic resonance spectrum were con-
sistent with toxoplasmosis.
106 Thurnher & Donovan Post

Aspergillosis difficulties in treating aspergillosis, it is important to

Aspergillus is a frequent pathogen in the CNS,
accounting for 18% to 28% of all fungal brain ab-
scesses, and is the most common CNS complication
after bone marrow transplantation [88]. Aspergillus
fumigatus is the most common human pathogen. Be-
cause of the high mortality rate of 85% to 100% and
raise suspicion early. Cerebral aspergillosis usually
occurs after hematogenous dissemination from an
extracerebral focus or is a result of contiguous spread
of the infection from the paranasal sinuses. Meningi-
tis, abscess or granuloma, vascular invasion with
thrombosis and infarction, and hemorrhage and

Fig. 13. 201TI SPECT in a case

of cerebral toxoplasmosis
and lymphoma. (A) Coro-
nal, sagittal, axial, and pla-
nar images from 201TI
SPECT of a patient who
had AIDS with multifocal
ring-enhancing lesions
seen on the postcontrast
CT scan. No focal uptake is
identified. (B) Coronal, sag-
ittal, axial, and planar im-
ages from 201TI SPECT of
a patient who had AIDS
with an enhancing lesion
in the frontal lobe. Focal
uptake is demonstrated in
the pericallosal region con-
sistent with neoplasm.
 Neuroimaging in the Brain in HIV-1–Infected Patients 107

aneurysm formation are manifestations of cerebral
aspergillosis [89].
Pathologically, hyphal elements invade cerebral
vessels, resulting in thrombosis and infarctions.
Sterile infarctions become septic when the fungus
erodes the wall of the vessel with extension into
the brain parenchyma, with inflammatory reactions
and necrosis. MR imaging is the method of choice
in detecting cerebral infarctions because of aspergil-
losis. In addition, a recent study has shown that dif-
fusion imaging allows early diagnosis of CNS
aspergillosis [90]. DWI revealed multiple signal in-
tensity abnormalities consistent with infarctions,
whereas conventional MR imaging sequences were
still normal [90]. Intracerebral parenchymal lesions
in aspergillosis have a central zone of hemorrhagic
necrosis with sparse presence of fungi. On MR im-
aging, these lesions usually have low signal cen-
trally or peripherally on T2-weighted images
(Fig. 9) [91]. Cox and colleagues [92] showed that
low peripheral signal is attributable to accumula-
tion of fungi containing iron, magnesium, and
manganese in addition to blood breakdown prod-
ucts. Low signal on T2-weighted MR imaging is
not specific for aspergillosis, and it may be seen in
tuberculomas or cysticercosis, for example. In one
series, 14 of 36 lesions showed areas of low signal
intensity located centrally, and in 8 of 36 lesions,
low signal was present peripherally [93]. Contrast
enhancement is usually not present, depending
on the severity of the immunocompetence. Dietrich
and colleagues [93] have observed faint enhance-
ment in 15 of 36 lesions in patients who had
bone marrow transplantation and cerebral
aspergillosis.
Parasitic infections
Toxoplasmosis
Cerebral toxoplasmosis results from infection by an
intracellular protozoan, Toxoplasma gondii. In the

Fig. 14. Toxoplasmosis reinfection in a noncompliant patient who had AIDS. (A) Postcontrast T1-weighted turbo
field echo (TFE) (repetition time [TR]/TE/flip angle 5 20 milliseconds/1.8 milliseconds/35 ) MR imaging in the axial
plane shows a ring-like enhancing lesion in the right basal ganglia region. (B) FDG-PETscan show no uptake. A high-
er dose of antitoxoplasma therapy was initiated; on a follow-up MR imaging scan, no enhancement was present.
108 Thurnher & Donovan Post

United States, 20% to 70% of adults are seroposi-
tive [94]. After the acute infection, the latent form,
called encysted bradyzoites, remains in the tissues
until a decline in immunity. Rupture of the cysts re-
leases the free tachyzoite, which causes acute illness.
Toxoplasma is found in 10% to 34% of all AIDS au-
topsies [95].
In patients who have AIDS, Toxoplasma causes
necrotizing encephalitis. The lesions have three
well-defined zones: an avascular necrotic center,
an intermediate zone with intense inflammatory re-
action, and a peripheral zone with an encysted form
of Toxoplasma [96].
On nonenhanced CT scans, toxoplasma lesions
are hypodense with edema and mass effect. Solid,
nodular-enhancing, or ring-enhancing lesions are
typically observed on postcontrast studies. The
most common locations are the basal ganglia and
the corticomedullary junction. The number of
detectable lesions significantly increases with a
double-dose delayed technique [97]. Pathologic-
radiologic correlation showed that the radiologic
appearance correlates well with the pathologic find-
ings; the ring-enhancing lesions correlate with an
inflammatory zone, the hypodense center correlates
with an avascular necrosis, and edema correlates
with the peripheral zone [96].
On T1-weighted MR imaging, toxoplasma lesions
have isointense to low signal centrally. Signal inten-
sity on T2-weighted images depends on the stage of
the lesion, which could be isointense, hypointense,
or hyperintense [97,98] (Fig. 10). Enhanced
T1-weighted images reveal ring or nodular enhance-
ment (Fig. 11).
Approximately 10 days after the initiation of anti-
toxoplasma therapy, a decrease in the number and
size of the lesions, with a reduction in edema and
mass effect, should be observed on follow-up MR
imaging examinations. Full resolution of the le-
sions may take 6 months [94], and healed foci
may calcify or show changes consistent with leuko-
malacia (see Fig. 10). Lifelong maintenance of ther-
apy is necessary, because discontinuation of
treatment results in recurrence. Encysted forms of
Toxoplasma cannot be treated with therapy; thus,
toxoplasma lesions are never entirely eradicated.
Based on findings on conventional MR imaging
sequences, cerebral toxoplasmosis cannot be distin-
guished from primary cerebral lymphoma. Early re-
ports about MR imaging findings of toxoplasmosis
and lymphoma in patients who had AIDS describe
solitary lesions, which suggest lymphoma, and
multiple lesions, which suggest toxoplasmosis
[99–101]. Further studies have shown that the num-
ber of the lesions, their signal intensity, their loca-
tion, and their appearance on postcontrast images
are not reliable factors in differentiation between
those two entities. New MR imaging methods
have been introduced to improve differentiation,
such as MRS and pMR imaging.
The MRS pattern of toxoplasma lesions is non-
specific, consistent with anaerobic inflammation
within the abscess (Fig. 12). In lymphoma, an in-
crease of lactate and lipids and an elevated Cho

Fig. 15. Primary CNS lymphoma in a 40-year-old female patient who had AIDS. (A) Nonenhanced axial CT scan of
the brain shows a slightly hyperdense lesion in the right basal ganglia region with mass effect and surrounding
edema. (B) On a contrast-enhanced axial CT scan, the lesion demonstrates intense enhancement with a hypo-
dense ventral portion, indicating the necrotic part of the tumor.
 Neuroimaging in the Brain in HIV-1–Infected Patients 109

peak have been described. Chinn and colleagues
[102] have studied MR imaging spectra from 18
toxoplasma lesions and nine lymphomas at 1.5 T
with a TE of 135 milliseconds. Visual analysis in
their study failed to differentiate between Toxo-
plasma and lymphoma. An important variable for
MR imaging spectra is the maturity of the lesions
and the presence of necrosis. At some stage, all in-
tracranial processes destroy brain parenchyma,
and in patients who have AIDS, lymphomas are
usually necrotic tumors. Therefore, necrotic lym-
phoma has compounds similar to necrotic toxo-
plasma abscess. The presence of lipids is seen in
both entities as a result of brain destruction. A rela-
tively immature toxoplasma lesion is more cellular,
resulting in a spectrum with no lipid, increased
Cho, and decreased NAA. It is crucial to place the
voxel for spectroscopic analysis over the cellular
portion of the lesion. In another series of 11 toxo-
plasma lesions and eight lymphomas of the brain
in patients who had AIDS, MRS was considered
a potentially specific noninvasive adjunctive
method for differential diagnosis of focal brain le-
sions in AIDS [25,103]. Toxoplasma was correctly di-
agnosed in 11 of 11 cases, and lymphoma was
correctly diagnosed in eight of eight cases. The

Fig. 16. Primary CNS lymphoma. (A) Axial FLAIR (repetition time [TR]/TE/time after inversion pulse [TI] 5 7000/150/
2100 milliseconds) MR imaging shows a large mass of inhomogeneous high signal intensity in the right basal ganglia
region with mass effect and perifocal edema. Note the additional lesion in the left basal ganglia region. (B) On un-
enhanced T1-weighted spin echo (SE) (TR/TE 5 550/20 milliseconds) MR imaging, the lesions are hypointense with
central hyperintensity, representing subacute hemorrhage. (C) Postcontrast T1-weighted SE (TR/TE 5 550/20 milli-
seconds) MR imaging demonstrates heterogeneous peripheral enhancement and irregular margin of the lesion.
110 Thurnher & Donovan Post

Fig. 17. Nonenhancing primary CNS lymphoma in patient who had AIDS. (A) High signal intensity lesion located
in the left parietal region is shown on axial FLAIR turbo spin echo (TSE) (repetition time [TR]/ TE/time after in-
version pulse [TI] 5 7384/130/2100 milliseconds) MR imaging. (B) Lesion is intense to slightly hyperintense on T1-
weighted spin echo (SE) MR imaging with magnetization transfer contrast (MTC) (TR/TE 5 904/15 milliseconds).
(C) On postcontrast T1-weighted MR imaging with MTC (TR/TE 5 904/15 milliseconds), the lesion shows minimal
central enhancement. Axial FLAIR TSE (TR/TE/TI 5 7384/130/2100 milliseconds) MR imaging at two other levels
shows an additional two lesions: one well-defined high signal intensity lesion in the lateral portion of the
left thalamus (D) and one lesion in the left temporal lobe (E). (F) Magnetic resonance spectrum of the lesion
shows decreased NAA, increased Cho, and appearance of lactate peaks, consistent with lymphoma. (G, H)
FDG-PET shows uptake in all three lesions, indicating neoplastic lesions. An autopsy confirmed primary CNS lym-
phoma in all three locations.

lactate peak was greatest in lymphoma in that study.
Although much work has been done, MRS must be
seen as a valuable adjunctive tool and cannot re-
place conventional MR imaging in differentiation
of toxoplasmosis and lymphoma.
pMR imaging is another potential noninvasive
method that may allow differentiation between
toxoplasmosis and lymphoma in patients who
have AIDS. Prospective evaluation of 13 patients
who had focal brain lesions with pMR imaging
showed reduced regional cerebral blood volume
(rCBV) in toxoplasma lesions and increased
rCBV in lymphoma [104]. Reduced rCBV in toxo-
plasmosis is probably attributable to a lack of
 Neuroimaging in the Brain in HIV-1–Infected Patients
Fig. 17 (continued)
vasculature within the abscess, whereas the hyper-
vascularity of lymphoma is the reason for increased
rCBV in lymphoma.
The use of thallium-201 (201TI) brain SPECT in
patients who have AIDS has been proved to be
helpful in distinguishing toxoplasmosis from lym-
phoma [103,105]. Thallium is a potassium ana-
logue with uptake in active tissue, with a half-life
of approximately 73 hours [105]. After intravenous
administration, 201TI rapidly disappears from the
blood and increased activity is usually seen in the
orbits, the base of the skull, the scalp, and the naso-
pharyngeal region. Normally, there is no uptake of
201
TI in the brain. Positive 201TI brain SPECT is sug-
gestive of CNS lymphoma, and negative uptake sug-
gests infection (toxoplasmosis) in patients who
have AIDS (Fig. 13) [105]. A study of 37 patients
who had AIDS and focal brain lesions evaluated
with 201TI SPECT has shown the benefit of 201TI
SPECT in the differentiation between lymphoma
and infectious lesions. All lymphomas in this series
showed uptake of 201TI in contrast to infections,
which showed negative uptake [105]. Contrary to
the results of Ruiz and colleagues [105], the results
from a recent prospective study on 14 patients who
had AIDS and focal brain lesions suggest the inabil-
ity of 201TI SPECT to differentiate lymphoma from
toxoplasmosis [106]. The accuracy was 57% in
that study, with a positive predictive value of 43%
and a negative predictive value of 71%. A combina-
tion of 201TI SPECT and toxoplasma serology may
improve diagnostic accuracy for toxoplasmosis
111
[107]. A combined approach with 201TI SPECT
and Epstein-Barr virus DNA polymerase chain reac-
tion in CSF provides high diagnostic accuracy for
cerebral lymphoma [108]. Thallium and gallium
scans were reviewed in 40 patients who had AIDS
with focal brain lesions. All patients who had lym-
phomas and gliomas had positive thallium and
gallium scans. Patients who had infections (toxo-
plasmosis and tuberculosis, mycobacterial infec-
tion, and cryptococcosis) had positive gallium
scans and negative thallium scans. Negative thal-
lium and gallium scans were also seen in patients
who had infarcts.
The potential use of F-18 fluorodeoxyglucose
(FDG) PET in differentiating lymphoma from toxo-
plasmosis in patients who have AIDS has been also
examined [109]. The results of the studies have
shown that FDG-PET can accurately differentiate
lymphoma from infections (Fig. 14) [110,111].
The standardized uptake values (SUVs) over cere-
bral lesions were much higher in lymphomas
than in toxoplasma lesions [112]. In another study,
the highest FDG uptake was found in patients who
had lymphoma [109]. Diagnostic problems may oc-
cur in cases of progressive multifocal leukoence-
phalopathy (PML), in which high metabolic
activity and FDG uptake may be found [110,113].
Two cases of PML had high metabolic activity in
a series of 18 patients who had AIDS and could
not be differentiated from lymphoma.
In hospitals with SPECT or PET facilities, a thal-
lium scan or an FDG scan in patients who have
112 Thurnher & Donovan Post
Fig. 17 (continued)
AIDS and focal brain lesions allows rapid evalua-
tion of the brain and, combined with Toxoplasma
IgG and Epstein-Barr virus DNA polymerase chain
reaction in CSF, improves diagnostic accuracy.
Neoplastic lesions
Lymphoma
Primary central nervous system lymphoma
(PCNSL) is of major importance because of its in-
creasing frequency, especially in immunocompro-
mised patients [114,115]. Up to 6% of all patients
who have AIDS develop high-grade lymphoma, al-
most always non-Hodgkin’s type [116]. Multicentric
lymphomas are a common finding as solitary le-
sions, with a frequency between 41% and 81%
[117–119]. The number of lesions on CT or MR
imaging, however, does not allow a definitive final
diagnosis. On nonenhanced CT scans, the
lymphomas are usually hyperdense, whereas on
MR imaging, lymphomas may have low, high, or
intermediate signal on T1- and T2-weighted se-
quences (Figs. 15 and 16) [120–123]. The enhance-
ment is variable, but peripheral or ring
enhancement is the most common pattern (see
Figs. 15 and 16). Solid homogeneous enhance-
ment has been described in some CT series [122].
Nonenhancing lymphomatous lesions have also
been reported, for example, in one study in which
15 lymphomatous lesions in four patients who
had AIDS did not enhance (Fig. 17) [119].
Approximately 3.4% of PCNSL lesions show no en-
hancement in immunocompetent patients [124],
especially in those receiving steroids before imag-
ing. The diffuse form of lymphoma has also been
described recently, presenting as nonenhancing,
diffuse, white matter lesions [119]. The differential
diagnosis would include HIV encephalopathy and
PML in those cases [125]. Lymphomas usually
demonstrate a moderate degree of edema and
 Neuroimaging in the Brain in HIV-1–Infected Patients
mass effect, and marked edema with midline shift
was observed in 25% of patients who had AIDS
and lymphoma in one series. The relatively mild
mass effect in 53% to 75% of cases is attributable
to the infiltrating nature of lymphoma [126]. Evi-
dence of hemorrhage does not exclude PCNSL in
patients who have AIDS, and 35% of untreated
lymphomas were hemorrhagic in the authors’ series
[119,127].
Lymphomatous involvement of the cranial vault
in patients who have AIDS is rare [128–130]. MR
imaging revealed a large scalp-enhancing lesion
with bone destruction and an epidural component
in the first HIV-positive patient in whom primary
lymphoma of the cranial vault was described
[128]. A recently published case of malignant lym-
phoma of the cranial vault was detected on CT or
MR imaging scans presenting as a large scalp lesion
in the left frontoparietal region with extension
through the bony calvarium, with an epidural com-
ponent [130]. The lesion showed peripheral en-
hancement on postcontrast MR imaging, and the
epidural lesion demonstrated homogeneous en-
hancement. Although it is a rare enitity, a prominent
soft tissue mass of the scalp associated with a bone
lesion and an epidural mass in an HIV-positive pa-
tient should suggest lymphoma of the cranial vault.
Differentiation between lymphoma and toxo-
plasmosis in patients who have AIDS remains a
diagnostic dilemma. The combination of a neurora-
diologic examination, a compatibleradionuclide
study, and CSF analysis (Epstein-Barr virus DNA)
should certainly aid in the correct diagnosis.
References
[1] Davis LE, Hjelle BL, Miller VE, et al. Early viral
brain invasion in iatrogenic human immunode-
ficiency virus infection. Neurology 1992;42:
1736–9.
[2] Rausch DM, Davis MR. HIV in the CNS: patho-
genic relationships to systemic HIV disease and
other CNS disease. J Neurovirol 2001;7:85–96.
[3] Arendt G, Hefter H, Elsing C, et al. Motor dys-
function in HIV-infected patients without clini-
cally detectable central nervous deficit. J Neurol
1990;237:362–8.
[4] Navia BA, Jordan BD, Price RW. The AIDS de-
mentia complex. I. Clinical features. Ann Neu-
rol 1986;19:517–24.
[5] Power C, Selnes OA, Grim JA, et al. HIV dementia
scale: a rapid screening test. J Acquir Immune
Defic Syndr Hum Retrovirol 1995;8:273–8.
[6] Price RW, Sidtis JJ. Evaluation of the AIDS de-
mentia complex in clinical trials. J Acquir Im-
mune Defic Syndr 1990;3:S51–60.
[7] Sacktor NC, Lyles RH, Skolasky MA, et al.
HIV-associated neurologic disease incidence
113
changes: Multicenter AIDS Cohort Study,
1990–1998. Neurology 2001;56:257–60.
[8] Budka H, Constanzi G, Cristina S, et al. Brain
pathology induced by infection with the human
immunodeficiency virus (HIV). Acta Neuropa-
thol 1987;75:185–98.
[9] Kleihues P, Lang W, Burger PC, et al. Progressive
diffuse leukoencephalopathy in patients with ac-
quired immune deficiency syndrome (AIDS).
Acta Neuropathol 1985;68:333–9.
[10] Arendt G, Hefter H, Neuen-Jacob E, et al. Elec-
trophysiological motor testing, MRI findings
and clinical course in AIDS patients with de-
mentia. J Neurol 1993;240:439–45.
[11] Bencherif B, Rottenberg DA. Neuroimaging of
the AIDS dementia complex. AIDS 1998;12:
233–44.
[12] Bursztyn EM, Lee BCP, Bauman J. CT of ac-
quired immunodeficiency syndrome. AJNR
Am J Neuroradiol 1984;5:711–4.
[13] Eloovara I, Poutiainen E, Raininko R, et al. Mild
brain atrophy in early HIV-1 infection: the lack
of association with cognitive deficits and HIV-
specific intrathecal immune response. J Neurol
Sci 1990;99:121–36.
[14] Levy RM, Rosenbloom S, Perrett LV. Neurora-
diologic findings in AIDS: a review of 200 cases.
AJR Am J Roentgenol 1986;147:977–83.
[15] Post MJD, Kursunoglu SJ, Hensley GT, et al.
Cranial CT in acquired immunodeficiency syn-
drome: spectrum of diseases and optimal con-
trast enhancement technique. AJNR Am J
Neuroradiol 1985;6:743–54.
[16] Poutiainen E, Eloovara I, Raininko R, et al. Cog-
nitive performance in HIV-1 infection: relation-
ship to severity of disease and brain atrophy.
Acta Neurol Scand 1993;87:88–94.
[17] Jacobsen J, Gyldensted C, Brun B, et al. Cerebral
ventricular enlargement relates to neuropsycho-
logical measures in unselected AIDS patients.
Acta Neurol Scand 1989;79:59–62.
[18] Aylward EH, Brettschneider PD, McArthur JC,
et al. Magnetic resonance imaging measure-
ment of gray matter volume reductions in
HIV dementia. Am J Psychiatry 1995;152:
987–94.
[19] Olsen WL, Longo FM, Mills CM, et al. White
matter disease in AIDS: findings at MR imaging.
Radiology 1988;169:445–8.
[20] Cohen WA, Maravilla KR, Gerlach R, et al. Pro-
spective cerebral MR study of HIV seropositive
and seronegative men: correlation of MR find-
ings with neurologic, neuropsychologic, and
cerebrospinal fluid analysis. AJNR Am J
Neuroradiol 1992;13:1231–40.
[21] Post MJD, Levin BE, Berger JR, et al. Sequen-
tial cranial MR findings of asymptomatic and
neurologically symptomatic HIV positive sub-
jects. AJNR Am J Neuroradiol 1992;13:
359–70.
[22] Post MJD, Berger JR, Duncan R, et al. Asymp-
tomatic and neurologically symptomatic HIV-
114 Thurnher & Donovan Post
seropositive subjects: results of long-term MR
imaging and clinical follow-up. Radiology
1993;188:727–33.
[23] Grafe MR, Press GA, Berthoty DP, et al. Abnor-
malities of the brain in AIDS patients: correla-
tion of postmortem MR findings with
neuropathology. AJNR Am J Neuroradiol
1990;11:905–11.
[24] Thurnher MM, Thurnher SA, Fleischmann D,
et al. Comparison of T2-weighted and fluid-
attenuated inversion-recovery fast spin-echo
MR sequences in intracerebral AIDS-associated
disease. AJNR Am J Neuroradiol 1997;18:
1601–9.
[25] Chang L, Miller BL, McBride D, et al. Brain le-
sions in patients with AIDS: H-1 MR spectros-
copy. Radiology 1995;197:525–31.
[26] Chang L, Ernst T, Leonido-Yee M, et al. Cerebral
metabolite abnormalities correlate with clinical
severity of HIV-1 cognitive motor complex.
Neurology 1999;52:100–8.
[27] Chang L, Itti I, Itti L, et al. Changes in cerebral
metabolism are detected prior to perfusion
changes in early HIV-CMC: a coregistered
(1)H MRS and SPECT study. J Magn Reson Im-
aging 2000;12:859–65.
[28] Jarvik JG, Lenkinski RE, Grossman RI, et al. Pro-
ton MR spectroscopy of HIV-infected patients:
characterization of abnormalities with imaging
and clinical correlation. Radiology 1993;186:
739–44.
[29] Laubenberger J, Häussinger D, Bayer S, et al.
HIV-related metabolic abnormalities in the
brain: depiction with proton MR spectroscopy
with short echo time. Radiology 1996;199:
805–10.
[30] Lopez-Villegas D, Lenkinski RE, Frank I. Bio-
chemical changes in the frontal lobe of HIV-
infected individuals detected by magnetic
resonance spectroscopy. Proc Natl Acad Sci
U S A 1997;94:9854–9.
[31] Marcus CD, Taylor-Robinson SD, Sargentoni J,
et al. 1H MR spectroscopy of the brain in HIV-
1-seropositive subjects: evidence for diffuse
metabolic abnormalities. Metab Brain Dis
1998;13:123–36.
[32] Moller HE, Vermathen P, Lentschig MG, et al.
Metabolic characterization of AIDS-dementia
complex by spectroscopic imaging. J Magn Re-
son Imaging 1999;9:10–8.
[33] Otake T, Mori H, Morimoto M, et al. Anti-HIV-1
activity of myo-inositol hexaphosphoric acid
(IP6) and myo-inositol hexasulphate (IS6). An-
ticancer Res 1999;19:3723–6.
[34] Salvan AM, Vion-Dury J, Confort-Gouny S,
et al. Brain proton magnetic resonance spec-
troscopy in HIV-related encephalopathy: identi-
fication of evolving metabolic patterns in
relation to dementia and therapy. AIDS Res
Hum Retroviruses 1997;13:1055–66.
[35] Suwanwela N, Phanuphak P,
Phanthumchinda K, et al. Magnetic resonance
spectroscopy of the brain in neurologically
asymptomatic HIV-infected patients. Magn Re-
son Imaging 2000;18:859–65.
[36] Tracey I, Carr CA, Guimaraes AR, et al. Brain
choline-containing compounds are elevated in
HIV-positive patients before the onset of AIDS
dementia complex: a proton magnetic reso-
nance spectroscopic study. Neurology 1996;
46:783–8.
[37] Von Giesen HJ, Wittsack HJ, Wenserski F, et al.
Basal ganglia metabolite abnormalities in mi-
nor motor disorders associated with human im-
munodeficiency virus type 1. Arch Neurol 2001;
58:1281–6.
[38] Le Bihan D, Mangin JF, Poupon C, et al. Diffu-
sion tensor imaging: concepts and applications.
J Magn Reson Imaging 2001;13:534–46.
[39] Ulug AM, Moore DF, Bojko AS, et al. Clinical
use of diffusion-tensor imaging for diseases
causing neuronal and axonal damage. AJNR
Am J Neuroradiol 1999;20:1044–8.
[40] Filippi CG, Ulug AM, Ryan E, et al. Diffusion-
tensor imaging of patients with HIV and nor-
mal-appearing white matter on MR images of
the brain. AJNR Am J Neuroradiol 2001;22:
277–83.
[41] Thurnher MM, Castillo M, Stadler A, et al. Dif-
fusion-tensor MR imaging of the brain in hu-
man immunodeficiency virus-positive patients.
AJNR Am J Neuroradiol 2005;26:2275–81.
[42] Entning RH, Hoetelmans MW, Lange JMA, et al.
Antiretroviral drugs and the central nervous sys-
tem. AIDS 1998;12:1941–55.
[43] Tozzi V, Balestra P, Galgani S, et al. Positive and
sustained effects of highly active antiretroviral
therapy on HIV-1-associated neurocognitive
impairment. AIDS 1999;13:1889–97.
[44] Von Giesen HJ, Hefter H, Jablonowski H, et al.
HAART is neuroprophylactic in HIV-1 infec-
tion. J Acquir Immune Defic Syndr 2000;23:
380–5.
[45] Chang L, Ernst T, Leonido-Yee M, et al. Highly
active antiretroviral therapy reverses brain me-
tabolite abnormalities in mild HIV dementia.
Neurology 1999;53:782–9.
[46] DeSimone JA, Pomerantz RJ, Babinchak TJ.
Inflammatory reactions in HIV-1-infected per-
sons after initiation of highly active antiretro-
viral therapy. Ann Intern Med 2000;133:
447–54.
[47] Filippi CG, Sze G, Farber SJ, et al. Regression of
HIV encephalopathy and basal ganglia signal
intensity abnormality at MR imaging in patients
with AIDS after initiation of protease inhibitor
therapy. Radiology 1998;206:491–8.
[48] Thurnher MM, Schindler EG, Thurnher SA,
et al. Highly active antiretroviral therapy for pa-
tients with AIDS dementia complex: effect on
MR imaging findings and clinical course.
AJNR Am J Neuroradiol 2000;21:670–8.
[49] Morgello S, Cho E, Nielsen S, et al. Cytomega-
lovirus encephalitis in patients with acquired
 Neuroimaging in the Brain in HIV-1–Infected Patients
immunodeficiency syndrome: an autopsy study
of 30 cases and a review of the literature. Hum
Pathol 1987;18:289–97.
[50] Setinek U, Wondrusch E, Jellinger K, et al. Cyto-
megalovirus infection of the brain in AIDS:
a clinicopathological study. Acta Neuropathol
1995;90:511–5.
[51] Holland N, Power C, Mathews V, et al. Cyto-
megalovirus encephalitis in acquired immuno-
deficiency syndrome (AIDS). Neurology 1994;
44:1892–900.
[52] Hassine D, Gray F, Chekroun R, et al. Encépha-
litides a CMV et VZV au cours du SIDA. J Neuro-
radiol 1995;22:184–92.
[53] Post MJD, Hensley GT, Moskowitz LB, et al. Cy-
tomegalic inclusion virus encephalitis in pa-
tients with AIDS: CT, clinical, and pathologic
correlation. AJNR Am J Neuroradiol 1986;7:
275–9.
[54] Dorfman LJ. Cytomegalovirus encephalitis in
adults. Neurology 1973;23:136–43.
[55] Hawley DA, Schaeffer JF, Schalz DM, et al. Cyto-
megalovirus encephalitis in acquired immuno-
deficiency syndrome. Am J Clin Pathol 1983;
80:874–7.
[56] Kalayijan RC, Cohen ML, Bonomo RA, et al.
Cytomegalovirus ventriculoencephalitis in
AIDS: a syndrome with distinct clinical and
pathologic features. Medicine (Baltimore)
1993;72:67–77.
[57] Salazar A, Podzamczer D, Reñe R, et al. Cyto-
megalovirus ventriculoencephalitis in AIDS pa-
tients. Scand J Infect Dis 1995;27:165–9.
[58] Dyer JR, French MAH, Mallal SA. Cerebral mass
lesions due to cytomegalovirus in patients with
AIDS: report of two cases. J Infect 1995;30:
147–51.
[59] Guermazi A, Miaux Y, Zagdanski AM, et al.
Chorioid plexitis caused by cytomegalovirus
in a patient with AIDS. AJNR Am J Neuroradiol
1996;17:1398–9.
[60] Arribas JR, Clifford DB, Fichtenbaum CJ, et al.
Level of cytomegalovirus (CMV) DNA in cere-
brospinal fluid of subjects with AIDS and
CMV infection of the central nervous system.
J Infect Dis 1995;172:527–31.
[61] Wilkinson ID, Miller RF, Paley MNJ, et al. Cere-
bral proton magnetic resonance spectroscopy in
cytomegalovirus encephalitis and HIV leukoen-
cephalopathy/encephalitis. AIDS 1996;10:
1443–4.
[62] Centers for Disease Control. Tuberculosis and
acquired immunodeficiency syndrome—New
York City. MMWR Morb Mortal Wkly Rep
1987;36:785–95.
[63] Moreno S, Baraia-Etxaburu J, Bouza E, et al.
Risk for developing tuberculosis among anergic
patients infected with HIV. Ann Intern Med
1993;119:194–8.
[64] Daley CL, Small PM, Schecter GF, et al. An out-
break of tuberculosis with accelerated progres-
sion among persons with the human
115
immunodeficiency virus. N Engl J Med 1992;
326:321–5.
[65] Berenguer J, Moreno S, Laguna F, et al. Tubercu-
lous meningitis in patients infected with the
human immunodeficiency virus. N Engl J Med
1992;326:668–72.
[66] Bishburg E, Sunderama G, Reichman LB, et al.
Central nervous system tuberculosis with the
acquired immunodeficiency syndrome and its
related complex. Ann Intern Med 1986;105:
210–3.
[67] Kiomehr F, Dadsetan MR, Rooholamini SA,
et al. Central nervous system tuberculosis.
MRI. Neuroradiology 1994;36:93–6.
[68] Tayfun C, Ücöz T, Tasar M, et al. Diagnostic
value of MRI in tuberculous meningitis. Neuro-
radiology 1995;6:380–6.
[69] Villoria MF, de la Torre J, Fortea F, et al. Intracra-
nial tuberculosis in AIDS: CT and MRI findings.
Neuroradiology 1992;34:11–4.
[70] Whiteman M, Espinosa L, Donovan Post JM, et al.
Central nervous system tuberculosis in HIV-in-
fected patients: clinical and radiographic findings.
AJNR Am J Neuroradiol 1995;16:1319–27.
[71] Gupta RK, Gupta S, Singh D, et al. MR imaging
and angiography in tuberculous meningitis.
Neuroradiology 1994;36:87–92.
[72] Rovira M, Romero F, Torrent O, et al. Study of
tuberculous meningitis by CT. Neuroradiology
1980;19:137–41.
[73] Welchman JM. Computerised tomography of
intracranial tuberculomata. Clin Radiol 1979;
30:567–73.
[74] Bargallo J, Berenguer J, Garcia-Barrionuevo J,
et al. The ‘‘target-sign’’: is it a specific sign of
CNS tuberculoma? Neuroradiology 1996;38:
547–50.
[75] Bowen BC, Post MJD. Intracranial infection. In:
Atlas SW, editor. Magnetic resonance imaging of
the brain and spine. 1st edition. New York:
Raven; 1991. p. 501–38.
[76] Kim TK, Chang KH, Goo JM, et al. Intracranial
tuberculoma: comparison of MR with patho-
logic findings. AJNR Am J Neuroradiol 1995;
16:1903–8.
[77] Fischl MA, Pitchenik AE, Spira TJ. Tuberculous
brain abscess and toxoplasma encephalitis in
a patient with the acquired immunodeficiency
syndrome. JAMA 1985;256:362–6.
[78] Yang PJ, Reger KM, Seeger JF, et al. Brain ab-
scess: an atypical CT appearance of CNS tuber-
culosis. AJNR Am J Neuroradiol 1987;8:
919–20.
[79] Gupta RK, Poptani H, Kohli A, et al. In vivo lo-
calized proton magnetic spectroscopy of intra-
cranial tuberculomas. Indian J Med Res 1995;
101:19–24.
[80] Gupta RK, Vatsal DK, Husain N, et al. Differen-
tiation of tuberculous from pyogenic abscess
with in vivo proton MR spectroscopy and mag-
netization transfer MR imaging. AJNR Am J
Neuroradiol 2001;22:1503–9.
116 Thurnher & Donovan Post
[81] Jayasundar R, Singh VP, Raghunathan P, et al.
Inflammatory granulomas: evaluation with pro-
ton MRS. NMR Biomed 1999;12:139–44.
[82] Jinkins JR. Focal tuberculous cerebritis. AJNR
Am J Neuroradiol 1988;9:121–4.
[83] Patankar T, Varma R, Krishnan A, et al. Radio-
graphic findings in tuberculosis of the calvar-
ium. Neuroradiology 2000;42:518–21.
[84] Arnder L, Castillo M, Heinz ER, et al. Unusual
pattern of enhancement in cryptococcal menin-
gitis: in vivo findings with postmortem correla-
tion. J Comput Assist Tomogr 1996;20:1023–6.
[85] Berkefeld J, Enzensberger W, Lanferman H.
Cryptococcus meningoencephalitis in AIDS: pa-
renchymal and meningeal forms. Neuroradiol-
ogy 1999;41:129–33.
[86] Ruiz A, Post MJD, Bundschu CC. Dentate nuclei
involvement in AIDS patients with CNS crypto-
coccosis: imaging findings with pathologic cor-
relation. J Comput Assist Tomogr 1997;21:
175–82.
[87] Kamezawa T, Shimozuru T, Niiro M, et al. MRI
demonstration of intracerebral cryptococcal
granuloma. Neuroradiology 2000;42:30–3.
[88] Miaux Y, Ribaud P, Williams M, et al. MR of ce-
rebral aspergillosis in patients who have had
bone marrow transplantation. AJNR Am J Neu-
roradiol 1995;16:555–62.
[89] Yuh WTC, Nguyen HD, Gao F, et al. Brain pa-
renchymal infection in bone marrow transplan-
tation patients. CT and MR findings. AJR Am J
Radiol 1994;62:425–30.
[90] Kami M, Shirouzu I, Mitani K, et al. Early diag-
nosis of central nervous system aspergillosis
with combination use of cerebral diffusion-
weighted echoplanar magnetic resonance image
and polymerase chain reaction of cerebrospinal
fluid. Intern Med 1999;38:45–8.
[91] Yamada K, Zoarski GH, Rothman MI, et al. An
intracranial aspergilloma with low signal on
T2-weighted images corresponding to iron accu-
mulation. Neuroradiology 2000;43:559–61.
[92] Cox J, Murtagh FR, Wilfong A, et al. Cerebral as-
pergillosis: MR imaging and histopathologic
correlation. AJNR Am J Neuroradiol 1992;13:
1489–92.
[93] Dietrich U, Hettmann M, Maschke M, et al. Ce-
rebral aspergillosis: comparison of radiological
and neuropathologic findings in patients with
bone marrow transplantation. Eur Radiol
2001;11:1242–9.
[94] Levy RM, Bredesen DE, Rosenblum S, et al.
Neurological manifestation of the acquired im-
munodeficiency syndrome (AIDS): experience
at UCSF and review of the literature. J Neuro-
surg 1985;62:475–95.
[95] Petito CK, Cho E-S, Lemann W, et al. Neu-
ropathology of acquired immunodeficiency
syndrome (AIDS): an autopsy review. J Neuro-
pathol Exp Neurol 1986;45:635–46.
[96] Post MJD, Chan JC, Hensley GT, et al.
Toxoplasma encephalitis in Haitian adults
with acquired immunodeficiency syndrome:
a clinical-pathological-CT correlation. AJR Am
J Roentgenol 1983;140:861–8.
[97] Post MJD, Sheldon JJ, Hensley GT, et al. Central
nervous system disease in acquired immunode-
ficiency syndrome: prospective correlation us-
ing CT, MR imaging, and pathological studies.
Radiology 1986;158:141–8.
[98] Post MJD, Tate LG, Quencer RM, et al. CT,
MR, and pathology in HIV encephalitis and
meningitis. AJR Am J Roentgenol 1988;151:
373–80.
[99] Dina TS. Primary central nervous system lym-
phoma versus toxoplasmosis in AIDS. Radiol-
ogy 1999;179:823–8.
[100] Kupfer MC, Zee CS, Colletti PM, et al. MRI eval-
uation of AIDS related encephalopathy: toxo-
plasmosis vs lymphomas. Magn Reson
Imaging 1990;8:51–7.
[101] Laissy JP, Lebtahi R, Cordoliani YS, et al. Diag-
nostic du lymphome cerebral primitif du
SIDA. J Neuroradiol 1995;22:207–17 [in
French].
[102] Chinn RJS, Wilkinson ID, Hall-Craggs MA,
et al. Toxoplasmosis and primary central ner-
vous system lymphoma in HIV infection: diag-
nosis with MR spectroscopy. Radiology 1995;
197:649–54.
[103] Miller RF, ll-Craggs MA, Costa DC, et al. Mag-
netic resonance imaging, thallium-210 SPECT
scanning, and laboratory analyses for discrimi-
nation of cerebral lymphoma and toxoplasmo-
sis in AIDS. Sex Transm Infect 1998;74:258–64.
[104] Ernst TE, Chang L, Witt MD, et al. Cerebral
toxoplasmosis and lymphoma in AIDS: perfu-
sion MR imaging experience in 13 patients. Ra-
diology 1998;208:663–9.
[105] Ruiz A, Ganz WI, Post MJD, et al. Use of thal-
lium-201 brain SPECT to differentiate cerebral
lymphoma from toxoplasma encephalitis in
AIDS patients. AJNR Am J Neuroradiol 1994;
15:1885–94.
[106] Licho R, Litofsky NS, Senitko M, et al. Inaccur-
acy of TI-201 brain SPECT in distinguishing ce-
rebral infections from lymphoma in patients
with AIDS. Clin Nucl Med 2002;27:81–6.
[107] Skiest DJ, Erdman W, Chang WE, et al. SPECT
thallium-201 combined with Toxoplasma serol-
ogy for the presumptive diagnosis of focal cen-
tral nervous system mass lesions in patients
with AIDS. J Infect 2000;40:274–81.
[108] Antinori A, De Rossi G, Ammassari A, et al.
Value of combined approach with thallium-
201 single-photon emission computed tomog-
raphy and Epstein-Barr virus DNA polymerase
chain reaction in CSF for the diagnosis of
AIDS-related primary CNS lymphoma. J Clin
Oncol 1999;17:554–60.
[109] Villringer K, Jager H, Dichgans M, et al. Differ-
ential diagnosis of CNS lesions in AIDS patients
by FDG-PET. J Comput Assist Tomogr 1995;19:
532–6.
 Neuroimaging in the Brain in HIV-1–Infected Patients
[110] Heald AE, Hoffman JM, Bartlett JA, et al. Differ-
entiation of central nervous system lesions in
AIDS patients using positron emission tomogra-
phy (PET). Int J STD AIDS 1996;7:337–46.
[111] Hoffman JM, Waskin HA, Schifter T, et al. FDG-
PET in differentiating lymphoma from nonma-
lignant central nervous system lesions in patients
with AIDS. J Nucl Med 1993;34:567–75.
[112] O’Doherty MJ, Barrington SF, Campbell M,
et al. PET scanning and the human immunode-
ficiency virus-positive patients. J Nucl Med
1997;38:1575–83.
[113] Provinciali L, Signorino M, Ceravolo G, et al.
Onset of primary brain T-lymphoma simulating
a progressive leukoencephalopathy. Ital J Neu-
rol Sci 1988;9:377–81.
[114] Ammassari A, Scoppettuolo G, Murri R, et al.
Changing disease patterns in focal brain le-
sion-causing disorders in AIDS. J Acquir Im-
mune Defic Syndr Hum Retroviro 1988;18:
365–71.
[115] So YT, Beckstead JH, Davis RL. Primary central
nervous system lymphoma in acquired immu-
nodeficiency syndrome: a clinical and patholog-
ical study. Ann Neurol 1986;20:566–72.
[116] Hainfellner JA, Budka H. Neuropathology of
human immunodeficiency virus-related oppor-
tunistic infections and neoplasms. In:
Berger JR, Levy RM, editors. AIDS and the ner-
vous system. 2nd edition. Philadelphia: Lippin-
cott-Raven Publishers; 1997. p. 461–515.
[117] Ciricillo SF, Rosenblum M. Use of CT and MR
imaging to distinguish intracranial lesions and
to define the need of biopsy in AIDS patients.
J Neurosurg 1990;73:720–4.
[118] Goldstein JD, Zeifer B, Chao C, et al. CT appear-
ance of primary CNS lymphoma in patients
with acquired immunodeficiency syndrome.
J Comput Assist Tomogr 1991;15:39–44.
[119] Thurnher MM, Rieger A, Kleibl-Popov Ch, et al.
Primary central nervous system lymphoma in
AIDS: a wider spectrum of CT and MRI findings.
Neuroradiology 2001;43:29–35.
117
[120] De La Blanchardiere A, Lesprit P, Molina JM,
et al. Lymphome cerebral primitif au cours du
SIDA. Presse Med 1997;26:940–4 [in French].
[121] Ferraresi S, Prosetti D, Griffini C, et al. Unusual
radiological presentation of primary CNS lym-
phoma. Ital J Neurol Sci 1989;10:583–6.
[122] Poon T, Matoso I, Tcherkoff V, et al. CT features
of primary cerebral lymphoma in AIDS and
non-AIDS patients. J Comput Assist Tomogr
1989;13:6–9.
[123] Schwaighofer BW, Hesselink JR, Press GA, et al.
Primary intracranial CNS lymphoma: MR man-
ifestations. AJNR Am J Neuroradiol 1989;10:
725–9.
[124] Johnson BA, Fram EK, Johnson PC, et al. The
variable MR appearance of primary lymphoma
of the central nervous system: comparison with
histopathologic features. AJNR Am J Neurora-
diol 1997;18:563–72.
[125] Sieb JP, van Roost D, Solymosi L. Zerebrales
B-Zell-Lymphom mit dem neuroradiologischen
Bild einer multifokalen Leukoenzephalopathie.
Fortschr Röntgenstr 1992;156:503–4 [in
German].
[126] Cordoliani YS, Derosier C, Pharaboz C, et al.
Primary cerebral lymphoma in patients with
AIDS: MR findings in 17 cases. AJR Am J Radiol
1992;159:841–7.
[127] Fukui MB, Livstone BJ, Meltzer CC, et al. Hem-
orrhagic presentation of untreated primary
CNS lymphoma in a patient with AIDS. AJR
Am J Roentgenol 1998;170:1114–5.
[128] Bhatia S, Smally AJ, Dekker P. Primary non-
Hodgkin’s lymphoma of the cranial vault.
Clin Oncol 1997;9:195–6.
[129] Moragas JM, Rodriguez SA, Camerino SR,
et al. Non-Hodgkin’s disease of the skull in
patients with AIDS. An Med Interna 1999;
16:186–8.
[130] Thurnher MM, Rieger A, Kleibl-Popov Ch, et al.
Malignant lymphoma of the cranial vault in an
HIV-positive patient: imaging findings. Eur Ra-
diol 2001;11:1506–9.