Imaging features of CNS involvement in AIDS.

Abstract

Patients with acquired immunodeficiency syndrome (AIDS) are the subjects of a large part of routine neuroradiological work in the Western world currently. The World Health Organization announced that Turkish authorities had reported a cumulative total of 2544 HIV cases from 1985 to 2006, of whom 623 had developed AIDS and 140 had died. It is estimated that approximately one-third of AIDS patients develop neurological complications. The spectrum of diseases affecting the central nervous system (CNS) in AIDS patients comprises predominantly opportunistic infections and primary CNS lymphoma. Although to a lesser degree when compared with Western countries, the incidence of AIDS and related neurological diseases are on the rise also in Turkey. Therefore radiologists should recognize HIV-associated problems and their imaging features. In this review, we focus on imaging features of more common CNS diseases in HIV-seropositive patients. This essay has been prepared using radiological studies of the patients who had been managed in our hospital which is a tertiary care center with a highly motivated medical team for this peculiar disease in the years between 2002 and 2008.

Full text

Page 1

© Turkish Society of Radiology 2009
H
symptoms. Upon entering the bloodstream, HIV infects the CD4+ T cells
and begins to replicate rapidly. Acquired immunodeficiency syndrome
(AIDS) is the final stage of HIV infection (1). The U.S. Centers for Disease
Control and Prevention established the definition of AIDS as a condi-
tion, which occurs in HIV-infected persons with fewer than 200/mm3
CD4+ T cells and/or persons with HIV who develop certain opportunis-
tic infections (2).
The brain may be affected by a variety of abnormalities in association
with HIV infection. The spectrum of central nervous system (CNS) ab-
normalities can be divided into three main categories: HIV-associated
lesions, opportunistic infections, and neoplasms. Although there is a
considerable overlap in the imaging characteristics of different entities,
some findings are found to be very suggestive of a particular disease and
imaging modalities, mainly magnetic resonance imaging (MRI), play
an important role in the diagnosis and follow up of AIDS patients with
neurological disorders (3). In addition to infections and neoplasms,
catabolic trend of the metabolism of these immunodeficient patients
with consecutive thiamine deficiency may result in Wernicke encepha-
lopathy (Fig. 1).
uman immunodeficiency virus (HIV) belongs to a subset of ret-
roviruses called lentiviruses (or slow viruses), which means that
there is an interval between the initial infection and the onset of
Pediatric HIV infection
Perinatal transmission is the most common route for HIV infection
in infants and children. The virus can be transmitted from an HIV-in-
fected mother to her child through pregnancy, birth or breastfeeding.
In children, opportunistic infections and tumors are less common than
in adults, occurring in 15% of cases (4). Reactivation is not often seen
in pediatric patients, owing to their lack of prior exposure to pathogens,
which results in a lower rate of infections. The most common CNS pres-
entation of AIDS in children is encephalitis (5). On computed tomogra-
phy (CT) and MRI, diffuse cerebral atrophy is the most common finding,
occurring in 90% of cases. On non-contrast CT studies, basal ganglia
calcifications are seen in one-third of infected children (Fig. 2) (4). These
calcifications can be observed as early as 2 months of age (5). Foci of in-
creased signal on T2-weighted (W) images that spare the U-fibers may be
seen in the peripheral and deep cerebral white matter on MRI. Contrast
enhancement is not a characteristic finding of these lesions and may be
absent. Isolated reports of cerebrovascular disease in children with HIV
have been described in the literature, including aneurysms, infarctions,
and hemorrhage. Because most of these patients are asymptomatic dur-
ing the early stages of the disease, screening of high-risk children is ad-
visable for the early detection of cerebrovascular abnormalities (6).
NEURORADIOLOGY
PICTORIAL ESSAY
Diagn Interv Radiol DOI 10.4261/1305-3825.DIR.2182-08.1
Imaging features of CNS involvement in AIDS
Efsun Şenocak, Kader Karlı Oğuz, Burçe Özgen, Aslı Kurne, Gülşen Özkaya, Serhat Ünal, Ayşenur Cila
From the Departments of Radiology (E.Ş.  eurger@yahoo.com,
K.K.O., B.Ö., A.C.), Neurology (A.K.), and Internal Medicine
[Division of Infectious Diseases] (G.Ö., S.Ü.), Hacettepe University
School of Medicine, Ankara, Turkey.
Received 6 August 2008; revision requested 23 October 2008; revision
received 10 November 2008; accepted 20 November 2008.
Published online 21 October 2009
DOI 10.4261/1305-3825.DIR.2182-08.1
ABSTRACT
Patients with acquired immunodeficiency syndrome (AIDS)
are the subjects of a large part of routine neuroradiological
work in the Western world currently. The World Health Or-
ganization announced that Turkish authorities had reported
a cumulative total of 2544 HIV cases from 1985 to 2006, of
whom 623 had developed AIDS and 140 had died. It is esti-
mated that approximately one-third of AIDS patients develop
neurological complications. The spectrum of diseases affecting
the central nervous system (CNS) in AIDS patients comprises
predominantly opportunistic infections and primary CNS lym-
phoma. Although to a lesser degree when compared with
Western countries, the incidence of AIDS and related neuro-
logical diseases are on the rise also in Turkey. Therefore radi-
ologists should recognize HIV-associated problems and their
imaging features. In this review, we focus on imaging features
of more common CNS diseases in HIV-seropositive patients.
This essay has been prepared using radiological studies of the
patients who had been managed in our hospital which is a
tertiary care center with a highly motivated medical team for
this peculiar disease in the years between 2002 and 2008.
Key words: • acquired immunodeficiency syndrome • magnetic
resonance imaging • central nervous system infections
• lymphoma

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Şenocak et al.
ii • Diagnostic and Interventional Radiology
HIV vasculitis
HIV-related vasculitis including a pri-
mary HIV vasculitis has been described
in pathologic studies of AIDS patients.
The lenticulostriate vessels are the most
vulnerable (7). Joshi et al. (8) have sug-
gested that the elastic lamina of vessels
may be injured by elastases because
of repeated infections. Shah et al. (5)
postulated that the inflammation be-
gins in the adventitia and involves the
vasa vasorum, which leads to ischemia
of the arterial wall, resulting in the de-
struction of elastic lamina and subin-
timal fibrosis. This panarteritis could
then lead to stenosis and/or aneurys-
mal dilatation (9). Resultant infarcts or
hemorrhages can occur (Fig. 3) (5).
HIV encephalitis
HIV encephalitis, also called AIDS-
dementia complex (ADC) or HIV-asso-
ciated dementia complex, is a progres-
sive subcortical dementia, attributed to
direct infection of the CNS with HIV
(10). HIV causes an encephalitic illness
in up to 60% of patients with AIDS and
frequently coexists with other AIDS-
related intracranial abnormalities (1).
The pathogenesis of ADC is not com-
pletely understood. It is suggested that
increased proliferation of HIV or a
macrophage-initiated cascade of events
even in the absence of a high viral load
in the brain may lead to brain dysfunc-
tion and clinical dementia (10). Both
CT and MRI have low sensitivity in
identification of early disease due to
the microscopic size of lesions. The
most frequent radiological finding is
atrophy of the brain (Fig. 4). On MRI,
unilateral hyperintense lesions are usu-
ally present on T2W images, mostly in
the frontal lobe, and progress to bilat-
eral involvement. In the later stages,
MRI reveals a diagnostic pattern of ab-
normalities: extensive and symmetric
involvement of the deep white matter
with typically spared cortical gray mat-
ter (Fig. 5). Contrast enhancement and
mass effect are not features of lesions
in HIV encephalitis (3). Among MRI
techniques, magnetization transfer ra-
tio (MTR) may be used to demonstrate
macromolecular destruction (myelin
and axonal loss) in HIV encephali-
tis and may help early diagnosis and
in differentiation between progres-
sive multifocal leukoencephalopathy
(PML) by showing a degree of destruc-
tion which is more pronounced in PML
(11). Wu et al. have proposed that dif-
Figure 1. Axial FLAIR image of an AIDS
patient with Wernicke encephalopathy shows
hyperintense signal of the mamillary bodies.
Figure 2. A 1-year-old girl with developmental
delay and fever. Axial non-enhanced CT
image shows basal ganglia calcifications.
b
a
Figure 3. a–d. A 41-year-old male with numbness of the whole left side. T1-weighted axial MR
images (a, b) demonstrate HIV vasculitis as hemorrhagic infarct of the right anterior temporal
lobe and lentiform nucleus. There is also chronic infarct of the posterior temporal lobe. A small
saccular small aneurysm at the middle cerebral artery (MCA) bifurcation is depicted (a). On
axial T2-weighted MR image obtained a few months later (c), chronic stage of the previous
hemorrhagic subacute infarct is seen with peripheral hemosiderin rim on the anterior temporal
lobe; posterior chronic infarct is depicted again. MR angiography (d) shows occluded right
MCA and a small saccular aneurysm on the anterior trunk of the left MCA.
d
c

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Imaging features of CNS involvement in AIDS • iii
fusion tensor imaging (DTI) measure-
ments acquired in the corpus callosum
splenium were significantly associated
with dementia severity and with motor
speed, a sensitive marker of early cog-
nitive decline in patients infected with
HIV (12). On CT scans, abnormal areas
of white matter may show decreased
attenuation (13).
Opportunistic infections
Toxoplasmosis
Toxoplasma encephalitis occurs in
15–50% of HIV-infected patients (3).
Any neurological sign indicative of
CNS involvement should lead to neu-
roimaging studies in HIV-infected pa-
tients, as toxoplasmosis is the most
frequent and easily treatable oppor-
tunistic infection (14). Until proven
otherwise, HIV/AIDS patients pre-
senting with focal neurological com-
plaints should be accepted as having
CNS toxoplasmosis (15). The corti-
comedullary junction, basal ganglia,
and thalamus are most frequently in-
volved; less commonly the brainstem
may be affected (1). Typical CT find-
ings of toxoplasmosis abscesses are
multiple iso- or hypodense lesions,
enhancing in a ring or nodular pat-
tern with perifocal vasogenic edema
and mass effect. The lesions may be
hyperdense if hemorrhagic (1). MRI
is superior to CT in detecting the le-
sions and identifying the disease ex-
tension. On T2W MRI, the majority of
the lesions are hyperintense; however,
iso- or hypointense lesions, as well as
a mixed pattern, may be found. T1 sig-
nal depends on lesion characteristics,
e.g., presence of hemorrhage or calci-
fication (Fig. 6). Pathological contrast-
enhancement on imaging is absent or
faint with CD4 counts below 50/mm3,
and becomes more pronounced as the
count increases—that is, when the pa-
tient becomes more able to develop an
immune/inflammatory response (1).
Imaging modalities are also important
in follow-up. If the lesions remain sta-
ble or increase in size 10–14 days after
beginning of a specific treatment, im-
mediate brain biopsy is indicated to
exclude lymphoma (3), as distinction
between lymphoma and toxoplasmo-
sis lesions is often difficult and may be
impossible in some cases on imaging
studies. Brain single photon emission
computed tomography (SPECT), 18F-
fluorodeoxyglucose positron emission
tomography (FDG-PET), or MR spec-
troscopy (MRS) may help in diagno-
sis. On thallium 201 (TI 201) SPECT,
in patients with lymphoma abnormal
increased uptake of TI 201 is usually
seen, whereas in toxoplasmosis no up-
take is found (3). On FDG-PET, high
FDG uptake most likely represents
lymphoma, which should be biopsied
for confirmation rather than treated
presumptively as infectious (16). On
MRS, lactate and lipids are elevated,
with reduction or absence of all nor-
mal brain metabolites in toxoplasmo-
sis lesions, whereas a prominent in-
crease in choline could be observed in
lymphoma (Fig. 7) (2).
Cryptococcosis
Cryptococcus neoformans is the most
common intracranial fungal infec-
tion and third commonest infecting
pathogen in AIDS (1). Cryptococcal
meningoencephalitis is still associated
with an overall mortality rate of 20%
Figure 4. A 34-year-old male with loss of
orientation to time. Axial T1-weighted
MR image shows cerebral cortical
atrophy, the most common finding of HIV
encephalopathy.
b
a
Figure 5. a–d. A 34-year-old male with loss of orientation to time. Axial T1-weighted
MR image (a) does not reveal any abnormal signal intensity. Symmetrical and diffuse
hyperintensity of the white matter is demonstrated on axial T2-weighted MR image (b); there
is a T2 shine-through effect on trace diffusion-weighted image (c), and no apparent change
of apparent diffusion coefficient (ADC) value on ADC map (d), and no mass affect compatible
with HIV encephalopathy.
d
c

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Şenocak et al.
iv • Diagnostic and Interventional Radiology
despite appropriate antifungal therapy
(17). Imaging findings are nonspecif-
ic, and most often CT and MR images
are normal. Nevertheless, meningitis
with mild dilatation of the ventricular
system or rarely nodular meningeal
enhancement on contrast-enhanced
images may be detected. Dilated Vir-
chow-Robin spaces filled with fungi
result in the formation of nonenhanc-
ing cystic lesions, predominantly seen
symmetrically in the basal ganglia
and thalamus. As expected, these le-
sions are of low density on CT scan,
hypointense on T1W MR images and
hyperintense on T2W MR images. An-
other pattern of cryptococcal CNS in-
fection is a solid or ring-like contrast-
enhancing parenchymal mass, crypto-
coccoma, which is extremely rare and
found preferentially in the ependyma
of the choroid plexus. These findings,
although nonspecific, are very sugges-
tive of CNS cryptococcosis in the ap-
propriate clinical setting (3). Between
2002 and 2008 we did not observe an
abnormal imaging finding attribut-
able to cryptococcal infection among
our AIDS patients.
Progressive multifocal
leukoencephalopathy
Progressive
cephalopathy (PML) is a fulminating
opportunistic infection of the brain
that occurs in approximately 4% of
AIDS patients; it is caused by the JC
papovavirus (18). Primary infection
with JC virus occurs in childhood
and remains latent. In the setting of
severely altered cellular immunity,
this virus causes extensive myelin
breakdown and white matter destruc-
tion, because of its targeting of the
oligodendrocytes, the cell responsi-
ble for the production of myelin (18).
The lesions are typically multifocal
hypodensities on CT scans, and hy-
perintense patchy areas on T2W MR
images, which start subcortically (the
site of highest blood flow), then ex-
tend into the deep white matter. They
demonstrate rapid progression in size,
resulting in confluence of the lesions
(3). Extensive white matter high sig-
nal on T2W /FLAIR imaging with spar-
ing of the cortical gray matter is the
hallmark of this infection (Fig. 8) (1).
There is a lack of mass effect (3). Con-
trast enhancement, however, especial-
ly when faint and peripheral, does not
exclude a PML diagnosis (14, 18) and
has been considered by Berger et al. to
be one of the factors predictive of pro-
longed survival in AIDS patients with
PML, along with higher CD4 counts,
possibly because of the patient’s abil-
ity to mount a better response (19).
The lesions may show a central area
of marked hypodensity on CT, or they
may show hyperintensity on T2W MR
images, resembling necrosis (3). While
a posterior location has been used as
an imaging sign favorable to the di-
multifocal leukoen-
b
a
Figure 6. a–d. A 39-year-old male with loss of consciousness. Axial FLAIR MR image shows
toxoplasmosis lesions in the corticomedullary junction of the right frontal and parietal lobes
and posterior periventricular white matter on the left, (a) which enhance peripherally after
gadolinium administration (b). Lesions show restricted diffusion on diffusion-weighted
imaging (c, d).
d
c
Figure 7. On MR spectroscopy of the right parietal lymphoma lesion, a prominent increase in
choline is observed with decrease in N-acetyl-aspartate. The lesion has a high lipid peak.

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Imaging features of CNS involvement in AIDS • v
agnosis of PML, such a location has
not been deemed pathognomonic of
PML (18). In PML, MTRs are very low
(11). DTI also allows quantification of
the degree of tissue injury, and these
measurements can be used to guide
and monitor treatment (20).
Cytomegalovirus infection
Cytomegalovirus (CMV) exists in la-
tent form in general population. As
many as 90% of adults have antibod-
ies to it; CMV infection is typically the
result of reactivation (1). Radiographic
studies of CMV infection in the CNS
are nonspecific and, in almost all cas-
es, CT and MRI do not reveal any ab-
normality (3). Atrophy and ventricular
enlargement are present in 40% of the
cases (14). Brain involvement is usu-
ally in the form of encephalitis, with
preferential involvement of periven-
tricular regions and brainstem. Ven-
triculitis, infarcts, and meningitis are
other manifestations. Less commonly,
spinal cord, cranial nerves, and the
peripheral nervous system may be af-
fected. CT findings, if present, include
diffuse white matter hypodensities,
ependymal enhancement, and focal
ring-enhancing or nodular-enhancing
lesions (1). Foci of increased signal on
T2W sequences are typical on MRI.
Necrotic ventriculitis may cause pe-
riventricular subependymal enhance-
ment around the lateral ventricles,
septum pellucidum, corpus callosum,
and the fornices (Fig. 9); or demyelina-
tion may result in diffuse white matter
abnormalities (3). Signs of ventriculi-
tis on imaging studies are supportive
of the diagnosis but are nonspecific as
they can also occur in Herpes virus ven-
triculitis or lymphoma (14). Because
of nonspecific neuroradiological fea-
tures, the diagnosis of CMV infection
must be confirmed by histological
identification of typical intranuclear
inclusions (owl’s eyes) (3).
Tuberculosis
CNS tuberculosis has a high mortality
(79%) among AIDS patients, underlin-
ing the necessity for an early diagnosis
(3). As in the non-AIDS population, ba-
sal meningitis usually presenting with
increased FLAIR intensity (suggestive
of exudate and meningeal enhance-
ment in the basal cisterns) and hydro-
cephalus are typical findings of CNS
tuberculosis (Fig. 10) (3). Rupture of
subependymal or subpial granulomata
into the cerebrospinal fluid (CSF) or
penetration of the walls of meningeal
vessels by hematogenous spread have
been proposed for the pathogenesis
of tuberculous meningitis (21). Com-
municating hydrocephalus, which is a
common sequela of tuberculous men-
ingitis, primarily results from obstruc-
tion of the basal cisterns by the dense
inflammatory exudates. Occasionally,
the hydrocephalus may be attributable
to a focal parenchymal lesion with
mass effect or entrapment of a ven-
tricle by granulomatous ependymitis
(3, 21). Tuberculomas may result from
extension of CSF infection into adja-
cent parenchyma via cortical veins or
small penetrating arteries or may result
from hematogenous spread of systemic
disease. They may be found anywhere
both in the intra- and extra-axial spac-
es; the majority are said to be supraten-
torial. Tuberculomas may be solitary
or multiple and may show nodular en-
hancement. Early tuberculomas appear
hypointense whereas mature tubercu-
lomas contain a hypointense center
Figure 8. A 12-year-old boy with seizures
and headache. Axial FLAIR MR image shows
hyperintense signal in the left frontal and
periventricular white matter consistent with
progressive multifocal leukoencephalopathy.
b
Figure 9. a–d. A 35-year-old male with tonic-clonic convulsions. Contrast-enhanced axial (a)
and coronal (b) T1-weighted MR images demonstrate ventriculitis caused by Cytomegalovirus
infection as periventricular ependymal enhancement. Diffusion-weighted MR image (c) and
apparent diffusion coefficient map (d) demonstrate periventricular restricted diffusion.
d
a
c

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Şenocak et al.
vi • Diagnostic and Interventional Radiology
surrounded by an isointense capsule
on T2W MRI sequences (Fig. 11) (21).
Tuberculous abscesses are rare, tend to
be larger than tuberculomas, and have
a more accelerated clinical course.
They are mostly multiloculated, and
central liquefaction with pus forma-
tion appears hyperintense on T2W
images. Significant edema and mass
effect favor abscess. These ring-like en-
hancing lesions can pose problems in
differentiation from abscesses of other
etiologies, especially in the absence of
associated findings such as basal men-
ingitis, hydrocephalus, and basal gan-
glia infarcts (3, 21). Infarction (Fig. 11)
is another common complication of
CNS tuberculosis, a result of spasm and
thrombosis as arterial vessels course
through the gelatinous basal exudates.
The most common locations are the
regions of basal ganglia (1, 3). We used
the MR images of a patient without
AIDS to demonstrate the imaging find-
ings of tuberculosis infection, as none
of our AIDS patients had tuberculosis;
however, one should keep in mind that
imaging features reported are similar to
those in the non-AIDS population.
Syphilis
It has been suggested that the natural
history of syphilis is altered by HIV in-
fection, because HIV-infected patients
are more likely to progress to clinical
neurosyphilis, and neurologic symp-
toms develop after shorter latent peri-
ods than in non-AIDS population (22).
Typical imaging findings are ischemic
infarcts in the perforator vessel territo-
ry of the basal ganglia or brainstem or
in the large vessel territory of the mid-
dle cerebral artery. Syphilitic cerebral
gummas are uncommon. They appear
as isolated, peripherally located nod-
ules on CT that appear isodense to cor-
tex and enhance intensely following
iodinated contrast material adminis-
tration (1). On MRI, they are isointense
to gray matter on T1W sequences, usu-
ally enhance homogeneously, and are
hyperintense on T2W sequences. Cra-
nial nerve involvement, particularly of
the optic and vestibulocochlear nerves,
has also been reported (1, 23).
Lymphoma
Parallel with the rising frequency of
AIDS, the prevalence of primary CNS
lymphoma (PCL) has increased to 6%
among AIDS patients (3). Unlike clas-
sical PCL, AIDS-related lymphoma can
Figure 10. a, b. A 42-year-old male with fever and loss of consciousness. Axial FLAIR MR image
(a) shows basal meningitis of tuberculosis infection presenting with increased signal intensity
suggestive of exudates. Contrast-enhanced axial T1-weighted MR image (b) shows nodular
meningeal enhancement in the basal cisterns; hydrocephalus is also depicted with dilatation of
the temporal horns of the lateral ventricles.
b
a
b
Figure 11. a–d. A 42-year-old male with fever and loss of consciousness. Axial T2-
weighted MR image (a) shows tuberculoma of the right parietal lobe with hypointense
center surrounded by hyperintense capsule that enhances peripherally on contrast
enhanced axial T1-weighted MR image (b). Acute infarct of the corpus callosum with
restricted diffusion is also depicted on diffusion-weighted MR image (c) and apparent
diffusion coefficient map (d).
d
a
c

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Imaging features of CNS involvement in AIDS • vii
be cortical, tends to involve gray and
white matter, is associated with lep-
tomeningeal thickening, and may in-
duce vasculitis (1). PCL predominantly
involves the basal ganglia, corpus cal-
losum, periventricular white matter,
frontal lobes, and thalamus; it is occa-
sionally confined to the subependymal
regions or can even be wholly intraven-
tricular (1, 3). It is typically isointense
to gray matter on T2W MR images, usu-
ally with a moderate peripheral edema.
The iso-/hypointensity of the central
areas is the result of necrosis due to the
coagulation necrosis and thrombosis of
the vessels. The lesion shows hetero-
geneous or ring-like, irregular nodular
type enhancement (3). Linear enhance-
ment at the margins of a lesion, track-
ing along Virchow-Robin perivascular
spaces, is highly specific for PCL (Fig.
12) (24). A large (more than 3.5 cm in
diameter) prominently enhancing le-
sion, localized in the deep white matter,
close to the midline, or a periventricu-
lar lesion, with a moderate degree of
edema and mass effect with rapid pro-
gression, should be suggestive of PCL
(3). The major differential diagnosis is
toxoplasmosis, and, as mentioned pre-
viously, biopsy may be often indicated.
SPECT, FDG-PET, and/or MRS may help
in diagnosis, before performing inter-
ventional procedures or surgery.
Conclusion
CT and MRI are both excellent means
of detection of cerebral lesions in AIDS
patients, useful in initial diagnosis and
in therapeutic follow-up evaluation.
MRI has a higher sensitivity. Imaging
findings of the lesions in HIV-infected
patients may overlap, and differential
diagnosis may be difficult; however,
certain imaging characteristics and lo-
calizations of lesions may favor the di-
agnosis. Adjunctive imaging tools such
as proton MRS, perfusion-weighted
MRI, CT, or MR angiography may help
to identify certain pathologic abnor-
malities to highlight the diagnosis.
References
1. Offiah CE, Turnbull IW. The imaging ap-
pearances of intracranial CNS infections in
adult HIV and AIDS patients. Clin Radiol
2006; 61:393–401.
2. Centers for Disease Control and Prevention
(CDC). Trends in HIV/AIDS diagnoses
among men who have sex with men--33
States, 2001-2006. MMWR Morb Mortal
Wkly Rep 2008; 57:681–686.
3. Thurnher MM, Thurnher SA, Schindler E.
CNS involvement in AIDS: spectrum of CT
and MR findings. Eur Radiol 1997; 7:1091–
1097.
4. Kauffman WM, Sivit CJ, Fitz CR, Rakusan
TA, Herzog K, Chandra RS. CT and MR
evaluation of intracranial involvement in
pediatric HIV infection: a clinical-imaging
correlation. AJNR Am J Neuroradiol 1992;
13:949–957.
5. Shah SS, Zimmerman RA, Rorke LB, Vezina
LG. Cerebrovascular complications of HIV
in children. AJNR Am J Neuroradiol 1996;
17:1913–1917.
6. Patsalides AD, Wood LV, Atac GK, Sandifer
E, Butman JA, Patronas NJ. Cerebrovascular
disease in HIV-infected pediatric pa-
tients: neuroimaging findings. AJR Am J
Roentgenol 2002; 179:999–1003.
7. Gillams AR, Allen E, Hrieb K, Venna N,
Craven D, Carter AP. Cerebral infarction in
patients with AIDS. AJNR Am J Neuroradiol
1997; 18:1581–1585.
8. Joshi VV, Pawel B, Connor E, et al.
Arteriopathy in children with acquired im-
mune deficiency syndrome. Pediatr Pathol
1987; 7:261–275.
9. O’Charoen P, Hesselink JR, Healy JF.
Cerebral aneurysmal arteriopathy in an
adult patient with acquired immunodefi-
ciency syndrome. AJNR Am J Neuroradiol
2007; 28:938–939.
10. Takeuchi M, Nobukuni K, Takata H, et al.
Rapidly progressed acquired immunode-
ficiency syndrome dementia complex as
an initial manifestation. Intern Med 2005;
44:757–760.
11. Dousset V, Armand JP, Lacoste D, et al.
Magnetization transfer study of HIV
encephalitis and
focal leukoencephalopathy.
d’Epidémiologie Clinique du SIDA en
Aquitaine. AJNR Am J Neuroradiol 1997;
18:895–901.
12. Wu Y, Storey P, Cohen BA, Epstein LG,
Edelman RR, Ragin AB. Diffusion altera-
tions in corpus callosum of patients with
HIV. AJNR Am J Neuroradiol 2006; 27:656–
660.
13. Balakrishnan J, Becker PS, Kumar AJ,
Zinreich SJ, McArthur JC, Bryan RN.
Acquired immunodeficiency syndrome:
correlation of radiologic and pathologic
findings in the brain. Radiographics 1990;
10:201–215.
progressive multi-
Groupe
b
Figure 12. a–d. A 54-year-old male with left-sided weakness. Frontal and parietal diffuse
edematous area is seen with hypointense nodular lesions on axial T2-weighted MR image
(a). On contrast enhanced axial T1-weighted MR image (b), these lesions show nodular
enhancement accompanied by linear enhancement at the margins of a lesion, tracking along
perivascular spaces, highly suggestive of primary central nervous system lymphoma. Posterior
larger lesion shows restricted diffusion on diffusion-weighted MR image (c) and apparent
diffusion coefficient map (d).
d
a
c

Page 8

Şenocak et al.
viii • Diagnostic and Interventional Radiology
14. Roullet E. Opportunistic infections of the
central nervous system during HIV-1 in-
fection (emphasis on cytomegalovirus dis-
ease). J Neurol 1999; 246:237–243.
15. Kurne A, Ozkaya G, Karli Oğuz K, et al. [The
colorful clinical spectrum of cerebral toxo-
plasmosis in five HIV positive cases: what
comes out of Pandora’s box?]. Mikrobiyol
Bul 2006; 40:85–92.
16. Hoffman JM, Waskin HA, Schifter T, et
al. FDG-PET in differentiating lymphoma
from nonmalignant central nervous sys-
tem lesions in patients with AIDS. J Nucl
Med 1993; 34:567–575.
17. Charlier C, Dromer F, Lévêque C, et al.;
French Cryptococcosis
Cryptococcal neuroradiological lesions cor-
relate with severity during cryptococcal
meningoencephalitis in HIV-positive pa-
tients in the HAART era. PLoS ONE 2008; 16:
e1950.
Study Group.
18. Post MJ, Yiannoutsos C, Simpson D, et al.
Progressive multifocal leukoencephalopa-
thy in AIDS: are there any MR findings use-
ful to patient management and predictive
of patient survival? AIDS Clinical Trials
Group, 243 Team. AJNR Am J Neuroradiol
1999; 20:1896–1906.
19. Berger JR, Levy RM, Flomenhoft D, Dobbs
M. Predictive factors for prolonged sur-
vival in acquired immunodeficiency syn-
drome-associated progressive multifocal
leukoencephalopathy. Ann Neurol 1998;
44:341–349.
20. Huisman TA, Boltshauser E, Martin E,
Nadal D. Diffusion tensor imaging in pro-
gressive multifocal leukoencephalopathy:
early predictor for demyelination? AJNR
Am J Neuroradiol 2005; 26:2153–2156.
21. Whiteman M, Espinoza L, Post MJ, Bell
MD, Falcone S. Central nervous system tu-
berculosis in HIV-infected patients: clini-
cal and radiographic findings. AJNR Am J
Neuroradiol 1995; 16:1319–1327.
22. Brightbill TC, Ihmeidan IH, Post MJ, Berger
JR, Katz DA. Neurosyphilis in HIV-positive
and HIV-negative patients: neuroimaging
findings. AJNR Am J Neuroradiol 1995;
16:703–711.
23. Osborn AG. Diagnostic neuroradiology.
1st ed. St. Louis: Mosby, 1994; 678–680.
24. Eichler AF, Batchelor TT. Primary central
nervous system lymphoma: presentation,
diagnosis and staging. Neurosurg Focus
2006; 21:E15.