Summary: A 58-year-old man presented with a 6-month history of progressive
blurring of vision and parosmia. Additional symptoms included an altered
taste and dizziness. He had past history of intravenous drug abuse, but
had not used drugs in many years. His human immunodeficiency virus
(HIV) status had been negative in the past. On admission he was afebrile
at 97°F. Neurological examination showed a left inferior quadrant field
defect. Motor and sensory examinations were normal. Deep tendon
reflexes were intact. Laboratory evaluations were unremarkable at the
time of admission. On the day of admission, computed tomography (CT)
without contrast was performed (not shown). An HIV test was sent under
the patient’s permission and had come back positive. The CD 4 count was
11 cells/µl. The toxoplasmosis IgG was positive.
Cerebral toxoplasmosis with necrotic and chronically inflamed brain parenchyma
CT without contrast (not shown) showed a 2-cm right parietal hypodense
lesion with surrounding edema. Magnetic resonance imaging (MRI) was
performed using a GE Signa LX 1.5T MRI scanner and magnevist was
injected intravenously (0.1 mmol/kg body weight).It showed several
enhancing lesions in the right parietal lobe, and the large, main mass
showed rim-enhancement (Figure 1). Diffusion-weighted (DW) imaging was
performed with an axial single-shot echoplanar sequences (TR/TE,
10000/99, section thickness = 5 mm, FOV= 38 cm) with an apparent
diffusion coefficient (ADC) map image, and a demonstrated heterogeneous
but relatively isointense mass to the unaffected white matter on DW
imaging, with a corresponding ADC map-image showing an iso/hyperintense
mass with surrounding vasogenic edema (Figure 2).
Toxoplasmosis, an infection with a worldwide distribution, is caused
by the intracellular protozoan parasite, Toxoplasma
gondii.Immunocompetent people with primary infection are usually
asymptomatic, but latent infection can persist for the life of the host.
Inimmunocompromised patients, especially patients with the acquired
immunodeficiency syndrome (AIDS), the parasite can reactivate and cause
disease, usually when the CD4 lymphocyte count falls below 100 cells/µl.
Patients with AIDS and < 100 CD4 cells/µl, who are toxoplasma
seropositive, have an approximately 30% probability of developing
reactivated toxoplasmosis if they are not receiving effective
prophylaxis. The most common site of reactivation is the central nervous
system (CNS), and toxoplasmosis is the most common CNS opportunistic
infection in AIDS patients.1
In the AIDS population,
differentiation of cerebral toxoplasmosis and lymphoma can be a
challenging clinical and radiological problem. These lesions are two of
the most common focal brain lesions in patients with AIDS, and they
typically occur when patients are severely immunocompromised. At
presentation, symptoms and signs of neurologic disease in HIV-positive
patients are frequently nonspecific. In radiologic terms, either disease
can present as a single mass or as multiple lesions that show
ring-shaped contrast enhancement on CT and MR images.2 Also, the two diseases occasionally have been documented to coexist, which further complicates diagnosis.3 Accurate
and early diagnosis is important because the treatment and prognosis
for these diseases are so different. Because of this diagnostic dilemma,
other radiologic techniques have been suggested as a means of
distinguishing between the two conditions.
are most commonly located in the cerebral hemispheric white matter and
subcortical gray matter, such as the thalamus and basal ganglia, and CT
and MR images show multiple ring-enhancing lesions.4 A focal
enhancing mass with subependymal spread on CT or MR images and
hyperattenuation on nonenhanced CT are features which favor the
diagnosis of primary CNS lymphoma.5 Recently
diffusion-weighted MR imaging with ADC maps has been used as a tool for
characterizing infectious and neoplastic brain lesions.Unlike pyogenic
abscesses, the core tissue of rim-enhancing toxoplasma abscesses shows
no restriction of water diffusion, and the signal intensity of the
abscess core on diffusion-weighted MRI is equal to or less than that of
normal, unaffected cerebral white matter. In addition, the measured
apparent diffusion coefficient is greater than that of unaffected white
matter.6 Some investigators also demonstrated that
toxoplasmosis lesions show significantly greater diffusion than that of
lymphoma lesions, and ADC ratios > 1.6 were associated solely with
A recent prospective study using
perfusion MR imaging showed that the regional cerebral blood volume
(rCBV) was decreased throughout the toxoplasmosis lesions and in the
surrounding edema of both lesion types, whereas all active lymphomas
displayed areas of increased rCBV.2 Proton MR spectroscopy
has been used to assess a variety of intracranial tumors, and diffuse
cerebral parenchymal abnormalities in HIV infection. However, the
application of spectroscopy to differentiate toxoplasmosis and lymphoma
is still questionable.8,9 Other diagnostic measures have been suggested, and 201Tl single photon emission computed tomography (SPECT) has been shown to be useful, but diagnostic inaccuracy persists.10 Similarly, 18F-fluoro-2-deoxyglucose positron emission tomography (PET) is also helpful in distinguishing between the two conditions.11,12
At most centers, however, the current clinical policy for AIDS patients
with intracranial mass lesions is a therapeutic trial with
antitoxoplasmosis chemotherapy for 2 to 3 weeks. Fortunately, the median
time to neurologic response is 5 days, with a significant improvement
present in > 90% of patients by day 14.4 If there is no clinical or radiologic response to the treatment at this stage, biopsy is considered.
- Porter, SB, Sande, MA. Toxoplasmosis of the central nervous system in the acquired immunodeficiency syndrome. N Engl J Med. 1992; 327: 1643-1648.
Ernst TM, Chang L, Witt MD, et al. Cerebral toxoplasmosis and lymphoma
in AIDS: perfusion MR imaging experience in 13 patients. Radiology. 1998; 208:663-669.
G, Parizel PM, Farber CM, et al. Nervous system manifestations and
neuroradiologic findings in acquired immunodeficiency syndrome (AIDS). Neuroradiology. 1989; 31: 33-39.
- Ramsey RG, Geremia GK. CNS complications of AIDS: CT and MR findings. Am J Roentgenol. 1988; 151:449-454.
- Dina TS. Primary central nervous system lymphoma versus toxoplasmosis in AIDS. Radiology. 1991; 179: 823-828.
- Chong-Han CH, Cortez C, Tung GA. Diffusion-weighted MRI of cerebral toxoplasma abscess. Am J Roentgenol. 2003; 181:1711-1714.
Camacho DLA, Smith JK, Castillo M. Differentiation of toxoplasmosis and
lymphoma in AIDS patients by using apparent diffusion coefficients. Am J Neuroradiol. 2003; 24: 633-637.