Approach To HIV-Infected Patients With Central Nervous System Lesions

30/10/2017 Approach to HIV-infected patients with central nervous system lesions - UpToDate
Official reprint from UpToDate

www.uptodate.com 2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Approach to HIV-infected patients with central nervous system lesions
Author: Igor J Koralnik, MD

Section Editor: John G Bartlett, MD
Deputy Editor: Jennifer Mitty, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Feb 09, 2017.
INTRODUCTION The evaluation and management of the HIV-infected patient who presents with a change in
mental status or abnormal neurologic examination is a challenging problem. Patients often have lesions on
computed tomography (CT) scan or magnetic resonance imaging (MRI), which may represent life-threatening
emergencies depending upon their size and location.
The most important factor in determining the differential diagnosis is the degree of immunosuppression in the
host.
In patients with CD4 cell counts >500/microL, benign and malignant brain tumors and metastases
predominate, as in immunocompetent hosts.
In moderately immunosuppressed patients with CD4 cell counts from 200 to 500/microL, HIV-associated
cognitive and motor disorders are common, but usually do not present with focal lesions.
CNS mass lesions are most common in severely immunosuppressed patients with CD4 cell counts
<200/microL. The most likely diagnostic considerations include opportunistic infections (OIs) and AIDS-
associated tumors, such as primary central nervous system lymphoma.
In addition, multiple etiologies can coexist in an immunosuppressed individual [1-3]. In one study of HIV-infected
patients undergoing brain biopsy for the diagnosis of focal CNS lesions, 6 percent had more than one etiology
established from histologic sampling of a single lesion [2].
EPIDEMIOLOGY A thorough knowledge of the various etiologies for CNS disease in the HIV-infected patient
is important for proper evaluation and management. The leading diagnostic considerations in a patient with
advanced immunosuppression are Toxoplasma encephalitis (TE), primary CNS lymphoma, progressive
multifocal leukoencephalopathy, HIV encephalopathy, and CMV encephalitis.
Patients who are not under medical supervision, or those who are not aware of their HIV status, may present
with their first opportunistic infection in the central nervous system. The clinical manifestations and the diagnostic
possibilities are similar to those seen in before the introduction of potent antiretroviral therapy (ART) era.
However, the effect of prophylaxis for Pneumocystis and the use of ART may alter the clinical spectrum of
disease and the diagnostic considerations in patients who are taking medications. Although the list of etiologies
is essentially the same, the incidence and the spectrum of disease has changed as illustrated by the following
points:
https://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/print?source=search_result&search=appro 1/13
The use of TMP-SMX prophylaxis against Pneumocystis is also effective for the prevention of TE. In one
study, the frequency of TE decreased from 72.2 to 18.6 percent from 1991 to 1996 [4].
The introduction of potent ART has been associated with a declining incidence of HIV encephalopathy,
primary CNS lymphoma, and progressive multifocal encephalopathy [5,6]. On the other hand, it is possible
that ART may be contributing to a new form of severe, demyelinating leukoencephalopathy characterized by
intense perivascular infiltration by HIV antigens and inflammatory cells with widespread myelin loss and
axonal injury [7].
RADIOLOGIC APPEARANCE OF CNS LESIONS The discovery of a CNS lesion is made by head CT or
MRI. These examinations must be performed before and after injection of contrast material to determine whether
a lesion enhances on neuroimaging. Enhancement usually signifies the presence of inflammation. Clinicians
need to be aware that steroid therapy, which reduces inflammatory responses, can convert enhancing into
nonenhancing lesions. (See 'Corticosteroids' below.)
MRI has a number of advantages compared to CT scan. It is much more sensitive than CT scan in determining if
a lesion is truly solitary; it has greater sensitivity for white matter disease or lesions in the posterior fossa [8]; and,
if a biopsy is being considered, it may identify a peripheral lesion that is more accessible for histologic sampling
[9] (image 1).
CNS mass lesions can be classified into two categories, according to the presence or absence of mass effect.
CNS lesions with mass effect CNS mass lesions are characterized by the presence of swelling, edema, and
mass effect on surrounding structures. In some cases, especially for lesions located in the posterior fossa,
cerebral herniation occurs. Mass lesions usually enhance after the injection of contrast material, indicating local
inflammation and breakdown of the blood-brain barrier.
Patients with mass effect can present with headache, nausea, vomiting, confusion, and lethargy, all of which may
reflect evidence of increased intracranial pressure.
The two leading diagnoses associated with mass effect in developed countries are Toxoplasma encephalitis and
primary central system lymphoma. In the developing world, tuberculomas are a leading diagnostic consideration
[10].
Toxoplasma encephalitis Toxoplasma encephalitis (TE) represents reactivation disease from prior
infection. Affected patients present with fever, headache, altered mental status, and focal neurologic complaints
or seizures. Supporting laboratory findings include the presence of Toxoplasma antibodies, which is consistent
with past exposure, and advanced immunosuppression with CD4 counts <100 cells/microL. (See "Toxoplasmosis
in HIV-infected patients".)
TE lesions are generally multiple and are localized in the parietal or frontal lobes, in the thalamus or basal
ganglia, or at the corticomedullary junction [11]. Ring enhancement is present in approximately 90 percent and
surrounding edema with mass effect is often seen (image 2). Uncommonly, TE can present as a diffuse
encephalitis, which is not associated with focal abscess formation [12].
The neuroradiologic characteristics of TE are not pathognomonic and may be observed in other conditions,
particularly lymphoma. If a single lesion is seen, an MRI should be obtained to determine whether the lesion is
truly solitary. Although single lesions can be seen in TE infection, solitary large (>4 cm) lesions are more
suspicious for primary CNS lymphoma. (See "AIDS-related lymphomas: Primary central nervous system
lymphoma".)
Primary central nervous system lymphoma Primary central nervous system lymphoma (PCNSL) can
present with confusion, lethargy, memory loss, hemiparesis, aphasia, and/or seizures. In addition, constitutional
symptoms, such as fever, night sweats, and weight loss, occur in over 80 percent of patients. (See "AIDS-related
lymphomas: Primary central nervous system lymphoma".)
In contrast to patients with toxoplasmosis, solitary and multiple mass lesions occur with approximately equal
frequency [13,14]. The majority of lesions display some degree of enhancement that is irregular or patchy (image
3). However, diffuse ring enhancement, identical to that commonly seen in TE, can occur.
The location and size may also be helpful to distinguish Toxoplasma infection from PCNSL. As an example,
lesions that involve the corpus callosum or the periventricular or periependymal areas are more likely to be due
to PCNSL, whereas posterior fossa lesions are more likely due to infection. Lesions that are larger than 4 cm in
size are more likely to be lymphoma. However, these neuroradiologic characteristics do not discriminate well
enough between TE and PCNSL [15].
Other infections Other opportunistic infections can be associated with focal CNS lesions with or without
mass effect, depending upon their size and location. These include brain abscesses secondary to
Staphylococcus, Streptococcus, Salmonella, Aspergillus, Nocardia, Rhodococcus, Listeria, unusual
granulomatous collections, such as cryptococcomas, and syphilitic gummas [16-20]. However, most of these
entities are much less common than TE or PCNSL and are often associated with evidence of disseminated
infection [21].
In the developing world, neurocysticercosis or tuberculosis can present as single or multiple mass lesions [10].
The appearance of neurocysticercosis depends upon the stage of the infection and the host immune response.
Tuberculomas can present as a focal lesion without evidence of systemic illness or meningeal infection. (See
"Clinical manifestations and diagnosis of cysticercosis" and "Central nervous system tuberculosis", section on
'Tuberculoma'.)
CNS lesions without mass effect Lesions without mass effect usually do not enhance after the injection of
contrast material and are not associated with a risk of herniation. The vast majority of these lesions are due to
progressive multifocal leukoencephalopathy or HIV-associated encephalopathy.
Progressive multifocal leukoencephalopathy Progressive multifocal leukoencephalopathy (PML) is a

demyelinating disease caused by the JC virus, a papovavirus that can be reactivated in the setting of severe
immunosuppression. Patients with PML characteristically present with rapidly progressive focal neurologic
deficits including hemiparesis, visual field deficits, ataxia, aphasia, and cognitive impairment. (See "Progressive
multifocal leukoencephalopathy: Epidemiology, clinical manifestations, and diagnosis".)
PML is usually characterized by multifocal areas of demyelination that are bilateral, asymmetric, and localized
preferentially to the periventricular areas and the subcortical white matter. The lesions are generally not contrast-
enhancing and are not surrounded by edema; as a result, substantial mass effect on surrounding structures is
absent. However, PML may occur in the setting of an immune reconstitution inflammatory syndrome (IRIS)
associated with increase of CD4+ T cell count and drop of HIV plasma viral load on antiretroviral therapy. In this
context, PML/IRIS can present with contrast enhancement on MRI, as well as focal edema and mass effect [22].
(See "Progressive multifocal leukoencephalopathy: Epidemiology, clinical manifestations, and diagnosis", section
on 'Inflammatory PML'.)
A detailed discussion of the appearance of PML on CT and MRI imaging is found elsewhere. (See "Progressive
multifocal leukoencephalopathy: Epidemiology, clinical manifestations, and diagnosis".)
The differential diagnosis of PML includes HIV encephalopathy, cytomegalovirus encephalitis, and PCNSL. (See
'Diagnostic approach' below.)
HIV encephalopathy HIV encephalopathy (HIVE) typically presents with the classic triad of symptoms of
subcortical dementia: memory and psychomotor speed impairment, depressive symptoms, and movement
disorders. Although this entity is not usually included in the category of CNS mass lesions, it can masquerade as
PML. (See "HIV-associated neurocognitive disorders: Epidemiology, clinical manifestations, and diagnosis".)
On MRI, multiple hyperintense signals are seen in T2-weighted images, which are generally non-enhancing and
localized bilaterally in the subcortical white matter (image 4). In contrast to the findings seen with PML, HIVE
lesions are usually symmetrical and less well-demarcated.
Cytomegalovirus encephalitis Encephalitis due to cytomegalovirus (CMV) results from reactivation in

patients with CD4 cell counts below 50 cells/microL. These patients present with delirium, confusion, and focal
neurologic abnormalities. (See "AIDS-related cytomegalovirus neurologic disease".)
MRI can show either diffuse micronodular encephalitis or ventriculoencephalitis. The former is characterized by
multifocal, diffusely scattered micronodules widely distributed in the cortex, basal ganglia, brainstem, and
cerebellum [23], while ventriculoencephalitis is characterized by progressive ventricular enlargement,
periventricular enhancement, and increased periventricular signal on T2-weighted images [24]. Rarely, CMV
causes focal ring-enhancing lesions with edema and mass effect [25].
Ancillary imaging studies Clinical and MRI/CT criteria alone are insufficient to lead to a diagnosis or to
direct appropriate treatment in HIV-infected patients with CNS lesions. As a result, a variety of specialized
imaging studies have been investigated, including thallium SPECT scans, perfusion MRI, MR spectroscopy, and
positron emission tomography.
These techniques are more sensitive than specific, and they may not be readily available outside of large
academic institutions. Thus, their role in helping the clinician establish the cause of a CNS lesion is unclear.
The following observations illustrate the range of findings:
Thallium 201 SPECT scan has been used to help differentiate CNS lymphoma from CNS toxoplasmosis,
since thallium is more avidly taken up to tumor cells [26-30]. In a study of 37 AIDS patients with intracranial
mass lesions on CT or MRI, all 12 patients with increased isotope uptake had biopsy proven PCNSL, while
24 of 25 without uptake had TE [27].
Perfusion MRI has been assessed to determine if changes in cerebral blood flow to CNS lesions can help
distinguish TE from PCNSL [31]. This imaging modality demonstrated decreased local blood flow in five
patients with TE; in contrast six patients with lymphoma had increased flow. Reduced perfusion in TE may
be related to lack of vasculature within an abscess compared to the relative hypervascularity of tumor tissue.
The utility of MR spectroscopy was assessed in 60 HIV-seropositive patients (25 with HIVE, 20 with TE, 8
with PML and 7 with PCNSL) and 22 HIV-seronegative controls. MRS demonstrated a high sensitivity in
detecting intracranial pathology, but poor sensitivity in the differential of CNS disease [32,33].
Positron emission tomography (PET) also may help differentiate PCNSL from CNS toxoplasmosis, as
demonstrated in two small studies [34,35].
DIAGNOSTIC APPROACH The diagnostic approach that we usually follow is summarized in the following
algorithm (algorithm 1). However, the algorithm is not as applicable in developing countries where alternative
strategies need to be considered that take into account tuberculosis as a common cause of CNS mass lesions
as well as any limitations in the availability of diagnostic testing [10].
CSF examination Lumbar puncture is contraindicated in patients with focal signs or with lesions producing
mass effect, especially in the posterior fossa, due to the risk of transtentorial herniation. If the patient does not
have any focality on examination and mass effect is not evident, then consideration should be given to
cerebrospinal fluid (CSF) examination, although its utility is limited.
In patients with Toxoplasma encephalitis (TE), progressive multifocal leukoencephalopathy (PML), or primary
central nervous system lymphoma (PCNSL), CSF analysis may demonstrate a mild pleocytosis and elevated
protein concentration, which are nonspecific. CSF cytology can help in the diagnosis of lymphoma if it is positive,
but this occurs in only 15 percent of cases with meningeal seeding. Cultures that are performed for isolated
abscesses are often negative.
The CSF findings in patients with brain abscess usually reflect a parameningeal pattern with <500
leukocytes/microL (predominantly lymphocytes), a normal glucose concentration, and a normal to mildly elevated
protein concentration. (See "AIDS-related lymphomas: Primary central nervous system lymphoma" and
"Toxoplasmosis in HIV-infected patients", section on 'Diagnosis' and "Pathogenesis, clinical manifestations, and
diagnosis of brain abscess", section on 'Lumbar puncture'.)
Polymerase chain reaction Polymerase chain reaction (PCR) analysis may assist in identifying the DNA
of JC virus (the causative agent of PML), Epstein-Barr virus (associated with PCNSL), and Toxoplasma gondii
[15,36].
PCR detection of JC virus DNA in PML had a sensitivity of 74 to 93 percent and a specificity of 92 to 100 percent
before the widespread use of potent ART [15,37-45]. Since then, the sensitivity of this test has dropped to 58
percent [46,47]. This is likely explained by ART-induced immune recovery, which may lower JCV replication
below the level of assay detection.
A patient with a positive PCR result who has a compatible radiologic picture can be presumed to have PML [8].
As a result, PCR has now become an established way to ascertain the diagnosis of PML. Nevertheless, HIV-
positive patients with low CD4+ T cell counts who present with clinical and radiologic findings consistent with
PML, should be considered as having "possible PML" even if JCV PCR is negative in the CSF, if other diagnoses
have been ruled out, based on consensus terminology criteria [48]. (See "Overview of JC polyomavirus, BK
polyomavirus, and other polyomavirus infections", section on 'Progressive multifocal leukoencephalopathy'.)
The utility of using PCR for EBV DNA is less clear, as the sensitivity and specificity have varied widely depending
upon whether the assay is performed in a research setting or a clinical laboratory [15,49]. Although a positive
EBV DNA PCR in an immunosuppressed patient with findings consistent with PCNSL is supportive of the
diagnosis, it does not exclude other causes of CNS disease. A conservative approach consists of confirming the
diagnosis with a brain biopsy, taking into account the risks inherent with this procedure. (See "AIDS-related
lymphomas: Primary central nervous system lymphoma".)
PCR has not been helpful for the detection of Toxoplasma gondii in CSF, with a sensitivity of only 50 percent,
although specificity ranges from 96 to 100 percent [8,15,43]. In contrast, PCR has become an important tool for
the diagnosis of CMV encephalitis, with a reported sensitivity exceeding 80 percent and a specificity of 90
percent [8,50]. (See "Toxoplasmosis in HIV-infected patients".)
Predictive value of clinical factors Investigators from Italy performed a decision analysis on 136
consecutive HIV patients presenting with focal CNS lesions between 1991 and 1995 (before the introduction of
effective ART) [15]. Following three weeks of empiric therapy for TE, patients with progressive disease
underwent a brain biopsy. In 66 patients, CSF PCR amplification for T. gondii, EBV, and JCV DNA was
performed. The following results were calculated:
The probability of TE was 0.87 in Toxoplasma seropositive patients with mass effect who were not on
trimethoprim-sulfamethoxazole (TMP-SMX), but only 0.59 for those receiving prophylaxis.
In Toxoplasma seropositive patients receiving TMP-SMX, the probability of PCNSL was 0.36.
In Toxoplasma seronegative patients with mass effect, the probability of PCNSL was 0.74, which increased
to 0.96 if EBV PCR was positive in the CSF.
Among focal brain lesions without mass effect, the probability of PML was 0.81, which increased to 0.99 if
JCV DNA was detected in the CSF.
Empiric Toxoplasma therapy A trial of empiric therapy for possible TE may be considered as an alternative
to brain biopsy when the above tests have not clearly identified a specific cause in a patient who presents with
focal CNS pathology but does not have manifestations of mass effect requiring early brain biopsy. Thus, clinical
symptoms and signs, neuroimaging, CD4 cell count, serologies, PCR results, and use of concomitant
medications, which could alter the diagnostic considerations, all need to be weighed:
Does the patient have advanced immunosuppression? If not, then tumors such as glioblastoma or
metastatic disease need to be excluded, as in HIV-seronegative patients. If the patient has severe
immunosuppression, then TE, PCNSL, and PML are the leading diagnostic considerations.
Does the patient have multiple lesions, which are radiologically consistent with TE or PCNSL? If serologic
studies show that the patient is seropositive for Toxoplasma, then TE becomes more likely [15]. However, as
noted in the previous section, the likelihood of TE is much lower if the seropositive patient is taking TMP-
SMX for prophylaxis for Pneumocystis [4,15]. The possibility of TE is also low (about 5 percent) if the patient
is seronegative for Toxoplasma [8]. In these settings, a brain biopsy should be pursued rapidly to make a
diagnosis.
Does the patient have a large solitary lesion greater than 4 cm in diameter? If so, then PCNSL is most likely
and tissue diagnosis is helpful. An empiric trial of treatment for TE is often employed if there is no immediate
concern for herniation risk. An imaging study should be repeated in approximately one week with plans for
early biopsy if no improvement is seen.
Does the patient have asymmetric lesions without mass effect that primarily involve white matter? In this
setting, PML is the leading diagnosis and CSF examination can help make a presumptive diagnosis if JC
virus can be isolated. Empiric Toxoplasma therapy is not warranted in such patients.
The empiric regimen for possible TE is discussed separately. Empiric therapy is usually given for 10 to 14 days.
(See "Toxoplasmosis in HIV-infected patients".)
It is critical to closely monitor the patient's neurologic examination during a trial of empiric therapy. Clinical
improvement is expected within one to two weeks [51]. The diagnosis of TE is established if the patient clinically
improves and there is a reduction in lesion size within two weeks. A brain biopsy should be considered in
patients who do not have clinical and radiologic improvement.
Corticosteroids Corticosteroid therapy should be considered in two settings:
When substantial mass effect can be demonstrated on imaging and the mental status is significantly
depressed. Such patients are at risk for cerebral herniation. (See "Evaluation and management of elevated
intracranial pressure in adults", section on 'Glucocorticoids' and "Management of vasogenic edema in
patients with primary and metastatic brain tumors", section on 'Glucocorticoids'.)
When the diagnosis of PCNSL has already been established, since steroids can cause false negative results
on a subsequent brain biopsy in patients with lymphoma. (See "Treatment and prognosis of primary central
nervous system lymphoma", section on 'Glucocorticoids'.)
The most common regimen is dexamethasone given intravenously as a 10 mg loading dose followed by 4 mg
Q6h; the drug should be discontinued as soon as possible. This regimen will decrease brain swelling whether or
not the mass is due to infection. As a result, a clear response to therapy is of no value in diagnosis. (See
"Evaluation and management of elevated intracranial pressure in adults".)
Brain biopsy Stereotactic brain biopsy is the gold standard for the diagnosis of focal CNS lesions in AIDS
[2,8], since several studies have demonstrated the inadequacy of clinical acumen alone [2,52]. However, biopsy
may not be possible with lesions in certain locations.
The overall reported complication rate has ranged from 0 to 3.1 percent mortality, 0.5 to 9 percent major
morbidity, and 2 to 4 percent minor morbidity [15,53-55]. The outcomes are better in centers with technical
expertise.
A definitive diagnosis is reached in as many as 93 to 96 percent patients [15,54]. This is important clinically,
since the prognosis of HIVE and PML has improved dramatically with the advent of ART [56-58].
SUMMARY AND RECOMMENDATIONS
The most important factor in determining the differential diagnosis in an HIV-infected patient with suspected
central nervous system (CNS) pathology is the degree of immunosuppression in the host. CNS mass lesions
are most common in severely immunosuppressed patients with CD4 cell counts <200/microL. (See
'Introduction' above.)
The leading diagnostic considerations in a patient with advanced immunosuppression are Toxoplasma
encephalitis, primary CNS lymphoma, progressive multifocal leukoencephalopathy, HIV encephalopathy,
and CMV encephalitis. (See 'Epidemiology' above.)
The discovery of a CNS lesion is made by head CT or MRI. These examinations must be performed before
and after injection of contrast material to determine whether a lesion enhances on neuroimaging.
Enhancement usually signifies the presence of inflammation. An MRI is more sensitive than a head CT in
determining if a lesion is truly solitary. (See 'Radiologic appearance of CNS lesions' above.)
CNS mass lesions are characterized by the presence of swelling, edema, and mass effect on surrounding
structures. The two leading diagnoses associated with mass effect in developed countries are Toxoplasma
encephalitis (TE) and primary central system lymphoma. In the developing world, tuberculomas are a
leading diagnostic consideration. (See 'CNS lesions with mass effect' above.)
Lesions without mass effect usually do not enhance after the injection of contrast material and are not
associated with a risk of herniation. The vast majority of these lesions are due to progressive multifocal
leukoencephalopathy or HIV-associated encephalopathy. (See 'CNS lesions without mass effect' above.)
Lumbar puncture is contraindicated in patients with focal signs or with lesions producing mass effect,
especially in the posterior fossa, due to the risk of transtentorial herniation. If the patient does not have any
focality on examination and mass effect is not evident, then consideration should be given to cerebrospinal
fluid (CSF) examination, although its utility is limited.
CSF cytology can help in the diagnosis of lymphoma if it is positive, but this occurs in only 15 percent of
cases with meningeal seeding. Polymerase chain reaction (PCR) analysis may assist in identifying the DNA
of JC virus (the causative agent of PML), Epstein-Barr virus (associated with lymphoma), and Toxoplasma
gondii. (See 'CSF examination' above.)
A trial of empiric therapy for possible TE may be considered as an alternative to brain biopsy when in a
patient who presents with focal CNS pathology but does not have manifestations of mass effect requiring
early brain biopsy. (See 'Empiric Toxoplasma therapy' above.)
Corticosteroid therapy should be considered in the presence of mass effect since these patients are at
increased risk of herniation. (See 'Corticosteroids' above.)
Stereotactic brain biopsy is the gold standard for the diagnosis of focal CNS lesions in AIDS, since several
studies have demonstrated the inadequacy of clinical acumen alone. However, biopsy may not be possible
with lesions in certain locations. (See 'Brain biopsy' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 3718 Version 7.0
GRAPHICS
AIDS patient with progressive multifocal

leukoencephalopathy (PML)
There is a focal area of low density on CT scan (A) which involves the right
periventricular white matter and extends peripherally to involve the subcortical white
matter. MRI of same patient shows the lesion to be hyperintense on T2-weighted (B)
and FLAIR (C) images, without contrast enhancement on post-contrast T1-weighted
image (D). Diffusion-weighted image (E) shows increased signal intensity with a more
hyperintense ring along the periphery, or advancing edge of the lesion. MR
Spectroscopy of this lesion (F) shows that this lesion has characteristic decreased NAA,
increased MI, increased choline, and elevated lactate/lipid peaks. (Refer to Izano et al).
MRI: magnetic resonance imaging; mI: myoinositol; Ch: choline; Cr: creatine; NAA: N-
acetyl-aspartate; Lac/Lip: lactate/lipids.
Courtesy of Eric D Schwartz, MD.
Graphic 74958 Version 4.0
MRI scan of patient with Toxoplasma encephalitis
Multiple ring enhancing lesions with mass effect are visible after injection of
gadolinium in this T1-weighted image.
https://www.uptodate.com/contents/approach-to-hiv-infected-patients-with-central-nervous-system-lesions/print?source=search_result&search=appr 10/13
MRI scan of a patient with primary central nervous

system lymphoma
A nodular enhancing lesion produces moderate mass effect on the frontal horn
of the right lateral ventricle in this T1-weighted image.
MRI: Magnetic resonance imaging.
MRI of the brain from a patient with HIV-associated

dementia
Bilateral symmetrical high T2 signals without mass effect are present in the
white matter of both frontal lobes, associated with subcortical atrophy.
MRI: Magnetic resonance imaging.
Algorithm for the management of HIV-infected patients with

central nervous system mass lesions
Elements in bold represent data which contribute to the decision-making process (see text
for details).
Toxo: Toxoplasma encephalitis; LP: lumbar puncture; CSF: cerebrospinal fluid; Rx: treatment.

Approach To HIV-Infected Patients With Central Nervous System Lesions - UpToDate

Загружено:

Сведения о документе

Оригинальное название

Авторское право

Доступные форматы

Поделиться этим документом

Поделиться или встроить документ

Параметры публикации

Этот документ был вам полезен?

Это неприемлемый материал?

Авторское право:

Доступные форматы

Approach To HIV-Infected Patients With Central Nervous System Lesions - UpToDate

Загружено:

Авторское право:

Доступные форматы

30/10/2017 Approach to HIV-infected patients with central nervous system lesions - UpToDate

Official reprint from UpToDate

Author: Igor J Koralnik, MD

Progressive multifocal leukoencephalopathy Progressive multifocal leukoencephalopathy (PML) is a

Cytomegalovirus encephalitis Encephalitis due to cytomegalovirus (CMV) results from reactivation in

The following observations illustrate the range of findings:

Corticosteroids Corticosteroid therapy should be considered in two settings:

SUMMARY AND RECOMMENDATIONS

early brain biopsy. (See 'Empiric Toxoplasma therapy' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 3718 Version 7.0

AIDS patient with progressive multifocal

Courtesy of Eric D Schwartz, MD.

Graphic 74958 Version 4.0

MRI scan of patient with Toxoplasma encephalitis

Graphic 74466 Version 3.0

MRI scan of a patient with primary central nervous

MRI: Magnetic resonance imaging.

Graphic 68209 Version 4.0

MRI of the brain from a patient with HIV-associated

MRI: Magnetic resonance imaging.

Graphic 82180 Version 4.0

Algorithm for the management of HIV-infected patients with

Graphic 50593 Version 2.0

Вам также может понравиться