Rationale and Objectives
The aim of this study was to assess the relationship between immune state and cerebral signal intensity abnormalities (SIAs) on T2-weighted magnetic resonance images in subjects with human immunodeficiency virus type 1 infection and highly active antiretroviral therapy.
Materials and Methods
Thirty-two subjects underwent a total of 109 magnetic resonance studies. The presence of human immunodeficiency virus–associated neurocognitive disorder, categorized CD4 + T lymphocyte count, and plasma viral load were assessed for relationship with the severity and interval change of SIAs for different anatomic locations of the brain.
Results
Subjects with multifocal patterns of SIAs had CD4 + cell counts < 200 cells/μL in 66.0%, whereas subjects with diffuse patterns of SIAs had CD4 + cell counts < 200 cells/μL in only 31.4% ( P < .001). Subjects without SIAs in the basal ganglia had CD4 + cell counts < 200 cells/μL in 37.0%, whereas subjects with minor and moderate SIAs in the basal ganglia had CD4 + cell counts < 200 cells/μL in 78.3% and 80.0%, respectively ( P < .005). The percentage of subjects with CD4 + cell counts < 200 cells/μL was 85.7% when there were progressive periventricular SIA changes and 45.5% when periventricular SIA changes were stable in follow-up ( P < .05).
Conclusions
The presence and progression of cerebral SIAs on T2-weighted magnetic resonance images reflecting cerebral infection with human immunodeficiency virus are significantly related to impaired immune state as measured by CD4 + cell count.
Central nervous system (CNS) involvement often occurs as part of human immunodeficiency virus (HIV) infection. This concerns not only the incidence of opportunistic CNS infections but in particular the direct CNS manifestation of HIV infection . Usually, in 10% of all HIV-infected and acquired immunodeficiency syndrome (AIDS) patients, neurologic complaints are the initial clinical manifestation, and an additional 30% to 60% of all patients will develop neurologic symptoms during the course of the infection . Cerebrospinal fluid analysis has demonstrated that HIV enters the CNS soon after exposure, even before antibodies are detectable in blood .
In the past, different patterns of changes in cerebral magnetic resonance (MR) imaging (MRI) in HIV infection have been described . MRI studies have provided in vivo evidence of white matter abnormalities on T2-weighted MR images in HIV type 1 , and reduced cerebral white matter volume has been reported in advanced disease stages . However, knowledge is limited about signal intensity abnormalities (SIAs) on T2-weighted MR images in subjects with HIV since the introduction of highly active antiretroviral therapy (HAART) in HIV treatment 15 years ago. In small study populations, MRI has been demonstrated to characterize cerebral changes during the course of HAART in patients with AIDS . Nevertheless, little information is available on the relationship of neuroclinical status and the distribution of white matter lesions in patients with HIV and AIDS receiving HAART.
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Materials and methods
Study Population
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Clinical Parameters
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Imaging Protocol
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Table 1
Scan Parameters of the MR Systems Used in the Study
Scanner TR (ms) TE (ms) FOV (mm) Matrix (mm) ST (mm) NSA Magnetom Impact 1.0 T ∗ 3000 85 230 × 230 250 × 256 5 2 Magnetom Expert 1.5 T ∗ 4000 90 230 × 230 252 × 256 5 2 Magnetom Vision 1.5 T ∗ 2700 90 230 × 230 192 × 256 5 2 Intera Gyroscan 1.5 T † 4500 100 230 × 230 299 × 512 6 2 Intera Gyroscan 3.0 T † 3000 80 230 × 230 319 × 512 4 1
FOV, field of view; MR, magnetic resonance; NSA, number of signal acquisitions; ST, slice thickness, TE, echo time; TR, repetition time.
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Image Analysis
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Table 2
Grading Scales of Image Analysis
Description Scale Pattern of signal intensity abnormalities None Multifocal Diffuse Severity of signal intensity abnormalities ∗ None Mild (<25%) Moderate (25%–75%) Severe (>75%)
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Statistical Analysis
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Results
Study Population
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Descriptive Statistics
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Table 3
Descriptive Statistics
Severity of Signal Intensity Abnormalities HAND χ 2 P Value Yes No Pattern .340 None 0 (0.0%) 0 (0.0%) Multifocal 36 (35.6%) 18 (17.8%) Diffuse 27 (26.7%) 20 (19.8%) Periventricular white matter .119 None 10 (9.9%) 14 (13.9%) Mild 36 (35.6%) 17 (16.8%) Moderate 9 (8.9%) 4 (4.0%) Severe 8 (7.9%) 3 (3.0%) Basal ganglia .083 None 40 (39.6%) 32 (31.7%) Mild 19 (18.8%) 5 (5.0%) Moderate 4 (4.0%) 1 (1.0%) Severe 0 (0.0%) 0 (0.0%) Posterior fossa .220 None 38 (37.6%) 29 (28.7%) Mild 24 (23.8%) 9 (8.9%) Moderate 1 (1.0%) 0 (0.0%) Severe 0 (0.0%) 0 (0.0%)
HAND, human immunodeficiency virus–associated neurocognitive disorder.
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Correlation Statistics
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Discussion
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Relationship with Pattern and Location of SIAs
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Relationship with Changes of SIA Severity on Follow-up
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Limitations of This Study
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Conclusions
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Appendix
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Table A1
Relationship Between Categorized CD4 + Cell Count and Pattern of SIAs for Subgroup with Identical Magnetic Resonance Scanner ∗ ( n = 39)
CD4 + Cell Count (cells/μL) Pattern of SIAs ≥500 200–499 <200 Multifocal ( n = 24) 8.3% 16.7% 75.0% Diffuse ( n = 15) 40.0% 26.7% 33.3%
Two-sided χ 2 test P = .021.
SIA, signal intensity abnormality.
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Table A2
Relationship Between Categorized CD4 + Cell Count and the Severity of BG SIAs for Subgroup with Identical Magnetic Resonance Scanner ∗ ( n = 39)
CD4 + Cell Count (cells/μL) Severity of BG SIAs ≥500 200–499 <200 None ( n = 24) 29.2% 29.2% 41.6% Mild ( n = 10) 0.0% 10.0% 90.0% Moderate ( n = 5) 20.0% 0.0% 80.0% Severe ( n = 0) 0.0% 0.0% 0.0%
Two-sided χ 2 test P = .072.
BG, basal ganglia; SIA, signal intensity abnormality.
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