|Clinical sy||motor, cognitive (aphasia, apraxia, agnosia, Gerstman, coma) sensitive, cerebellar, brain stem. Visual field defects, Epileptic seizures||epileptic seizures, cognitive and memory deficit, motor, sensitive.||altered mental status (aphasia), motor, limb and gait ataxia, visual symptoms: homonymous hemianopia, cortical blindness, diplopia. Epileptic seizures. No optic nerve and spinal cord involvement.||altered mental status (aphasia), motor, limb and gait ataxia, visual symptoms: hemianopia, cortical blindness, diplopia. Epileptic seizures. No optic nerve and spinal cord involvement||[8–14], |
Unilateral or bilateral. Frontal, parietal. Periventricular, juxta cortical. 2 cm, large lesion with little mass effect and edema
Variable rate of hyper-intensity.
Central dilated vessel.
Irregular border. Supra-tentorial WM, partially GM involvement.
Hyper or hypo intense.
Irregular border. Central necrosis.
Intensive vascular edema and mass effect
Bilateral. Supra-Intra-tentorial. Cortex, deep gray matter. (Frontal, parietal, occipital. Subcortical location, U-fibers, cortex, basal ganglia). 3 cm.
Early new lesions. Hyper-intense. Ill-defined to WM, sharp to GM.
No mass effect. Punctuate perilesional lesions.
|Bilateral, spreading. Cortex and subcortical WM. Edema||[11–18], [16, 26, 54]|
|Hypo-intense with hyper- intense rim||[11–18], [26, 54]|
|MRI Gd +||incomplete rim enhancement||complete rim enhancement||negative or variable, punctuate and rim like||positive or variable, punctate and rim like||[11–18], [26, 54]|
|MRI - PWI, DWI||decreased PWI in lesions, increased DWI in active demyelination||increased PWI, increased DWI in central necrosis||DWI always hyper-intense, with peripheral rim.||+/− restricted DWI||[9–18, 26]|
increased Cho, lipids, lactate, mildly decreased NAA and NAA/Cr (differ from malignant GT)
elevation of the β,γ-Glx peaks
|increased Cho and Cho/Cr, lipids, lactate, decreased NAA, lack of β,γ-Glx elevation||A decrease of NAA/Cr ratio, NAA and Cr. An increase of Lac/Cr, Cho/Cr, Cho, lipids/Cr, mIns, Lac, Lip.||
increased Cho, decreased NAA, the presence of Lac/lipids at 1.3 ppm, and the presence of mIns, Higher Cho/Cr, mIns/Cr, Lip1/Cr, and Lip2/Cr in PML-IRIS than PML .
Lower NAA/Cr than PML.
|, [13, 14], [28,29,30,31]|
normal or mild increased proteinorhachia and white blood count.
Positive oligoclonal bands, elevated IgG index
|GFAP+ cells||mildly increased cellularity, normal proteinorhachia||mild to moderate increase of lymphocytes and protein levels||[10, 11], [14, 15]|
|CSF JCV DNA||negative, infrequently low positivity (less than 25)||negative? unknown||JCV-specific IgG, DNA copies, infrequently negative||JCV-specific IgG, DNA copies. Sometimes negative||[12–18, 31]|
|Response to corticoids||very good||only partial||none||good||[2, 9,10,11], [15, 27]|
|Histology||Hyper-cellularity, myelin protein-laden macrophages, variable lymphocytic inflammation, reactive gliosis and relative axonal preservation.||
moderate cellularity, bizarre cells with hyperchromatic nuclei, moderate pleomorphic, gemistocytes, perivascular lymphocytes, rare areas of necrosis, neo-vascularization|
GFAP + cells: immature,
reactive, and neoplastic astrocytes and ependymal cells
swelling of oligodendrocyte and multi-lobular astrocytes, basophilic nuclei, eosinophilic inclusion bodies,|
2/3 of number of T cells in PML-IRIS.
Positive DNA JCV staining in all types of cells. Active gene copies in high numbers of virally infected cells, as well as a low inflam- matory infiltrate.
Hyper-cellularity, CD8+ positive T cells dominate - their number the same as in active MS lesions, fewer CD4+ and CD20+ T cells in perivascular cuffs.
High plasma and B cells in PML-IRIS-lesions.
No or low number JCV-infected cells.
[2, 10], [15, 17,18,19,20, 49], [41,42,43, 46,47,48],|
|Outcome||as typical MS||progressive worsening||progressive worsening||worsening, regression possible||[6, 10–20, 49], [24, 25], [47, 48], |
|Immunological markers in peripheral blood||upregulation of transcription factors of Th1 (pSTAT1 and T-bet) and Th17 (pSTAT3) in circulating CD4+, CD8 + T-cells and monocytes. CD4+ T-cells with a proinflammatory Th1 and Th17 phenotype,||
lower T-bet, pSTAT1, and pSTAT3 in CD4+, CD8 + T-cells, and monocytes. Lower CD4 Th1 and Th17. Increased IL-10, TGF-β, PGE2, down modulation of co-stimulation molecules by APCs. Tumor angiogenesis, expression of CD34+ progenitor cells.
Deficit of NK cells
|variable data: stable CD4+ and CD8+, non-significant decrease or increased T cells but unchanged CD4/CD8 ratio. Decrease expression of CD49d, CD29 (VLA-4), CD11a, CD62L, CXCR3 on T cells. Decreased expression of VLA4 on myeloid dendritic cells, decreased count of dendritic cells. Production of CD34+ cells, increase of memory B cells. Increased IL-10.||
Increased IFN-γ, IL-12p70, IL-4, IL-10, IL-5, IL-13.|
CD4+,T1 + PSTAT3+, CD8+, PSTAT1+,T-bet + .
Decreased CD4+, CD25+ FoxP3+
|[36,37,38,39,40,41,42,43,44,45,46,47,48, 56] |