Table 3:
Summary of Hypothesized Radiographic Changes During Radiation Response: Pseudoprogression (PsP) or Radionecrosis (RN), Inflammatory/Immune Response (IR), and Progressive Disease (PD)
| Conventional MRI | Diffusion MRI | Perfusion MRI | PET Imaging | |
|---|---|---|---|---|
| Radiation Response: Pseudoprogression (PSP) / Radionecrosis (RN) |
Subacute ↑(Increased contrast enhancement (T1w) and vasogenic edema (T2w) with increased vascular permeability from direct epithelial damage or indirect through cytokines) Chronic ↓ (After resolution of transient changes there is lack of contrast enhancement due to decreased abnormal “new” or “co-opted” vasculature) Potential Distinctions: Temporal changes (e.g. rates of change in volume) in enhancement and/or texture features, relative to any changes in T2/FLAIR (e.g. “shagginess” of tumor boundaries) |
Subacute ↓(?) (decreased ADC due to inflammatory cell infiltrate) Chronic ↑ (Decreased tumor cell membranes during apoptosis and/or demyelination from cytotoxic effects resulting in decreased boundaries for water diffusion) Potential Distinctions: Temporal patterns in ADC (?) |
Subacute ↑(?) (Inflammation, increased CBF; swelling, increased Ktrans) Chronic ↓ (lower CBV and Ktrans (permeability) due to lack of “established” tumor neovasculature) Potential Distinctions: Temporal patterns in CBV, Ktrans, or CBF (?) |
Subacute ↑(?) (Increased permeability = increased tracer accumulation) Chronic ↓ (lower uptake after BBB normalization in areas of less tumor “activity”) |
| Inflammatory/Immune Response (IR) |
Subacute ↑(Increased contrast enhancement (T1w) and vasogenic edema (T2w) with increased vascular permeability from cytokines) Chronic ↓ (After resolution of transient changes there is lack of contrast enhancement due to decreased abnormal “new” or “co-opted” vasculature) Potential Distinctions: Temporal changes in enhancement, relative to T2/FLAIR changes, and texture features. Pre-contrast T1 shortening may suggest high concentrations of tumor cell infiltrate. |
Subacute ↓(?) (decreased ADC due to inflammatory cell infiltrate) Chronic ↓↑ (?) (Questionable whether decreased ADC will occur due to prolonged inflammatory cell infiltrate, or whether increased ADC will occur after tumor cell death and clearance of cellular debris.) Potential Distinctions: Temporal patterns in ADC (?) |
Subacute ↑ (?) (Inflammation, increased CBF; swelling, increased Ktrans) Chronic ↓ (lower CBV and Ktrans (permeability) due to lack of “established” tumor neovasculature) Potential Distinctions: Temporal patterns in CBV, Ktrans, or CBF (?) |
Subacute ↑(?) (Increased permeability = increased tracer accumulation) Chronic ↓ (lower uptake after BBB normalization in areas of less tumor “activity”) |
| Progressive Disease (PD) |
Subacute ↑(Increased contrast enhancement from leaky “new” or “co-opted” vasculature. Induced by irregular levels of pro-angiogenic factors) Chronic ↑ (Continual increases in the extent of contrast enhancement due to constant recruitment of existing vasculature and formation of new, abnormal vasculature) |
Subacute ↓ (decreased ADC due to increased cellularity and proliferation rate) Chronic ↓ (decreased ADC due to uncontrolled proliferation and maximum cell packing) |
Subacute ↑ (Higher CBV and Ktrans due to uncontrolled angiogenesis) Chronic ↑ (Higher CBV and Ktrans due to uncontrolled angiogenesis) Potential Distinctions: Temporal patterns in CBV, Ktrans, or CBF, indicating continual increased neovascularity over time |
Subacute ↑(Increased uptake due to lack of effect on tumor “activity”) Chronic ↑(Increased uptake due to increased tumor “activity”) |