“…RT-induced brain injury can be divided into acute, early delayed, and late-delayed (Table 1) [11,13]. Acute brain injury is rare with conventional dose fractionation schemes and no changes are generally observed on MRI [11,14].…”
Section: Rt-induced Neurotoxicitymentioning
confidence: 99%
“…Acute brain injury is rare with conventional dose fractionation schemes and no changes are generally observed on MRI [11,14]. In early delayed brain injury, T2-hyperintense areas and new abnormal enhancement patterns may be detected, a phenomenon known as pseudoprogression and classically described in high-grade gliomas after initiation of treatment with RT and ChT, most commonly temozolomide [13]. Advanced MRI techniques allow to differentiate true progression from these transient post-treatment changes, with the latter showing higher ADC signal and lower rCBV on perfusion compared with viable tumor, as well as a decrease in total tumor burden during follow-up (Figs.…”
Section: Rt-induced Neurotoxicitymentioning
confidence: 99%
“…Axial FLAIR (upper row) and contrast-enhanced T1-weighted (lower row) images before (a, d), during (b, e), and 3 months after treatment (c, f) showed initial occurrence of increasing size and enhancement of the lesion, followed by reduction of both signal changes and enhancement at the 3-month follow-up T2-hyperintensities involving occipital and parietal lobes without diffusion restriction (Fig. 5) [11,13]. Cerebrovascular disorders may be either ischemic or hemorrhagic (i.e., after antiangiogenic drugs, such as bevacizumab); L-asparaginase may lead to venous sinus thrombosis [12].…”
Section: Cht-induced Neurotoxicitymentioning
confidence: 99%
“…According to the imaging pattern, late-delayed reactions can be classified as follows. RT-induced vascular injury: Progressive cerebral arteriopathy with vessel narrowing and irregularity can be observed, sometimes associated with moyamoya disease [ 13 ]. Further, RT may induce capillary telangiectasias and cavernous malformations demonstrated as hypointensities on T2/T2*-weighted images (Fig.…”
Section: Imaging Findingsmentioning
confidence: 99%
“…Further, RT may induce capillary telangiectasias and cavernous malformations demonstrated as hypointensities on T2/T2*-weighted images (Fig. 3 ), and mineralizing microangiopathy that can be detected on nonenhanced CT as calcifications in the affected region [ 11 , 13 ]. …”
Newer biologic drugs and immunomodulatory agents, as well as more tolerated and effective radiation therapy schemes, have reduced treatment toxicity in oncology patients. However, although imaging assessment of tumor response is adapting to atypical responses like tumor flare, expected changes and complications of chemo/radiotherapy are still routinely encountered in post-treatment imaging examinations. Radiologists must be aware of old and newer therapeutic options and related side effects or complications to avoid a misinterpretation of imaging findings. Further, advancements in oncology research have increased life expectancy of patients as well as the frequency of long-term therapy-related side effects that once could not be observed. This pictorial will help radiologists tasked to detect therapy-related complications and to differentiate expected changes of normal tissues from tumor relapse.
“…RT-induced brain injury can be divided into acute, early delayed, and late-delayed (Table 1) [11,13]. Acute brain injury is rare with conventional dose fractionation schemes and no changes are generally observed on MRI [11,14].…”
Section: Rt-induced Neurotoxicitymentioning
confidence: 99%
“…Acute brain injury is rare with conventional dose fractionation schemes and no changes are generally observed on MRI [11,14]. In early delayed brain injury, T2-hyperintense areas and new abnormal enhancement patterns may be detected, a phenomenon known as pseudoprogression and classically described in high-grade gliomas after initiation of treatment with RT and ChT, most commonly temozolomide [13]. Advanced MRI techniques allow to differentiate true progression from these transient post-treatment changes, with the latter showing higher ADC signal and lower rCBV on perfusion compared with viable tumor, as well as a decrease in total tumor burden during follow-up (Figs.…”
Section: Rt-induced Neurotoxicitymentioning
confidence: 99%
“…Axial FLAIR (upper row) and contrast-enhanced T1-weighted (lower row) images before (a, d), during (b, e), and 3 months after treatment (c, f) showed initial occurrence of increasing size and enhancement of the lesion, followed by reduction of both signal changes and enhancement at the 3-month follow-up T2-hyperintensities involving occipital and parietal lobes without diffusion restriction (Fig. 5) [11,13]. Cerebrovascular disorders may be either ischemic or hemorrhagic (i.e., after antiangiogenic drugs, such as bevacizumab); L-asparaginase may lead to venous sinus thrombosis [12].…”
Section: Cht-induced Neurotoxicitymentioning
confidence: 99%
“…According to the imaging pattern, late-delayed reactions can be classified as follows. RT-induced vascular injury: Progressive cerebral arteriopathy with vessel narrowing and irregularity can be observed, sometimes associated with moyamoya disease [ 13 ]. Further, RT may induce capillary telangiectasias and cavernous malformations demonstrated as hypointensities on T2/T2*-weighted images (Fig.…”
Section: Imaging Findingsmentioning
confidence: 99%
“…Further, RT may induce capillary telangiectasias and cavernous malformations demonstrated as hypointensities on T2/T2*-weighted images (Fig. 3 ), and mineralizing microangiopathy that can be detected on nonenhanced CT as calcifications in the affected region [ 11 , 13 ]. …”
Newer biologic drugs and immunomodulatory agents, as well as more tolerated and effective radiation therapy schemes, have reduced treatment toxicity in oncology patients. However, although imaging assessment of tumor response is adapting to atypical responses like tumor flare, expected changes and complications of chemo/radiotherapy are still routinely encountered in post-treatment imaging examinations. Radiologists must be aware of old and newer therapeutic options and related side effects or complications to avoid a misinterpretation of imaging findings. Further, advancements in oncology research have increased life expectancy of patients as well as the frequency of long-term therapy-related side effects that once could not be observed. This pictorial will help radiologists tasked to detect therapy-related complications and to differentiate expected changes of normal tissues from tumor relapse.
Due to the rising use of chemotherapy in cancer patients and growing survival rates, therapy-induced neurotoxic side effects are increasingly reported. Given the ambiguity about the prevalence and severity of leukoencephalopathy, one of such toxic side effects, in non-central nervous system (CNS) cancer patients, we performed a systematic literature search using the PubMed/Medline database to summarize existing literature regarding leukoencephalopathy epidemiology in non-CNS cancer patients and its potential cognitive sequelae. The search was based on the following terms: ('MRI' OR 'T2-weighted MRI' OR 'FLAIR') AND ('cancer' OR 'tumor' OR 'leukemia' OR 'neoplasms') AND ('chemotherapy' OR 'radiotherapy') AND ('posterior reversible encephalopathy' OR 'leukoencephalopathy' OR 'cerebral ischemia' OR 'stroke'). Thirtytwo studies discussing the occurrence of leukoencephalopathy in cancer patients were included, of which the majority investigated Acute Lymphoblastic Leukemia (ALL) patients (n=22).Regularly scanned ALL patients showed a prevalence of leukoencephalopathy between 17 -87%, and 15 -83% of patients presented with leukoencephalopathy when only scanned after a CNS event. When diagnosed with posterior reversible encephalopathy syndrome, 100% of patients showed leukoencephalopathy because its diagnosis is based in part on observable lesions. An increased prevalence was observed in ALL patients treated with higher doses of methotrexate (5 g/m2 MTX, 42 -87%) when compared to lower doses (< 5 g/m2, 32 -67%). By contrast, in breast cancer patients, white matter lesions were mainly detected in case of neurological symptoms, but not (yet) clearly associated with chemotherapy administration in general. However, chemotherapy treatment was associated with more infratentorial microbleeds in breast cancer patients. Up to 50% of other (neurologically asymptomatic) solid tumor patients presented white matter lesions, even years after treatment. When cognitive data were investigated, lesioned patients showed lower scores on neurocognitive tests in 50% of studies, years after ending therapy.In conclusion, leukoencephalopathy is well-documented for ALL patients (with a focus on methotrexate), but there is a lack of knowledge for other intravenous chemotherapeutics, other oncological populations, wider age ranges and risk factors (e.g. history of CNS event). Furthermore, the long-term neuropsychological impact and potential risk for neurodegenerative processes due to leukoencephalopathy remains inconclusive.Hence, large international databanks, epidemiological and prospective case-control studies are necessary to stratify risk groups for CNS-related side effects.
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