Article

Key clinical point: A molecular subtype-guided treatment based on four triple-negative breast cancer (TNBC) subtypes nearly doubled progression-free survival (PFS) outcomes compared with control therapy with nab-paclitaxel and had a favorable safety profile in patients with metastatic TNBC.

Major finding: Patients who received nab-paclitaxel + subtype-based therapy vs only nab-paclitaxel had significantly longer progression-free survival (median 11.3 months vs 5.8 months; hazard ratio 0.44; P < .0001). Neutropenia (30% vs 23%), anemia (7% vs none), and increased alanine aminotransferase (6% vs 1%) were the most common types of grade 3-4 treatment-related adverse events in the subtype-based group vs control group.

Study details: Findings are from the ongoing phase 2 FUTURE-SUPER trial that included 139 women age 18-70 years with metastatic or recurrent TNBC who were randomly assigned to receive a nab-paclitaxel + subtype-based regimen or only nab-paclitaxel.

Disclosures: This study was supported by Jiangsu Hengrui Pharmaceuticals, the National Key Research and Development Project of China, and other sources. Two authors declared being employees of Jiangsu Hengrui Pharmaceuticals.

Source: Fan L et al. Optimising first-line subtyping-based therapy in triple-negative breast cancer (FUTURE-SUPER): A multi-cohort, randomised, phase 2 trial. Lancet Oncol. 2024 (Jan 8). doi: 10.1016/S1470-2045(23)00579-X

Key clinical point: A molecular subtype-guided treatment based on four triple-negative breast cancer (TNBC) subtypes nearly doubled progression-free survival (PFS) outcomes compared with control therapy with nab-paclitaxel and had a favorable safety profile in patients with metastatic TNBC.

Major finding: Patients who received nab-paclitaxel + subtype-based therapy vs only nab-paclitaxel had significantly longer progression-free survival (median 11.3 months vs 5.8 months; hazard ratio 0.44; P < .0001). Neutropenia (30% vs 23%), anemia (7% vs none), and increased alanine aminotransferase (6% vs 1%) were the most common types of grade 3-4 treatment-related adverse events in the subtype-based group vs control group.

Study details: Findings are from the ongoing phase 2 FUTURE-SUPER trial that included 139 women age 18-70 years with metastatic or recurrent TNBC who were randomly assigned to receive a nab-paclitaxel + subtype-based regimen or only nab-paclitaxel.

Disclosures: This study was supported by Jiangsu Hengrui Pharmaceuticals, the National Key Research and Development Project of China, and other sources. Two authors declared being employees of Jiangsu Hengrui Pharmaceuticals.

Source: Fan L et al. Optimising first-line subtyping-based therapy in triple-negative breast cancer (FUTURE-SUPER): A multi-cohort, randomised, phase 2 trial. Lancet Oncol. 2024 (Jan 8). doi: 10.1016/S1470-2045(23)00579-X

Key clinical point: A molecular subtype-guided treatment based on four triple-negative breast cancer (TNBC) subtypes nearly doubled progression-free survival (PFS) outcomes compared with control therapy with nab-paclitaxel and had a favorable safety profile in patients with metastatic TNBC.

Major finding: Patients who received nab-paclitaxel + subtype-based therapy vs only nab-paclitaxel had significantly longer progression-free survival (median 11.3 months vs 5.8 months; hazard ratio 0.44; P < .0001). Neutropenia (30% vs 23%), anemia (7% vs none), and increased alanine aminotransferase (6% vs 1%) were the most common types of grade 3-4 treatment-related adverse events in the subtype-based group vs control group.

Study details: Findings are from the ongoing phase 2 FUTURE-SUPER trial that included 139 women age 18-70 years with metastatic or recurrent TNBC who were randomly assigned to receive a nab-paclitaxel + subtype-based regimen or only nab-paclitaxel.

Disclosures: This study was supported by Jiangsu Hengrui Pharmaceuticals, the National Key Research and Development Project of China, and other sources. Two authors declared being employees of Jiangsu Hengrui Pharmaceuticals.

Source: Fan L et al. Optimising first-line subtyping-based therapy in triple-negative breast cancer (FUTURE-SUPER): A multi-cohort, randomised, phase 2 trial. Lancet Oncol. 2024 (Jan 8). doi: 10.1016/S1470-2045(23)00579-X

Key clinical point: Higher levels of leisure-time physical activity reduced the risk for premenopausal breast cancer (BC) significantly, with more prominent effects observed for human epidermal growth factor receptor 2 (HER2)-enriched BC.

Major finding: At a median follow-up of 11.5 years, higher vs lower levels (90^th vs 10^th percentile) of leisure-time physical activity were associated with a 10% reduced risk for overall BC (adjusted hazard ratio [aHR] 0.90; P < .001) and a substantial 45% reduction in the risk for HER2-enriched BC (aHR 0.55; 95% CI 0.37-0.82).

Study details: Findings are from a pooled analysis of the data from 19 prospective cohorts that included a total of 547,601 premenopausal women with 10,231 incident cases of in situ or invasive BC.

Disclosures: This study was supported by the Intramural Research Program of the US National Cancer Institute and US National Institutes of Health, and other sources. Some authors declared employment with; holding patents, stocks, and other ownership interests in; serving in consulting or advisory roles for; or receiving honoraria or research funding from various sources.

Source: Timmins IR et al. International pooled analysis of leisure-time physical activity and premenopausal breast cancer in women from 19 cohorts. J Clin Oncol. 2023 (Dec 11). doi: 10.1200/JCO.23.01101

Key clinical point: Higher levels of leisure-time physical activity reduced the risk for premenopausal breast cancer (BC) significantly, with more prominent effects observed for human epidermal growth factor receptor 2 (HER2)-enriched BC.

Major finding: At a median follow-up of 11.5 years, higher vs lower levels (90^th vs 10^th percentile) of leisure-time physical activity were associated with a 10% reduced risk for overall BC (adjusted hazard ratio [aHR] 0.90; P < .001) and a substantial 45% reduction in the risk for HER2-enriched BC (aHR 0.55; 95% CI 0.37-0.82).

Study details: Findings are from a pooled analysis of the data from 19 prospective cohorts that included a total of 547,601 premenopausal women with 10,231 incident cases of in situ or invasive BC.

Disclosures: This study was supported by the Intramural Research Program of the US National Cancer Institute and US National Institutes of Health, and other sources. Some authors declared employment with; holding patents, stocks, and other ownership interests in; serving in consulting or advisory roles for; or receiving honoraria or research funding from various sources.

Source: Timmins IR et al. International pooled analysis of leisure-time physical activity and premenopausal breast cancer in women from 19 cohorts. J Clin Oncol. 2023 (Dec 11). doi: 10.1200/JCO.23.01101

Key clinical point: Higher levels of leisure-time physical activity reduced the risk for premenopausal breast cancer (BC) significantly, with more prominent effects observed for human epidermal growth factor receptor 2 (HER2)-enriched BC.

Major finding: At a median follow-up of 11.5 years, higher vs lower levels (90^th vs 10^th percentile) of leisure-time physical activity were associated with a 10% reduced risk for overall BC (adjusted hazard ratio [aHR] 0.90; P < .001) and a substantial 45% reduction in the risk for HER2-enriched BC (aHR 0.55; 95% CI 0.37-0.82).

Study details: Findings are from a pooled analysis of the data from 19 prospective cohorts that included a total of 547,601 premenopausal women with 10,231 incident cases of in situ or invasive BC.

Disclosures: This study was supported by the Intramural Research Program of the US National Cancer Institute and US National Institutes of Health, and other sources. Some authors declared employment with; holding patents, stocks, and other ownership interests in; serving in consulting or advisory roles for; or receiving honoraria or research funding from various sources.

Source: Timmins IR et al. International pooled analysis of leisure-time physical activity and premenopausal breast cancer in women from 19 cohorts. J Clin Oncol. 2023 (Dec 11). doi: 10.1200/JCO.23.01101

Key clinical point: In patients with human epidermal growth factor receptor 2-negative (HER2−) inflammatory breast cancer (BC), the estrogen receptor-positive (ER+)/progesterone receptor-negative (PR−) vs ER+/PR+ phenotype was associated with significantly worse survival outcomes.

Major finding: Patients with ER+/PR‒ vs ER+/PR+ phenotype had significantly worse BC-specific survival (hazard ratio [HR] 1.764; P < .001) and overall survival (HR 1.675; P < .001) outcomes.

Study details: This retrospective study analyzed the data of 1553 women with ER+/HER2− inflammatory BC from the Surveillance, Epidemiology, and End Results (SEER) database, of whom 25.5% and 74.5% of patients presented with ER+/PR− and ER+/PR+ phenotypes, respectively.

Disclosures: This study was supported by grants from the North Sichuan Medical College Scientific Research and Development Project and Guigang Science and Technology Project. The authors declared no conflicts of interest.

Source: Luo Y et al. ER+/PR− phenotype exhibits more aggressive biological features and worse outcome compared with ER+/PR+ phenotype in HER2-negative inflammatory breast cancer. Sci Rep. 2024;14:197 (Jan 2). doi: 10.1038/s41598-023-50755-4

Key clinical point: In patients with human epidermal growth factor receptor 2-negative (HER2−) inflammatory breast cancer (BC), the estrogen receptor-positive (ER+)/progesterone receptor-negative (PR−) vs ER+/PR+ phenotype was associated with significantly worse survival outcomes.

Major finding: Patients with ER+/PR‒ vs ER+/PR+ phenotype had significantly worse BC-specific survival (hazard ratio [HR] 1.764; P < .001) and overall survival (HR 1.675; P < .001) outcomes.

Study details: This retrospective study analyzed the data of 1553 women with ER+/HER2− inflammatory BC from the Surveillance, Epidemiology, and End Results (SEER) database, of whom 25.5% and 74.5% of patients presented with ER+/PR− and ER+/PR+ phenotypes, respectively.

Disclosures: This study was supported by grants from the North Sichuan Medical College Scientific Research and Development Project and Guigang Science and Technology Project. The authors declared no conflicts of interest.

Source: Luo Y et al. ER+/PR− phenotype exhibits more aggressive biological features and worse outcome compared with ER+/PR+ phenotype in HER2-negative inflammatory breast cancer. Sci Rep. 2024;14:197 (Jan 2). doi: 10.1038/s41598-023-50755-4

Key clinical point: In patients with human epidermal growth factor receptor 2-negative (HER2−) inflammatory breast cancer (BC), the estrogen receptor-positive (ER+)/progesterone receptor-negative (PR−) vs ER+/PR+ phenotype was associated with significantly worse survival outcomes.

Major finding: Patients with ER+/PR‒ vs ER+/PR+ phenotype had significantly worse BC-specific survival (hazard ratio [HR] 1.764; P < .001) and overall survival (HR 1.675; P < .001) outcomes.

Study details: This retrospective study analyzed the data of 1553 women with ER+/HER2− inflammatory BC from the Surveillance, Epidemiology, and End Results (SEER) database, of whom 25.5% and 74.5% of patients presented with ER+/PR− and ER+/PR+ phenotypes, respectively.

Disclosures: This study was supported by grants from the North Sichuan Medical College Scientific Research and Development Project and Guigang Science and Technology Project. The authors declared no conflicts of interest.

Source: Luo Y et al. ER+/PR− phenotype exhibits more aggressive biological features and worse outcome compared with ER+/PR+ phenotype in HER2-negative inflammatory breast cancer. Sci Rep. 2024;14:197 (Jan 2). doi: 10.1038/s41598-023-50755-4

Key clinical point: Combining radiotherapy with pyrotinib and capecitabine led to improved intracranial survival outcomes and an acceptable radiation necrosis rate in patients with human epidermal growth factor receptor 2-positive (ERBB2+) breast cancer (BC) with brain metastases.

Major finding: The 1-year central nervous system (CNS) progression-free survival (PFS) rate was 74.9% (95% CI 61.9%-90.7%), and the median CNS PFS was 18.0 months (95% CI 15.5-not reached). Diarrhea (7.5%) was the most common grade ≥ 3 treatment-related adverse event. Asymptomatic radiation necrosis was identified in only 6% of the 67 lesions treated with fractionated stereotactic radiotherapy.

Study details: Findings are from a phase 2 trial that included 40 women with ERBB2+ BC and brain metastases who received fractionated stereotactic or whole-brain radiotherapy and initiated treatment with pyrotinib and capecitabine.

Disclosures: This study was supported by the National Natural Science Foundation of China (NSFC). Three authors declared receiving grants or personal fees from various sources, including the NSFC.

Source: Yang Z et al. Brain radiotherapy with pyrotinib and capecitabine in patients with ERBB2-positive advanced breast cancer and brain metastases: A nonrandomized phase 2 trial. JAMA Oncol. 2024 (Jan 4). doi: 10.1001/jamaoncol.2023.5791

Key clinical point: Combining radiotherapy with pyrotinib and capecitabine led to improved intracranial survival outcomes and an acceptable radiation necrosis rate in patients with human epidermal growth factor receptor 2-positive (ERBB2+) breast cancer (BC) with brain metastases.

Major finding: The 1-year central nervous system (CNS) progression-free survival (PFS) rate was 74.9% (95% CI 61.9%-90.7%), and the median CNS PFS was 18.0 months (95% CI 15.5-not reached). Diarrhea (7.5%) was the most common grade ≥ 3 treatment-related adverse event. Asymptomatic radiation necrosis was identified in only 6% of the 67 lesions treated with fractionated stereotactic radiotherapy.

Study details: Findings are from a phase 2 trial that included 40 women with ERBB2+ BC and brain metastases who received fractionated stereotactic or whole-brain radiotherapy and initiated treatment with pyrotinib and capecitabine.

Disclosures: This study was supported by the National Natural Science Foundation of China (NSFC). Three authors declared receiving grants or personal fees from various sources, including the NSFC.

Source: Yang Z et al. Brain radiotherapy with pyrotinib and capecitabine in patients with ERBB2-positive advanced breast cancer and brain metastases: A nonrandomized phase 2 trial. JAMA Oncol. 2024 (Jan 4). doi: 10.1001/jamaoncol.2023.5791

Key clinical point: Combining radiotherapy with pyrotinib and capecitabine led to improved intracranial survival outcomes and an acceptable radiation necrosis rate in patients with human epidermal growth factor receptor 2-positive (ERBB2+) breast cancer (BC) with brain metastases.

Major finding: The 1-year central nervous system (CNS) progression-free survival (PFS) rate was 74.9% (95% CI 61.9%-90.7%), and the median CNS PFS was 18.0 months (95% CI 15.5-not reached). Diarrhea (7.5%) was the most common grade ≥ 3 treatment-related adverse event. Asymptomatic radiation necrosis was identified in only 6% of the 67 lesions treated with fractionated stereotactic radiotherapy.

Study details: Findings are from a phase 2 trial that included 40 women with ERBB2+ BC and brain metastases who received fractionated stereotactic or whole-brain radiotherapy and initiated treatment with pyrotinib and capecitabine.

Disclosures: This study was supported by the National Natural Science Foundation of China (NSFC). Three authors declared receiving grants or personal fees from various sources, including the NSFC.

Source: Yang Z et al. Brain radiotherapy with pyrotinib and capecitabine in patients with ERBB2-positive advanced breast cancer and brain metastases: A nonrandomized phase 2 trial. JAMA Oncol. 2024 (Jan 4). doi: 10.1001/jamaoncol.2023.5791

Key clinical point: In patients with early breast cancer (BC) who were undergoing breast-conserving surgery and sentinel lymph node detection (SLND), a combination of paramagnetic seed + superparamagnetic iron oxide (SPIO) led to comparable rates of re-excision and resection ratios as the more standard approach with guidewire + SPIO.

Major finding: Paramagnetic seed + SPIO and guidewire + SPIO showed comparable re-excision rates (2.87% vs 2.84%; P = .99) and median resection ratios (2.01 vs 1.93; P = .70). The rate of failed breast lesion localizations was significantly more in the guidewire vs paramagnetic seed group (10.1% vs 1.9%; P < .001).

Study details: Findings are from the phase 3 MAGTOTAL trial that included 426 patients with early BC scheduled to undergo breast-conserving surgery and SLND who were randomly assigned to either lesion localization using paramagnetic seed + SPIO or guidewire + SPIO.

Disclosures: This study was supported partly by Uppsala University Hospital. Sweden, and institutional grants from Uppsala University and other sources. A Karakatsanis declared receiving grants and honoraria from various sources outside the study.

Source: Pantiora E et al. Magnetic seed vs guidewire breast cancer localization with magnetic lymph node detection: A randomized clinical trial. JAMA Surg. 2023 (Dec 27). doi: 10.1001/jamasurg.2023.6520

Key clinical point: In patients with early breast cancer (BC) who were undergoing breast-conserving surgery and sentinel lymph node detection (SLND), a combination of paramagnetic seed + superparamagnetic iron oxide (SPIO) led to comparable rates of re-excision and resection ratios as the more standard approach with guidewire + SPIO.

Major finding: Paramagnetic seed + SPIO and guidewire + SPIO showed comparable re-excision rates (2.87% vs 2.84%; P = .99) and median resection ratios (2.01 vs 1.93; P = .70). The rate of failed breast lesion localizations was significantly more in the guidewire vs paramagnetic seed group (10.1% vs 1.9%; P < .001).

Study details: Findings are from the phase 3 MAGTOTAL trial that included 426 patients with early BC scheduled to undergo breast-conserving surgery and SLND who were randomly assigned to either lesion localization using paramagnetic seed + SPIO or guidewire + SPIO.

Disclosures: This study was supported partly by Uppsala University Hospital. Sweden, and institutional grants from Uppsala University and other sources. A Karakatsanis declared receiving grants and honoraria from various sources outside the study.

Source: Pantiora E et al. Magnetic seed vs guidewire breast cancer localization with magnetic lymph node detection: A randomized clinical trial. JAMA Surg. 2023 (Dec 27). doi: 10.1001/jamasurg.2023.6520

Key clinical point: In patients with early breast cancer (BC) who were undergoing breast-conserving surgery and sentinel lymph node detection (SLND), a combination of paramagnetic seed + superparamagnetic iron oxide (SPIO) led to comparable rates of re-excision and resection ratios as the more standard approach with guidewire + SPIO.

Major finding: Paramagnetic seed + SPIO and guidewire + SPIO showed comparable re-excision rates (2.87% vs 2.84%; P = .99) and median resection ratios (2.01 vs 1.93; P = .70). The rate of failed breast lesion localizations was significantly more in the guidewire vs paramagnetic seed group (10.1% vs 1.9%; P < .001).

Study details: Findings are from the phase 3 MAGTOTAL trial that included 426 patients with early BC scheduled to undergo breast-conserving surgery and SLND who were randomly assigned to either lesion localization using paramagnetic seed + SPIO or guidewire + SPIO.

Disclosures: This study was supported partly by Uppsala University Hospital. Sweden, and institutional grants from Uppsala University and other sources. A Karakatsanis declared receiving grants and honoraria from various sources outside the study.

Source: Pantiora E et al. Magnetic seed vs guidewire breast cancer localization with magnetic lymph node detection: A randomized clinical trial. JAMA Surg. 2023 (Dec 27). doi: 10.1001/jamasurg.2023.6520

Key clinical point: Induction treatment with bevacizumab, etoposide, and cisplatin (BEEP) before whole-brain radiotherapy (WBRT) vs WBRT alone improved brain-specific progression-free survival (PFS) outcomes in patients with brain metastases from breast cancer (BMBC).

Major finding: Patients who received BEEP + WBRT vs WBRT alone had significantly longer median brain-specific PFS based on a predefined α level of ≤0.20 (8.1 vs 6.5 months; hazard ratio 0.71; P = .15) and higher 8-month brain-specific PFS rate (48.7% vs 26.3%; P = .03). Neutropenia, nausea, anemia, and leukopenia were the most common adverse events in the BEEP induction arm.

Study details: Findings are from the phase 2 A-PLUS trial that included 118 WBRT-naive patients with invasive breast cancer who had ≥1 metastatic brain tumors and were randomly assigned to receive BEEP induction followed by WBRT or only WBRT.

Disclosures: This study received investigational product support and grants funding from Roche Taiwan, Chugai Pharma Taiwan, and other sources. Four authors declared receiving personal fees, lecture fees, consulting or speakers’ bureau fees, travel support, or grants from Roche and other sources.

Source: Chen TW et al. Whole-brain radiotherapy alone vs preceded by bevacizumab, etoposide, and cisplatin for untreated brain metastases from breast cancer: A randomized clinical trial. JAMA Oncol. 2023 (Dec 21). doi: 10.1001/jamaoncol.2023.5456

Key clinical point: Induction treatment with bevacizumab, etoposide, and cisplatin (BEEP) before whole-brain radiotherapy (WBRT) vs WBRT alone improved brain-specific progression-free survival (PFS) outcomes in patients with brain metastases from breast cancer (BMBC).

Major finding: Patients who received BEEP + WBRT vs WBRT alone had significantly longer median brain-specific PFS based on a predefined α level of ≤0.20 (8.1 vs 6.5 months; hazard ratio 0.71; P = .15) and higher 8-month brain-specific PFS rate (48.7% vs 26.3%; P = .03). Neutropenia, nausea, anemia, and leukopenia were the most common adverse events in the BEEP induction arm.

Study details: Findings are from the phase 2 A-PLUS trial that included 118 WBRT-naive patients with invasive breast cancer who had ≥1 metastatic brain tumors and were randomly assigned to receive BEEP induction followed by WBRT or only WBRT.

Disclosures: This study received investigational product support and grants funding from Roche Taiwan, Chugai Pharma Taiwan, and other sources. Four authors declared receiving personal fees, lecture fees, consulting or speakers’ bureau fees, travel support, or grants from Roche and other sources.

Source: Chen TW et al. Whole-brain radiotherapy alone vs preceded by bevacizumab, etoposide, and cisplatin for untreated brain metastases from breast cancer: A randomized clinical trial. JAMA Oncol. 2023 (Dec 21). doi: 10.1001/jamaoncol.2023.5456

Key clinical point: Induction treatment with bevacizumab, etoposide, and cisplatin (BEEP) before whole-brain radiotherapy (WBRT) vs WBRT alone improved brain-specific progression-free survival (PFS) outcomes in patients with brain metastases from breast cancer (BMBC).

Major finding: Patients who received BEEP + WBRT vs WBRT alone had significantly longer median brain-specific PFS based on a predefined α level of ≤0.20 (8.1 vs 6.5 months; hazard ratio 0.71; P = .15) and higher 8-month brain-specific PFS rate (48.7% vs 26.3%; P = .03). Neutropenia, nausea, anemia, and leukopenia were the most common adverse events in the BEEP induction arm.

Study details: Findings are from the phase 2 A-PLUS trial that included 118 WBRT-naive patients with invasive breast cancer who had ≥1 metastatic brain tumors and were randomly assigned to receive BEEP induction followed by WBRT or only WBRT.

Disclosures: This study received investigational product support and grants funding from Roche Taiwan, Chugai Pharma Taiwan, and other sources. Four authors declared receiving personal fees, lecture fees, consulting or speakers’ bureau fees, travel support, or grants from Roche and other sources.

Source: Chen TW et al. Whole-brain radiotherapy alone vs preceded by bevacizumab, etoposide, and cisplatin for untreated brain metastases from breast cancer: A randomized clinical trial. JAMA Oncol. 2023 (Dec 21). doi: 10.1001/jamaoncol.2023.5456

Key clinical point: Adding atezolizumab to carboplatin improved overall survival (OS) outcomes in patients with metastatic triple-negative breast cancer (TNBC).

Major finding: Compared with carboplatin alone, carboplatin + atezolizumab demonstrated significant improvement in OS outcomes (hazard ratio [HR] 0.60; log-rank P = .03) even though the improvement in the primary endpoint of progression-free survival was not statistically significant (HR 0.66; log-rank P = .05). The prevalence of grade 3/4 serious adverse events was higher with carboplatin + atezolizumab vs carboplatin alone (41% vs 8%).

Study details: Findings are from the phase 2 TBCRC 043 trial that included 106 patients with metastatic TNBC who were randomly assigned to receive either carboplatin alone or in combination with atezolizumab.

Disclosures: This study was supported by a US National Cancer Institute grant, Susan G. Komen grants, and other sources. Some authors declared receiving grants or personal fees from or having other ties with various sources, including the funding agencies.

Source: Lehmann BD et al. Atezolizumab in combination with carboplatin and survival outcomes in patients with metastatic triple-negative breast cancer: The TBCRC 043 phase 2 randomized clinical trial. JAMA Oncol. 2023 (Dec 14). doi: 10.1001/jamaoncol.2023.5424

Key clinical point: Adding atezolizumab to carboplatin improved overall survival (OS) outcomes in patients with metastatic triple-negative breast cancer (TNBC).

Major finding: Compared with carboplatin alone, carboplatin + atezolizumab demonstrated significant improvement in OS outcomes (hazard ratio [HR] 0.60; log-rank P = .03) even though the improvement in the primary endpoint of progression-free survival was not statistically significant (HR 0.66; log-rank P = .05). The prevalence of grade 3/4 serious adverse events was higher with carboplatin + atezolizumab vs carboplatin alone (41% vs 8%).

Study details: Findings are from the phase 2 TBCRC 043 trial that included 106 patients with metastatic TNBC who were randomly assigned to receive either carboplatin alone or in combination with atezolizumab.

Disclosures: This study was supported by a US National Cancer Institute grant, Susan G. Komen grants, and other sources. Some authors declared receiving grants or personal fees from or having other ties with various sources, including the funding agencies.

Source: Lehmann BD et al. Atezolizumab in combination with carboplatin and survival outcomes in patients with metastatic triple-negative breast cancer: The TBCRC 043 phase 2 randomized clinical trial. JAMA Oncol. 2023 (Dec 14). doi: 10.1001/jamaoncol.2023.5424

Key clinical point: Adding atezolizumab to carboplatin improved overall survival (OS) outcomes in patients with metastatic triple-negative breast cancer (TNBC).

Major finding: Compared with carboplatin alone, carboplatin + atezolizumab demonstrated significant improvement in OS outcomes (hazard ratio [HR] 0.60; log-rank P = .03) even though the improvement in the primary endpoint of progression-free survival was not statistically significant (HR 0.66; log-rank P = .05). The prevalence of grade 3/4 serious adverse events was higher with carboplatin + atezolizumab vs carboplatin alone (41% vs 8%).

Study details: Findings are from the phase 2 TBCRC 043 trial that included 106 patients with metastatic TNBC who were randomly assigned to receive either carboplatin alone or in combination with atezolizumab.

Disclosures: This study was supported by a US National Cancer Institute grant, Susan G. Komen grants, and other sources. Some authors declared receiving grants or personal fees from or having other ties with various sources, including the funding agencies.

Source: Lehmann BD et al. Atezolizumab in combination with carboplatin and survival outcomes in patients with metastatic triple-negative breast cancer: The TBCRC 043 phase 2 randomized clinical trial. JAMA Oncol. 2023 (Dec 14). doi: 10.1001/jamaoncol.2023.5424

Key clinical point: Compared with the general population, the risk for overall breast cancer (BC) was nearly double in women with benign breast disease (BBD) diagnosed by percutaneous biopsies.

Major finding: Patients with BBD vs the general population were at a significantly higher risk for overall BC (standard incidence ratio [SIR] 1.95; 95% CI 1.76-2.17), including invasive BC (SIR 1.56; 95% CI 1.37-1.78) and ductal carcinoma in situ (SIR 3.10; 95% CI 2.54-3.77). The SIR for overall BC increased progressively with increasing BBD severity (nonproliferative 1.42; 95% CI 1.19-1.71; proliferative disease without atypia 2.19; 95% CI 1.88-2.54; atypical hyperplasia 3.91; 95% CI 2.97-5.14).

Study details: Findings are from a retrospective cohort study including 4819 female patients who underwent a BBD biopsy, of whom 338 patients had incident BC.

Disclosures: This study was supported by a grant from the US National Institutes of Health (NIH). Four authors declared receiving grants, research support, or personal fees from NIH and other sources.

Source: Sherman ME et al. Benign breast disease and breast cancer risk in the percutaneous biopsy era. JAMA Surg. 2023 (Dec 13). doi: 10.1001/jamasurg.2023.6382

Key clinical point: Compared with the general population, the risk for overall breast cancer (BC) was nearly double in women with benign breast disease (BBD) diagnosed by percutaneous biopsies.

Major finding: Patients with BBD vs the general population were at a significantly higher risk for overall BC (standard incidence ratio [SIR] 1.95; 95% CI 1.76-2.17), including invasive BC (SIR 1.56; 95% CI 1.37-1.78) and ductal carcinoma in situ (SIR 3.10; 95% CI 2.54-3.77). The SIR for overall BC increased progressively with increasing BBD severity (nonproliferative 1.42; 95% CI 1.19-1.71; proliferative disease without atypia 2.19; 95% CI 1.88-2.54; atypical hyperplasia 3.91; 95% CI 2.97-5.14).

Study details: Findings are from a retrospective cohort study including 4819 female patients who underwent a BBD biopsy, of whom 338 patients had incident BC.

Disclosures: This study was supported by a grant from the US National Institutes of Health (NIH). Four authors declared receiving grants, research support, or personal fees from NIH and other sources.

Source: Sherman ME et al. Benign breast disease and breast cancer risk in the percutaneous biopsy era. JAMA Surg. 2023 (Dec 13). doi: 10.1001/jamasurg.2023.6382

Key clinical point: Compared with the general population, the risk for overall breast cancer (BC) was nearly double in women with benign breast disease (BBD) diagnosed by percutaneous biopsies.

Major finding: Patients with BBD vs the general population were at a significantly higher risk for overall BC (standard incidence ratio [SIR] 1.95; 95% CI 1.76-2.17), including invasive BC (SIR 1.56; 95% CI 1.37-1.78) and ductal carcinoma in situ (SIR 3.10; 95% CI 2.54-3.77). The SIR for overall BC increased progressively with increasing BBD severity (nonproliferative 1.42; 95% CI 1.19-1.71; proliferative disease without atypia 2.19; 95% CI 1.88-2.54; atypical hyperplasia 3.91; 95% CI 2.97-5.14).

Study details: Findings are from a retrospective cohort study including 4819 female patients who underwent a BBD biopsy, of whom 338 patients had incident BC.

Disclosures: This study was supported by a grant from the US National Institutes of Health (NIH). Four authors declared receiving grants, research support, or personal fees from NIH and other sources.

Source: Sherman ME et al. Benign breast disease and breast cancer risk in the percutaneous biopsy era. JAMA Surg. 2023 (Dec 13). doi: 10.1001/jamasurg.2023.6382

Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.

Myth: Migraine Is the Most Common Type of Headache

This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.

When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.

Myth: Only Adults Get Headaches

False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.

Myth: Migraines Are Just Really Bad Headaches

False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache. 

Myth: More Women Than Men Experience Migraine 

This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.

While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.

Myth: All Headaches Are Psychological

This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.

Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems). 

Myth: Migraines Aren’t Serious

Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.

Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences. 

Myth: Lack of Sleep Causes Migraine 

Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.

Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.

Myth: Caffeine Causes Migraine

This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.

Myth: Headache Medicine Will Cure Migraine

False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers. 

Myth: You Cannot Take Any Migraine Medications During Pregnancy

Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects. 

Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant. 

Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.

Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.

Myth: “Migraine Diets” Cure Migraine

This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.

Myth: Dietary Supplements Can Cure Migraine

This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.

Myth: It’s Not a Migraine Unless You Experience Aura

This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.

Myth: Researchers No Longer Investigate Migraine

False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.                                                                                                                                                         

Several migraine studies of note include the following:

• OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.

• Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.

• The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.

• Metformin is being investigated as a treatment for the prevention of episodic migraine.

Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam

This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.

Summary

Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.

Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.

Myth: Migraine Is the Most Common Type of Headache

This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.

When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.

Myth: Only Adults Get Headaches

False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.

Myth: Migraines Are Just Really Bad Headaches

False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache. 

Myth: More Women Than Men Experience Migraine 

This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.

While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.

Myth: All Headaches Are Psychological

This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.

Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems). 

Myth: Migraines Aren’t Serious

Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.

Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences. 

Myth: Lack of Sleep Causes Migraine 

Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.

Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.

Myth: Caffeine Causes Migraine

This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.

Myth: Headache Medicine Will Cure Migraine

False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers. 

Myth: You Cannot Take Any Migraine Medications During Pregnancy

Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects. 

Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant. 

Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.

Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.

Myth: “Migraine Diets” Cure Migraine

This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.

Myth: Dietary Supplements Can Cure Migraine

This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.

Myth: It’s Not a Migraine Unless You Experience Aura

This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.

Myth: Researchers No Longer Investigate Migraine

False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.                                                                                                                                                         

Several migraine studies of note include the following:

• OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.

• Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.

• The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.

• Metformin is being investigated as a treatment for the prevention of episodic migraine.

Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam

This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.

Summary

Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.

Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.

Myth: Migraine Is the Most Common Type of Headache

This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.

When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.

Myth: Only Adults Get Headaches

False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.

Myth: Migraines Are Just Really Bad Headaches

False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache. 

Myth: More Women Than Men Experience Migraine 

This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.

While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.

Myth: All Headaches Are Psychological

This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.

Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems). 

Myth: Migraines Aren’t Serious

Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.

Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences. 

Myth: Lack of Sleep Causes Migraine 

Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.

Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.

Myth: Caffeine Causes Migraine

This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.

Myth: Headache Medicine Will Cure Migraine

False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers. 

Myth: You Cannot Take Any Migraine Medications During Pregnancy

Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects. 

Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant. 

Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.

Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.

Myth: “Migraine Diets” Cure Migraine

This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.

Myth: Dietary Supplements Can Cure Migraine

This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.

Myth: It’s Not a Migraine Unless You Experience Aura

This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.

Myth: Researchers No Longer Investigate Migraine

False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.                                                                                                                                                         

Several migraine studies of note include the following:

• OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.

• Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.

• The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.

• Metformin is being investigated as a treatment for the prevention of episodic migraine.

Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam

This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.

Summary

Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.

The Diagnosis: Superior Vena Cava Syndrome

Computed tomography angiography of the chest confirmed a diagnosis of superior vena cava (SVC) syndrome due to external pressure of the indwelling catheter. Upon diagnosis, the left indwelling catheter was removed. Further testing to assess for a potential pulmonary embolism was negative. Resolution of the ectatic spider veins and patientreported intermittent facial swelling was achieved after catheter removal.

Superior vena cava syndrome occurs when the SVC is occluded due to extrinsic pressure or thrombosis. Although classically thought to be due to underlying bronchogenic carcinomas, all pathologies that cause compression of the SVC also can lead to vessel occlusion.¹ Superior vena cava syndrome initially can be detected on physical examination. The most prominent skin finding includes diffusely dilated blood vessels on the central chest wall, which indicate the presence of collateral blood vessels.¹ Imaging studies such as abdominal computed tomography can provide information on the etiology of the condition but are not required for diagnosis. Given the high correlation of SVC syndrome with underlying lung and mediastinal carcinomas, imaging was warranted in our patient. Imaging also can distinguish if the condition is due to external pressure or thrombosis.² For SVC syndrome due to thrombosis, endovascular therapy is first-line management; however, mechanical thrombectomy may be preferred in patients with absolute contraindication to thrombolytic agents.³ In the setting of increased external pressure on the SVC, treatment includes the removal of the source of pressure.⁴

In a case series including 78 patients, ports and indwelling catheters accounted for 71% of benign SVC cases.⁵ Our patient’s SVC syndrome most likely was due to the indwelling catheter pressing on the SVC. The goal of treatment is to address the underlying cause—whether it be pressure or thrombosis. In the setting of increased external pressure, treatment includes removal of the source of pressure from the SVC.⁴

Other differential diagnoses to consider for newonset ectatic vessels on the chest wall include generalized essential telangiectasia, scleroderma, poikiloderma vasculare atrophicans, and caput medusae. Generalized essential telangiectasia is characterized by red or pink dilated capillary blood vessels in a branch or lacelike pattern predominantly on the lower limbs. The eruption primarily is asymptomatic, though tingling or numbness may be reported.⁶ The diagnosis can be made with a punch biopsy, with histopathology showing dilated vessels in the dermis.⁷

Scleroderma is a connective tissue fibrosis disorder with variable clinical presentations. The systemic sclerosis subset can be divided into localized systemic sclerosis and diffuse systemic sclerosis. Physical examination reveals cutaneous sclerosis in various areas of the body. Localized systemic sclerosis includes sclerosis of the fingers and face, while diffuse systemic sclerosis is notable for progression to the arms, legs, and trunk.⁸ In addition to sclerosis, diffuse telangiectases also can be observed. Systemic sclerosis is a clinical diagnosis based on physical examination and laboratory studies to identify antibodies such as antinuclear antibodies.

Poikiloderma vasculare atrophicans is a variant of cutaneous T-cell lymphoma. The initial presentation is characterized by plaques of hypopigmentation and hyperpigmentation with atrophy and telangiectases. The lesions may be asymptomatic or mildly pruritic and classically involve the trunk and flexural areas.⁹ The diagnosis is made with skin biopsy and immunohistochemical studies, with findings reflective of mycosis fungoides.

Caput medusae (palm tree sign) is a cardinal feature of portal hypertension characterized by grossly dilated and engorged periumbilical veins. To shunt blood from the portal venous system, cutaneous collateral veins between the umbilical veins and abdominal wall veins are used, resulting in the appearance of engorged veins in the anterior abdominal wall.¹⁰ The diagnosis can be made with abdominal ultrasonography showing the direction of blood flow through abdominal vessels.

The Diagnosis: Superior Vena Cava Syndrome

Computed tomography angiography of the chest confirmed a diagnosis of superior vena cava (SVC) syndrome due to external pressure of the indwelling catheter. Upon diagnosis, the left indwelling catheter was removed. Further testing to assess for a potential pulmonary embolism was negative. Resolution of the ectatic spider veins and patientreported intermittent facial swelling was achieved after catheter removal.

Superior vena cava syndrome occurs when the SVC is occluded due to extrinsic pressure or thrombosis. Although classically thought to be due to underlying bronchogenic carcinomas, all pathologies that cause compression of the SVC also can lead to vessel occlusion.¹ Superior vena cava syndrome initially can be detected on physical examination. The most prominent skin finding includes diffusely dilated blood vessels on the central chest wall, which indicate the presence of collateral blood vessels.¹ Imaging studies such as abdominal computed tomography can provide information on the etiology of the condition but are not required for diagnosis. Given the high correlation of SVC syndrome with underlying lung and mediastinal carcinomas, imaging was warranted in our patient. Imaging also can distinguish if the condition is due to external pressure or thrombosis.² For SVC syndrome due to thrombosis, endovascular therapy is first-line management; however, mechanical thrombectomy may be preferred in patients with absolute contraindication to thrombolytic agents.³ In the setting of increased external pressure on the SVC, treatment includes the removal of the source of pressure.⁴

In a case series including 78 patients, ports and indwelling catheters accounted for 71% of benign SVC cases.⁵ Our patient’s SVC syndrome most likely was due to the indwelling catheter pressing on the SVC. The goal of treatment is to address the underlying cause—whether it be pressure or thrombosis. In the setting of increased external pressure, treatment includes removal of the source of pressure from the SVC.⁴

Other differential diagnoses to consider for newonset ectatic vessels on the chest wall include generalized essential telangiectasia, scleroderma, poikiloderma vasculare atrophicans, and caput medusae. Generalized essential telangiectasia is characterized by red or pink dilated capillary blood vessels in a branch or lacelike pattern predominantly on the lower limbs. The eruption primarily is asymptomatic, though tingling or numbness may be reported.⁶ The diagnosis can be made with a punch biopsy, with histopathology showing dilated vessels in the dermis.⁷

Scleroderma is a connective tissue fibrosis disorder with variable clinical presentations. The systemic sclerosis subset can be divided into localized systemic sclerosis and diffuse systemic sclerosis. Physical examination reveals cutaneous sclerosis in various areas of the body. Localized systemic sclerosis includes sclerosis of the fingers and face, while diffuse systemic sclerosis is notable for progression to the arms, legs, and trunk.⁸ In addition to sclerosis, diffuse telangiectases also can be observed. Systemic sclerosis is a clinical diagnosis based on physical examination and laboratory studies to identify antibodies such as antinuclear antibodies.

Poikiloderma vasculare atrophicans is a variant of cutaneous T-cell lymphoma. The initial presentation is characterized by plaques of hypopigmentation and hyperpigmentation with atrophy and telangiectases. The lesions may be asymptomatic or mildly pruritic and classically involve the trunk and flexural areas.⁹ The diagnosis is made with skin biopsy and immunohistochemical studies, with findings reflective of mycosis fungoides.

Caput medusae (palm tree sign) is a cardinal feature of portal hypertension characterized by grossly dilated and engorged periumbilical veins. To shunt blood from the portal venous system, cutaneous collateral veins between the umbilical veins and abdominal wall veins are used, resulting in the appearance of engorged veins in the anterior abdominal wall.¹⁰ The diagnosis can be made with abdominal ultrasonography showing the direction of blood flow through abdominal vessels.

The Diagnosis: Superior Vena Cava Syndrome

Computed tomography angiography of the chest confirmed a diagnosis of superior vena cava (SVC) syndrome due to external pressure of the indwelling catheter. Upon diagnosis, the left indwelling catheter was removed. Further testing to assess for a potential pulmonary embolism was negative. Resolution of the ectatic spider veins and patientreported intermittent facial swelling was achieved after catheter removal.

Superior vena cava syndrome occurs when the SVC is occluded due to extrinsic pressure or thrombosis. Although classically thought to be due to underlying bronchogenic carcinomas, all pathologies that cause compression of the SVC also can lead to vessel occlusion.¹ Superior vena cava syndrome initially can be detected on physical examination. The most prominent skin finding includes diffusely dilated blood vessels on the central chest wall, which indicate the presence of collateral blood vessels.¹ Imaging studies such as abdominal computed tomography can provide information on the etiology of the condition but are not required for diagnosis. Given the high correlation of SVC syndrome with underlying lung and mediastinal carcinomas, imaging was warranted in our patient. Imaging also can distinguish if the condition is due to external pressure or thrombosis.² For SVC syndrome due to thrombosis, endovascular therapy is first-line management; however, mechanical thrombectomy may be preferred in patients with absolute contraindication to thrombolytic agents.³ In the setting of increased external pressure on the SVC, treatment includes the removal of the source of pressure.⁴

In a case series including 78 patients, ports and indwelling catheters accounted for 71% of benign SVC cases.⁵ Our patient’s SVC syndrome most likely was due to the indwelling catheter pressing on the SVC. The goal of treatment is to address the underlying cause—whether it be pressure or thrombosis. In the setting of increased external pressure, treatment includes removal of the source of pressure from the SVC.⁴

Other differential diagnoses to consider for newonset ectatic vessels on the chest wall include generalized essential telangiectasia, scleroderma, poikiloderma vasculare atrophicans, and caput medusae. Generalized essential telangiectasia is characterized by red or pink dilated capillary blood vessels in a branch or lacelike pattern predominantly on the lower limbs. The eruption primarily is asymptomatic, though tingling or numbness may be reported.⁶ The diagnosis can be made with a punch biopsy, with histopathology showing dilated vessels in the dermis.⁷

Scleroderma is a connective tissue fibrosis disorder with variable clinical presentations. The systemic sclerosis subset can be divided into localized systemic sclerosis and diffuse systemic sclerosis. Physical examination reveals cutaneous sclerosis in various areas of the body. Localized systemic sclerosis includes sclerosis of the fingers and face, while diffuse systemic sclerosis is notable for progression to the arms, legs, and trunk.⁸ In addition to sclerosis, diffuse telangiectases also can be observed. Systemic sclerosis is a clinical diagnosis based on physical examination and laboratory studies to identify antibodies such as antinuclear antibodies.

Poikiloderma vasculare atrophicans is a variant of cutaneous T-cell lymphoma. The initial presentation is characterized by plaques of hypopigmentation and hyperpigmentation with atrophy and telangiectases. The lesions may be asymptomatic or mildly pruritic and classically involve the trunk and flexural areas.⁹ The diagnosis is made with skin biopsy and immunohistochemical studies, with findings reflective of mycosis fungoides.

Caput medusae (palm tree sign) is a cardinal feature of portal hypertension characterized by grossly dilated and engorged periumbilical veins. To shunt blood from the portal venous system, cutaneous collateral veins between the umbilical veins and abdominal wall veins are used, resulting in the appearance of engorged veins in the anterior abdominal wall.¹⁰ The diagnosis can be made with abdominal ultrasonography showing the direction of blood flow through abdominal vessels.