Published online Aug 15, 2026. doi: 10.4251/wjgo.119679
Revised: March 14, 2026
Accepted: May 9, 2026
Published online: August 15, 2026
Processing time: 185 Days and 19.3 Hours
Colorectal cancer (CRC) typically manifests initially with gastrointestinal symptoms. The incidence of brain metastasis from CRC is extremely low, and most cases are accompanied by lung or liver metastases. Isolated brain metastasis from CRC presenting with headache as the initial symptom is relatively rare, with few reported cases, and is thus prone to being overlooked and underdiagnosed. The prognosis of CRC with brain metastasis is poor, and comprehensive multidisciplinary treatment is crucial.
This article reports the case of a 71-year-old woman with a 20-day history of headache. Imaging examinations revealed a lesion in the right frontal lobe. Positron emission tomography-computed tomography further identified the primary intestinal lesion, with no evidence of extracranial metastases. Based on imaging and pathological findings, the patient was ultimately diagnosed with brain metastasis from CRC. Treatment involved surgical resection of the brain metastasis, followed by radiotherapy to the frontal lobe tumor bed and a newly developed cerebellar metastasis, with subsequent systemic chemotherapy after radiotherapy. This was followed by laparoscopic radical resection of rectal cancer. The patient is currently recovering well, demonstrating the effectiveness of the multidisciplinary treatment strategy and providing insights into the comprehensive management of similar cases.
For unexplained intracranial masses, evaluation for CRC metastasis, multidisciplinary management, and regular follow-up are crucial.
Core Tip: Given the rarity of brain metastasis from colorectal cancer in the absence of extracranial spread or typical gastrointestinal symptoms, few such cases have been reported, and clinicians have limited diagnostic and therapeutic experience with this condition. This article presents a case of colorectal cancer brain metastasis and summarizes the diagnostic challenges and multidisciplinary treatment strategy for this disease.
- Citation: Xu JL, Ge ZW, Wu CW, Wang YH, Mao JD. Multidisciplinary care for colorectal cancer brain metastases with headache as initial symptom: A case report and literature review. World J Gastrointest Oncol 2026; 18(8): 119679
- URL: https://www.wjgnet.com/1948-5204/full/v18/i8/119679.htm
- DOI: https://dx.doi.org/10.4251/wjgo.119679
Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. Epidemiological statistics indicate that the annual number of new CRC cases worldwide exceeds 1.9 million, ranking third among all malignancies, and that both the incidence and mortality rates have increased over time[1]. According to data from the National Cancer Center, CRC ranks fifth in both incidence and mortality among all malignant tumors in China[2]. Approximately 20% to 30% of patients already have distant metastases at the time of CRC diagnosis[3]. Brain metastasis from CRC is relatively rare, with an incidence ranging from approximately 0.59% to 1.40%[4,5], and it occurs mainly in patients with advanced-stage disease who have already had distant metastases to organs such as the liver and lungs[6]. Brain-only metastasis without involvement of other organs is even rarer.
The initial symptoms in patients with CRC are primarily gastrointestinal, such as hematochezia, abdominal pain, and changes in stool characteristics or bowel habits. Therefore, CRC presenting with headache as the initial symptom due to brain-only metastasis, together with normal tumor marker levels, is clinically extremely rare and prone to underdiagnosis. Clinicians must maintain a high index of suspicion when encountering similar cases.
Furthermore, the prognosis of patients with CRC brain metastasis is poor. Scientifically standardized diagnosis and treatment are crucial to improving survival rates in this population. However, there is currently no consensus, and the goals and modalities of multidisciplinary treatment remain under debate. This article reports the clinical data of a case of CRC with brain-only metastasis initially presenting with headache and discusses the multidisciplinary management of CRC brain metastasis in conjunction with the treatment strategy employed.
A 71-year-old woman presented with a 20-day history of headache.
The patient presented with a 20-day history of headache of no apparent cause. No other specific discomfort was reported.
The patient had no notable past medical history.
No significant personal or family history was reported.
The physical examination findings were unremarkable.
Laboratory examinations revealed a positive fecal occult blood test. Other laboratory findings were unremarkable.
Head computed tomography (CT) revealed an abnormal density lesion in the right frontal lobe (Figure 1A). Brain magnetic resonance imaging (MRI) demonstrated a space-occupying lesion in the right frontal cortex with heterogeneous enhancement after contrast administration, measuring approximately 3.1 cm × 2.4 cm. A mass effect was noted, with compression of both lateral ventricles and a local midline shift of approximately 1.1 cm to the left. Metastasis was thus suspected (Figure 1B). A follow-up brain MRI scan performed before radiotherapy revealed a new small nodular lesion, approximately 0.6 cm in diameter, in the right cerebellar hemisphere (Figure 1C). This lesion exhibited ring enhancement after contrast administration and was considered a new metastasis. Whole-body positron emission tomography-CT (PET-CT) (Figure 2) showed focal wall thickening with increased FDG uptake at the rectosigmoid junction, suggestive of a primary malignancy. A hypermetabolic nodule with surrounding edema was identified in the right frontal lobe and was considered likely to represent a malignant metastasis. No evidence of metastasis to other organs was detected.
Pathological examination of the brain lesion indicated moderately differentiated adenocarcinoma (Figure 3A). Immunohistochemical analysis showed positivity for AE1/AE3, partial positivity for CK20, and positivity for caudal-type homeobox transcription factor 2 and P53 (mutant type). Staining was negative for CK7, thyroid transcription factor-1, and Napsin A. The Ki-67 index was 80%. These findings supported a gastrointestinal origin (Figure 3B-F). Colonoscopy performed before radiotherapy identified a cauliflower-like mass measuring 4 cm × 3 cm in the rectum (Figure 4A). Pathology of the biopsy confirmed moderately differentiated adenocarcinoma (Figure 4B). Following laparoscopic radical resection of rectal cancer, pathological examination of the surgical specimen confirmed invasive, moderately to poorly differentiated adenocarcinoma (Figure 4C).
Based on imaging, pathological, and other relevant examinations, the patient was ultimately diagnosed with brain metastasis from rectal cancer.
This case was discussed by a multidisciplinary team consisting of specialists in neurosurgery, radiation oncology, medical oncology, and digestive surgery at our hospital. After a comprehensive evaluation, a staged treatment plan was formulated. Priority was given to the life-threatening intracranial space-occupying lesions, and after stabilization of the intracranial condition, radiotherapy, chemotherapy, and radical surgery for the primary tumor were performed sequentially.
The patient has been followed up for 3 months after completion of all treatments. Tumor marker levels remained within the normal range both before and after resection of the primary tumor. The patient's neurological symptoms, including headache, nausea, and vomiting, resolved completely, and she can care for herself. A follow-up brain MRI scan performed approximately 1 month after resection of the primary tumor revealed that the previously observed right cerebellar metastasis had disappeared, and no new metastases were detected. These preliminary follow-up findings suggest a favorable initial response to treatment.
The common sites of distant metastasis in CRC include the liver, lungs, and peritoneum. Brain metastasis occurs less frequently, accounting for approximately 3.4% of all metastatic cases[7], and is associated with a poor prognosis. The median survival of patients with CRC brain metastasis is approximately 6.8 months[8]. Notably, rectal cancer is more likely to metastasize to the brain than colon cancer[9], possibly because venous drainage from the rectum enters the vertebral venous system and bypasses the portal circulation. Most patients diagnosed with brain metastasis already have concurrent lung or liver metastases[6]. Brain-only metastasis is even rarer, accounting for only approximately 10%-15% of brain metastasis cases[10]. In the present case, the patient was confirmed to have distant metastasis confined to the brain, with no other sites identified. CRC lesions are more commonly located in the cerebellum[11], which may be related to the pattern of hematogenous dissemination.
Notably, the occurrence and development of brain metastases from CRC have unique molecular biological characteristics. The frequency of RAS mutations in CRC patients with brain metastases is higher than in those without. The KRAS mutation rate in the primary tumor of patients with metastatic CRC is approximately 40%, whereas in patients with brain metastases, it is approximately 60%. RAS mutation status is not fully concordant between brain metastases and primary tumors (85% vs 62%). Some differences have also been observed in the expression of CD3, CD8, programmed death 1 (PD-1), and its ligand programmed death-ligand 1 between these sites[5,12]. RAS mutation status is a negative predictive marker for anti-epidermal growth factor receptor (EGFR) therapy. Patients with metastatic CRC harboring RAS mutations do not benefit from anti-EGFR therapy. Therefore, if wild-type RAS is detected in this patient, anti-EGFR agents should be considered as part of systemic therapy. Unfortunately, financial constraints prevented this patient from undergoing testing for RAS/KRAS, BRCA, and more comprehensive next-generation sequencing. In addition, defects in the DNA damage response play an important role in CRC brain metastases. Patients with brain metastases show increased mutations associated with homologous recombination defects and mismatch repair defects, which are more pronounced in brain metastases, suggesting that DNA damage response defects may be an early event in CRC brain metastasis and may exist independently of primary tumor progression. Among these defects, homologous recombination deficiency is most common in breast cancer with BRCA1 and BRCA2 mutations, and functional BRCA1/BRCA2 mutations have also been identified in patients with CRC brain metastases, suggesting a potential association between CRC brain metastases and BRCA mutations[13]. In summary, the molecular pathological mechanisms underlying brain metastases from CRC are complex and diverse. A comprehensive understanding of these pathological features will help guide the diagnosis and treatment of brain metastases.
The typical symptoms of CRC are predominantly gastrointestinal manifestations, such as hematochezia and changes in bowel habits. Brain metastasis from CRC is usually detected 22-36 months after diagnosis of the primary tumor[14]. In this case, neurological symptoms such as headache were the initial presentation, which is clinically rare, increases diagnostic difficulty, and may lead to delayed diagnosis of the primary tumor. This finding highlights that, for intracranial space-occupying lesions of unknown origin, the differential diagnosis should be actively broadened to include metastatic tumors. Systematic evaluation involving endoscopy, PET-CT, and pathological examination should be performed early to promptly identify the primary tumor and formulate targeted treatment, thereby avoiding delays in both diagnosis and precise treatment of the primary lesion. The role of serum tumor markers in this case also warrants comment. Although carcinoembryonic antigen (CEA) and carbohydrate antigen (CA) 19-9 are established biomarkers for CRC, the patient’s CEA levels, measured both before and after resection of the primary tumor, remained within the normal range. While this finding is based on limited measurements, it reinforces a critical clinical message: Normal CEA levels do not exclude aggressive metastatic CRC. Unfortunately, because of specific circumstances in clinical practice, CA19-9 testing was not performed, which represents a limitation of this case report. Interestingly, this case provides a unique opportunity to observe the dynamic changes in CA50, a less commonly used marker, throughout the entire therapeutic course, from initial presentation through brain surgery, radiotherapy, systemic chemotherapy, and finally radical rectal surgery. Although CA50 levels remained within the normal range throughout, a transient elevation was observed during chemotherapy, with a mean value of 6.86 U/mL (< 25) across three determinations. Before and after chemotherapy, CA50 levels showed minimal fluctuation, with a mean value of 3.79 U/mL across four determinations. This transient yet normal-range elevation may reflect treatment-related release of tumor antigens or nonspecific inflammatory responses. One study[15] indicated that the preoperative positive rate of CA50 in CRC was 8.1%, and that elevated CA50 levels were significantly associated with more aggressive tumor features. Patients with high CA50 levels had a significantly increased risk of recurrence and metastasis, and CA50 was an independent prognostic factor for overall survival and disease-free survival. In this patient, the CA50 level was normal and low, yet distant metastasis still occurred, suggesting marked aggressiveness. This finding contrasts with that study’s conclusion but is consistent with the view regarding a favorable prognosis. Another study suggested that combining CA50 testing with fecal occult blood testing could significantly improve the sensitivity and accuracy of CRC diagnosis[16]. Currently, because of limited sensitivity, especially for early-stage lesions, the primary clinical value of tumor markers lies in monitoring treatment response and providing early warning of recurrence. Therefore, when brain metastasis is encountered in the presence of abnormal intestinal tumor markers, a colorectal origin should be suspected; even when tumor marker levels are normal, a multidisciplinary diagnostic approach remains necessary to establish a definitive diagnosis. In this case, the tumor origin was clarified on time by preoperative imaging and postoperative pathology, facilitating subsequent systemic treatment.
The management of brain metastasis from CRC should primarily focus on control of the primary disease, supplemented by local treatment of the brain metastases. An individualized treatment plan should be formulated according to the patient’s specific condition, involving surgery, radiotherapy, chemotherapy, and molecular targeted therapy, either alone or in combination, under multidisciplinary guidance. The treatment goals are to improve quality of life, prolong survival, preserve neurological function as much as possible, and minimize treatment-related adverse effects and complications.
The patient first underwent surgical resection of the brain metastasis. Surgical resection of brain metastases is primarily performed to obtain a definitive pathological diagnosis and relieve neuropsychiatric symptoms, and the indications for surgery require a comprehensive assessment based on factors such as the number, size, and location of the tumors, as well as the overall patient condition. This patient presented with intractable headache on admission, and the neurological symptoms worsened during hospitalization, manifesting as vomiting, limb weakness, choking while drinking, and worsening symptoms of intracranial hypertension. Therefore, prioritizing treatment of the symptomatic and neurologically threatening brain metastasis was urgently necessary and was consistent with neuro-oncological principles. The advantage of this approach lies in avoiding life-threatening complications such as intracranial hypertension or brain herniation, while also providing a therapeutic window for subsequent systemic treatment. Second, detection of a new lesion 1 month after surgery necessitated adjustment of the radiotherapy strategy, leading to the use of tomotherapy (TOMO) technology for precise multitarget irradiation. Finally, after effective control of the intracranial disease was achieved, three cycles of systemic chemotherapy were administered first. The purpose of this sequence was not to delay treatment, but rather to use chemotherapy as a systemic “bridge” therapy—aimed not only at treating visible lesions but also at controlling micrometastases in the circulation to reduce the future risk of distant metastases, such as to the liver or lungs, thereby creating a safer systemic environment with a lower tumor burden for subsequent radical surgery for rectal cancer. Additionally, because the patient had undergone resection of the brain metastasis first, the physical condition was not suitable for another operation in the short term. Therefore, the entire treatment sequence represents an active and proactive strategy based on the evolving disease course rather than a passive delay. Multiple studies have shown that, for CRC patients with brain metastases, a combined treatment approach centered on surgery can improve overall survival and quality of life when the brain metastases are resectable and favorable prognostic factors are present[17-19].
The patient underwent cranial radiotherapy 1 month after resection of the brain metastasis. Unexpectedly, a follow-up brain MRI scan performed before radiotherapy revealed a new lesion in the right cerebellar hemisphere. This finding warrants further consideration. One possibility is that the lesion was already present preoperatively but was not detectable on PET-CT, potentially because of its small size and masking by the high metabolic background of the brain, and became detectable only after tumor growth. This possibility suggests that even a negative PET-CT scan cannot completely exclude intracranial micrometastases. Another possibility is that this was a truly new lesion that developed within a short postoperative period, which may be related to surgical stress or the inherently aggressive nature of the tumor. If the former is correct, it suggests that the therapeutic window for systemic chemotherapy may need to be shifted earlier; if the latter is correct, it indicates a highly aggressive tumor phenotype that may warrant more intensive systemic regimens, such as combination therapy with anti-angiogenic agents. This finding also highlights the importance of close imaging follow-up and timely adjustment of systemic treatment strategies for this highly aggressive form of CRC presenting with brain metastases.
The primary radiotherapy modalities for CRC brain metastasis include whole-brain radiotherapy (WBRT) and stereotactic radiosurgery (SRS). WBRT is a conventional radiotherapy technique suitable for multiple lesions or for situations requiring rapid palliative relief of symptoms. However, the clinical application of WBRT remains controversial. Because this approach delivers radiation to the entire brain, it inevitably damages normal brain tissue, particularly structures such as the hippocampus, which is closely associated with learning and memory. As a result, patients may develop significant mid- to long-term neurocognitive impairment, which is often irreversible. The risk of WBRT-related neurocognitive decline increases with higher single-fraction doses[20]. Furthermore, no statistically significant difference in survival has been observed between patients treated with SRS plus WBRT and those treated with SRS alone; instead, patients in the combination group exhibited more pronounced declines in short-term memory and cognitive function[21]. Therefore, WBRT is currently used primarily in specific palliative settings. SRS involves the precise delivery of a high, conformal radiation dose to the target while minimizing damage to the surrounding normal tissue. It is suitable for patients in good general condition who have a limited number of brain metastases (< 4), small lesions (< 35 mm), deep-seated lesions, or lesions located within or near eloquent areas (e.g., the motor or speech cortex). Compared with WBRT, SRS is associated with fewer adverse effects and provides better local control[18], with local control rates ranging from 84% to 94%[22,23]. This approach is particularly effective in patients with small lesions receiving high doses (e.g., 25 Gray)[24,25]. In addition, the volume of brain metastases is closely related to local control outcomes. For lesions with a volume of less than 5 cm3, the local control rate is 86%, whereas it decreases to 52% for lesions with a volume of 20 cm3[26]. The median survival with SRS alone is approximately 5.1 to 9.5 months[27,28]. However, SRS targets visible lesions and provides limited prophylactic or therapeutic benefit against microscopic metastases that are undetectable on imaging or against established leptomeningeal dissemination.
In this case, the patient developed metastases in both the frontal lobe and the cerebellum. To achieve multitarget irradiation while protecting normal brain tissue, TOMO was used. TOMO can provide the broad coverage characteristic of WBRT while achieving the targeting precision of SRS through dose modulation, thereby accurately sparing critical structures such as the hippocampus and optic nerves. Furthermore, tumors may change during radiotherapy due to factors such as volume reduction or positional shifts, which are difficult to accommodate with traditional radiotherapy plans. In contrast, TOMO supports adaptive radiotherapy, enabling dynamic assessment of tumor and normal tissue changes, real-time optimization of dose distribution and treatment plans, and maintaining precision throughout the entire treatment course. This approach reduces the radiation dose to the hippocampus, a structure crucial for memory function, to below safe thresholds, thereby potentially mitigating the risk of cognitive impairment associated with traditional WBRT[20,28,29]. One study[29] indicated that TOMO performed best in terms of the homogeneity index for the planning target volume of the metastases. For the planning target volume of the brain, TOMO provided the lowest mean D2% (37.5 ± 2.8 Gray), the highest mean D98% (25.2 ± 2.0 Gray), and the best target coverage (92.6% ± 2.1%) and conformity index (0.79 ± 0.06). Furthermore, TOMO demonstrated optimal performance in minimizing the radiation dose to the hippocampus, indicating more effective hippocampal sparing. TOMO also showed the best performance in whole-brain target coverage and dose uniformity. However, this study also found that, despite its optimal dose distribution, TOMO typically requires longer treatment times, making it less efficient than volumetric-modulated arc therapy for treatment delivery. The application of TOMO radiotherapy in this case reflects a paradigm shift in modern precision radiotherapy from “single-target” to “multitarget” approaches and from “mere irradiation” to “precision protection”, offering valuable insights into selecting radiotherapy strategy for similar cases. In addition, combined surgical and radiotherapeutic treatment yields superior outcomes compared with surgery alone, with a median survival of 14 months vs 4.8 months in the surgery-only group[30]. This finding highlights the importance for clinicians of striving for a more delicate balance between effective control of intracranial lesions and maximal preservation of neurological function when formulating radiotherapy plans for brain metastases.
Following completion of radiotherapy, the patient received systemic chemotherapy. Because of the presence of the blood-brain barrier, the efficacy of traditional chemotherapy for CRC brain metastasis is limited. In this case, local control had been achieved through surgery and radiotherapy, and the patient's condition was relatively stable. To reduce the risk of systemic recurrence and progression, particularly to prevent new lesions in extracranial organs and to control potential micrometastases that might have been present but were undetectable on imaging, chemotherapy with the XELOX regimen was administered under multidisciplinary guidance. The XELOX regimen is one of the globally recognized first-line standard chemotherapy protocols for metastatic CRC, and its efficacy and safety are well established. Given the crucial role of angiogenesis in tumor brain metastasis, vascular endothelial growth factor inhibitors such as bevacizumab can be considered for combination therapy in patients with CRC and brain metastasis. Maintenance therapy with XELOX/FOLFIRI combined with bevacizumab may, to some extent, help control disease progression[31]. Concern about an increased risk of intracranial hemorrhage with bevacizumab in patients with brain metastases was common in earlier clinical practice. Although recent studies have shown that bevacizumab is relatively safe for the treatment of brain metastases that have been treated and are stable[31], at the time of the treatment of this patient, the clinician took a relatively conservative attitude and the patient's economic conditions were limited, so bevacizumab was not used after communication with the patient. Although the antineoplastic agent temozolomide can readily cross the blood-brain barrier, its efficacy in CRC brain metastasis remains controversial, and it may increase toxicities, such as myelosuppression[32]. Nevertheless, in certain circumstances, temozolomide may serve as an option for palliative treatment. After completing three cycles of chemotherapy, the patient underwent laparoscopic radical resection of rectal cancer.
Currently, combination immunotherapy offers advantages in the treatment of refractory advanced CRC, particularly for patients in whom prior treatments have failed, and provides new therapeutic strategies and directions. However, there is a lack of clinical studies specifically focused on brain metastasis, and conclusions can be drawn only by reference to studies on liver and lung metastases. Previous studies have demonstrated that combining immunotherapy with chemotherapy, radiotherapy, targeted therapy, or multichannel immune checkpoint therapy can enhance efficacy and increase patient benefit[33]. Nevertheless, at present, only microsatellite instability-high/deficient mismatch repair CRC benefits from anti-PD-1 immunotherapy[34], whereas immunotherapy has limited efficacy in microsatellite-stable CRC. In this case, molecular pathological testing indicated microsatellite stability, making the patient unsuitable for anti-PD-1 immunotherapy. As understanding of the immune mechanisms underlying distant metastasis in CRC continues to deepen, future advances may significantly improve the prognosis of this disease.
This case involved a rare presentation of CRC with brain-only metastasis, in which headache was the initial symptom. This presentation is clinically uncommon and prone to underdiagnosis. During the diagnostic process, broadening the differential diagnosis and integrating multiple examinations were crucial. In terms of management, symptoms were rapidly relieved through surgery, and precise radiotherapy with preservation of neurological function was achieved using TOMO technology, supplemented by systemic chemotherapy to effectively control the disease. This approach illustrates the principles of multidisciplinary collaboration and individualized treatment. For brain tumors of unknown origin, the possibility of CRC metastasis should be actively investigated, even in the presence of normal tumor marker levels, absence of extracranial metastases, and lack of typical gastrointestinal symptoms, to achieve early diagnosis and treatment and improve patient prognosis. Furthermore, patients with CRC brain metastasis should undergo regular follow-up after surgery to prevent recurrence or to ensure prompt detection of any potential metastatic lesions.
The authors extend their gratitude to all the investigators who contributed to this article. We also thank the patient’s family for their cooperation.
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