Magnetic resonance imaging (MRI) is the cornerstone of neuroimaging and plays an essential role in detecting and characterizing intracranial pathologies. Contrast-enhanced MRI is widely employed to assess lesion vascularity, blood-brain barrier disruption, and pathological enhancement patterns, which are critical for diagnosis and therapeutic planning [1]. Traditionally, contrast-enhanced T1-weighted imaging (CE-T1WI) has been considered the gold standard for evaluating enhancement in intracranial lesions such as neoplasms, infections, demyelinating disorders, and postoperative residual tumors [2]. However, recent studies have highlighted limitations of CE-T1WI, particularly in detecting subtle leptomeningeal or subarachnoid enhancement, and in differentiating certain pathologies in complex anatomical regions [3].

Fluid Attenuated Inversion Recovery (FLAIR) is an inversion recovery sequence that nullifies cerebrospinal fluid (CSF) signal, thereby improving visualization of periventricular and cortical lesions [4]. Traditionally used for demyelinating plaques and edema detection, FLAIR imaging has evolved to include contrast-enhanced FLAIR (CE-FLAIR), which utilizes gadolinium-based contrast agents to highlight areas of blood-brain barrier breakdown [5]. CE-FLAIR offers superior detection of meningeal and subarachnoid enhancements due to suppression of bright CSF signal, providing a high lesion-to-background contrast ratio compared to CE-T1WI [6].

Recent clinical studies suggest that CE-FLAIR is highly sensitive for detecting leptomeningeal carcinomatosis, infectious meningitis, and inflammatory disorders such as neurosarcoidosis, where CE-T1WI may yield false-negative results [7]. It is also reported to improve visualization of cortical lesions in early meningitis and low-grade gliomas [8]. Furthermore, CE-FLAIR demonstrates reduced vascular enhancement artifacts, making it preferable in specific diagnostic scenarios [9].

Despite these advantages, CE-FLAIR is not yet a routine part of standard neuroimaging protocols in many centers, and its diagnostic value compared to CE-T1WI remains underutilized. Current literature emphasizes its utility in complementing conventional sequences, particularly in conditions involving leptomeningeal spread and subtle parenchymal enhancement [10].

Given the evolving role of CE-FLAIR, this study aims to assess its efficacy in evaluating intracranial pathologies and determine whether its inclusion improves lesion detection and characterization in comparison to traditional contrast-enhanced sequences.

This prospective observational study was conducted in the Department of Radiology at a GMERS Medical College, Gandhinagar over a period of 18 months. A total of 120 patients referred for MRI brain with suspected intracranial pathology, such as neoplasms, infections, inflammatory conditions, or suspected meningeal involvement, were included in the study after obtaining informed consent. Inclusion criteria comprised patients aged above 18 years undergoing MRI brain with intravenous contrast administration for clinical indications. Exclusion criteria included patients with contraindications to MRI, those with impaired renal function (eGFR <30 ml/min/1.73 m²) precluding gadolinium use, pregnant women, and those unwilling to participate.

All examinations were performed on a 1.5 Tesla MRI scanner using a standardized imaging protocol. Pre-contrast sequences included T1-weighted, T2-weighted, FLAIR, and diffusion-weighted imaging in axial, sagittal, and coronal planes. Post-contrast imaging involved conventional T1-weighted sequences in multiple planes followed by Fluid Attenuated Inversion Recovery (FLAIR) sequences acquired after intravenous administration of gadolinium-based contrast agent at a dose of 0.1 mmol/kg body weight. Post-contrast FLAIR images were obtained after a delay of 5–10 minutes to allow for adequate contrast uptake and distribution in the subarachnoid space and parenchymal lesions.

Two experienced neuroradiologists, blinded to clinical details and each other’s interpretations, independently evaluated all images. Each lesion was assessed for location, size, pattern, and degree of contrast enhancement on both post-contrast T1-weighted and FLAIR sequences. Enhancement was graded visually and categorized as mild, moderate, or marked. The presence of meningeal, subarachnoid, ependymal, and parenchymal enhancement was recorded. Discrepancies between observers were resolved by consensus.

The diagnostic contribution of post-contrast FLAIR in addition to conventional post-contrast T1-weighted imaging was evaluated in terms of detection of additional lesions, better delineation of margins, and improved characterization of meningeal involvement. Final diagnosis was confirmed through correlation with clinical findings, cerebrospinal fluid analysis, histopathology (where available), or follow-up imaging. Statistical analysis was performed using IBM SPSS version 27. Sensitivity, specificity, positive predictive value, and negative predictive value were calculated for both sequences, taking the final clinical or histopathological diagnosis as reference. McNemar’s test was applied to compare the diagnostic yield of the two techniques, and interobserver agreement was assessed using Cohen’s kappa coefficient. A p-value of less than 0.05 was considered statistically significant. Ethical approval was obtained from the Institutional Ethics Committee prior to the commencement of the study, and written informed consent was obtained from all participants.

Table 1 presents the distribution of the total number of lesions detected on post-contrast T1-weighted (T1PC) and post-contrast FLAIR (CE-FLAIR) sequences among 120 patients. The majority of patients (70.8%) had a single lesion on both sequences, while 9.2% had two lesions. Multiple lesions were observed in a smaller proportion, with a few cases showing more than four lesions. Both sequences demonstrated identical counts across all categories, indicating comparable lesion detection capability in terms of lesion count.

Table 2 summarizes the highest degree of contrast enhancement for T1PC and CE-FLAIR sequences across all intracranial pathologies. The median enhancement value for T1PC was 0.95, which was higher compared to CE-FLAIR (0.39), indicating that T1PC showed stronger enhancement intensity overall. However, the lower interquartile range for CE-FLAIR suggests reduced variability and potentially better delineation of subtle enhancements.

Table 3 shows the correlation between enhancement values obtained from T1PC and CE-FLAIR using Spearman’s Rho. A moderate positive correlation (r=0.468, p<0.01) was observed, indicating that although both sequences follow a similar trend in detecting enhancement, CE-FLAIR provides additional complementary information rather than duplicating T1PC findings.
Table 4 compares contrast enhancement between intra-axial and extra-axial lesions on T1PC and CE-FLAIR. Extra-axial lesions exhibited significantly higher enhancement on T1PC (median 1.14) compared to CE-FLAIR (0.59), while intra-axial lesions demonstrated lower enhancement on both sequences but retained statistical significance (p<0.0001). These findings suggest that although CE-FLAIR shows less absolute enhancement intensity, it still highlights key areas of pathological involvement, especially in subtle extra-axial and meningeal lesions.

Table 5 provides an analysis based on lesion etiology. Neoplasms constituted the largest group, demonstrating significantly higher enhancement on T1PC compared to CE-FLAIR (p<0.0001), while infectious lesions did not show significant differences between sequences. Interestingly, postoperative lesions showed extremely high CE-FLAIR enhancement (median 4.7), highlighting the sequence’s sensitivity for detecting residual inflammatory or vascular changes.

Table 6 outlines the distribution of various intracranial pathologies in the study population. Meningitis was the most frequent diagnosis, accounting for 18.3% of cases, followed by meningioma (16.6%) and schwannoma (8.3%). Other common pathologies included metastasis, cerebral abscess, gliomas, and a wide range of less frequent lesions such as pituitary macroadenoma, ependymoma, and hemangioblastoma. This diversity ensures that the findings are generalizable to multiple clinical scenarios.

Table 7 examines the degree of contrast enhancement for specific pathologies. For meningiomas, T1PC showed significantly higher enhancement (median 1.30) compared to CE-FLAIR (0.31) with p<0.0001, while schwannomas and metastases also showed similar trends with significant p-values. Conversely, in cases such as meningitis and cerebral abscess, CE-FLAIR often demonstrated comparable or slightly higher enhancement than T1PC, although without statistical significance. These observations suggest that CE-FLAIR adds diagnostic value in infections and inflammatory lesions, whereas T1PC remains superior for solid tumors.

Table 1: Total number of lesions on T1PC and CE-FLAIR

Table 2: Highest Degree of Contrast Enhancement

Table 3: Spearman’s Rho Correlation

Table 4: Degree of Contrast Enhancement for Intra-axial and Extra-axial Pathologies

Table 5: Degree of Contrast Enhancement by Etiology

Table 6: Various Intracranial Pathologies

Table 7: Degree of Contrast Enhancement for Various Pathologies

The current study assessed the role of contrast-enhanced FLAIR (CE-FLAIR) imaging compared to the conventional post-contrast T1-weighted (T1PC) sequence in evaluating intracranial pathologies. Findings indicated that while T1PC demonstrated a higher median degree of enhancement across most pathologies, CE-FLAIR contributed significantly to the detection and delineation of certain lesions, particularly infectious and meningeal processes. These observations align with recent literature suggesting that CE-FLAIR provides superior lesion conspicuity in the presence of blood-brain barrier disruption, particularly within the subarachnoid and meningeal spaces, owing to CSF signal suppression [11].

One of the most clinically relevant findings in our study was the additional value of CE-FLAIR in infectious etiologies such as meningitis, where CE-FLAIR highlighted subtle meningeal enhancement more clearly than T1PC. This supports the results of Kamble et al., who reported CE-FLAIR as more sensitive than T1PC for early leptomeningeal involvement in tubercular meningitis [12].

Similarly, its ability to detect low-grade meningeal inflammation, which may remain inconspicuous on conventional sequences, has been recognized as critical for early diagnosis and timely intervention.

Conversely, for solid extra-axial and intra-axial tumors such as meningiomas and schwannomas, T1PC retained a statistically significant superiority in enhancement quantification compared to CE-FLAIR, consistent with recent evidence that CE-FLAIR may under-represent tumor enhancement relative to T1PC [13]. Nonetheless, CE-FLAIR contributed additional diagnostic value in postoperative cases, showing pronounced enhancement that potentially reflects residual inflammatory changes or subarachnoid seeding, which could be masked on conventional imaging [14].

Another important observation from this study was the moderate positive correlation between enhancement values on the two sequences (r=0.468), implying that CE-FLAIR does not duplicate T1PC findings but rather provides complementary information. This synergy has been highlighted in recent studies recommending CE-FLAIR as an adjunct rather than a replacement for T1PC in comprehensive neuroimaging protocols [15]. Therefore, adopting CE-FLAIR into routine practice may enhance diagnostic confidence, particularly in suspected infectious and meningeal pathologies, without significantly increasing acquisition time or cost.

Contrast-enhanced FLAIR is a valuable adjunct to conventional post-contrast T1-weighted imaging in evaluating intracranial pathologies. While T1PC remains superior for characterizing solid tumors, CE-FLAIR enhances detection of meningeal and subarachnoid involvement, contributing to more accurate diagnosis in infections, inflammatory disorders, and postoperative states. Incorporating CE-FLAIR into standard imaging protocols can improve diagnostic sensitivity and provide a more comprehensive assessment of intracranial disease.

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