Idiopathic intracranial hypertension (IIH) features elevated intracranial pressure (ICP) without a secondary cause. Trigeminal neuralgia (TN), usually attributed to neurovascular conflict (NVC), has been reported only rarely in association with IIH. We reviewed the literature and present three institutional cases to better characterize this association while explicitly acknowledging the limits of case-based causal inference. We systematically searched PubMed, Ovid Medline, Ovid Embase, Scopus, and Web of Science from inception through August 2025, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The core search combined terms for idiopathic intracranial hypertension or pseudotumor cerebri with trigeminal neuralgia, trigeminal neuropathy, and facial pain. Because causal attribution from case reports is limited, we applied a qualitative framework based on temporality, objective evidence of raised ICP, exclusion of more convincing alternative causes, especially definite NVC, and response to ICP-lowering therapy. Methodological quality was appraised using the Joanna Briggs Institute case report checklist. Quantitative summaries were restricted to published TN phenotypes; trigeminal neuropathy without pain and persistent idiopathic facial pain were summarized separately. Out of 1302 records, 12 case reports met the criteria. Nine described TN, two involved trigeminal neuropathy without pain, and one involved a persistent idiopathic facial pain phenotype. Across the nine TN cases, all patients were female (mean age 38.7 ± 12.5 years). Reported opening pressure ranged from 220 to 480 mmH2O (mean 393.0 ± 89.2 mmH2O), although diagnostic certainty varied, and not all cases fulfilled the full Friedman criteria for definite IIH. Maxillary (V2) and mandibular (V3) involvement predominated, and multidivisional pain was common. Imaging features of raised ICP and improvement after ICP-lowering therapy were recurrent themes, but standardized high-resolution trigeminal magnetic resonance imaging (MRI) sequences were inconsistently reported, limiting exclusion of coexisting classical TN. We additionally describe three institutional cases: two with documented elevated opening pressure (290 and 320 mmH2O) and one probable ICP-related case with suggestive imaging but unavailable opening pressure. In the institutional cohort, dedicated Constructive Interference in Steady State (CISS) or Fast Imaging Employing Steady-state Acquisition (FIESTA) assessment was not uniformly available; in one case, venous contact was of uncertain significance, and in another, microvascular decompression was performed without operative confirmation of arterial compression or pain relief. TN associated with IIH is a rarely reported association. Given the limited case-based evidence, the available data should be regarded as hypothesis-generating rather than definitively causal. When objective intracranial hypertension is present, careful evaluation of both ICP-related markers and alternative TN mechanisms, including NVC, is essential. ICP-lowering therapy has been reported to improve pain in some cases and may address a potential contributing mechanism.