Traumatic brain injury (TBI) initiates secondary injury processes that include neuroinflammation, oxidative stress, blood-brain barrier disruption, cerebral edema, synaptic dysfunction, and cell death. These interacting processes contribute to persistent motor, cognitive, and neurobehavioral impairments. This review aims to summarize the major techniques, functional effects, and mechanistic networks of non-invasive neuromodulation in animal models of TBI. It also evaluates current limitations and future directions from the perspective of causal evidence. Published animal studies were qualitatively synthesized by stimulation modality, injury model, functional outcome, and mechanistic target, with particular attention to whether pathway involvement was supported by causal interventions or only by correlated changes. In recent years, transcranial magnetic stimulation (TMS), transcranial electrical stimulation (tES), low-intensity transcranial ultrasound stimulation (LITUS), and non-invasive vagus nerve stimulation have been investigated in animal models of TBI. TMS primarily regulates cortical excitability and activity-dependent network reorganization through magnetically induced electric fields. Different forms of tES modulate neuronal membrane potentials, corticospinal excitability, and inflammatory responses through weak electrical currents. LITUS provides relatively high spatial precision and penetration depth. It can affect both cortical and deep brain structures. Non-invasive vagus nerve stimulation acts indirectly through vagal afferent pathways and associated central and peripheral regulatory networks. Although these techniques have different physical inputs and stimulation targets, their effects may converge on several interconnected mechanistic hubs. These hubs include neurotrophic signaling and synaptic remodeling, neuroimmune regulation, endogenous antioxidant defense, and neurovascular unit protection. Brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB)-cyclic adenosine monophosphate response element binding protein (CREB) signaling is associated with neuronal survival, synaptic protein expression, cortical excitability, and neural circuit reorganization. LITUS studies have provided interventional support for this pathway through BDNF neutralization. A LITUS study has provided interventional support for BDNF/TrkB signaling through BDNF neutralization. Evidence from repetitive TMS and transcranial direct current stimulation is mainly based on parallel molecular, electrophysiological, structural, and behavioral changes. Neuroimmune regulation commonly involves reduced microglial activation and shifts toward repair-associated microglial phenotypes. It also involves decreased production of pro-inflammatory mediators. Transcranial pulsed current stimulation and low-intensity focused ultrasound stimulation have been linked to orexin-A (OX-A)/orexin receptor type 1 (OX1R) signaling. This signaling may inhibit nuclear factor-κB (NF-κB) and the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Receptor antagonism and inflammasome reactivation have strengthened the causal evidence for this pathway. However, OX-A/OX1R-related evidence currently covers only specific electrical and ultrasound paradigms. It should not be regarded as a universal mechanism shared by all four neuromodulation techniques. Antioxidant effects have been associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. They are also associated with reduced reactive oxygen species production and inhibition of neuronal death. This evidence has mainly been established in studies of transcutaneous auricular vagus nerve stimulation (taVNS). Neurovascular effects may include preservation of tight-junction and endothelial proteins, reduction of cerebral edema, improvement of cerebral perfusion, and promotion of angiogenesis. However, the evidence supporting these mechanisms is unevenly distributed among stimulation techniques. Some studies have provided causal support through receptor antagonism, pathway activation or inhibition, neurotrophic factor neutralization, and chemogenetic manipulation. Most available evidence still relies on simultaneous changes in molecular expression, histopathology, and functional outcomes. Direct comparisons among stimulation paradigms are also scarce. Differences in animal species, injury models, skull conditions, stimulation doses, intervention windows, and outcome measures further limit cross-study comparisons. Overall, non-invasive neuromodulation shows the potential to promote functional recovery after TBI by modulating interconnected repair mechanisms. However, current evidence therefore cannot establish the overall superiority of a single technique. It also cannot identify a mechanism that is indispensable across all stimulation paradigms. Future studies should standardize injury and stimulation parameters. Behavioral, electrophysiological, imaging, histological, and molecular outcomes should be assessed together. Direct comparative studies, cell-type-specific manipulation, rescue experiments, long-term safety assessments, and adaptive closed-loop stimulation are also needed. These approaches may strengthen causal inference and improve clinical translation. This review summarizes the major techniques, functional effects, and mechanistic networks of non-invasive neuromodulation in animal models of TBI. It also evaluates current limitations and future directions from the perspective of evidence hierarchy.