Pain is a sensory, emotional and subjective experience, which may or may not be associated with tissue damage, being possible to divide it into 3 categories: nociceptive, inflammatory, and pathological pain, which may be neuropathic or dysfunctional. Neuropathic pain will appear after a nervous injury, or even due to a disease in the nervous system, including peripheral fibers (Abeta, Adelta and C) and central neurons. These injuries and diseases can lead to altered and disordered transmission of sensory signals in the spinal cord and brain. Negative emotions have been reported to exacerbate chronic pain, resulting in refractory disease. A wide variety of areas in the brain can be constituted as the pain matrix, these regions are activated during concentration on the location, intensity, duration, quality and emotional associations of nociceptive pain, and will show how pain can be influenced by mood. And several evidences indicate that chronic pain shares many characteristics with neurodegenerative diseases, including the development of major depression and anxiety, with anxiety disorders being one of the most prevalent psychiatric conditions nowadays. Pain experiments using human subjects are quite challenging, subjective and ethically self-limiting, so when the aim is to better understand pain mechanisms, animal models are more widely used, offering an advantage over human studies in terms of standardizing genetic and environmental backgrounds. The spared nerve injury (SNI) model is a classic animal model for pain that will exhibit typical behavioral manifestations of neuropathic pain. It proved to be an effective method that showed substantial and prolonged sensory, mechanical and thermal changes in responses that closely mimic those configured in clinical neuropathic pain. This work, therefore, is a systematic review of a descriptive nature. A systematic search was conducted in MEDLINE/PubMed, Embase and Web of Science, and was performed according to PRISMA guidelines. The inclusion criteria was mainly the mention of neuropathic pain, an anxiety disorder and the spared nerve injury model in the same study. Quality of studies was evaluated according to the table of risk of bias from SYRCLE. From 21 eligible studies, 18 were included. Research in rats and mice shows that a few days after the SNI, the animals presented both neuropathic pain and anxiety-like behavior. And some studies presented interventions that were able to attenuate both neuropathic pain and the anxiety-like behavior. The administration of 2-OHOA had analgesic potential, in addition to reducing behavioral anxiety associated with SNI, the Ylang-ylang essential oil (YEO) in analgesic doses increases the pain threshold, has an anxiolytic effect related to the anxiety, a low dose of paracetamol reduced nerve damage associated with anxiety, treating the central amygdaloid nucleus with tetrapentylammonium (TPA), attenuated the development of neuropathic pain and anxiety-like behavior, 5HT1 receptors were necessary for the anxiolytic effect of Cannabidiol (CBD), UR13870 had analgesic potential in SNI, in addition to reducing comorbid anxiety, enriched environment reduced anxious and depressive behavior in adolescence, the inhibition of P2X7R, could improve pain symptoms, and P2X7ko had potential to prevent anxiety-like behavior, elemene administration reduced neuropathic pain and was shown to reduce anxiety-like behavior, Anxiety-like behavior was suppressed by local application of serotonin to the medial prefrontal córtex. Electroacupuncture and specific inhibition of the rACCGlu-vlPAG pathway can alleviate anxiety-like behaviors.