Abstract
Congenital insensitivity to pain (CIP) is a rare genetic neurological disorder which is full-blown PID, in which they are permanently unable to feel physical pain, despite being conscious to and sense of touch are often spared. CIP patients have no sense of pain, which results in increased risk in significant health, due to the fact that pain can be seen as a vital response to the body that signals the body to damage or illness. Recurrence of strains, guys, destruction of castles, joint infusion, and disease and largely undiagnosed until severe, are not uncommon in people living with this disease. Problems arise. Changes in the genes required for the development and function of nociceptors, are associated with CIP, most commonly as NTRK1, SCN9A, and PRDM12, in an autosomal recessive manner. These genetic alterations either restrict sodium channel sends activity in sensory neurons or blocks nerve growth factor signals that disrupt pain signaling pathways. The clinical presentation is dependent on the underlying genetic mutation, such as anhidrosis, recurrent hyperthermia, and autonomic dysfunctions, which may be underlying clefts of types such as cleft palate. Poor temperature perception. Higher rates have been reported in groups of CIP is also still rare, thus the global frequency remains hugely uncertain, especially in populations that practice consanguineous marriages. In both syndromic and non-syndromic cases, careful clinical evaluation supported by molecular genetic testing is required for the diagnosis. Currently, there is no cure for CIP therefore, long-term multidisciplinary follow-up. Management is typically based on patient and caregiver teaching, and injury prevention. The development of new pain killers depends on some findings regarding CIP which led to a large role in our understanding of how pain works.