It may be that the condition is caused by increased production of endorphins in the brain. In this case, naloxone may be a treatment, but it does not always work. In all cases, this disorder can be in the voltage-gated sodium channel SCN9A (Nav1.7). Patients with such mutations are<unk> ly insensitive to<unk>  and lack other neuropathies. There are three mutations in SCN9A: W897X, located in the P-loop of domain 2; I767X, located in the S2 segment of domain 2; and S459X, located in the linker region between domains 1 and 2. This results in a truncated non-functional protein. Nav1.7 channels are expressed at high levels in nociceptive neurons of the dorsal root ganglia. As these channels are likely involved in the formation and propagation of action potentials in such neurons, it is expected that a loss of function mutation in SCN9A leads to abolished nociceptive<unk>  propagation. PRDM12 gene is normally switched on during the development of<unk> -sensing nerve cells. People with homozygous mutations of the PRDM12 gene experience<unk>  (CIP). Homozygous microdeletion in the FAAH-OUT pseudogene of the fatty acid amide hydrolase chromosomal region that is expressed in the brain and dorsal root ganglia was identified as the cause of<unk>  analgesia in a single individual (as of 2019). The individual experienced lifelong<unk>  to<unk>  and was oblivious to cuts and burns, did not experience<unk>  during childbirth, did not experience<unk>  from degeneration of a hip that required hip replacement surgery, and did not require analgesics for postoperative<unk> . Furthermore, the individual exhibited expedited wound healing and reduced scarring, could not sense heat from chili peppers, did not experience depression, fear, and anxiety and lacked a normal fear response to erratic and aggressive behaviour. However, the individual also experienced slight memory impairment (was prone to losing the trail of thought while speaking, and experienced some forgetfulness), and could not experience thrill ("adrenaline rush"). Another gene implicated in human<unk> <unk>  is ZFHX2, which encodes zinc finger homeobox 2. A 2018 study analysed six members of a family with inherited<unk> <unk>  and identified a "novel point mutation in ZFHX2, encoding a putative transcription factor expressed in small diameter sensory neurons", as the cause. As a therapeutic application, the study further discuses how "the ZFHX2 variant and downstream regulated genes associated with a human<unk> -insensitive phenotype are ... potential novel targets for the development of new analgesic drugs". Developmental disabilities such as autism can include varying degrees of<unk> <unk>  as a sign. However, since these disorders are characterized by dysfunction of the sensory system in general, autism is not in itself an indicator of<unk> .
Congenital insensitivity to pain
Hereditary neuralgic amyotrophy
Hereditary neuropathy with liability to pressure palsy
Hereditary sensory and autonomic neuropathy
Accessory nerve disorder
Monomelic amyotrophy
Split hand syndrome
Dissociated sensory loss