Pain

Gene therapy for reducing pain

gene therapy that targets opioid-sensitive neurons in the cingulate using a synthetic μ-opioid receptor promoter to drive inhibition of pain (ref)

Intramuscular electroporation with the pro-opiomelanocortin gene in rat adjuvant arthritis (2003)

Analgesics

acetaminophen, ibuprofen, naproxen, ketorolac, diclofenac, morphine, fentanyl, hydromorphone, oxycodone, hydrocodone, codeine, tramadol, methadone, ketamine, dexmedetomidine, bupivacaine, lidocaine, celecoxib, aspirin, gabapentin, ziconotide

next-gen analgesics might include: suzetrigine, cebranopadol, G protein-biased MOR agonists (e.g., SR-17018, PZM21, ...), TRPV1 as a target, ...

Anesthetics

propofol, sevoflurane, isoflurane, desflurane, nitrous oxide, ketamine, etomidate, midazolam, fentanyl, remifentanil

next-gen anesthetics might include: remimazolam, ciprofol (HSK3486) (propofol analogue), ...

Surgical methods

Surgical methods in pain management: neuroablative methods, neuromodulatory methods.. focused ultrasound in general, but also focused ultrasound thalamotomy. Various peripheral nerve stimulation techniques, dorsal root ganglion stimulation with transforaminal electrode placement.

selective neuretomy in general. microsurgical neurolysis.

adjunctive distal nerve crush (Clark's procedure)

For pain see also

opiod receptors (μ, δ, κ) are a common target for analgesics.

MC1R gene variants like R151C, R160W, and D294H are associated with higher anesthetic requirements (e.g., more anesthetic needed for sedation) and sometimes altered pain sensitivity. people with loss-of-function CYP2D6 variants metabolize certain opioids (like codeine or tramadol) very poorly. variations in drug-metabolizing enzymes and transporters (e.g., CYP3A4, CYP2C9, ABCB1) can reduce plasma clearance or alter effective concentrations of analgesics, resulting in variable pain control. some mutations in RYR1 greatly increase susceptibility to a severe reaction to volatile anesthetics (malignant hyperthermia). (ref -- TODO: needs more processing)

Various germline genetic modifications for pain are proposed on the ?human germline genetic engineering page inside the pain section.

Pain insensitivity

A novel human pain insensitivity disorder caused by a point mutation in ZFHX2

A pathological missense mutation in the deubiquitinase USP5 leads to insensitivity to pain

various mutations in SCN9A can result in low pain and also total pain insensitivity. also FAAH pseudogene microdeletion. there are other congenital mutations leading to congenital insensitivty to pain. Again see the pain insensitivity section for more info.