The Role of Special K in Pain Management

Author: Courtney Kominek

Ketamine, known on the street as “special K,” is a dissociative anesthetic with hallucinogenic properties and is classified as a controlled substance. Its unique mechanism as an N-methyl-D-aspartate (NMDA) receptor antagonist is thought to be responsible for many of the drug’s most promising properties. Stimulation of the NMDA receptor results in central sensitization (wind up phenomenon), hyperalgesia, reduced sensitivity to opioids, and the development of opioid tolerance. This can result in allodynia, hyperalgesia, and prolonged pain response. Ketamine partially reverses the previously mentioned complications that can restore the effectiveness of opioids in various settings and often allows for reduced opioid doses and improved pain control. With appropriate clinical knowledge and patient monitoring, ketamine at subanesthetic doses can play a role in the treatment of complex regional pain syndrome (CRPS), cancer pain, and even neuropathic or chronic pain refractory to typical treatment options. Depending on the clinical setting, ketamine can be administered via intravenous (IV) or oral (PO) routes, among others. Clinical monitoring is required to ensure that side effects, such as dysphoria, do not adversely impact the patient.

Ketamine, an anesthetic structurally related to phencyclidine (PCP), is a Schedule III controlled substance, according to the Controlled Substances Act, that has both licit and illicit uses. Special K refers to one of the many street names for ketamine when used illicitly via various routes for its dissociative and hallucinatory effects. In addition to its dissociative anesthetic properties, ketamine also has analgesic, sedative, and amnesic characteristics. Anesthetic doses of ketamine range from 0.5 to 4.5 mg/kg/h while subanesthetic doses are generally in the range of 0.1 to 0.3 mg/kg/h.

Though ketamine interacts with multiple receptors in the central and peripheral nervous systems, ketamine’s primary mechanism of action is through noncompetitive NMDA receptor antagonism. This reduces the release of the excitatory neurotransmitter, glutamate, involved in afferent pain transmission. It is through the antagonistic effects on NMDA receptors that ketamine is thought to reverse hyperalgesia, opioid tolerance, and central sensitization. In addition, ketamine binds to mu-, kappa-, and delta-opioid receptors. Hirota et al 1996 suggested that ketamine is a mu-opioid receptor antagonist and a kappa-opioid receptor agonist. Later in 2011 Hirota et al proposed that ketamine is a mu-opioid receptor antagonist and a kappa-receptor antagonist at anesthetic doses. However, others classify ketamine as a mu-opioid receptor agonist. The analgesic effect of ketamine is stereoselective with the S(+)-enantiomer yielding more analgesia than the R(-)-enantiomer.

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