• The Korean Journal of Pain
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• v.23 no.1
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• pp.70-73
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• 2010

Complex regional pain syndrome (CRPS) is a painful and disabling disorder that can affect one or more extremities. Unfortunately, the knowledge concerning its natural history and mechanism is very limited and many current rationales in treatment of CRPS are mainly dependent on efficacy originated in other common conditions of neuropathic pain. Therefore, in this study, we present a case using a total spinal block (TSB) for the refractory pain management of a 16-year-old male CRPS patient, who suffered from constant stabbing and squeezing pain, with severe touch allodynia in the left upper extremity following an operation of chondroblastoma. After the TSB, the patient’s continuous and spontaneous pain became mild and the allodynia disappeared and maintained decreased for 1 month.

• Journal of Oral Medicine and Pain
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• v.25 no.2
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• pp.229-234
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• 2000

The patient, 62-years-old woman, had a constant dull pain in the right mandible and an intermittent spontaneous burning sensation of the mouth. The pain began 6 months ago. About 5 years ago, a trauma in her right mandible which was so severe that kept her in the hospital for 2 days. This was followed by mouth opening disturbance with pain for about 2 years. However, she did not have a treatment for the temporomandibular disorder symptoms. After then, she experienced the trigeminal neuralgia characterized by an electrical pain which lasted about 30 minutes in her right face and head when touching the skin or hair. After taking a year course treatment of trigeminal neuralgia, the symptom disappeared. The pain was a constant dull pain and a intermittent burning pain which are contradictory. And the pain responded to various modalities such as physical therapy, anti-inflammatory drug, carbamazepine, and amitriptyline, among which carbamazepine was most effective. The diagnosis was clinically made as an atypical trigeminal neuralgia. The term 'atypical' is used when there is something unknown and the problem is not identified. It is thought that an atypical pain may be approached in the perspective of chronic pain, neuropathic pain, and myofascial pain, the mchanisms of which are poorly understood. As the knowledge of pain physiology improves, there needs to be modification and re-evaluation. Pain disorders must be classified on the basis of an understanding of the underlying mechanism and etiology.

• The Korean Journal of Pain
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• v.25 no.2
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• pp.75-80
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• 2012

Hypnosis is an altered state of consciousness that comprises of heightened absorption in focal attention, dissociation of peripheral awareness, and enhanced responsiveness to social cues. Hypnosis has a long tradition of effectiveness in controlling somatic symptoms, such as pain. Pain, the most common symptom in clinical practice, is a multi-dimensional experience, which includes sensory-discriminative, affective-emotional, cognitive and behavioral components. There is a growing recognition for hypnosis and related techniques in pain management. Psychological approaches to pain control, such as hypnosis, can be highly effective analgesics, but are underused in Korea. In this article, we would like to review the basic concepts of hypnosis, the mechanism, and the outcome data of the analgesic effects of hypnosis, and also, its limitations.

• The Journal of Korean Medicine
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• v.16 no.1 s.29
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• pp.36-50
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• 1995

Acupuncture is so effective and simple to use in the pain and dysfunction syndrome of TMD. Acupuncture treatment is a point-specific. So, the selection of acupuncture point is very important. According to the traditional meridian theory, we select the points; local points around TMJ and mastication muscles(ST6, ST7, GB20, GB21) and remote point(LI4). And if there is another pain, one or two other points are added. Both neural and humoral mechanism play an important role in acupuncture analgesia. The discovery of spinal gate mechanisms shows somatic stimulation can induce pain inhibition. Humoral mechanism has been established from the discovery of opioid receptors and endogenous opioids. Acupuncture induces a relaxation in the patient, which further decreases the muscle tension.

• The Korean Journal of Pain
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• v.31 no.2
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• pp.73-79
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• 2018

All drugs have both favorable therapeutic and untoward adverse effects. Conventional opioid analgesics possess both analgesia and adverse reactions, such as nausea, vomiting, and respiratory depression. The opioid ligand binds to ${\mu}$ opioid receptor and non-selectively activates two intracellular signaling pathways: the G protein pathway induce analgesia, while the ${\beta}$-arrestin pathway is responsible for the opioid-related adverse reactions. An ideal opioid should activate the G protein pathway while deactivating the ${\beta}$-arrestin pathway. Oliceridine (TRV130) has a novel characteristic mechanism on the action of the ${\mu}$ receptor G protein pathway selective (${\mu}$-GPS) modulation. Even though adverse reactions (ADRs) are significantly attenuated, while the analgesic effect is augmented, the some residual ADRs persist. Consequently, a G protein biased ${\mu}$ opioid ligand, oliceridine, improves the therapeutic index owing to increased analgesia with decreased adverse events. This review article provides a brief history, mechanism of action, pharmacokinetics, pharmacodynamics, and ADRs of oliceridine.

• The Korean Journal of Pain
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• v.12 no.2
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• pp.246-249
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• 1999

Postherpetic neuralgia (PHN) is defined as the persistence of pain after recovery from herpes zoster (HZ), when the rash has healed, usually after about 4 weeks. PHN is the most feared complication of herpes zoster and remains one of the most common and intractable chronic pain disorders. Recent evidence has shed some light on the possible mechanism of pain, and on the prophylactic and treatment approaches to PHN, but there is no secure therapy. This report is a case of a 70-year-old male with PHN, affecting the 8th to 10th thoracic dermatomes. Patient complains of allodynia and hyperalgesia on the affected skins. After sympathectomy, antidepressant, anticonvulsant, and capsaicin ointment application, much pain relief was achieved, but allodynia remained at the subcostal area about $7\times3 cm^2$ in size. We decided to remove the painful area. Skin excision was done under local anesthesia. After skin excision, the pain was decreased and patient did not complain of pain for 10 months.

• The Korean Journal of Pain
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• v.9 no.1
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• pp.229-231
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• 1996

Spinal cord stimulation(SCS) was first attempted to relieve intractable pain in 1966. SCS has evolved into percutaneously implanted electrode with aim of activating spinal pain-inhibiting mechanism via dorsal columns. SCS is valuable for the treatment of many painful and difficult to treat conditions such as postamputation pain, painful peripheral neuropathies, chronic sciatic pain and so on. We treated a case of causalgia of the right lower extremity with successful outcome of 90% sustained relief of pain. And patient has satisfied using SCS(Model MNR-94, Neuromed) for 6 months follow-up.

• Journal of Acupuncture Research
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• v.20 no.3
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• pp.117-130
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• 2003

To study the analgesic and effect and its mechanism of eletroacupunture(EA) on the chronic inflammatory pain 50 rats were induced with arthralgesia by injecting complete freund's adjuvant(CFA). Two weeks after the injection of CFA, EA stimulation(2Hz, 0.07mA, 0.3ms) was delivered to Jogsamni($ST_{36}$) for 20 minutes. Analgesic effect was evaluated by using the tail flick latency(TFL) and the analgesic mechanism was observed by applying TFL with the pretreatment with naloxone and yohimbine. The results were as follows ; 1. TFL level for the model of adjuvant-induced arthritis decreased as time went by and it induced the hyperalgesia. 2. EA stimulation delivered to Jogsamni($ST_{36}$) for 20 minutes in the rat model of adjuvant-induced arthritis brought analgesic effect and its effect had lasted for 40 minutes after the stimulation. 3. The analgesic effect of Jogsamni($ST_{36}$) EA in the rat model of adjuvant-induced arthritis was blocked by pretreatment with naloxone(2mg/kg,i.p). This result suggests that the EA effect on the chronic inflammatory pain can be related to the endogenous opioid mechanism. 4. The analgesic effect of Jogsamni($ST_{36}$) EA in the rat model of adjuvant-induced arthritis was blocked by pretreatment with naloxone(2mg/kg,i.p). This result suggests that the EA effect on the chronic inflammatory pain can be related to the ${\alpha}_2$-adrenergic mechanism.

• 경락경혈학회:학술대회논문집
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• 2006.11a
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• pp.141-141
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• 2006

• The Korean Journal of Pain
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• v.28 no.1
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• pp.4-10
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• 2015

Etifoxine (etafenoxine, $Stresam^{(R)}$) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by $GABA_A{\alpha}2$ receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to ${\beta}2$ or ${\beta}3$ subunits of the $GABA_A$ receptor complex. It also modulates $GABA_A$ receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates $GABA_A$ receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.