• The Korean Journal of Pain
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• v.4 no.2
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• pp.186-190
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• 1991

Causalgia is an extremely incapacitating disease often associated with a major peripheral nerve injury, which is characterized by sustained diffuse burning pain, allodynia and hyperpathia. The condition follows traumatic nerve lesions, often combined with vasomotor and sudomotor disturbances and later trophic changes. While sympathectomy has been the classical treatment of causalgia, others nonsurgical therapies such as regional sympathetic block, IV regional sympathetic block, oral adrenolytic drugs, transcutaneous electrical nerve simulation, physical theraphy, cryotheraphy and psychotheraphy have been used. Causalgia is rare in children and early treatment is controversial because of the possibility of many different complications following aggressive treatment. This is a report of a 6-year-old girl with causalgia suffered after a right posterior tibial nerve injury following an intragluteal injection of an antipyretics. We successfully treated this syndrome with continuous epidural block using 0.5% lidocaine and no specific complication was encountered.

• The Korean Journal of Pain
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• v.11 no.1
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• pp.109-112
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• 1998

The sympathetic nervous system has been implicated as an important factor contributing to causalgia. Basis on reports of presence of opioid receptors in sympathetic autonomic ganglia, including human stellate ganglion, we administered morphine in stellate ganglion block for a patient with causalgia. The patient suffering from brachial plexus injury treated with stellate ganglion block in conjunction with physical therapy. Stellate ganglion block was performed in a paratracheal approach by injection of 1% lidocaine, or 0.25% bupivacaine 8 ml, with morpine 1 mg. Patient's symptoms were dramatically improved after 13 stellate ganglion blocks.

• The Korean Journal of Pain
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• v.7 no.2
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• pp.263-269
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• 1994

Causaliga is a syndrome of sustained burning pain, allodynia and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes. Various treatments of causalgia contain sympathetic blockade, sympathectomy, transcutaneous electrical nerve stimulation, physical therapy, cryotherapy and psychotherapy. Repeated stellate ganglion blocks with 6ml of 0.25% bupivacaine provided good results for 2 patients. We recommand sympathetic blocks for treatment of causalgia.

• The Korean Journal of Pain
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• v.5 no.1
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• pp.80-84
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• 1992

49세 여자 환자가 경부 추간판 탈출증의 치료를 받기위하여 전신 마취하에 우측의 추궁 절제술과 전방 추체간 접합술을 받고난 즉시 회복실에서 부터 양측 상지에 작열통이 발생하였다. 환자는 양측 상지에 전형적인 작열통의 증상인 allodynia, 통각 과민(hyperalgesia), 통각 이상 과민증 (hyperpathia)을 보였으며 특히 우측 상지에는 심한 부종을 보이고 있었다. 환자는 일련의 성상 신경절 차단과 disposable $Daymate^{TM}$ portable elastomeric infusor를 이용한 연속적 상완신경총 차단으로 작열통이 완치되었다.

• 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.

• The Korean Journal of Pain
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• v.7 no.1
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• pp.96-99
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• 1994

Causalgia is a symptom complex usually consisting of burning pain, hyperesthesia and atrophy of the involved extremity. The pain may be aggravated by contact, motion of extremity or emotional excitement. It occurs following incomplete nerve injury. The patient was a 58-year-old male with a 3-year history of causalgic pain of left lower extremity. He had multiple fractures with degloving injury of left lower extremity in an automobile accident. The pain was exacerbated by movement, and he experienced knee joint and ankle joint contracture. The patient's pain decreased after continuous epidural block with 1% lidocaine and 0.25% bupivacaine. He also received lumbar sympathetic ganglion alcohol block resulting in much improvement of level of pain and walking disturbance.

• The Korean Journal of Pain
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• v.13 no.2
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• pp.156-163
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• 2000

Background: Peripheral nerve injury sometimes leads to chronic neuropathic pain such as causalgia. A subset of patients with causalgia have a sympathetically maintained pain which is often evoked by cooling stimuli. However, our knowledge on adrenergic receptor types responsible for cold-evoked pain that is sympathetically dependent is lacking. The present study was conducted to investigate subtypes of adrenoceptors involved in mediating cold-evoked pain that developed following peripheral nerve injury. Methods: Neuropathic surgery was performed by a unilateral ligation of L5 and L6 spinal nerves of rats. Behavioral sign of cold-evoked pain was examined for 5 min by measuring cumulative duration of time that the rat lifted its foot off a metal plate held at cold temperature ($5^{\circ}C$). Whether cold-evoked pain behavior was affected by antagonists of various subtypes of adrenoceptors, which were administered intraperitoneally before and after the ligation, was investigated. Results: After ligation, duration of foot lifting on the ligated side at cold temperature increased as compared to the pre-operative period. This increase maintained for the entire 40-day test period. Pretreatment with alpha-antagonist phentolamine produced a suppression of cold-evoked pain behavior that was not affected by beta-antagonist propranolol pretreatment. Prazosin, alpha-1 antagonist, suppressed cold- evoked pain behavior when treated either before or after nerve ligation. On the other hand, alpha-2 antagonist yohimbine was without effect on cold-evoked pain behavior whether it was treated before or after the ligation. Conclusions: The results suggest that peripheral nerve injury develops cold-evoked pain that is sympathetically dependent, and that alpha-1 adrenoreceptor plays a critical role for the generation of this type of pain in its initiation as well as maintenance.

• The Korean Journal of Pain
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• v.3 no.2
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• pp.101-107
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• 1990

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.35-45
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• 2022

Complex regional pain syndrome (CRPS) is a chronic regional pain disorder that most frequently affects the limbs. It is characterized by hyperalgesia, allodynia, edema, motor disturbance, and vasomotor instability, and typically occurs following surgery or trauma. In type-I CRPS there is no confirmed nerve injury, while peripheral nerve injury is present in type-II CRPS. The multifactorial pathophysiological etiology of CRPS includes inflammation, autoimmune responses, abnormal cytokine production, autonomic dysfunction, altered blood flow, psychological factors, and central cortical reorganization. There are no specific laboratory diagnostic tools for CRPS, and so it is diagnosed clinically. The Budapest criteria are currently the most-accepted diagnostic criteria.

• Clinical Pain
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• v.18 no.2
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• pp.133-137
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• 2019

The long-term prognosis of complex regional pain syndrome is difficult to predict because of its unclear pathophysiology. The syndrome can spontaneously spread to other regions in the body. We report a case in which a complex regional pain syndrome that occurred in a 75-year-old male patient after a stroke spread to the opposite side.