Li L

Chongqing Institute of Green and Intelligent Technology

EM Publications

h-index

(3,972 citations, 226 total works)

Research Topics

Neuroscience and Neuropharmacology Research (55) Neuroinflammation and Neurodegeneration Mechanisms (45) Anesthesia and Neurotoxicity Research (43) Pain Mechanisms and Treatments (31) Intensive Care Unit Cognitive Disorders (18)

Erythromelalgia Publications

Between fire and ice: refractory hypothermia and warmth-induced pain in inherited erythromelalgia.

Tham SW, Li L, Effraim P, Waxman S

BMJ case reports • 2017-Jul-26

Inherited erythromelalgia (IEM) is a well-described pain disorder caused by mutations of sodium channel Na1.7, a peripheral channel expressed within dorsal root ganglion and the sympathetic ganglion neurons. Clinically, IEM is characterised by paroxysmal attacks of severe pain, usually in the distal extremities, triggered by warmth or exercise. Pain is not adequately treated by existing pharmacological agents. Individuals with IEM classically cool their limbs for relief, in some cases resulting in tissue injury. We describe a patient from a family with IEM due to the L858F mutation of Na1.7 who presented with refractory hypothermia due to overcooling. This presentation of refractory hypothermia necessitating warming strategies, complicated by severe warmth-induced pain, posed a substantial therapeutic challenge. We report our experience in overcoming hypothermia lasting 3 weeks in a child with IEM, discuss possible pathophysiological mechanisms underlying this unusual complication and suggest potential therapeutic interventions.

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Long-term remission of primary erythermalgia with R1150W polymorphism in SCN9A after chemical lumbar sympathectomy.

Zhang L, Wang WH, Li LF, Dong GX, Zhao J , et al.

European journal of dermatology : EJD • 2010-01-01

Primary erythermalgia (PEM) is recalcitrant and long-term remission is difficult to achieve. Favorable results of treatment using carbamazepine or mexiletine have been identified in some PEM patients with SCN9A gene mutations. However, no therapeutic studies regarding patients without pathogenic SCN9A gene mutation have been reported. Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy (CLS). A 15-year-old girl with severe PEM attacks in both feet and lower legs was treated with CLS and followed up for five years. The encoding exons and their flanking sequences in the SCN9A gene were amplified and sequenced. A 50% immediate pain reduction was achieved after CLS. Burning pain, erythema and swelling in the lower legs disappeared in four days, and all ulceration healed in a month. The patient resumed normal exercise five months after CLS. There were no relapses in the following five years. R1150W polymorphism in SCN9A was detected in the patient and her healthy father. Long-term remission was achieved after CLS in this PEM case with R1150W polymorphism in SCN9A. The effectiveness of CLS and phenotype/genotype of PEM should be further studied in larger samples.

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