title: [Pathophysiological, molecular and metabolic changes at the neuromuscular junction and the peripheral nerve after central nervous system lesions in humans].
abstract: From the elaborate information processing that takes place in the brain to the contraction of skeletal muscles, the neurotransmission pathways involve, at least in part, (1) in tissue, Na+, K+-ATPase electrogenesis making action potential (AP) propagation possible and (2) in the cell, the synthesis, maturation, and renewal of an amazing number of molecules concentrated at the neuromuscular junction (NMJ). Our aim is to clarify CNS and peripheral nerve system (PNS) interactions by determining whether the partial motor recovery sometimes observed after a lesion of the first motoneuron is related to (1) changes in active transportation of the ions in peripheral nerve and/or muscle and (2) morphological and/or molecular changes at the NMJ, illustrating a dysfunction. Peripheral nerve surgery is proposed to some spastic patients who have recovered partially after CNS lesions to improve their gait. During these surgical procedures, the nerve and muscle samples that are usually resected can be collected and analyzed. Here, we report on eight patients who showed strictly similar motor recovery 2 years after massive CNS lesions and who underwent a selective tibial neurotomy for a spastic equinus foot. In these eight spastic patients, we performed a pathophysiological, molecular, and metabolic study of their neuromuscular junctions and peripheral nerves to characterize the dysfunction of the neuromuscular transmission after a permanent CNS injury.
authors.affiliation: Service de neurochirurgie, CHU La-Milètrie, 2, rue de La-Milètrie, BP 577, 86021 Poitiers cedex, France. p.rigoard@chu-poitiers.fr
authors.forename: P
authors.initials: P
authors.lastname: Rigoard
authors.forename: S
authors.initials: S
authors.lastname: Bauche
authors.forename: K
authors.initials: K
authors.lastname: Buffenoir
authors.forename: L
authors.initials: L
authors.lastname: Da Costa
authors.forename: N
authors.initials: N
authors.lastname: Boildieu
authors.forename: F
authors.initials: F
authors.lastname: Seguin
authors.forename: J
authors.initials: J
authors.lastname: Koenig
authors.forename: F
authors.initials: F
authors.lastname: Lapierre
authors.forename: J-M
authors.initials: JM
authors.lastname: Maixent
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000328:Adult; D000368:Aged; D001693:Biological Transport, Active / Q000502:physiology; D002493:Central Nervous System Diseases / Q000150:complications*; D004594:Electrophysiology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D009128:Muscle Spasticity / Q000209:etiology / Q000473:pathology* / Q000601:surgery*; D009469:Neuromuscular Junction / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D010525:Peripheral Nerves / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D010523:Peripheral Nervous System Diseases / Q000209:etiology* / Q000473:pathology* / Q000601:surgery; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012583:Schwann Cells / Q000473:pathology / Q000648:ultrastructure; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000502:physiology; D009435:Synaptic Transmission
chemical_list: D011950:Receptors, Cholinergic; D000254:Sodium-Potassium-Exchanging ATPase