Motor Unit Populations in Healthy and Diseased Muscles

Abstract

Avaibbb at k t ! Previously offered only through AFTAS risk management workshop, this hefty guide to risk management issues shares information every PT professional needs to know. ..on preventive recording ... malpractice and other bases of potential liabiliq..the judicial process when dealing with malpractice ... informed consent ... and more! In a handy, usable format. Numerous expert contributors. (21 7 pages, tabbed 3-ring binder, 1990) Order No. P-95 s.

Motoneuron Death after Human Spinal Cord Injury

“…Each spinal cord was removed within 24 h of death, preserved in 10% neutral buffered formalin for at least 2 weeks, and then stored in 0.1 M phosphate buffer. 1 Ventral roots were taken for the present study provided that: 1) the person was between 18-61 years when they died, which avoided the motoneuron death associated with aging 25 ; 2) the ventral roots were intact for at least 30 mm after exiting the cord, which avoided motoneuron death from root avulsion 10 and Wallerian degeneration of motor axons in our root samples 26,27 ; and 3) the root levels could be identified clearly by anatomical landmarks. For each root, 5-10 mm samples were taken, beginning at the point where the rootlets entered the cord caudal to the corresponding spinal segment, since motor axons take a caudal intramedullary course in the spinal cord before exiting into the ventral root.…”

Measures and markers in Amyotrophic Lateral Sclerosis

“…No technique has been universally accepted, but 4 have emerged as the most commonly used. The original incremental technique described by McComas [81][82][83] relied on stimulating at one location, using a stimulus that varied slightly from near-threshold levels. Initially, an all-or-none response was generated, representing the response of a single unit.…”

Muscle histone deacetylase 4 upregulation in amyotrophic lateral sclerosis: potential role in reinnervation ability and disease progression

“…In ALS, loss of functional motor neurons is initially followed by compensatory collateral reinnervation of denervated muscle fibres by the remaining motor neurons (Hansen and Ballantyne, 1978;McComas et al, 1993). Consequently, clinical muscle weakness results from the dynamic interaction between primary loss of lower motor neurons and secondary compensation by collateral reinnervation (Bromberg et al, 1993).…”