Muscle Action Potential Reduction Research Articles

1. Diagnosing polyneuropathy – Achievements and perspectives

The lecture aims at summarizing latest possibilities and trends in the diagnostics of polyneuropathy with stress laid on neurophysiological methods. Diagnostics of polyneuropathy is traditionally based on clinical findings and electromyography (EMG). EMG confirms diffuse involvement of peripheral nervous system (PNS) usually detected clinically; in addition, it more closely characterizes PNS involvement (distribution, degree, duration of involvement, its dynamics, type of involvement including differentiation between axonal and demyelinating neuropathy), and it may detect subclinical involvement. Standardization, reproducibility and availability are among advantages of the EMG. On the other hand, EMG reflects the involvement of large myelinated fibres (with a diameter >7 μm), that form about 15% of nerve fibres only and they usually did not serve as the initial target in most of polyneuropathies. Diagnosing demyelinating polyneuropathy is reliable in motor fibres only and is based on the detection of conduction slowing, temporal dispersion and conduction block. Criteria of conduction block have been changing last decades and with respect to experimental findings they have finally been agreed on >50% area of a proximal compound muscle action potential reduction relative to a distal one. Differential diagnosis of demyelinating conduction block in addition to inadequate stimulation especially from Erb’s point from technical reasons comprises blocks of other than demyelinating origin (such as in multifocal motor neuropathy). In axonal neuropathies, s.c. pseudoblock (“length dependent conduction block”) due to ongoing Wallerian degeneration, or axonal block (“reversible acute conduction failure”) due to dysfunction of sodium channels in nodal region caused by autoantibodies (for instance in acute motor axonal neuropathy – AMAN) could be encountered. The presence of axonal block could lead to underestimation of AMAN in Guillain–Barre syndrome (GBS) that is falsely marked as acute inflammatory demyelinating polyneuropathy (AIDP) during one-time examination. This fact indicates the necessity of repeated neurophysiological evaluation of GBS. There are, however, no generally accepted neurophysiological criteria for both GBS and chronic inflammatory demyelinating neuropathy (CIDP). Involvement of small sensory and autonomic fibres – s.c. small fibre neuropathy (SFN) is a prevalent and usually initial type of involvement in diabetic polyneuropathy and most polyneuropathies of other origin. Valid diagnostic methods detecting SFN, however, have been lacking until recently. Involvement of sensory small fibres manifests itself by positive sensory symptoms including neuropathic pain. Validated screening methods, such as DN4, PainDETECT or recently validated Czech version of the Neuropathic Pain Symptom Inventory are used for differentiation between neuropathic and nociceptive pain. Verification of thermal and pain perception is a necessary part of clinical evaluation. Semi-quantitative bedside sensory tests are easily available, but offers rough estimate only. Quantitative sensory testing, especially psychophysical method of evaluation of thermal sensory perception, is much more valid. Recently proposed diagnostic criteria for diabetic polyneuropathy, in addition to the evidence of large fibre involvement proved by EMG, also comprises proof of SFN with a validated class A marker, represented currently by the decrease of intra-epidermal nerve fibre density obtained with skin biopsy. Corneal confocal microscopy quantifying sensory small fibres in the Bowman layer of corneal becomes a promising non-invasive alternative of skin biopsy in the detection of SFN. The only neurophysiological method that showed ability to detect SFN are contact heat-evoked potentials.

Intermittent Cauda Equina Compression An Experimental Study of the Porcine Cauda Equina With Analyses of Nerve Impulse Conduction Properties

Neurophysiologic reactions of cauda equina nerve roots to intermittently applied compression were assessed for two different modes of compression using a porcine model. To assess the neurophysiologic reactions of cauda equina nerve roots to intermittently applied compression. A number of experimental studies have been presented recently regarding the reaction pattern of spinal nerve roots to compression. These studies have used a continuous pressure level. For studies of pathophysiologic mechanisms behind neurogenic claudication, however, it would be more relevant to study the effects of intermittently applied compression. The cauda equina was exposed and compression was applied by two inflatable balloons. Two different modes of compression were used. Either the two balloons were inflated and deflated simultaneously (intermittent compression), or just the caudal balloon was inflated and deflated while the cranial balloon was kept continuously inflated (continuous/intermittent compression). The experimental series were: intermittent compression at 10 mm Hg (n = 5) and 50 mm Hg (n = 5), and continuous/intermittent compression at 10 mm Hg (n = 5) and 50 mm Hg (n = 5). For both modes of compression the pressure in the balloons with intermittent inflation was maintained for 10 minutes and deflated for 5 minutes. This procedure was repeated in 8 cycles for 2 hours. Muscle action potentials were recorded in the tail muscles. Compression at 10 mm Hg induced similar reductions of muscle action potentials for both compression modes. At 50 mm Hg, the effects were more pronounced at continuous/intermittent compression than at intermittent compression. The reduction of muscle action potentials was slightly more pronounced for 50 than for 10 mm Hg at intermittent compression. However, a statistically significant difference in the results was found only between 10 and 50 mm Hg at the continuous/intermittent compression mode. The established model allows investigation of the effects of intermittent cauda equina compression, which might be clinically more relevant than continuous compression regarding the pathophysiologic mechanisms behind neurogenic claudication.