CLASSIFICATION OF HUMAN PERIPHERAL-NERVE FIBER GROUPS BY CONDUCTION-VELOCITY AND NERVE-FIBER DIAMETER IS PRESERVED FOLLOWING SPINAL-CORD LESION

(1) Single nerve fibre action potentials (APs) of lower sacral nerve r oots were recorded extracellularly with two pairs of wire electrodes d uring an operation in which an anterior root stimulator for bladder co ntrol was implanted in 9 humans with a spinal cord lesion and dyssyner gia of the urinary bladder. Roots that were not saved and that were us ed to record from were later used for morphometry. (2) Nerve fibre gro ups were identified by conduction velocity distribution histograms of single afferent and efferent fibres and partly by nerve fibre diameter distribution histograms, and correlation analysis was performed. Grou p conduction velocity values were obtained additionally from compound action potentials (CAPs) evoked by electrical stimulation of nerve roo ts and the urinary bladder. (3) The group conduction velocities and gr oup nerve fibre diameters had the following pair-values at 35.5 degree s C: Spindle afferents: SP1 (65 m/s/13.1 mu m), SP2 (51/12.1); touch a fferents: T1 (47/11.1), T2 (39/10.1), T3 (27/9.1), T4 (19/8.1); urinar y bladder afferents: S1 (41 m/s/-), ST (35/-); alpha-motoneurons: alph a(13) (-/14.4), alpha(12) (65m/s/13.1 mu m), alpha(11) (60?/12.1)(FF), alpha(2) (51/10.3)(FR), alpha(3) (41/8.2)(S); gamma-motoneurons: gamm a(beta) (27/7.1), gamma(1) (21/6.6), gamma(21) (16/5.8), gamma(22) (14 /5.1); preganglionic parasympathetic motoneurons: (10 m/s/3.7 mu m). ( 4) The values of group conduction velocity and group nerve fibre diame ter measured in the paraplegics were very similar to those obtained ea rlier from brain-dead humans and patients with no spinal cord lesions. Also, the number and the density of myelinated fibres were preserved in the roots. Thus, the classification and identification of nerve fib re groups remained preserved following spinal cord lesion. A direct co mparison can thus be made of natural impulse patterns of afferent and efferent nerve fibres between paraplegics (pathologic) and brain-dead humans (supraspinal destroyed CNS, in many respects physiologic). (5) When changing the root temperature from 32 degrees C to 35.5 degrees C , the group conduction velocities changed in the following way in one case: SP2: 40 m/s (32 degrees C) to 50 m/s (35.5 degrees C), S1: 31.3 to 40, ST: 25 to 33.8, M: 12.5 to 13.8; alpha(2): 40 to 50, alpha(3): 33 to 40. The group conduction velocities showed different temperature dependence apart from SP2 fibres and alpha(2)-motoneurons. (6) Upon r etrograde bladder filling the urinary bladder stretch (S1) and tension receptor afferent (ST) activity levels were undulating and increased. As compared to activity levels detected in a brain-dead human, S1 (de signates afferents, not cord segment) and ST afferents fired, even whe n the bladder was empty, with an activity level similar to that observ ed in a brain-dead human with the bladder half filled. Two reasons are brought forward for a too small storage volume of the urinary bladder in paraplegics: too high afferent activity of the bladder due to chan ged receptor field signal transduction mechanisms and too low complian ce.