The classification and identification of human somatic and parasympathetic nerve fibres including urinary bladder afferents and efferents is preserved following spinal cord injury.
Single-fibre extracellular action potentials were recorded with 2 pairs of wire electrodes from lower human sacral nerve roots during surgery. The roots from which was recorded from were used for morphometry. Nerve fibre groups were identified by conduction velocity distribution histograms of single afferent and efferent fibres and partly by nerve fibre diameter distribution histograms. The values of group conduction velocity and group nerve fibre diameter measured in the paraplegics were very similar to those obtained from brain-dead humans and patients with no spinal cord injury. Thus the classification and identification of nerve fibre groups remained preserved following spinal cord injury. Upon retrograde bladder filling the urinary bladder stretch and tension receptor afferent activities were increased; on two occasions they even fired when the bladder was empty. 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 changed receptor field transduction mechanisms and too low compliance.


CONCLUSIONS
1. Single nerve fibre action potentials (APs) of lower sacral nerve roots were recorded extracellularly with 2 pairs of wire electrodes during an operation for implanting an anterior root stimulator for bladder control in 9 humans with a spinal cord injury and a dyssynergia of the urinary bladder. Roots that were not saved and that were used to record from were later used for morphometry. 2. Nerve fibre groups 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. Group conduction velocity values were obtained additionally from compound action potentials (CAPs) evoked by electrical stimulation of nerve roots and the urinary bladder. 3. The group conduction velocities and group nerve fibre diameters had the following pair-values at 35.5 degrees C: Spindle afferents: SP1 (65 m/s / 13.1 microm), SP2 (51/12.1); touch afferents: T1 (47/11.1), T2 (39/10.1), T3 (27/9.1), T4 (19/8.1); urinary bladder afferents: S1 (41 m/s / -), ST (35/-); alpha-motoneurons: alpha 13 (-/14.4), alpha 12 (65 m/s /13.1 microm), alpha 11 (60?/12.1)[FF], alpha 2 (51/10.3)[FR], alpha 3 (41/8.2)[S]; gamma-motoneurons: gamma(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 microm). 4. The values of group conduction velocity and group nerve fibre diameter measured in the paraplegics were very similar to those obtained earlier from brain-dead humans and patients with no spinal cord injury. Also, the axon number and the axon density of myelinated fibres of lower sacral nerve roots remain unchanged following spinal cord injury. Thus the classification and identification of nerve fibre groups remained preservedfollowing spinal cord injury. A direct comparison 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%), 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 retrograde 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 (designates afferents, not cord segment) and ST afferents fired even when the bladder was empty, with an activity level similar to those observed in a brain-dead human with the bladder half filled. Two reasons are brought forward for an too small storage volume of the urinary bladder in paraplegics: too high afferent activity of the bladder due to changed receptor field signal transduction mechanisms and too low compliance. 7. With the newly developed 'coordination dynamics therapy', applied early after spinal cord injury, such complications of bladder functioning can be avoided; the bladder can causally be cured in severe spinal cord injury.
g_schalow@hotmail.com
G
G
Schalow
D000200:Action Potentials / Q000502:physiology; D000328:Adult; D000344:Afferent Pathways / Q000502:physiology; D004525:Efferent Pathways / Q000502:physiology; D004558:Electric Stimulation; D006801:Humans; D009046:Motor Neurons / Q000502:physiology*; D009412:Nerve Fibers / Q000145:classification* / Q000502:physiology*; D009431:Neural Conduction / Q000502:physiology*; D010275:Parasympathetic Nervous System / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013126:Spinal Nerve Roots / Q000503:physiopathology*; D001743:Urinary Bladder / Q000294:innervation*; D001750:Urinary Bladder, Neurogenic / Q000503:physiopathology*