脊髓损伤后,保留了人体躯体神经纤维和副交感神经纤维的分类和识别,包括膀胱传入神经和传出神经。

G Schalow
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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.</p><p><strong>Summary: </strong>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. 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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. 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引用次数: 0

摘要

未标记:术中用2对丝电极记录骶神经根下段单纤维细胞外动作电位。所记录的根被用于形态测定。通过单个传入和传出纤维的传导速度分布直方图和部分神经纤维直径分布直方图来识别神经纤维组。截瘫患者的组传导速度和组神经纤维直径与脑死亡患者和无脊髓损伤患者的组传导速度和组神经纤维直径非常相似。因此脊髓损伤后神经纤维群的分类和鉴定得以保留。膀胱逆行充盈后,膀胱张力受体传入活动增加;有两次他们甚至在膀胱空了的情况下开枪。截瘫患者膀胱储藏量过小的原因主要有两方面:一是由于受体场转导机制改变导致膀胱传入活性过高,二是依从性过低。总结:1。本文对9例脊髓损伤伴膀胱协同功能障碍患者行前神经根刺激器膀胱控制术时,用2对丝电极记录下骶下神经根单神经纤维动作电位(APs)。没有保存下来的根和用来记录的根后来被用于形态测定。2. 通过单个传入和传出纤维的传导速度分布直方图和部分神经纤维直径分布直方图来识别神经纤维组,并进行相关性分析。另外,通过电刺激神经根和膀胱引起的复合动作电位(cap)获得组传导速度值。3.在35.5℃时,组神经传导速度和组神经纤维直径有以下成对值:纺锤体传入:SP1 (65 m/s / 13.1微米),SP2 (51/12.1);触觉事件:T1(47/11.1)、T2(39/10.1)、T3(27/9.1)、T4 (19/8.1);膀胱传入:S1 (41 m/s /-), ST (35 m/ -);α -运动神经元:α 13(-/14.4)、α 12 (65 μ m/s /13.1 μ m)、α 11 (60 μ m/ 12.1)[FF]、α 2 (51/10.3)[FR]、α 3 (41/8.2)[s];-运动神经元:γ (β) (27/7.1), γ 1 (21/6.6), γ 21 (16/5.8), γ 22 (14/5.1);节前副交感神经运动神经元:(10 m/s / 3.7微米)。4. 截瘫患者的组传导速度和组神经纤维直径与早期脑死亡患者和无脊髓损伤患者的组传导速度和组神经纤维直径非常相似。脊髓损伤后,骶下神经根髓鞘纤维的轴突数量和轴突密度保持不变。因此,脊髓损伤后神经纤维群的分类和鉴定得以保留。因此,可以直接比较截瘫患者(病理性)和脑死亡患者(在许多生理方面脊髓上中枢神经系统受损)之间传入和传出神经纤维的自然冲动模式。5. 当根温从32℃变化到35.5℃时,组传导速度的变化规律如下:SP2从40 m/s(32℃)到50 m/s (35.5%), S1从31.3到40,ST: 25到33.8,m: 12.5到13.8;Alpha 2:40到50,Alpha 3:33到40。除SP2纤维和α 2运动神经元外,各组传导速度表现出不同的温度依赖性。6. 膀胱逆行充盈后,膀胱拉伸(S1)和张力受体传入(ST)活性水平呈波动和升高。与在脑死亡的人身上检测到的活动水平相比,S1(指传入事件,而不是脊髓段)和ST传入事件即使在膀胱空的情况下也会被激发,其活动水平与在膀胱半满的脑死亡的人身上观察到的活动水平相似。截瘫患者膀胱储藏量过小的原因主要有两方面:一是由于受体场信号转导机制改变导致膀胱传入活性过高,二是依从性过低。7. 新发展的“协调动力学疗法”,在脊髓损伤后早期应用,可以避免膀胱功能的并发症;严重脊髓损伤的膀胱是可以治愈的。
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The classification and identification of human somatic and parasympathetic nerve fibres including urinary bladder afferents and efferents is preserved following spinal cord injury.

Unlabelled: 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.

Summary: 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.

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