脊髓损伤患者实施间歇导尿指征的研究

Objective To know the indication for patients with spinal cord injury during the course of intermittent urethral catheterization.Methods Divided 33 patients with spinal cord injury into the experimental group(18 cases)and control group(15 cases)randomly.The indication of beginning in the experiment group was less than 500 ml transfusion per day,without press ulcer,more than 150 ml bladder capacity.The indication in the control group was＞28 cm H2O pressure of bladder.Compared the effects between the two groups.Results The incidence rate of infection in the experiment group was lower than control group,all the indexes of uretharal catheterization were better in the experiment group than those of in the control group.Conclusions The indication of less than 500ml transfusion per day,without press ulcer,more than 150 ml bladder capacity are proper.     

Short latency cutaneous reflex responses of γ-efferents in the decerebrate cat

Summary The effect of single shock stimulation, up to 20 × threshold (T), of the sural nerve on the discharges of triceps surae -efferents was investigated in decerebrate cats. Units were classified as static (12) or dynamic (7) on the basis of their resting discharge rates (Murphy et al. 1984). All neurones were excited at short latency by sural nerve stimulation and response size was graded with stimulus intensity. Short latency mixed or inhibitory responses were not evident. Although reflex effects first occurred at low stimulus strengths (<-1.5T) in both types of efferent, most responses appeared at higher intensities (> 1.5T). The estimated central delays of the responses of static (3.0 ±1.1 ms, mean± SD) and dynamic (3.4 ± 1.0 ms) -motoneurones were not significantly different and are consistent with spinal oligosynaptic pathways. The present results differ from those of the only previous study (Johansson and Sojka 1985) of the short latency responses of triceps surae static and dynamic -motoneurones to sural nerve stimulation, in which mixed and inhibitory effects were common in anaesthetised cats. Although differences in recording techniques and sampling may account for the apparent disparity between these studies, it is also feasible that a difference in the setting of interneuronal pathways in the two types of preparation is responsible. The results are discussed in relation to the control of -motoneurones with particular reference to the final common input hypothesis (Johansson 1981; Appelberg et al. 1983).     

Bulbospinal inhibition of PAD elicited by stimulation of afferent and motor axons in the isolated frog spinal cord and brainstem

Summary 1. In the isolated spinal cord and brainstem of the frog, stimulation of the brainstem (BS) with trains of 3–4 pulses at 60–400 Hz produced dorsal root potentials (DRPs). The lowest threshold sites eliciting DRPs were located at the level of the obex up to about 2.5 mm rostrally, 0.5–1.2 mm laterally, between 0.5 and 1.6 mm depth. This region corresponds to the bulbar reticular formation (RF). 2. Stimulation of the RF with strengths below those required to produce DRPs, very effectively inhibited the DRPs produced by stimulation of a neighboring dorsal root (DR-DRPs) as well as the DRPs produced by antidromic stimulation of the central end of motor nerves (VR-DRPs). The inhibition was detectable 20 ms after the first pulse of the conditioning train, attained maximal values between 50 and 100 ms and lasted more than 250ms. 3. Stimulation of the bulbar RF increased the negative response (N₁ response) produced in the motor pool by antidromic activation of motoneurons. The time course of the facilitation of the N₁ response resembled that of the reticularly-induced inhibition of the VR-DRPs and DR-DRPs. 4. The present series of observations supports the existence of reticulospinal pathways that are able to inhibit the depolarization elicited in afferent fibers by stimulation of other afferent fibers or by antidromic activation of motor axons. This inhibition appears to be exerted on the PAD mediating interneurons and is envisaged as playing an important role in motor control.     

Transplantation of nasal olfactory tissue promotes partial recovery in paraplegic adult rats

Recent reports have highlighted the potential therapeutic role of olfactory ensheathing cells for repair of spinal cord injuries. Previously ensheathing cells collected from the olfactory bulbs within the skull were used. In humans a source of these cells for autologous therapy lies in the nasal mucosa where they accompany the axons of the olfactory neurons. The aim of the present study was to test the therapeutic potential of nasal olfactory ensheathing cells for spinal cord repair. Olfactory ensheathing cells cultured from the olfactory lamina propria or pieces of lamina propria from the olfactory mucosa were transplanted into the transected spinal cord. Three to ten weeks later these animals partially recovered movement of their hind limbs and joints which was abolished by a second spinal cord transection. Control rats, receiving collagen matrix, respiratory lamina propria or culture medium, did not recover hind limb movement. Recovery of movement was associated with recovery of spinal reflex circuitry, assessed using the rate-sensitive depression of the H-reflex from an interosseous muscle. Histological analysis of spinal cords grafted with olfactory tissue demonstrated nerve fibres passing through the transection site, serotonin-positive fibres in the spinal cord distal to the transection site, and retrograde labelling of brainstem raphe and gigantocellularis neurons from injections into the distal cord, indicating regeneration of descending pathways. Thus, olfactory lamina propria transplantation promoted partial restoration of function after relatively short recovery periods. This study is particularly significance because it suggests an accessible source of tissue for autologous grafting in human paraplegia.     

Expression of 5-HT2A receptor mRNA in rat spinal dorsal horn and some nuclei of brainstem after peripheral inflammation

The expression of 5-hydroxytryptamine 5-HT2A receptor mRNA was studied in the lumbar spinal dorsal horn, nucleus of raphe magnus (NRM), ventrolateral periaqueductal gray (vlPAG) and dorsal raphe nucleus (DRN) following carrageenan inflammation using in situ hybridization technique. The findings of this study demonstrated that 5-HT2A receptor mRNA was expressed with low to moderate levels in lumbar spinal dorsal horn, NRM, vlPAG and DRN. Following carrageenan inflammation, the expression of 5-HT2A receptor mRNA in ipsilateral dorsal horn, bilateral NRM, vlPAG and DRN was significantly increased. The peak occurred at 3 h and then there was a clear decrease but still a substantial number of labeled cells at 24 h after injection of carrageenan. This result suggested that the synthesis of 5-HT2A receptor is enhanced in spinal dorsal horn, NRM, vlPAG and DRN during inflammatory pain.     

Sympathetic skin response in incomplete spinal cord injury with urinary incontinence

Objectives:

Sympathetic skin response (SSR) is a test for evaluation of the sympathetic sweat gland pathways, and it has been used to study the central sympathetic pathways in spinal cord injury (SCI). This study aimed to assess the autonomic pathways according to normal or abnormal SSR in urinary incontinence patients due to incomplete spinal cord injury.

Materials and Methods:

Suprapubic, palmar, and plantar SSR to the peripheral nerve electrical stimulation were recorded in 16 urinary incontinence patients with incomplete spinal cord injury at various neurological levels and in 30 healthy control subjects.

Results:

All the recordings of SSR from the incomplete SCI patients with urinary incontinence as compared with their counterparts in the control group showed significantly reduced amplitudes with more prominent reduction in the suprapubic area recording site (P value < 0.0004). SSR with significantly prolonged latencies were recorded from palm and plantar areas in response to suprapubic area and tibial N stimuli, respectively (P value < 0.02). In this study, a significantly higher stimulus intensity (P value < 0.01) was needed to elicit SSR in the cases compared with the control group.

Conclusion:

This study showed abnormal SSR in urinary incontinence patients due to incomplete SCI. In addition, for the first time we have described recording of abnormal SSR from the suprapubic area as another way to show bladder sympathetic system involvement.     

上矢状窦旁脑膜瘤致上矢状窦阻塞时侧支静脉通路的意义

目的 分析上矢状窦旁脑膜瘤致上矢状窦(SSS)阻塞时其侧支静脉通路的建立情况，确定其在肿瘤切除术中的意义。方法 总结归纳86例上矢状窦旁脑膜瘤行MRA及DSA检查时的静脉系表现。结果 27例发生SSS完全阻塞，59例部分阻塞。18例在阻塞的SSS周围出现了由表浅皮层静脉所形成的侧支静脉环；通过表浅皮层静脉与蝶顶窦及小脑幕静脉系建立端—端吻合的16例；通过与Troland或Labbe静脉建立吻合的14例；通过大脑镰与下矢状窦吻合的9例；通过脑膜静脉并经板障静脉引流到颈外静脉系的17例；混合型12例。结论 上矢状窦旁脑膜瘤致SSS阻塞时，肿瘤周围存在广泛侧支静脉通路，术中应注意保护。脑DSA及MRA检查对术前了解SSS通畅性及侧支静脉通路建立有帮助。     

The nature of conditioned anti-analgesia: spinal cord opiate and anti-opiate neurochemistry

The central nervous system contains circuitry that inhibits pain sensitivity (analgesia), as well as circuitry that opposes pain inhibition (anti-analgesia). Activation of analgesia systems and anti-analgesia systems can each be brought under environmental control using classical conditioning procedures. Analgesia can be produced by cues present before and during aversive events such as electric shock, while active inhibition of analgesia comes to be produced by cues never present immediately before or during shock and therefore signal safety. We have recently reported that these analgesia and anti-analgesia systems interact at the level of the spinal cord. A series of 3 experiments were performed to examine how such interactions occur. First, potential opioid mediation of conditioned analgesia was investigated using systemic and intrathecal (i.t.) delivery of opiate antagonists. Conditioned analgesia was found to be mediated by activation of spinal μ and δ opiate receptors. Second, analgesia produced by each of these receptor subtypes was challenged by environmental signals for safety. Analgesias produced by μ and δ opiate agonists were each abolished by safety signals. Third, antagonists/antisera directed against several putative anti-opiate neurotransmitters were tested i.t. to identify which mediate conditioned anti-analgesia at the level of the spinal cord. A cholecystokinin antagonist abolished conditioned anti-analgesia. In contrast, neuropeptide FF antiserum and a κ opiate antagonist were without effect.     

The antinociceptive action of an α2-adrenoceptor agonist in the spinal dorsal horn is due to a direct spinal action and not to activation of Descending Inhibition

In this electrophysiological study we tried to find out whether the spinal antinociceptive effect of a supraspinaly administered α₂-adrenoceptor agonist is due to a direct spinal effect or to activation of descending inhibition. The responses to wide-dynamic range (WDR) neurons of the spinal dorsal horn were studied following application of medetomidine, a selective α₂-adrenergic agonist, into the rostroventromedial medulla (RVM) or directly onto the spinal cord of the Intact and in spinal rats. The noxious electrical stimuli were applied to the ipsilateral receptive field in the plantar region of the hind paw, and responses mediated by A- and C-fibers to WDR neurons were separately evaluated. The reversal of medetomidine-induced effects was attempted by a systemic administration of atipamezole, a selective α₂-adronoceptor antagonist. Medetomldine injection into the RVM produced a dose-dependent, atipamezole-reversible attenuation of the C-fiber-mediated responses to WDR neurons of the spinal dorsal horn in both intact and spinal rats. Paradoxically, the spinal aMFnociceptive effect of supraspinally administered medstomidine was stronger in spinal rats. The A-fiber-mediated responses were significantly less attenuated by medetomidine than the C-fiber-mediated responses to the WDR neurons. Also a direct application of medetomidine onto the spinal cord produced a dose-dependent, atipamezole-reversible attenuation of the C-fiber-mediated responses, and this effect was identical in intact and in spinal rats. The medetomidins doses producing spinal antinociception were considerably lower with a direct spinal application than with a supraspinal application. These results indicate that spinal antinocicsption following spinal or supraspinal application of an α₂-adrenergic agonist is due to a direct activation of spinal α₂-adrenoceptors and not to descending inhibition. Activation of supraspinal α₂-adrenoceptors counteracts the spinal antinociceptive effect.