Radiation-induced cellular changes in traumatic spinal cord injury

Summary Left dorsal cordotomy at the 11th thoracic vertebra was performed in mature female rats. Local exposures of 1,000 R of 280 kvp x rays were made within 10 min, 12, 24 36 or 48 hrs after injury. Tritiated thymidine (1 Ci/g body wt.) was injected i. v. 1 hr before death and necropsy examination 5, 18 or 30 days after surgery. Hematoxylin-stained sagittal sections (5 ) of the spinal cord were prepared for radioautographic examination. The parameters of magnitude and duration of changes in cell numbers and numbers of cells incorporating tritiated thymidine were determined for scar parenchymal cells (neuroglia and fibroblasts), macrophage, endothelia and mitotic cells.Irradiation modified the cellular composition of the developing scar tissue. These changes were due to a delay of proliferation in scar parenchymal and endothelial cell populations. A concomitant suppression of the number of cells incorporating tritiated thymidine occurred in 5-day old irradiated lesions. The magnitude and duration of these delays varied with the cell type and the time of irradiation after injury.These changes indicate that scar parenchymal and endothelial cells proliferatein situ from progenitor cell populations that were in the lesions at the time of irradiation.Macrophage cell numbers and numbers of these cells incorporating tritiated thymidine were not decreased after irradiation. It is, therefore, probable that the majority of the macrophage cells did not originate from a local progenitor cell population.

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Zusammenfassung Bei erwachsenen weiblichen Ratten wurde eine linksseitige dorsale Chordotomie in Höhe des 11. BWK durchgeführt. Lokale Röntgenbestrahlung mit einer Dosis von 1000 r bei 280 KVP binnen 10 min wurde 12, 24, 36 und 48 Std nach dem Trauma durchgeführt.³H-markiertes Thymidin (1 Ci/kg) wurde 1 Std vor der Tötung i.v. appliziet. Die autoptische Untersuchung erfolgte 5, 18 und 30 Tage nach dem Eingriff. Mit Hämatoxylin gefärbte Sagittalschnitte (5 Dicke) des Rückenmarks wurden autoradiographisch untersucht. Die Parameter der Größe und Dauer der Veränderungen der Zellzahl sowie dez Zahl der³H-Thymidin-markierten Zellen wurden für die Narbenparenchymzellen (Neuroglia und Fibroblasten), Makrophagen, Endothelzellen und Mitosen in der Narbe bestimmt.Die Bestrahlung veränderte die Zellzusammensetzung in dem sich entwickelnden Narbengewebe infolge verzögerter Proliferation der Parenchym- und Endothelzellen. In 5 Tage alten bestrahlten Läsionen erfolgte eine gleichzeitige Verminderung der³H-Thymidin inkorporierenden Zellen. Die Stärke und Dauer dieser Verzögerung schwankte je nach Zelltyp und Bestrahlungszeit nach dem Trauma.Die Befunde sprechen dafür, daß Narbenparenchyn- und Endothelzellen bei der Narbenbildung in situ aus ortsständigen Zellpopulationen gebildet werden, die bereits zum Zeitpunkt der Bestrahlung in der Läsion vorliegen.Die Zahl der Makrophagen sowie der³H-Thymidin-inkorporierenden Zellen war nach der Bestrahlung nicht vermindert. Es ist daher wahrscheinlich, daß die Mehrzahl der Makrophagen nicht aus ortsständigen Zellvorläufern entsteht.

     

Changes in galanin immunoreactivity in rat lumbosacral spinal cord and dorsal root ganglia after spinal cord injury

Alterations in the expression of the neuropeptide galanin were examined in micturition reflex pathways 6 weeks after complete spinal cord transection (T8). In control animals, galanin expression was present in specific regions of the gray matter in the rostral lumbar and caudal lumbosacral spinal cord, including: (1) the dorsal commissure; (2) the superficial dorsal horn; (3) the regions of the intermediolateral cell column (L1-L2) and the sacral parasympathetic nucleus (L6-S1); and (4) the lateral collateral pathway in lumbosacral spinal segments. Densitometry analysis demonstrated significant increases (P < or = 0.001) in galanin immunoreactivity (IR) in these regions of the S1 spinal cord after spinal cord injury (SCI). Changes in galanin-IR were not observed at the L4-L6 segments except for an increase in galanin-IR in the dorsal commissure in the L4 segment. In contrast, decreases in galanin-IR were observed in the L1 segment. The number of galanin-IR cells increased (P < or = 0.001) in the L1 and S1 dorsal root ganglia (DRG) after SCI. In all DRG examined (L1, L2, L6, and S1), the percentage of bladder afferent cells expressing galanin-IR significantly increased (4-19-fold) after chronic SCI. In contrast, galanin expression in nerve fibers in the urinary bladder detrusor and urothelium was decreased or eliminated after SCI. Expression of the neurotrophic factors nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) was altered in the spinal cord after SCI. A significant increase in BDNF expression was present in spinal cord segments after SCI. In contrast, NGF expression was only increased in the spinal segments adjacent and rostral to the transection site (T7-T8), whereas spinal segments (T13-L1; L6-S1), distal to the transection site exhibited decreased NGF expression. Changes in galanin expression in micturition pathways after SCI may be mediated by changing neurotrophic factor expression, particularly BDNF. These changes may contribute to urinary bladder dysfunction after SCI.     

Dorsal root potentials and afferent input to the spinal cord in rats with an experimental peripheral neuropathy.

Compound action potentials (CAPs), dorsal root potentials (DRPs) and cord dorsum potentials evoked by stimulating the sciatic nerves have been measured in 4 control rats and in 19 rats with a constriction injury of one sciatic nerve produced by loose ligation of the nerve at mid-thigh level 5 days (n = 8) or 10 days (n = 11) before the acute experiments. The contralateral nerve was exposed but not ligated in a sham procedure. In all cases, the nerve was stimulated proximal to the lesion. At 5 days post-operative (PO) the maximal A-fibre CAPs on the nerve-injured side were not significantly different from those on the sham-operated side. At 10 days PO all animals showed a decrease in the CAP on the nerve-injured side. The mean CAP area on the nerve-injured side was 74.0% +/- 4.2 of the sham-operated side, which was significantly different (P less than 0.005). The sciatic nerves and L5 dorsal roots from 4 of the 10 day PO animals were examined histologically and showed no signs of demyelination or degeneration. The amplitude and area of the maximal DRPs were significantly smaller on the nerve-injured side than on the sham-operated side in all of the nerve-injured animals (P less than 0.01 at 5 days PO; P less than 0.05 at 10 days PO). The mean area of DRPs from the nerve-injured side was 61.7% +/- 10.1 and 46.8% +/- 7.5 of the DRPs from the sham-operated side in the 5 and 10 day PO animals, respectively. The DRPs evoked by sub-maximal afferent volleys were also measured. In all of the nerve-injured animals the CAP-DRP curve on the nerve-injured side was shifted to the right compared to that of the sham-operated side, such that a given size of CAP evoked a smaller DRP on the nerve-injured side than on the sham-operated side. We conclude that the constriction injury produces a decrease in the DRP generated by a volley in the injured nerve and that this change is independent of the decrease in the CAP seen in the injured nerve. We propose that the constriction injury affects the central mechanism responsible for generating primary afferent depolarization (PAD), and thus the pre-synaptic inhibitory control of the afferent input from the injured nerve is impaired.     

实验性糖尿病周围神经病大鼠脊髓及背根神经节CGRP、VIP表达变化

目的通过观察糖尿病大鼠周围神经形态学的变化以及脊髓、背根神经节中降钙素基因相关肽(CGRP)、血管活性肠肽(VIP)表达变化,以探讨神经肽在糖尿病性神经病中所起的作用。方法Wistar大鼠模型的建立:采用腹腔一次性注射pH4.4枸橼酸钠缓冲液配制的1.25%链脲佐菌素(Streptozotocin STZ)制成糖尿病周围神经病大鼠。用ABC免疫组化方法观察8周和12周大鼠降钙素基因相关肽(CGRP)、血管活性肠肽(VIP)在脊髓及背根神经节的表达。结果糖尿病大鼠8周和12周时背根神经节、12周时脊髓CGRP、VIP表达下降(P<0.05),糖尿病大鼠脊髓8周时CGRP、VIP表达与正常大鼠比无明显差别。结论CGRP和VIP参与了糖尿病周围神经病的发病,糖尿病对大鼠背根神经节CGRP、VIP的表达影响更早。     

Localization of NADPH diaphorase in the lumbosacral spinal cord and dorsal root ganglia of the cat

The distribution of NADPH-d activity in the spinal cord and dorsal root ganglia of the cat was studied to evaluate the role of nitric oxide in lumbosacral afferent and spinal autonomic pathways. At all levels of the spinal cord NADPH-d staining was present in neurons and fibers in the superficial dorsal horn and in neurons around the central canal and in the dorsal commissure. In addition, the sympathetic autonomic nucleus in the rostral lumbar segments exhibited prominent NADPH-d cellular staining whereas the parasympathetic nucleus in the sacral segments was not well stained. The most prominent NADPH-d activity in the sacral segments occurred in fibers extending from Lissauer's tract through laminae I along the lateral edge of the dorsal horn to lamina V and the region of the sacral parasympathetic nucleus. These fibers were very similar to VIP-containing and pelvic nerve afferent projections in the same region. They were prominent in the S₁–S₃ segments but not in adjacent segments (L₆–L₇ and Cx₁) or in thoracolumbar and cervical segments. NADPH-d activity and VIP immunoreactivity in Lissauer's tract and the lateral dorsal horn were eliminated or greatly reduced after dorsal-ventral rhizotomy (S₁–S₃), indicating the fibers represent primary afferent projections. A population of small diameter afferent neurons in the L₇–S₂ dorsal root ganglia were intensely stained for NADPH-d. The functional significance of the NADPH-d histochemical stain remains to be determined; however, if NADPH-d is nitric oxide synthase then this would suggest that nitric oxide may function as a transmitter in thoracolumbar sympathetic preganglionic efferent pathways and in sacral parasympathetic afferent pathways in the cat. © 1994 Wiley-Liss, Inc.     

Giganto-cellular glioblastoma of the lumbosacral spinal cord

Summary A case of giganto-cellular glioblastoma multiforme occurring in the lumbosacral spinal cord is described.Supported in part by US Public Health Grant NS06239 from the National Institute of Neurological Diseases and Stroke     

Morphological characteristics of the lumbosacral spinal cord urogenital center in Sprague Dawley rats

BACKGROUND： Studies have demonstrated that selective innervation of the sacral nerve tract to the bladder plays an important role in bladder functional reconstruction following spinal cord injury. However, there are very few studies reporting detailed morphological characteristics of urogenital center and lumbosacral nerve roots. OBJECTIVE： To analyze the spinal cord segment of the lumbosacral spinal cord urogenital center, and to observe morphological characteristics. DESIGN, TIME AND SETTING： A neuroanatomical study was performed at the Laboratory of Neuroanatomy, Peking University Health Science Center between September 2007 and March 2008. MATERIALS： Horseradish peroxidase-conjugated cholera toxin B subunit （CB-HRP） was purchased from Sigma, USA; surgical microscope was purchased from Zhenjian Zhongtian Optical Instrument, Jiangsu Province, China; BCL-420 biological and functional experimental system was purchased from Taimeng Science and Technology, Sichuan Province, China. METHODS： A total of 36 adult, Sprague Dawley rats were randomly assigned to groups A （n = 10）, B （n = 10）, C （n = 10）, and D （n = 6）. CB-HRP （3%, 10-15 μL） was injected into the bladder detrusor muscle （group A）, external urethral sphincter （group B）, and perineal muscles （group C）, respectively. Rats in group D were not given any treatments. MAIN OUTCOME MEASURES： At 72 hours after CB-HRP injection, CB-HRP-positive neurons were analyzed in lumbosacral segments using 3, 3＇, 5, 5＇-tetramethylbenzidine staining and an Olympus optic microscope, while anatomical structures in the respective spinal nerve tract were observed using a surgical microscope. RESULTS： CB-HRP-positive neurons were distributed in the L6-S1 segments of the spinal cord, and neurons primarily innervating the bladder detrusor muscle were located at the sacral parasympathetic nucleus and the intermediolateral nucleus. In addition, neurons that primarily innervate the external urethral sphincter and perineal muscles were observed in the ventrolateral portion （Onuf＇s nucleus）. The lumbar-sacral nerve roots were composed of varying nerve tracts, Le., they were typically divided into 1-2 sub-bundles, and the sub-bundles were then divided into 2-3 tiny bundles. There were extensive fibro-connections between the rootlets. CONCLUSION： The urogenital center in Sprague Dawley rats was located in the L6 -S1 segments of the spinal cord, and the rootlets were clearly observed. Therefore, this rat experimental model could be utilized for highly selective anterior/posterior rhizotomy.     

Activation and circuitry of uterine-cervix-related neurons in the lumbosacral dorsal root ganglia and spinal cord at parturition

Stimulation of the uterine cervix at parturition activates neural circuits involving primary sensory nerves and supraspinally projecting neurons of the lumbosacral spinal cord, resulting in output of hypothalamic neurohormones. Dorsal root ganglia (DRG) and spinal neurons of these circuits are not well-characterized. The objectives of this study were to detail the activation of DRG and spinal neurons of the L6/S1 levels that are stimulated at late pregnancy, verify hypothalamic projections of activated spinal neurons, and determine whether activated neurons express estrogen receptor-alpha (ERalpha). Expression of phosphorylated cyclic-AMP response element-binding protein (PCREB) and Fos immunohistochemistry were used to "mark" activated DRG and spinal neurons, respectively. Retrograde tracing identified uterine-cervix-related and spinohypothalamic neurons. Baseline PCREB expression in the DRG increased during pregnancy and peaked during the last trimester. Some PCREB-expressing neurons contained retrograde tracer identifying them as cervix-related neurons. Fos-expressing neurons were few in spinal cords of nonpregnant and day 22 pregnant rats but were numerous in parturient animals. Some Fos-expressing neurons located in the dorsal half of the spinal cord contained retrograde tracer identifying them as spinohypothalamic neurons. Some DRG neurons expressing PCREB also expressed ERalpha, and some spinal neurons activated at parturition projected axons to the hypothalamus and expressed ERalpha. These results indicate that DRG and spinal cord neurons are activated at parturition; that those in the spinal cord are present in areas involved in autonomic and sensory processing; that some spinal neurons project axons to the hypothalamus, ostensibly part of a neuroendocrine reflex; and that sensory and spinal neurons can respond to estrogens. Moreover, some activated sensory neurons may be involved in the animal's perception of labor pain.     

The development of descending and dorsal root connections in the lumbosacral spinal cord of the postnatal rat.

Light and electron microscopy were used to study degenerating axons and synaptic endings in the lumbosacral spinal cord at different stages of postnatal development in the rat. After dorsal root section (L5-S1) or mid-thoracic hemisection of the spinal cord (T6-T8), the distribution and type of degeneration argyrophilia were studied with the light microscope over varied post-operative survival periods using a modified Fink-Heimer method (Leonard, '74). The light microscopic results were correlated with the appearance of electron dense degeneration seen using the electron microscope. The distribution of degeneration found in the lumbosacral spinal cord after dorsal root section was similar at the neonatal (4d), weanling (21d) and adult stages. At the neonatal stage, the type of degeneration argyrophilia appeared at an earlier postoperative survival period (12 hours), and was maximal at an earlier time (12-18 hours) than in older animals. The appearance of electron dense degeneration using the electron microscope matched the light microscopic findings. Electron dense degenerating synaptic knobs were found at the neonatal stage making asymmetrical contact with small dendrites in areas of the dorsal horn showing degeneration argyrophilia. No degeneration was found in the dorsal funiculus, dorsal horn or intermediate nucleus of Cajal (INC) after mid-thoracic hemisection at the neonatal stage although degeneration was present elsewhere in the intermediate gray, in the ventral gray, and in the ventral and lateral funiculi. At this stage, the type of degeneration argyrophilia and time course of degeneration in the gray and white matter was identical to that found after dorsal root section in neonatal animals. The distribution of degeneration was not mature in the lumbosacral enlargement until 15d of age and the degeneration was still immature in the dorsal horn and INC at 21d of age. Although degeneration argyrophilia and electron dense degeneration was found in the ventromedial gray (lamina VIII) and lateral gray (laminae VI-VII) at the neonatal stage, electron dense degenerating synaptic knobs were not observed in these areas until 12d of age for the ventromedial and 18d of age for the lateral gray matter even using a large number of different survival periods. Degenerating synaptic endings were first observed after mid-thoracic hemisection during the period when behavioral maturation is nearing completion in the hindlimbs, and when response depression (spinal shock) increases and response recovery decreases after mid-thoracic spinal transection (Weber and Stelzner, '77). Our data suggest that either the number of connections from descending sources increases markedly in the gray matter of the lumbosacral spinal cord during this period or connections, already present, reach a state of maturity where they can first be observed using the degeneration method of analysis.     

Development changes in the distribution of gamma-aminobutyric acid-immunoreactive neurons in the embryonic chick lumbosacral spinal cord

The development of γ-aminobutyric acid (GABA)-immunoreactive neurons was investigated in the embryonic and posthatch chick lumbosacral spinal cord by using pre- and postembedding immunostaining with an anti-GABA antiserum. The first GABA-immunoreactive cells were detected in the ventral one-half of the spinal cord dorsal to the lateral motor exception of the lateral motor column, appeared throughout the entire extent of the ventral one-half of the spinal gray matter by E6. Thereafter, GABA-immunoreactive neurons extended from ventral to dorsal regions. Stained perikarya first appeared at E8 and then progressively accumulated in the dorsal horn, while immunoreactive neurons gradually declined in the ventral horn. The general pattern of GABA immunoreactivity characteristic of mature animals had been achieved by E12 and was only slightly altered afterwards. In the dorsal horn, most of the stained neurons were observed in laminae I–III, both at the upper (LS 1–3) and at the lower (LS 5–7) segments of the lumbosacral spinal cord. In the ventral horn, the upper and lower lumbosacral segments showed marked differences in the distribution of stained perikarya. GABAergic neurons were scattered in a relatively large region dorsomedial to the lateral motor column at the level of the upper lumbosacral segments, whereas they were confined to the dorsalmost region of lamina VII at the lower segments. The early expression of GABA immunoreactivity may indicate a trophic and synaptogenetic role for GABA in early phases of spinal cord development. The localization of GABAergic neurons in the ventral horn and their distribution along the rostrocaudal axis of the lumbosacral spinal cord coincide well with previous physiological findings, suggesting that some of these GABAergic neurons may be involved in neural circuits underlying alternating rhythmic motor activity of the embryonic chick spinal cord. © 1994 Wiley-Liss, Inc.     

At-level neuropathic pain is induced by lumbosacral ventral root avulsion injury and ameliorated by root reimplantation into the spinal cord

Neuropathic pain is common after traumatic injuries to the cauda equina/conus medullaris and brachial plexus. Clinically, this pain is difficult to treat and its mechanisms are not well understood. Lesions to the ventral roots are common in these injuries, but are rarely considered as potential contributors to pain. We examined whether a unilateral L6-S1 ventral root avulsion (VRA) injury in adult female rats might elicit pain within the dermatome projecting to the adjacent, uninjured L5 spinal segment. Additionally, a subset of subjects had the avulsed L6-S1 ventral roots reimplanted (VRA+Imp) into the lateral funiculus post-avulsion to determine whether this neural repair strategy elicits or ameliorates pain. Behavioral tests for mechanical allodynia and hyperalgesia were performed weekly over 7 weeks post-injury at the hindpaw plantar surface. Allodynia developed early and persisted post-VRA, whereas VRA+Imp rats exhibited allodynia only at 1 week post-operatively. Hyperalgesia was not observed at any time in any experimental group. Quantitative immunohistochemistry showed increased levels of inflammatory markers in laminae III-V and in the dorsal funiculus of the L5 spinal cord of VRA, but not VRA+Imp rats, specific to areas that receive projections from mechanoreceptive, but not nociceptive, primary afferents. These data suggest that sustained at-level neuropathic pain can develop following a pure motor lesion, whereas the pain may be ameliorated by acute root reimplantation. We believe that our findings are of translational research interest, as root implantation surgery is emerging as a potentially useful strategy for the repair of cauda equina/conus medullaris injuries.     

Subacute combined degeneration of spinal cord. Significance of peripheral nerve involvement

A 36 year old woman was admitted to the hospital in November 1983 because of her inability to walk. For 3 months prior to admission, she took oral contraceptives (OCs) as a treatment for amenorrhea. 2 months prior to admission, she had general malaise, anorexia, and unsteady gait. 1 month before her admission, tingling and numbness began in the fingertips and spread up to the forearms, a tight feeling around the waist developed, and walking became ataxic. On admission to the hospital, she was thin and pale with greying hair. Her mind was clear and there were no abnormalities of the cranial nerves. Her extremities were hypotonic but not wasted. Slight muscle weakness of the hands and feet was noted. There was myokymia in both legs. Deep tendon reflexes of the extremities were absent. The plantar responses were extensor and lack of coordination in the extremities was noted. There was a definite glove and stocking type of hypesthesia to pinprick and cotton wool. Vibration sense was decreased below T11 and lost in both legs. There was a marked loss of position sense to passive movement in the legs and some impairment in the hands. Laboratory examination revealed mild magaloblastic anemia, elevated LDH, borderline low concentration of vitamin B12 in the serum, increased excretion of methylmalonate in the urine, achylia, positive antiparietal cell antibody and positive anti-intrinsic factor antibody. Cyanocobalamin absorption by the Schilling test was 5.6% after intrinsic factor, 11.3%. The diagnosis of pernicious anemia was made. Upper gastrointestinal studies showed typical carcinoid tumors of the stomach. Cerebrospinal fluid was normal. Peripheral nerve conduction studies demonstrated normal or slightly decreased motor conduction velocities and absent sensory action potential. Sural nerve biopsy was performed. Myelinated fibers were moderately decreased in number to 5554/mm squared and pronounced loss of large myelinated fibers was demonstrated in fiber histogram. Teased method of the single fiber showed mainly axonal degeneration. Anemia and neurologic function improved rapidly with parenteral hydroxocobalamin therapy and 1 month after treatment commenced, she was able to walk without assistance. The clinical significance of peripheral nerve involvement of subacute combined degeneration of the spinal cord was discussed, as the peripheral nerve affection is only poorly understood in contrast to the myelopathy. This was followed by discussion of the possible effect of the OCs and gastric carcinoid to neurological manifestation of pernicious anemia. (author's modified)     

Changes in carbohydrate expression in the cervical spinal cord of rats during aging

Aging is a process where histochemical changes occur. Some of these may consist of age‐dependent loss of expression of some cell markers. Conversely, cell markers not expressed in young animals may be detectable in their older counterparts. Histochemical age changes in carbohydrate profiles in the spinal cord have not been documented. In order to fill this information gap lectin histochemistry and image analysis were used to characterize the histochemical age changes occurring in the cervical segments of the rat spinal cord. From a battery of 11 lectins, the more important age changes were detected with Glicine maximus (SBA)‐lectin. Thus, SBA‐lectin neuronal staining which was moderately positive in the cervical segments of young animals was negative in old rats. In contrast the same lectin which did not react with the ependyma of young animals strongly bound to the ependyma of senescent rats. None of the tested lectins bound to glial cells, either in young or old animals. In no case the senile animals evidenced anatomopathological changes. We conclude that although in the aged spinal cord changes in lectin histochemical binding patterns occur, they do not reflect a pathologic situation.     

Local spinal cord glucose utilization and extracellular potassium activity changes after spinal cord injury in rats

Spinal microenvironment and metabolic alterations after experimental contusional injury of the spinal cord were evaluated in the same Wistar rats. Severe spinal cord injury was made under light GOF anesthesia with a 10 g weight drop onto the exposed Th-8 spinal cord from a 10 cm height and then halothane was ceased. The author studied extracellular potassium activity ([K+]e) and DC potential for 2 hours after paraplegic spinal cord injury in conscious rats. Furthermore, at 2 hours after cord injury, local spinal cord glucose utilization (1-SCGU) was measured with quantitative autoradiographic 2-[14C] deoxy-glucose method (Sokoloff et al.). [K+]e in injured spinal cords was 59 +/- 5 (mean +/- S.E.M.) mEq at 10 min after injury and was cleared with an exponential half-life of 1 hour. At 2 hours after injury [K+]e was still high with a value of 16 +/- 1 mEq compared with 4 mEq of control animals. DC potential changes was a mirror image of that of [K+]e. DC potential changed by a mean of 10.7 mV positively from 10 min. to 2 hours after injury. 1-SCGU at the impact site was extremely low in both white and gray matters. At 6mm rostral from the impact center 1-SCGU was remarkably reduced in the gray matter, and in the lateral white matter. But at 3 mm rostral 1-SCGU was well preserved. And at 20 mm rostral there was no difference in 1-SCGU with control animals. Massive potassium efflux from the injured spinal cord to the adjacent spinal segment was clarified at this experiment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of lumbosacral nerve root conduction in chickens by electrophysiological testing including high-resolution spinal magnetic stimulation

The value of avian models in peripheral nerve research recently became substantiated by the immunobiological similarity of avian inflammatory demyelinating polyradiculoneuropathy to human Guillain-Barré syndrome providing an alternative animal model for experimental autoimmune neuritis. As electrophysiologic evaluation of nerve roots is essential part of the diagnosis of polyradiculoneuropathies in humans, it would be favourable to have similar research methods available for juvenile chickens. Hence, this study was performed (1) to establish a tool-set that allows for reproducible evaluation of the tibial/sciatic nerve and its nerve roots, (2) to achieve age-matched reference values, and (3) to trace the kinetics of peripheral nerve maturation within chickens. Nine chickens underwent serial electrodiagnostic examinations between the age of 6 and 15 weeks. Several methods of sensory and motor nerve fiber stimulation of the tibial/sciatic nerve were tested and modified or established. Ultimately, scalp-recorded somatosensory evoked potentials, compound muscle action potentials elicited by tibial/sciatic nerve electrical as well as spinal magnetic stimulation and motor nerve conduction velocity were available for tibial/sciatic nerve and nerve root evaluation in chickens. Base values were obtained for all investigations and parameters. Results indicated that the maturation of the nerve fibers is incomplete up to the age of 15 weeks. The methods tested here provide an excellent tool-set for quantitative tibial/sciatic nerve and nerve root assessment in avian polyradiculoneuropathies, especially within the scope of longitudinal monitoring of the disease course.