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Cervical Spinal Cord (cervical + spinal_cord)
Selected AbstractsCervical spinal cord injury following cephalic presentation and delivery by Caesarean sectionDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2001C Morgan MD MRCP MRCPCH We describe a term infant with an acute spinal cord injury following emergency Caesarean section. Foetal movements were normal on the day that the mother was admitted for postterm induction of labour. Caesarean section was performed because of foetal distress and failure to progress during labour. The initial clinical picture suggested acute birth asphyxia. The presence of a high cervical spine injury became more obvious as the clinical picture evolved over the next 7 days. A discontinuity of the cervical spinal cord at C4,5 was confirmed on MRI. Spontaneous respiration failed to develop and intensive care was withdrawn on day 15. No evidence of trauma, or a vascular, neurological, or congenital anomaly of the cervical spinal cord was found at post mortem. The absence of a similar case following cephalic presentation and Caesarean section made bereavement couselling of the parents especially difficult. [source] Evaluation of decision criteria for detection of spinal cord compression based on cervical myelography in horses: 38 cases (1981,2001)EQUINE VETERINARY JOURNAL, Issue 1 2004J. Van Biervliet Summary Reasons for performing study: Different criteria have been described based on height reduction of the total myelographic contrast column and components of it as tests for compression of the spinal cord due to cervical stenotic myelopathy (CSM). Fifty percent height reduction of the dorsal myelographic column (DMC), <2 mm empiric height of the DMC and a 40% reduction of the ratio of stenosis calculated based on the height reduction of the entire dural diameter (DD) have been described as decision criteria for considering the test result positive. The reasons for selecting these decision criteria or their accuracies have rarely been reported. Objectives: To evaluate the accuracy of diagnostic criteria based on reduced height of the total myelographic column and components of it for diagnosing extradural spinal cord compression using different decision criteria, and make recommendations for consistent myelographic interpretation in horses suspected of having CSM. Methods: Four measurements were obtained by 2 readers in a retrospective sample population of 38 horses in which both cervical myelography and histopathological examination of the cervical spinal cord were performed. The prevalence of CSM in the sample was 50%. At intervertebral sites, the minimum heights of the DD and DMC were measured. At intravertebral sites, the maximum heights of the entire DD and DMC were obtained. Percent height reductions of the DMC and DD were determined as the ratio of minimum intervertebral height to maximum intravertebral height within the next cranial vertebra. Histological examination was used as the gold standard for determining the actual site of spinal cord compression. Sensitivity and specificity for the diagnostic criteria were estimated at each site in neutral and flexed neck positions using several different decision criteria. Conclusions: At C6-C7, in neutral or flexed neck position and using 20% reduction of DD, the test was highly sensitive and specific for CSM. At other sites, reduced height of the myelographic column generally was not accurate for diagnosing extradural spinal cord compression. Using 20% reduction of DD in neutral position at the mid-cervical sites, the test had only low sensitivity and high specificity. Flexion of the neck appeared to increase detection of spinal cord compression in the mid-cervical region, but also substantially increased the frequency of false-positive diagnoses. Potential relevance: By using the reported sensitivity and specificity estimates, readers may decide on a decision criterion for diagnosis of extradural spinal cord compression due to CSM. However, in planning a surgical correction, it is difficult to define a decision criterion that combines acceptable sensitivity and specificity, especially at the mid-cervical sites. [source] Adult neural progenitor cells provide a permissive guiding substrate for corticospinal axon growth following spinal cord injuryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2004Katharina Pfeifer Abstract Adult neural progenitor cells (NPC) are an attractive source for cell transplantation and neural tissue replacement after central nervous system (CNS) injury. Following transplantation of NPC cell suspensions into the acutely injured rat spinal cord, NPC survive; however, they migrate away from the lesion site and are unable to replace the injury-induced lesion cavity. In the present study we examined (i) whether NPC can be retained within the lesion site after co-transplantation with primary fibroblasts, and (ii) whether NPC promote axonal regeneration following spinal cord injury. Co-cultivation of NPC with fibroblasts demonstrated that NPC adhere to fibroblasts and the extracellular matrix produced by fibroblasts. In the presence of fibroblasts, the differentiation pattern of co-cultivated NPC was shifted towards glial differentiation. Three weeks after transplantation of adult spinal-cord-derived NPC with primary fibroblasts as mixed cell suspensions into the acutely injured cervical spinal cord in adult rats, the lesion cavity was completely replaced. NPC survived throughout the graft and differentiated exclusively into glial cells. Quantification of neurofilament-labeled axons and anterogradely labeled corticospinal axons indicated that NPC co-grafted with fibroblasts significantly enhanced axonal regeneration. Both neurofilament-labeled axons and corticospinal axons aligned longitudinally along GFAP-expressing NPC-derived cells, which displayed a bipolar morphology reminiscent of immature astroglia. Thus, grafted astroglial differentiated NPC promote axon regrowth following spinal cord injury by means of cellular guidance. [source] Somatic and visceral afferents to the ,vasodepressor region' of the caudal midline medulla in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2003Jason R. Potas Abstract Previous research has found that the integrity of a restricted region of the caudal midline medulla (including caudal portions of nucleus raphé obscurus and nucleus raphé pallidus) was critical for vasodepression (hypotension, bradycardia, decreased cardiac contractility) evoked either by haemorrhage or deep pain. In this anatomical tracing study we found that the vasodepressor part of the caudal midline medulla (CMM) receives inputs arising from spinal cord, spinal trigeminal nucleus (SpV) and nucleus of the solitary tract (NTS). Specifically: (i) a spinal,CMM projection arises from neurons of the deep dorsal horn, medial ventral horn and lamina X at all spinal segmental levels, with approximately 60% of the projection originating from the upper cervical spinal cord (C1,C4); (ii) a SpV,CMM projection arises primarily from neurons at the transition between subnucleus caudalis and subnucleus interpolaris; (iii) a NTS,CMM projection arises primarily from neurons in ventrolateral and medial subnuclei. In combination, the specific spinal, SpV and NTS regions which project to the CMM receive the complete range of somatic and visceral afferents known to trigger vasodepression. The role(s) of each specific projection is discussed. [source] Proton MR spectroscopic imaging of the medulla and cervical spinal cord,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2007Richard A.E. Edden PhD Abstract Purpose To demonstrate the feasibility of quantitative, one-dimensional proton MR spectroscopic imaging (1D-MRSI) of the upper cervical spine and medulla at 3.0 Tesla. Materials and Methods A method was developed for 1D-point-resolved spectroscopy sequence (PRESS)-MRSI, exciting signal in five voxels extending from the pontomedullary junction to the level of the C3 vertebra, and performed in 10 healthy volunteers to generate control data. Results High-resolution 1D-MRSI data were obtained from all 10 subjects. Upper cervical spine concentrations of choline, creatine, and N-acetyl aspartate were estimated to be 2.8 ± 0.5, 8.8 ± 1.8, and 10.9 ± 2.7 mM, respectively, while in the medulla they were 2.6 ± 0.5, 9.1 ± 1.7, and 10.8 ± 0.9 mM. Conclusion Quantitative 1D-MRSI of the upper cervical spine has been shown to be feasible at 3.0 Tesla. J. Magn. Reson. Imaging 2007;26:1101,1105. © 2007 Wiley-Liss, Inc. [source] Enterovirus 71-induced autophagy detected in vitro and in vivo promotes viral replicationJOURNAL OF MEDICAL VIROLOGY, Issue 7 2009Shu-Chen Huang Abstract Enterovirus 71 (EV71) is an important pathogen causing death in children under 5 years old worldwide. However, the underlying pathogenesis remains unclear. This study reveals that EV71 infection in rhabdomyosarcoma (RD) and neuroblastoma (SK-N-SH) cells stimulated the autophagic process, which was demonstrated by an increase of punctate GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3), the level of autophagosome-bound LC3-II protein and double-membrane autophagosome formation. EV71-induced autophagy benefited EV71 replication, which was confirmed by the autophagic inducer rapamycin and the inhibitor 3-methyladenine. Signaling pathway investigation revealed that the decreased expression of phosphorylated mTOR and phosphorylated p70S6K is involved in EV71-induced autophagy in a cell-specific manner. The expression of phosphorylated extracellular signal-regulated kinase (Erk) was suppressed consistently in EV71-infected cells. However it did not participate in the autophagic response of the cell. Other signaling pathway molecules, such as Erk, PI3K/Akt, Bcl-2, BNIP3, and Beclin-1 were not affected by infection with EV71. Electron microscopy showed co-localization of autophagosome-like vesicles with either EV71-VP1 or LC3 protein in neurons of the cervical spinal cord in ICR mice infected with EV71. In conclusion, EV71 infection triggered autophagic flux and induced autophagosome formation both in vitro and in vivo. Autophagy induced by EV71 is beneficial for viral replication. Understanding the role of autophagy induced by EV71 in vitro and the formation of autophagosome-like vesicle in vivo provide new insights into the pathogenesis of EV71 infection. J. Med. Virol. 81:1241,1252, 2009. © 2009 Wiley-Liss, Inc. [source] Regulation of development of oligodendrocytesJOURNAL OF NEUROCHEMISTRY, Issue 2002K. Ikenaka Oligodendrocyte (OL) is the myelin-forming glial cell in the central nervous system. In the spinal cord, molecular markers for OL precursor cells (OPCs), such as PDGF a-receptor (PDGFR a), are first expressed in a strictly restricted focus of the ventral ventricular lumen at E12.5 in mouse and later spread throughout the cord. To investigate how they originate from these specific regions, we used an explant culture system of E12 mouse cervical spinal cord. When we cultured the ventral and dorsal spinal cords separately, a robust increase in the number of O4+ cells was observed in the ventral fragment. This phenomenon suggests the presence of factors inhibiting OL development from dorsal spinal cord. BMP4 is secreted from dorsal spinal cord and is a strong candidate for this factor; however, it did not affect OL development in our system. Here we show that Wnt-1 and Wnt-3a, in contrast, may have a role in OL maturation. The developmental profile of wnt-1/3a gene expressions in the dorsal spinal cord showed a significant correlation with that of the dorsal activity, which was very strong at E11, and then reduced to an undetectable level by E14. When Wnt-3a was added to the dissociation culture prepared from E14 mouse ventral cervical cords, the numbers of OL decreased. b-Catenin and LEF family proteins are known to form a transcription factor complex at the down stream of Wnt signalling. OL,like differentiation of CG4 cells was inhibited by constitutively active LEF-b-Catenin, supporting the idea that Wnt signalling directly inhibits OL differentiation. [source] Peripheral nervous system involvement as presenting symptom of systemic B-cell lymphomaJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004C Casellato Peripheral nervous system involvement has been reported in systemic B or T cell lymphoma and may result from intraneural localization of lymphoma resulting in meningo-radiculopathy or mononeuropathies, or manifest as a sensory-motor polyneuropathy sometimes mimicking chronic inflammatory demyelinating polyneuropathy. We report two patients with a previously unknown NHL presenting in both with a stepwise progressive asymmetric multiradiculoneuropathy initially misdiagnosed as inflammatory radiculopathy. A 58-year-old man presented with a 2 year history of stepwise progressive peroneal sensory loss, impotence, and lower limb painful asymmetric neuropathy. Lumbosacral MRI was normal. Electrophysiological studies were consistent with an axonal multiradiculoneuropathy while CSF examinations repeatedly showed increased protein levels (80,91 mg/dl) with slightly increased white cells (<10 mm3) but no malignant cell. The patient repeatedly failed to respond to steroids although he consistently deteriorated at their suspension. An MRI performed 2 years later when multiple cranial nerve palsies appeared showed bilateral T1 and T2 hyperintensities in the brain and cervical spinal cord. An extensive investigation for neoplasm was negative. The patient died from an intracranial hemorrhage during anticoagulant therapy for deep vein thrombosis. Autoptic studies revealed a widespread non-Hodgkin's type B lymphoma with massive systemic and neural involvement including cauda equina and spinal cord. A 54-year-old man presented with a 1 year history of impotence, urinary incontinence, progressive asymmetric painful distal sensorimotor impairment at four limbs and prominent weight loss. Four previous CSF examinations revealed increased protein levels (80,100 mg/dl), and slightly but inconsistently increased white cells (1,11/mm3) but no malinant cells. Steroids were repeatedly ineffective although the patient consistently deteriorated whenever steroids were discontinued. On admission electrophysiological studies showed an axonal asymmetric polyradiculoneuropathy. Brain and spinal MRI was normal while bone marrow biopsy and aspiration disclosed a B cell lymphoma. [source] ANTI-SULFATIDE IgM ANTIBODIES DETECTED IN A PATIENT DIAGNOSIS OF MOTOR NEURON DISEASEJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002Article first published online: 11 MAR 200 D'Avino C., Del Corona A., Bacci A., Calabrese R., Siciliano G. Department of Neuroscience-Clinical Neurology-University of Pisa-Italy Case report. The patient, a 66-year-old man with a 5-year diagnosis of diabetes mellitus, in Sep. 2000 started complaining of language disturbances as rhinolalia. In Jan. 2001, because of generalized fatigue and difficulties in walking, he was hospitalized in Internal Medicine and a diagnosis of diabetic angiopathy and neuropathy was made. Since discharge patient clinical conditions gradually deteriorated and a neurological evaluation showed tongue atrophy, dysarthria, dysphagia, fasciculations in the four limbs, increased deep tendon reflexes with bilateral foot clonus and paraparetic spastic deambulation. He underwent spinal MRI that showed mild arthrosic abnormalities in cervical spinal cord and limb EMG that showed denervation spontaneous activity with neurogenic MUAP modifications, with normal sensory and motor conduction velocity. MEP showed bilateral pyramidal track involvement. A significantly increased anti-sulphatide IgM antibodies titer (1:32,000) in the serum was detected. The diagnosis at discharge was "probable motor neuron disease" and the patient is under riluzole therapy at the moment. Discussion. Anti-sulfatide IgM antibodies are currently associated with several subtypes of peripheral neuropathy. In most cases it is a chronic dysimmune sensory or sensorimotor neuropathy in which electrophysiological and morphological studies are usually con- sistent with a predominant demyelination frequently associated with prominent axonal loss. Although rare, an association between motor neuron disease and IgM anti-sulfatide has been described in a recent paper by Latov and coworkers that reviewed electrophysiologic, morphologic and laboratory data of 25 patients with elevated antisulfatide antibodies. It seems interesting to follow-up the clinical course of the patient, the response to therapy and its correlation to antibodies titer, while the opportunity of high dose IVIg therapy is under discussion at the moment. [source] Meningioangiomatosis in Young Dogs: A Case Series and Literature ReviewJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2004Todd M. Bishop Meningioangiomatosis (MA) is a proliferative disorder of the central nervous system (CNS) that has been reported rarely in humans and sporadically in dogs. Meningioangiomatosis may occur in the brainstem or cervical spinal cord of young dogs and can be identified tentatively by magnetic resonance imaging. The histopathologic hallmark of MA is a leptomeningeal plaque that extends along the CNS microvasculature and invades the adjacent neural parenchyma. This case series describes the neurologic signs, clinical progression, diagnostic imaging, and neuropathology of 4 dogs with MA. The 4 dogs with MA are compared and contrasted with 4 previously reported cases in dogs as well as with their human counterpart. [source] Measurement of T1 and T2 in the cervical spinal cord at 3 teslaMAGNETIC RESONANCE IN MEDICINE, Issue 1 2008Seth A. Smith Abstract T1 and T2 were measured for white matter (WM) and gray matter (GM) in the human cervical spinal cord at 3T. T1 values were calculated using an inversion-recovery (IR) and B1 -corrected double flip angle gradient echo (GRE) and show significant differences (p = 0.002) between WM (IR = 876 ± 27 ms, GRE = 838 ± 54 ms) and GM (IR = 973 ± 33 ms, GRE = 994 ± 54 ms). IR showed significant difference between lateral and dorsal column WM (863 ± 23 ms and 899 ± 18 ms, respectively, p = 0.01) but GRE did not (p = 0.40). There was no significant difference (p = 0.31) in T2 between WM (73 ± 6 ms) and GM (76 ± 3 ms) or between lateral and dorsal columns (lateral: 73 ± 6 ms, dorsal: 72 ± 7 ms, p = 0.59). WM relaxation times were similar to brain structures with very dense fiber packing (e.g., corpus callosum), while GM values resembled deep GM in brain. Optimized sequence parameters for maximal contrast between WM and GM, and between WM and cerebrospinal fluid (CSF) were derived. Since the spinal cord has rostral-caudal symmetry, we expect these findings to be applicable to the whole cord. Magn Reson Med 60:213,219, 2008. © 2008 Wiley-Liss, Inc. [source] Venous congestive myelopathy of the cervical spinal cord: An autopsy case showing a rapidly progressive clinical courseNEUROPATHOLOGY, Issue 3 2007Akio Kimura We report a rapidly progressive myelopathy in a 74-year-old Japanese man who was admitted to our hospital with a 4-month history of progressive gait disturbance and died of pneumonia followed by respiratory failure on the 22nd day of admission. During the course of his illness, magnetic resonance imaging (MRI) revealed intramedullary lesions with edematous swelling from the medulla oblongata to the spinal cord at the level of the fourth vertebra. After administration of contrast medium, the ventral portion of the lesion was mildly and irregularly enhanced and a dilated vessel was recognized along the ventral surface of the upper cervical cord. At autopsy, ischemic changes were observed in the upper-to-middle cervical cord segments, with so-called arterialized veins in the subarachnoid space. No neoplastic lesions were found within or outside the brain and spinal cord. These pathological findings were essentially those of venous congestive myelopathy (VCM) associated with dural arteriovenous fistulae (AVF), formerly known as Foix,Alajouanine syndrome. VCM associated with dural AVF, which is now considered to be treatable in the early stages, is rare found in the cervical spinal cord. The present autopsy case, with MRI findings, provides further information that might be useful for recognition and diagnosis. [source] Epidural haemorrhage of the cervical spinal cord: a post-mortem artefact?NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2005G. N. Rutty Spinal epidural haemorrhage is a rare entity that occurs uncommonly in adults and rarely in children. It has a typical clinical presentation, although to date, the cause for the majority of cases remains unknown. We present a series of cases where epidural haemorrhage was identified at post-mortem, principly to the cervical cord, in cases outside the age range usually reported for clinical epidural haemorrhage, and with no underlying pathology to account for the finding. We present a hypothesis for a post-mortem cause for this finding and consider that, in the absence of any other identifiable causation, then this is a post-mortem occurrence similar to that of the Prinsloo,Gordon artefact of the soft tissues of the neck. This finding must be interpreted with care so as not to make the mistaken diagnosis of a nonaccidental head injury based on its finding, especially in the absence of intracranial, cranial nerve, optic nerve or eye pathologies. [source] The extent of axonal loss in the long tracts in hereditary spastic paraplegiaNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2004G. C. DeLuca Hereditary spastic paraplegia (HSP) comprises a group of inherited neurodegenerative disorders with the shared characteristics of progressive weakness and spasticity predominantly affecting the lower limbs. Limited pathological accounts have described a ,dying back' axonal degeneration in this disease. However, the distribution and extent of axonal loss has not been elucidated in a quantitative way. We have studied post-mortem material from six HSP patients and 32 controls in detail. The population of axons was examined quantitatively in the corticospinal tracts from the medulla to the lumbar spinal cord and the sensory tracts from the lumbar to upper cervical spinal cord. Myelin and axon-stained sections were employed to estimate the notional area and axonal density, respectively, of both tracts. Our results indicate that in the corticospinal tracts there is a significant reduction in area and axonal density at all levels investigated in HSP compared to controls. In the corticospinal tracts, the ratio of medulla and lumbar total axonal number was significantly greater in HSP cases compared to controls suggesting more pronounced axonal loss in the distal neuraxis in HSP than in controls. The sensory tracts in HSP, in contrast, showed a significant reduction in area and axonal density only in the upper regions of the spinal cord. Similar to the corticospinal tracts, the ratio of lumbar and upper cervical cord total axonal number in the sensory tracts was increased in HSP cases compared to controls. These findings are consistent with a length-dependent ,dying back' axonopathy. Nerve fibre loss was not size-selective with both small and large diameter fibres affected. In HSP, axonal loss is widespread and symmetrical and its extent tract-specific. The characterization of the nature of axonal loss in HSP, where this is a primary phenomenon, may help the interpretation of axonal loss in conditions such as multiple sclerosis where the sequence of events is less clear. [source] The effects of MRI signal intensity changes and clinical manifestations on prognosis after surgical intervention for cervical spondylotic myelopathyORTHOPAEDIC SURGERY, Issue 2 2009Ying-ze Zhang MD Objective:, To investigate whether the magnetic resonance (MR) T2 image signal intensity ratio and clinical manifestations can predict the prognosis in patients with cervical spondylotic myelopathy (CSM). Methods:, A total of 73 patients treated with anterior, posterior, or posterior-anterior combined surgery for compressive cervical myelopathy were enrolled retrospectively in this study. 1.5 T magnetic resonance imaging (MRI) was performed on all patients before surgery. T2-weighted images (T2WI) of sagittal signal intensity were obtained of the cervical spinal cord, and the regions of interest (ROI) were taken by 0.05 cm2. MR T2WI of sagittal normal cord signal at the C7-T1 disc level were also obtained, and the ROI were taken by 0.3 cm2. Signal value was measured by computer and the signal ratio between regions 0.05 cm2 and 0.3 cm2 calculated. Where no intramedullary high signal intensity was noted on MR T2WI, the ROI were taken by 0.05 cm2 of the region of most severe spinal cord compression. The 73 patients were divided into three groups by hierarchical clustering analysis with signal intensity ratio (group 1: low signal intensity ratio; group 2: middle signal intensity ratio; group 3: high signal intensity ratio). Statistical analyses were performed with SPSS 11.0. Results:, There were significant differences between the three groups according to the recovery rate (P < 0.001), age (P= 0.003), duration of disease (P= 0.001), Babinski sign (P < 0.001), pre- and postoperative Japanese Orthopaedic Association (JOA) score (P= 0.006). With increases in both signal intensity ratio grade and age, the recovery rate and pre- and postoperative JOA scores gradually decreased, and the incidence of Babinski sign increased. There was no significant difference in sex among the three groups (P= 0.387). Multiple comparison tests further supported the above-mentioned results. Conclusion:, Patients with light or no intramedullary signal changes on T2WI had a good surgical outcome. However, increase of signal intensity ratio and occurrence of the pyramidal sign were associated with a poor prognosis after surgery. [source] Intraspinally mediated state-dependent enhancement of motoneurone excitability during fictive scratch in the adult decerebrate catTHE JOURNAL OF PHYSIOLOGY, Issue 15 2010Kevin E. Power This is the first study to report on the increase in motoneurone excitability during fictive scratch in adult decerebrate cats. Intracellular recordings from antidromically identified motoneurones revealed a decrease in the voltage threshold for spike initiation (Vth), a suppression of motoneurone afterhyperpolarization and activation of voltage-dependent excitation at the onset of scratch. These state-dependent changes recovered within 10,20 s after scratch and could be evoked after acute transection of the spinal cord at C1. Thus, there is a powerful intraspinal system that can quickly and reversibly re-configure neuronal excitability during spinal network activation. Fictive scratch was evoked in spinal intact and transected decerebrate preparations by stroking the pinnae following topical curare application to the dorsal cervical spinal cord and neuromuscular block. Hyperpolarization of Vth occurred (mean ,5.8 mV) in about 80% of ipsilateral flexor, extensor or bifunctional motoneurones during fictive scratch. The decrease in Vth began before any scratch-evoked motoneurone activity as well as during the initial phase in which extensors are tonically hyperpolarized. The Vth of contralateral extensors depolarized by a mean of +3.7 mV during the tonic contralateral extensor activity accompanying ipsilateral scratch. There was a consistent and substantial reduction of afterhyperpolarization amplitude without large increases in motoneurone conductance in both spinal intact and transected preparations. Depolarizing current injection increased, and hyperpolarization decreased the amplitude of rhythmic scratch drive potentials in acute spinal preparations indicating that the spinal scratch-generating network can activate voltage-dependent conductances in motoneurones. The enhanced excitability in spinal preparations associated with fictive scratch indicates the existence of previously unrecognized, intraspinal mechanisms increasing motoneurone excitability. [source] | |||||||||||||||||||||||||