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PubMed2004

Neurogenesis of corticospinal motor neurons extending spinal projections in adult mice.

The adult mammalian CNS shows a very limited capacity to regenerate after injury. However, endogenous precursors, or stem cells, provide a potential source of new neurons in the adult brain. Here, we induce the birth of new corticospinal motor neurons (CSMN), the CNS neurons that die in motor neuron degenerative diseases, including amyotrophic lateral sclerosis, and that cause loss of motor function in spinal cord injury. We induced synchronous apoptotic degeneration of CSMN and examined the fates of newborn cells arising from endogenous precursors, using markers for DNA replication, neuroblast migration, and progressive neuronal differentiation, combined with retrograde labeling from the spinal cord. We observed neuroblasts entering the neocortex and progressively differentiating into mature pyramidal neurons in cortical layer V. We found 20-30 new neurons per mm(3) in experimental mice vs. 0 in controls. A subset of these newborn neurons projected axons into the spinal cord and survived >56 weeks. These results demonstrate that endogenous precursors can differentiate into even highly complex long-projection CSMN in the adult mammalian brain and send new projections to spinal cord targets, suggesting that molecular manipulation of endogenous neural precursors in situ may offer future therapeutic possibilities for motor neuron degenerative disease and spinal cord injury.

Animals↗
PubMed1997

Activation of the cAMP transduction cascade contributes to the mechanical hyperalgesia and allodynia induced by intradermal injection of capsaicin.

1. The spinal role of the cAMP transduction cascade in nociceptive processing was investigated in awake behaving rats (male, Sprague-Dawley) by activating or inhibiting this pathway spinally. Microdialysis fibres were implanted into the dorsal horn to infuse drugs directly to the spinal cord. 2. Animals, without peripheral tissue injury, were tested for responses to repeated applications (10 trials) of von Frey filaments and threshold to mechanical stimulation before and after infusion of 8-bromo-cAMP. In this group of animals treated spinally with 8-br-cAMP (1-10 mM) a dose-dependent hyperalgesia and allodynia were produced. This was manifested as an increased number of responses to 10 trials of von Frey filaments (10, 50, 150, 250 mN) and a decrease in mechanical threshold. 3. A second series of experiments studied the manipulation of the cAMP pathway spinally in a model of tissue injury induced by intradermal injection of capsaicin. Animals were either pre- or post-treated spinally with the adenylate cyclase inhibitor, tetrahydrofuryl adenine (THFA) or the protein kinase A inhibitor, myrosilated protein kinase (14-22) amide (PKI). Injection of capsaicin resulted in an increased number of responses to repeated applications of von Frey filaments and a decrease in threshold to mechanical stimuli outside the site of injection, secondary mechanical hyperalgesia and allodynia. 4. Pre-treatment with either THFA (1 mM) or PKI (5 mM) had no effect on the capsaicin-evoked secondary hyperalgesia and allodynia. 5. In contrast, post-treatment spinally with THFA (0.01-1 mM) or PKI (0.05-50 mM) dose-dependently reduced the mechanical hyperalgesia and allodynia produced by capsaicin injection. Furthermore, the mechanical hyperalgesia and allodynia blocked by the adenylate cyclase inhibitor, THFA (1 mM), was reversed by infusion of 8-bromo-cAMP (0.01-10 mM) in a dose-dependent manner. 6. Thus, this study demonstrates that activation of the cAMP transduction cascade at the spinal cord level results in mechanical hyperalgesia and allodynia and that the secondary mechanical hyperalgesia and allodynia following intradermal injection of capsaicin is mediated by this same transduction cascade.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Chiropractic management of a patient with lumbar spinal stenosis.

OBJECTIVES: To discuss the case of a patient with severe, multilevel central canal stenosis who was managed conservatively with flexion-distraction manipulation; to introduce a cautious approach to the application of treatment, which can reduce the risk of adverse effects and might make an apprehensive doctor more comfortable treating this condition; and to propose a theoretic mechanism for relief of symptoms through use of chiropractic manipulation. CLINICAL FEATURES: A 78-year-old man had low back pain and severe bilateral leg pains. Objective findings were minimal, yet magnetic resonance imaging demonstrated severe degenerative lumbar stenosis at L3-L4 and L4-L5 and to a lesser degree at L2-L3. INTERVENTION AND OUTCOME: Flexion-distraction manipulation of the lumbar spine was performed. Incremental increases in traction forces were applied as the patient responded positively to care. He experienced a decrease in the frequency and intensity of his leg symptoms and a resolution of his low back pain. These improvements were maintained at a 5-month follow-up visit. CONCLUSION: Successful management of symptoms either caused by or complicated by lumbar spinal stenosis is presented. Manipulation of the spine shows promise for relief of symptoms through improving spinal biomechanics. Further study in the form of a randomized clinical trial is warranted.

Aged↗
PubMed2005

Endocannabinoids at the spinal level regulate, but do not mediate, nonopioid stress-induced analgesia.

Recent work in our laboratories has demonstrated that an opioid-independent form of stress-induced analgesia (SIA) is mediated by endogenous cannabinoids [Hohmann et al., 2005. Nature 435, 1108]. Non-opioid SIA, induced by a 3-min continuous foot shock, is characterized by the mobilization of two endocannabinoid lipids--2-arachidonoylglycerol (2-AG) and anandamide--in the midbrain periaqueductal gray (PAG). The present studies were conducted to examine the contributions of spinal endocannabinoids to nonopioid SIA. Time-dependent increases in levels of 2-AG, but not anandamide, were observed in lumbar spinal cord extracts derived from shocked relative to non-shocked rats. Notably, 2-AG accumulation was of smaller magnitude than that observed previously in the dorsal midbrain following foot shock. 2-AG is preferentially degraded by monoacylglycerol lipase (MGL), whereas anandamide is hydrolyzed primarily by fatty-acid amide hydrolase (FAAH). This metabolic segregation enabled us to manipulate endocannabinoid tone at the spinal level to further evaluate the roles of 2-AG and anandamide in nonopioid SIA. Intrathecal administration of the competitive CB1 antagonist SR141716A (rimonabant) failed to suppress nonopioid SIA, suggesting that supraspinal rather than spinal CB1 receptor activation plays a pivotal role in endocannabinoid-mediated SIA. By contrast, spinal inhibition of MGL using URB602, which selectively inhibits 2-AG hydrolysis in the PAG, enhanced SIA through a CB1-selective mechanism. Spinal inhibition of FAAH, with either URB597 or arachidonoyl serotonin (AA-5-HT), also enhanced SIA through a CB1-mediated mechanism, presumably by increasing accumulation of tonically released anandamide. Our results suggest that endocannabinoids in the spinal cord regulate, but do not mediate, nonopioid SIA.

Analgesia↗
PubMed1991

Functional innervation of spinal cord tissue by fetal neocortical grafts in oculo: an electrophysiological study.

The ability of fetal neocortex transplants, to functionally innervate maturated cervical spinal cord grafts in oculo, was investigated in rats. We found that a neocortex co-graft will grow and develop in contact with a spinal cord graft, and will generate a functional input to maturated spinal cord tissue which can be activated by electrical stimulation of the neocortex graft. Our data suggest that orthodromic stimulation of this pathway causes short latency, transient excitations of spinal graft neurons. These appear to be mediated by an excitatory amino acid receptor since the response was noncompetitively antagonized by kynurenic acid. Kynurenic acid also noncompetitively antagonized the excitatory effects of glutamate superfused over single spinal cord grafts. The mechanism of the excitation probably does not involve an NMDA (N-methyl-D-aspartate) receptor since APV (2-amino-5-phosphonovalerate) did not alter the spinal graft neuronal responses to neocortical co-graft stimulation. These data suggest that fetal neocortex can functionally innervate maturated cervical spinal cord in the in oculo graft preparation. The in oculo spinal cord graft model may thus provide a unique test system for studies of the influence of drugs and other manipulations that might alter cortico-spinal pathway development as well as influence reestablishment of neuronal pathways after spinal cord injury.

Action Potentials↗
PubMed1993

Limiting ischemic spinal cord injury using a free radical scavenger 21-aminosteroid and/or cerebrospinal fluid drainage.

Traumatic spinal cord injury occurs in two phases: biomechanical injury, followed by ischemia and reperfusion injury. Biomechanical injury to the spinal cord, preceded or followed by various pharmaceutical manipulations or interventions, has been studied, but the ischemia/reperfusion aspect of spinal cord injury isolated from the biomechanical injury has not been previously evaluated. In the current study, ischemia to the lumbar spinal cord was induced in albino rabbits via infrarenal aortic occlusion, and two interventions were analyzed: the use of U74006F (Tirilazad mesylate), a 21-aminosteroid, and cerebrospinal fluid (CSF) drainage. These treatment modalities were tested alone or in combination. In Phase 1 of this study, the rabbits received 1.0 mg/kg of Tirilazad or an equal volume of vehicle (controls) prior to the actual occlusion, three doses of Tirilazad (1 mg/kg each) during the occlusion, then several doses after the occlusion. Of the Tirilazad-treated animals, 30% became paraplegic while 70% of the control animals became paraplegic. Phase 2 involved the same doses of Tirilazad as in Phase 1 and, in addition, CSF pressure monitoring and drainage were performed. The paraplegia rate was 79% in the control animals, 36% in the group receiving Tirilazad alone, 25% in the group with CSF drainage alone, and 20% in the Tirilazad plus CSF drainage group. This rate also correlated with changes noted in CSF pressure; both Tirilazad administration alone and CSF drainage alone induced a decrease in CSF pressure and the two combined produced a further decrease. There was marked improvement in the perfusion pressure when using Tirilazad alone, CSF drainage alone, and Tirilazad therapy in combination with CSF drainage, with the last group producing the largest increase. This change in CSF pressure and perfusion pressure correlated with improved functional neurological outcome. Pathological examination revealed that Tirilazad therapy reduced the extensive and diffuse neuronal, glial, and endothelial damage to (in its most severe form) a more patchy focal region of damage in the gray matter. Cerebrospinal fluid drainage resulted in pyknosis of some motor neurons, and some eosinophilia. The combination of CSF drainage and Tirilazad administration resulted in the least abnormality, with either normal or near-normal spinal cords. It is concluded that Tirilazad administration decreased CSF pressure during spinal cord ischemia and reperfusion and, like CSF drainage, increased and improved the perfusion pressure to the spinal cord, decreased spinal cord damage, and improved functional outcome.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Staged spinal cord decompression through posterior approach for thoracic myelopathy caused by ossification of posterior longitudinal ligament.

STUDY DESIGN: Prospective clinical study of the effect of staged elimination of anatomic factors inhibiting posterior shift of the thoracic spinal cord on the degree of posterior shift of the thoracic spinal cord and its significance in augmenting the safety of ossification of posterior longitudinal ligament (OPLL) manipulation in thoracic OPLL myelopathy. OBJECTIVES: To develop a comprehensive method that enables safe and sufficient decompression of the spinal cord for thoracic OPLL myelopathy. SUMMARY OF BACKGROUND DATA: Decompression of the spinal cord by direct manipulations of thoracic OPLLs, via either anterior or posterior approach, caused some iatrogenic catastrophic spinal cord injuries, and methods to prevent such injuries during surgery have not yet been developed. METHODS: Procedures of elimination of anatomic factors inhibiting posterior shift of the thoracic spinal cord were performed in stages at intervals of between 1 month and 11 years depending on patients' neurologic status. The first stage operation consisted of extensive cervicothoracic laminoplastic decompression with or without posterior longitudinal durotomy, and if the decompression were insufficient, measures for OPLL-spinal cord separation with or without OPLL manipulation were added. RESULTS: All 17 patients with thoracic OPLL myelopathy showed improvements of neurology comparable with those with successful anterior approaches after decompression. The mean follow-up period was 42 months (range 6-101 months). Neurologic improvements persisted for the entire follow-up period in all patients except one patient who developed arachnoid cyst compressing the dorsum of the once-decompressed spinal cord 30 months after surgery. CONCLUSIONS: Staged posterior decompression to eliminate anatomic factors inhibiting posterior shift of the thoracic spinal cord is the safest and the most reliable method of spinal cord decompression to treat thoracic OPLL myelopathy, so far. However, long-term results are required before the methods can be established.

Adult↗
PubMed1983

Diagnostic palpation of the spine: a review of procedures and assessment of their reliability.

Spinal palpation as employed by practitioners of manipulative therapy is a common diagnostic tool used to identify manipulable lesions. Three methods of diagnostic palpation are static palpation, active motion palpation and passive motion palpation. As a diagnostic technique, spinal palpation suffers from a lack of research on its statistical reliability. Assessment of the clinical efficacy of manipulative therapy would be better addressed if a statistically reliable method of palpatory diagnosis were developed.

Chiropractic↗
PubMed1997

Spinal cord injury and anti-NGF treatment results in changes in CGRP density and distribution in the dorsal horn in the rat.

Spinal cord injury (SCI) results in chronic pain states in which the underlying mechanism is poorly understood. To begin to explore possible mechanisms, calcitonin gene-related peptide (CGRP), a neuropeptide confined to fine primary afferent terminals in laminae I and II in the dorsal horn of the spinal cord and implicated in pain transmission, was selected. Immunocytochemical techniques were used to examine the temporal and spatial distribution of CGRP in the spinal cord following T-13 spinal cord hemisection in adult male Sprague-Dawley rats compared to that seen in sham controls. Spinal cords from both hemisected and sham control groups (N = 5, per time point) were examined on postoperative day (POD) 3, 5, 7, 14, and 108 following surgery. Sham operated rats displayed CGRP immunoreaction product in laminae I and II outer, Lissauer's tract, dorsal roots, and motor neurons of the ventral horn. In the hemisected group, densiometric data demonstrated an increased deposition of reaction product that was statistically significant, in laminae III and IV, both ipsilateral and contralateral to the lesion that extended at least two segments rostral and caudal to the hemisection site by POD 14, and remained significantly elevated as long as POD 108. Since upregulation alone of CGRP would occur in an acute temporal window (by 2 to 3 days following spinal injury), these results are interpreted to be invasion of laminae III and IV by sprouting of CGRP containing fine primary afferents. Intrathecal delivery of antibodies against purified 2.5S nerve growth factor for 14 days to the hemisected group resulted in CGRP density in laminae I through IV that was significantly less than that seen in untreated or vehicle treated hemisected groups and to sham controls. These data indicate changes in density and distribution of CGRP following spinal hemisection that can be manipulated by changes in endogenous levels of NGF. These observations suggest possible strategies for intervention in the development of various pain states in human SCI.

Afferent Pathways↗
PubMed1989

Electrophysiological recordings during spinal surgery.

Experience with electrophysiological monitoring during surgery of the spinal vertebrae and spinal cord is reviewed. The cerebral somatosensory evoked potential (CSEP) is used to monitor spinal cord conductivity during mechanical manipulation of the vertebrae, most commonly during correction of the curvature of the spine. Abnormal CSEPs were recorded in 11 out of approximately 700 cases of scoliosis surgery. During percutaneous cordotomy, intracord evoked and spontaneous potentials are recorded in order to identify the cord structure. Experiment models are also discussed.

Brain↗
PubMed2003

Differential regulation of GABA B receptor subunit expression and function.

The GABA(B) receptor is a G protein-coupled heterodimer composed of GABA(B1) and GABA(B2) subunits. In the present study, experiments were undertaken to examine the relationship between GABA(B) receptor function and subunit expression in the rat lumbar spinal cord following pharmacological and physiological manipulation of this receptor system. Although formalin-induced hind paw inflammation increases the production of GABA(B1) and GABA(B2) protein in the spinal cord within 24 h, there is no change in receptor function, as measured by the baclofen-stimulated guanosine 5'-O-(3-[(35)S]thiotriphosphate) ([(35)S]GTPgammaS) binding assay. Conversely, although chronic (7 days) administration of baclofen, a GABA(B) receptor agonist, abolishes baclofen-stimulated [(35)S]GTPgammaS binding in the spinal cord tissue, causes tolerance to the sedative and antinociceptive effects of the drug, increases the number of formalin-induced hind paw flinches, and induces mechanical hyperalgesia, this treatment had no effect on the levels of GABA(B1) or GABA(B2) mRNAs in the lumbar spinal cord. The results indicate a lack of concordance between expression of GABA(B1) and GABA(B2) subunits and GABA(B) receptor function, suggesting these subunit proteins may serve multiple functions in the cells. Moreover, these findings indicate that nongenomic mechanisms are primarily responsible for the GABA(B) receptor desensitization that occurs during prolonged exposure to receptor agonist.

Animals↗
PubMed1977

Compensatory responses in the development of the brachial lateral motor column in triploid Rana pipiens.

Responses of the lateral motor column (LMC) in the frog spinal cord to various experimental manipulations generally are manifested in an adjustment of the number and sizes of the motor neurons. Analysis of the brachial LMC in induced-triploid Rana pipiens larvae as compared to diploid controls revealed a significant increase in nuclear size with a concomitant reduction in cell counts at all stages of development examined. These compensatory responses of the LMC to polyploidy in normal size frog larvae are consistent with results reported for other amphibian polyploid tissues and serve as a basis for exploring mechanisms of plasticity in the developing central nervous system.

Age Factors↗
PubMed2001

Consequences of neck manipulation performed by a non-professional.

Case report. Documentation of complication of neck manipulation by an untrained person. Tertiary care referral teaching hospital at Lucknow, India. Clinical evaluation, plain radiography of cervical spine, spinal MRI.A 30-year-old man who fainted after neck manipulation by a barber and developed spinal cord and brainstem dysfunction. His MRI revealed an extramedullary, intradural dumbbell shaped mass on the right side at C1 and C2 level compressing the spinal cord. Public awareness should be increased about the danger of neck manipulation by an untrained person especially in the communities where it is commonly practiced.

Adult↗
PubMed1996

Noradrenergic neurotransmission in the ventral spinal cord: basic characteristics and effects of denervating lesions, as studied in the awake rat by microdialysis.

Extracellular levels of noradrenaline (NA) were measured in the ventral horn of the lumbar spinal cord in awake unrestrained rats using in vivo microdialysis coupled to a highly sensitive radioenzymatic assay. In normal animals, baseline NA output averaged 13.4 +/- 2.2 fmol/30 microliters. KCl (100 mM) or desipramine (5 microM) added to the perfusion fluid increased NA levels 11.2-fold and 2.2-fold, respectively, whereas neuronal impulse blockade by tetrodotoxin (1 microM) added in the presence of desipramine stimulation produced a 88% reduction of extracellular NA levels. Noradrenergic denervation of the spinal cord by either electrolytic destruction of the noradrenaline-containing axon terminals or intraventricular 6-hydroxydopamine produced, 3-4 weeks later, dramatic 84 and 91% reductions in baseline NA release associated to a marked loss of immunoreactive noradrenergic fibers throughout the spinal cord or caudal to the site of electrolytic damage and almost completely abolished responses to pharmacological manipulations. The results support the view that spinal extracellular NA levels are neuronally derived, also suggesting that noradrenergic neurotransmission in the ventral spinal cord largely (by at least 85%) depends on the integrity of descending brainstem afferents. The microdialysis technique, thus, appears to be a useful tool for future studies on strategies aimed at promoting reinnervation and functional recovery in the deafferented spinal cord.

Adrenergic Uptake Inhibitors↗