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At least 19 recordsLinked to original sources
PubMed1979

Local tetanus in rats; concentration of amino acids as studied in spinal cord segments, spinal roots, and dorsal root ganglia.

1. The effect of tetanus toxin injected into one gastrocnemius muscle on the steady state concentration of several amino acids was investigated in spinal cord half segments, spinal roots and dorsal root ganglia of rats. Care was taken to ensure a symmetrical afferent input to the spinal cord and to localize the segment with the highest concentration of tetanus toxin. 2. In the spinal cord segments containing the highest concentration of tetanus toxin the steady state concentration of glycine was higher on the side of the tetanus than on the contralateral control side. Results obtained after intravenous injection of 14C-glycine do not indicate that the higher concentration of glycine on the side of the tetanus was due to a higher uptake of glycine. 3. The results obtained in the spinal cord contradict previous findings of other authors but lend support to the prevailing concept about the action of tetanus toxin in local and general tetanus.

Amino Acids↗
PubMed1979

Arteriovenous malformations of the spinal cord.

Spinal AVM's are not rare, and are diagnosed today with increasing frequency by utilization of moedern neuroradiological techniques. Their relationship to the spinal medulla is related to vascular embryological anatomy, and the only effective treatment is directed at obliteration of the fistula. Males are affected more frequently in the middle years of life. Symptoms may mimic spinal cord tumors and demyelinating disorders. The pathogenesis of symptoms, classification, and methods of diagnosis are reviewed, and the various methods of treatment discussed.

Arteriovenous Malformations↗
PubMedDate not supplied

[Effect of spinal cord and spinal injuries on the phagocytic activity of neutrophils].

Study of neutrophil phagocytic activity in injuries to the spinal cord and spine and in damage to the spine without involvement of the spinal cord showed that injuries to the spinal cord have no specific effect on this activity. True, the phagocytic reaction is inhibited in the first 2-3 weeks after the trauma both in patients with injury to the spinal cord and spine and in those with injury only to the spine. In later periods after the trauma, however, with the neurological status remaining the same, the values of the phagocytic reaction do not differ from those in healthy persons. The level at which the spinal cord is injured hardly affects the activity of phagocytosis. The examination was conducted in 117 patients with spinal fractures 94 of whom had also sustained injury to the spinal cord.

Acute Disease↗
PubMed1977

The mechanism of spinal cord cavitation follwing spinal cord transection. Part 2. Electron microscopic observations.

The authors report their findings by electron microscopy after microsurgical subpial spinal cord transection in dogs. After cord transection, conspicuous myelin microcysts are formed in a background of otherwise intact cord tisue at a distance of 1 to 2 mm from the cut end of the cord, both proximal and distal to the transection, Seen through the electron microscope, the microcysts iss a myelin sac distended by fluid under pressure, containing a swollen axon filled with excessive axoplasmic organelles; that is, a terminal club. Later the microcysts and terminal clubs rupture. The large spaces within the microcysts are opened to heretofore small extracellular spaces and the spinal cord tissues are destroyed. Thus, microcysts are precursors of large cavitites seen at the ends of transcreted cord stumps. The formation of microcysts and their subsequent rupture, which leads to cord cavitation, is interpreted as an inherent response of cord tissue to injury, and the result of an abortive attempt at cord regeneration.

Animals↗
PubMed1976

Further characterization of the anti-encephalitogenic protein (SCP): isolation from bovine spinal cord and spinal roots.

The three molecular forms of the anti-encephalitogenic protein, beta-SCP, gamma-SCP, and SCP-peptide were isolated in higher yield by a shortened procedure, which involved 1) extraction of bovine spinal cord (BSC) or bovine spinal roots (BSR) with 0.05 M sodium acetate buffer, pH 4.5, 2) batch absorption on CM-52 cellulose, 3) stepwise elution with sodium acetate buffers, pH 5.8, containing increasing concentrations of sodium chloride and finally, 4) removal of trace contaminants by gel-exclusion chromatography on Sephadex G-50 superfine. The m.w. of the purified proteins determined by sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis was 13,200 daltons. The same value for the molecular sizes was obtained by gel-exclusion chromatography by using 0.1% SDS in 0.05M sodium chloride as eluant. In the absence of SDS the molecular sizes estimated by gel exclusion chromatography ranged from 14,000 to 18,500. The amino acid compositions of the beta-SCP and gamma-SCP from BSC and BSR were similar except that beta-SCP from BSR lacked half-cystine whereas gamma-SCP from BSR contained three times as much half-cystine as the SCP forms prepared from BSC. All forms of SCP showed reactions of identity when compared by immunodiffusion analyses with a rabbit anti-bovine SCP serum; none formed precipitin lines with a rabbit anti-bovine myelin basic protein (MyBP) serum.

Amino Acids↗
PubMed1977

Effects of Ro 4-1284 on electrically-induced spinal cord seizures and on spinal cord norepinephrine and 5-hydroxytryptamine levels.

The time course effects of the benzoquinolizine Ro 4-1284 on spinal cord norepinephrine (NE) and 5-hydroxytryptamine (5-HT) levels were compared to the effects of this same drug on electrically-induced spinal cord seizures. The data show that a significant decrease in spinal cord NE levels and a facilitating effect on spinal cord seizures are apparent 15 minutes after Ro 4-1284 (10 mg/kg s.c.) and that both of these effects persist for at least 24 hours. Forty-eight hours after injection, the effects of Ro 4-1284 on seizure and on NE levels are completely dissipated. A significant decrease in 5-HT levels is not apparent until 1 hour after Ro 4-1284. These data suggest that noradrenergic neurons of the spinal cord act as attenuators of seizure activity. The possibility that spinal cord 5-HT also subserves a seizure attenuating function is not precluded.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMedDate not supplied

[Spinal cord influences on immune responses demonstrated following interruption of the spinal cord as a result of injury].

Specific and nonspecific immunity reactions were studied in dynamics in 126 patients with injury to the spinal cord, in 162 healthy persons (controls), and in 30 persons who had suffered injury to other organs. The serum agglutinins against the causative agents of infection of the urinary system (colibacillus, Proteus, enterococcus) and C-reactive protein were studied. Phases were revealed in the course of the immunologic reactions depending on the neurodynamics of the damaged spinal cord. The correlation established between the character of changes in the immunologic reactivity and the time elapsed after the injury, the level and the degree of damage to the spinal cord allows the conclusion that cerebrospinal effects are one of the links in the complex chain of central control of immunogenesis.

Agglutinins↗
PubMed1979

Xenon enhancement for computed tomography of the spinal cord.

The spinal cord is not consistently shown by plain computed tomography or with iodide enhancement. Xenon enhancement increases the attenuation of the spinal cord and visualization is improved considerably; fluid-filled cavities, including syringohydromyelia, do not enhance and are clearly defined.

Cysts↗
PubMed1979

[Infarction of the spinal cord in the posterior spinal arterial supply area as a result of intervertebral disc embolism (author's transl)].

A female patient aged 49 developed an acute transverse lesion of the spinal cord from D11 downwards. Autopsy revealed spinal cord infarcts mainly in the dorsal parts corresponding to the posterior spinal arterial supply area, caused by multiple arterial and venous fibrocartilaginous emboli. This particular cause of spinal vascular syndrome has been reported previously only in 11 patients, all outside Austria. This case report serves to stress the poor clinical delineation of a distinct "posterior spinal syndrome". The source of the emboli is the intervertebral disc, mainly the nucleus pulposus. The spinal cord vessels are probably entered by the following route: extrusion of disc material into the venous bone marrow sinus (probably favoured by trauma or endocrine factors) yield basivertebral veins yield internal vertebral venous plexus; the spread is supported by blood stream changes caused by increased intraabdominal/intrathoracic pressure; there is also the possibility of direct penetration of disc material into the internal vertebral plexus, as demonstrated in dogs yield radicular veins yield meningeal and cord veins; sometimes entry occurs through arteriovenous shunts into cord arteries. The true incidence of this condition is unknown since cases are likely to be overlooked in the absence of extensive histopathological investigation.

Accidents, Home↗
PubMed1979

Electron microscopy of synapses in reptile spinal cord.

The spinal cord of the reptile Anolis carolinensis was examined by electron microscopy. Motor neurons appear as multipolar cells 30-60 micrometer in diameter. Two types of synaptic endings are endings are present on motor neurons. The first type is characterized by distinct synaptic clefts measuring 15-20 nm between pre- and postsynaptic membranes, and by clear presynaptic vesicles. The second type of synapse, which is less common, is characterized by gap junctions between pre- and postsynaptic membranes. At these synapses, there are also clusters of clear vesicles close to the presynaptic membrane adjacent to the gap junction. These findings indicate that both chemical and electrical synaptic transmission are present in the spinal cord of Anolis.

Animals↗
PubMed1979

Studies of experimental cervical spinal cord transection. Part II: Plasma norepinephrine levels after acute cervical spinal cord transection.

Plasma concentrations of norepinephrine (NE) were measured by a radioenzymatic assay technique before and serially after laminectomy at the C-6 level in 14 anesthetized dogs. In half the animals, no further procedures were carried out (control group); in the other dogs, cervical cord transection was performed in addition to laminectomy (experimental group). Mean plasma NE levels were similar in both groups after laminectomy and before cord interruption. In the control group, NE levels increased gradually for 2 hours after the procedure. In the group with cord transection, however, NE rose immediately after transection to 267% of the baseline value, then fell to 25% of the plasma NE level in the control group at 30 minutes, 29% at 60 minutes, and 15% at 120 minutes. Cervical spinal cord transection, therefore, results in an abrupt but short-lived increase in plasma NE concentrations. These changes in plasma NE levels may explain, at least in part, the hemodynamic alterations and the acute central hemorrhagic necrosis that occur after high spinal cord trauma.

Animals↗
PubMed1979

Studies of experimental cervical spinal cord transection. Part III: Effects of acute cervical spinal cord transection on cerebral blood flow.

Regional cerebral blood flow (CBF) was measured by the microsphere technique in anesthetized, mechanically ventilated dogs before and after cervical laminectomy in four (control group), or cervical laminectomy followed by cervical cord transection (CCT) at the C-6 level in six (experimental group). No significant differences in arterial pH, pO2 or pCO2 were observed between control and experimental dogs. Baseline values for mean arterial pressure (MAP) were also similar in the two groups, but MAP fell in all experimental dogs after CCT (p less than 0.025). At 120 minutes after CCT, three of the six dogs had an MAP greater than 60 torr (66 +/- 4 torr), and in three the MAP was greater than 50 torr (45 +/- 3 torr). Regional CBF in cortical gray matter, white matter, and medulla did not change significantly after CCT in dogs with MAP greater than 60 torr. The CBF fell significantly at 120 minutes after CCT in all regions sampled in the dogs with MAP less than 50 torr (p less than 0.025). At 30 and 120 minutes after CCT, cerebellar blood flow fell significantly in all experimental animals (p less than 0.05). These findings indicate that, despite hypotension and sympathetic denervation of cerebral vessels, CBF in cortical gray matter, white matter, and medulla is maintained at normal levels after CCT by autoregulation as long as MAP exceeds 60 torr. Decreased cerebellar blood flow in the experimental group suggests redistribution of CBF after CCT with relative preservation of flow to gray matter, white matter, and medulla. Reduced CBF in the acutely cord-injured patient with significant hypotension (MAP less than 60 torr) may stimulate or complicate coexistent head injury.

Animals↗
PubMedDate not supplied

Current status of spinal cord monitoring.

Spinal cord monitoring, as currently practiced, requires a source of sensory stimulus, transmitted through filters and amplifiers, to result in an enhanced signal, which is recorded and studied. Three techniques are under investigation. In one, the stimulation and responses are recorded directly from the dura. In another, the stimulus is applied to a peripheral nerve and the response is gathered from vertebral bone. The third utilizes responses in the form of cortical evoked potentials, with the stimulus applied to peripheral nerves.

Cerebral Cortex↗
PubMed2026

The investigation of human cerebrospinal fluid exosome in spinal cord injury.

Spinal cord injury (SCI) leads to severe neurological and functional impairments, yet reliable biomarkers for assessing injury severity and predicting recovery remain limited. Cerebrospinal fluid (CSF) is in direct contact with the central nervous system and provides a valuable source for detecting molecular changes after SCI. Although exosomal microRNAs (miRNAs) and proteins are increasingly recognized as mediators of intercellular communication, the role of human CSF exosomes in SCI has not been systematically investigated. To identify exosome-based biomarkers and potential therapeutic targets, we analyzed CSF and serum exosomes from patients with acute SCI using RNA sequencing and proteomic profiling. Weighted gene co-expression network analysis identified 6 gene modules significantly associated with injury severity and neurological recovery at 3 months. Proteomic analysis revealed a 5-protein panel that distinguished complete from incomplete SCI and a 4-protein panel that predicted neurological improvement. Additionally, 15 CSF-specific and 9 serum-specific exosomal miRNAs were identified independent of injury severity. Among 10 tested miRNAs associated with neurological recovery, 7 regulated astrocyte proliferation, and 6 promoted neurite extension and synapse formation. Overall, this study provides a comprehensive characterization of CSF exosomal miRNAs and proteins in human SCI and identifies molecular signatures associated with injury severity and recovery.

Humans↗