scholarly journals Correction to: The Histopathology of Severe Graded Compression in Lower Thoracic Spinal Cord Segment of Rat, Evaluated at Late Post-injury Phase

2021 ◽  
Author(s):  
Jana Fedorova ◽  
Erika Kellerova ◽  
Katarina Bimbova ◽  
Jaroslav Pavel
Keyword(s):  
Spinal Cord ◽  
Post Injury ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Spinal Cord Segment

scholarly journals The Histopathology of Severe Graded Compression in Lower Thoracic Spinal Cord Segment of Rat, Evaluated at Late Post-injury Phase

2021 ◽  
Author(s):  
Fedorova Jana ◽  
Kellerova Erika ◽  
Bimbova Katarina ◽  
Pavel Jaroslav
Keyword(s):  
Spinal Cord ◽  
Spontaneous Recovery ◽  
Traumatic Injury ◽  
Blue Dye ◽  
Post Injury ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Severe Traumatic Injury ◽  
Spinal Cord Segment ◽  
Cord Injury

AbstractSpontaneous recovery of lost motor functions is relative fast in rodent models after inducing a very mild/moderate spinal cord injury (SCI), and this may complicate a reliable evaluation of the effectiveness of potential therapy. Therefore, a severe graded (30 g, 40 g and 50 g) weight-compression SCI at the Th9 spinal segment, involving an acute mechanical impact followed by 15 min of persistent compression, was studied in adult female Wistar rats. Functional parameters, such as spontaneous recovery of motor hind limb and bladder emptying function, and the presence of hematuria were evaluated within 28 days of the post-traumatic period. The disruption of the blood-spinal cord barrier, measured by extravasated Evans Blue dye, was examined 24 h after the SCI, when maximum permeability occurs. At the end of the survival period, the degradation of gray and white matter associated with the formation of cystic cavities, and quantitative changes of glial structural proteins, such as GFAP, and integral components of axonal architecture, such as neurofilaments and myelin basic protein, were evaluated in the lesioned area of the spinal cord. Based on these functional and histological parameters, and taking the animal’s welfare into account, the 40 g weight can be considered as an upper limit for severe traumatic injury in this compression model.

The histopathology of experimental spinal cord trauma

1978 ◽  
Vol 48 (6) ◽  
pp. 1002-1007 ◽  
Author(s):  
Stephen E. Rawe ◽  
William A. Lee ◽  
Phanor L. Perot
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Systemic Blood Pressure ◽  
Post Injury ◽  
Systemic Blood ◽  
Edema Formation ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Marked Enhancement

✓ The early sequential histopathological alterations following a concussive paraplegic injury to the posterior thoracic spinal cord in cats were studied. The lack of significant progression of hemorrhages over a 4-hour period after injury indicates that most hemorrhages probably occur within the first hour. The marked enhancement or retardation of hemorrhages in the post-injury period, when the blood pressure was increased or decreased, respectively, demonstrates the loss of autoregulation of spinal cord vasculature at the trauma site after a concussive paraplegic injury. Progressive edema formation was evident over a 4-hour period following injury, and it could be enhanced or retarded by elevation or reduction of the systemic blood pressure.

Adrenergic receptors (α1 and α2) modulate different potassium conductances in sympathetic preganglionic neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S92-S97 ◽  
Author(s):  
Hiroe Inokuchi ◽  
Megumu Yoshimura ◽  
Canio Polosa ◽  
Syogoro Nishi
Keyword(s):  
Spinal Cord ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Extracellular Potassium ◽  
Thoracic Spinal Cord ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Thoracic Spinal ◽  
Spinal Cord Segment

Intracellular recordings were made from 168 sympathetic preganglionic neurons in the slice of the second or third thoracic spinal-cord segment of the adult cat to study the actions of noradrenaline on these neurons. Noradrenaline, applied by superfusion (0.5–50 μM), produced membrane depolarization in 73 neurons and membrane hyperpolarization in 39 neurons. In 26 neurons noradrenaline produced a biphasic response (depolarization–hyperpolarization or vice versa). The depolarization was blocked by prazosin, while the hyperpolarization was blocked by yohimbine. The noradrenaline-induced depolarization was associated with an increase in neuron input resistance, while the noradrenaline-induced hyperpolarization was associated with a decrease in neuron input resistance. Both responses decreased in amplitude with membrane hyperpolarization and were nullified at around the potassium equilibrium potential EK. The null potential of both responses became more and less negative with a decrease and an increase, respectively, in the extracellular potassium concentration. When the membrane potential was made more negative than EK, the noradrenaline-induced hyperpolarization reversed to depolarization in all cases, whereas in only 4 of 12 cases did the noradrenaline-induced depolarization reverse to hyperpolarization. These data suggest that the noradrenaline-induced depolarization is a result of a decrease, while the noradrenaline-induced hyperpolarization is a result of an increase in K+ conductance. Cobalt (2 mM), low calcium – high magnesium, and intracellular EGTA markedly reduced or abolished the noradrenaline-induced depolarization but had no significant effect on the noradrenaline-induced hyperpolarization. Barium (2 mM) depressed both responses. Tetraethylammonium (10–30 mM), 4-aminopyridine (3 mM), and cesium (2 mM) had no effect on either response. These data suggest that the noradrenaline-induced depolarization is a result of an inactivation of a background calcium-sensitive K+ conductance, while the noradrenaline-induced hyperpolarization is due to activation of a calcium-insensitive potassium conductance.Key words: K+ conductances, catecholamines, Ca2+ dependent, K+ current, spinal cord.

scholarly journals Urinary Tract Infections in Spinal Cord Injury Patients Undergoing Intermittent Catheterization Procedures

1992 ◽  
Vol 3 (3) ◽  
pp. 129-133
Author(s):  
Teresa Kirkland ◽  
Geoffrey D Taylor
Keyword(s):  
Spinal Cord ◽  
Urinary Tract ◽  
Intermittent Catheterization ◽  
Infection Rates ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Spinal Cord Segment ◽  
Significant Downward Trend ◽  
Cord Injury ◽  
Tract Infections

A prospective study was organized to assess whether feeding back infection rates to staff performing intermittent catheterization in spinal cord-injured patients would produce a fall in urinary tract infection rates. Over a 12 month period, infection rates for such procedures were reported to unit staff: reporting was combined with educational programs emphasizing aseptic catheterization techniques and the importance ofhandwashing. Overall infection rates for the 12 month period were 13.3 per 1000 days of intermittent catheterization - unchanged from the preceding six months (15.1 per 1000 days) by retrospective chart review. Likewise, there was no statistically significant downward trend during the prospective phase of the study. A wide variety of infecting organisms were found, of whichKlebsiellaspecies (39%),Escherichia coli(18%) andEnterobacterspecies (17%) were most common: most infections were asymptomatic. Patients with complete cord lesions at or above the sixth thoracic spinal cord segment (T6) had a much higher incidence of infection (73%) than those with incomplete lesions below T6 (33%).

scholarly journals Relationship of American Spinal Injury Association Impairment Scale Grade to Post-injury Hospitalization and Costs in Thoracic Spinal Cord Injury

Neurosurgery ◽  
2017 ◽  
Vol 83 (3) ◽  
pp. 445-451 ◽  
Author(s):  
Ellen M Dukes ◽  
Steven Kirshblum ◽  
Alex A Aimetti ◽  
Sarah S Qin ◽  
Rebecca K Bornheimer ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Injury ◽  
American Spinal Injury Association ◽  
Economic Costs ◽  
Present Value ◽  
Post Injury ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cord Injury

Abstract BACKGROUND The lifetime economic burden of thoracic spinal cord injury (SCI) is known to be high, but evidence of variability of costs in relation to the American Spinal Injury Association Impairment Scale (AIS) grade is limited. OBJECTIVE To estimate lifetime economic costs of hospitalization by AIS grade in thoracic SCI. METHODS Using SCI Model Systems data from January 2000 to March 2016 from the National Spinal Cord Injury Statistical Center, we estimated mean total annual days of all-cause hospitalization by AIS grade among persons with thoracic SCI, based on assessments 1, 5, and 10 yr post-injury. We combined this information with secondary cost data and projections of life expectancy to estimate lifetime economic costs of hospitalization by AIS grade in persons aged 35 yr at time of thoracic SCI. Future costs were discounted to present value at 3% annually. RESULTS One year post-injury, mean total annual days of hospitalization ranged from 2.1 for persons with AIS-D injuries to 5.9 for those who were AIS-A. Similar differences were noted 5 and 10 yr post-SCI. The estimated net present value of expected lifetime costs of hospitalization following thoracic SCI at age 35 yr was $321 534, $249 514, $188 989, and $68 120 (2015 US$) for AIS-A, AIS-B, AIS-C, and AIS-D injuries, respectively. CONCLUSION Persons with less severe thoracic SCI, as reflected in AIS grade, spend fewer days in hospital over their lifetimes, leading to lower costs of inpatient care. Therapies improving AIS grade following thoracic SCI may provide cost savings in addition to addressing substantial unmet need.

scholarly journals Peripheral Immune Dysfunction: A Problem of Central Importance after Spinal Cord Injury

Biology ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 928
Author(s):  
Marisa A. Jeffries ◽  
Veronica J. Tom
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Immune Dysfunction ◽  
Lymphocyte Function ◽  
Immune Functions ◽  
Thoracic Spinal Cord ◽  
Susceptibility To Infection ◽  
Thoracic Spinal ◽  
Spinal Cord Segment ◽  
Cord Injury

Individuals with spinal cord injuries (SCI) exhibit increased susceptibility to infection, with pneumonia consistently ranking as a leading cause of death. Despite this statistic, chronic inflammation and concurrent immune suppression have only recently begun to be explored mechanistically. Investigators have now identified numerous changes that occur in the peripheral immune system post-SCI, including splenic atrophy, reduced circulating lymphocytes, and impaired lymphocyte function. These effects stem from maladaptive changes in the spinal cord after injury, including plasticity within the spinal sympathetic reflex circuit that results in exaggerated sympathetic output in response to peripheral stimulation below injury level. Such pathological activity is particularly evident after a severe high-level injury above thoracic spinal cord segment 6, greatly increasing the risk of the development of sympathetic hyperreflexia and subsequent disrupted regulation of lymphoid organs. Encouragingly, studies have presented evidence for promising therapies, such as modulation of neuroimmune activity, to improve regulation of peripheral immune function. In this review, we summarize recent publications examining (1) how various immune functions and populations are affected, (2) mechanisms behind SCI-induced immune dysfunction, and (3) potential interventions to improve SCI individuals’ immunological function to strengthen resistance to potentially deadly infections.

Spontaneous Herniation of the Thoracic Spinal Cord: A Case Report

2001 ◽  
Vol 45 (4) ◽  
pp. 353 ◽  
Author(s):  
Sung Chan Jin ◽  
Seoung Ro Lee ◽  
Dong Woo Park ◽  
Kyung Bin Joo
Keyword(s):  
Spinal Cord ◽  
Case Report ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Spontaneous Herniation

Lipomeningocele associated with diplomyelia in a dog

2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze
Keyword(s):  
Spinal Cord ◽  
Neurological Status ◽  
Split Cord Malformation ◽  
Lumbar Spinal Cord ◽  
Histopathological Diagnosis ◽  
Type I ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Subcutaneous Mass ◽  
Lumbar Spinal

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.

Superficial siderosis due to dural defect with thoracic spinal cord herniation

2012 ◽  
Vol 312 (1-2) ◽  
pp. 170-172 ◽  
Author(s):  
Giorgio B. Boncoraglio ◽  
Elena Ballabio ◽  
Alessandra Erbetta ◽  
Francesco Prada ◽  
Mario Savoiardo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Superficial Siderosis ◽  
Dural Defect ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Spinal Cord Herniation
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