A clinician's view of spinal cord injury

Harkey, H. Louis; White, Elbert A.; Tibbs, Robert E.; Haines, Duane E.

doi:10.1002/ar.b.10012

Cited by 34 publications

(24 citation statements)

References 31 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…10,11 Individuals with incomplete SCI represent over half of the SCI population. [12][13][14] However, there are few reports describing their muscle adaptations compared to individuals with complete SCI. Although skeletal muscle atrophy can adversely affect individuals with both complete and incomplete SCI, 2,3 the degree of atrophy may lead to more serious implications among those with incomplete injury because it can limit their functional performance and their ability to attain independent ambulation.…”

Section: Introductionmentioning

confidence: 99%

Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury

Gorgey

Dudley

2007

Spinal Cord

View full text Add to dashboard Cite

Design: Cross-sectional. Objectives: (1) To determine the effects of the level of spinal cord injury (SCI) on skeletal muscle, intramuscular fat (IMF) cross-sectional areas (CSAs) and relative IMF; (2) to determine the relation, if any, of spasticity to each of these variables after incomplete SCI. Settings: In-patient study at the Shepherd Center, Atlanta, GA, USA. Methods: Thirteen individuals with incomplete SCI were classified according to their level of injury into a high level of injury group (HLI, C5-C7, n ¼ 8) and a low level of injury group (LLI, T12-L2, n ¼ 5). Spasticity was determined for thigh muscles using a modified Ashworth scale at 6 weeks post-injury. T1-weighted magnetic resonance (MR) images were taken 6 weeks post-injury to measure thigh skeletal muscle and IMF CSAs. Results: Spasticity was significantly evident in the HLI group compared to the LLI group (P ¼ 0.023). Six weeks post-injury, muscle CSA was 103718 cm 2 in the HLI group and 80720 cm 2 in the LLI group (P ¼ 0.042). Relative IMF was 3.672.0% in HLI and 7.574.0% in LLI (P ¼ 0.021). Additionally, spasticity accounted for 54% of the variability in muscle CSA for all subjects (r 2 ¼ 0.54, P ¼ 0.006). Conclusions: Spasticity may be an important factor in defending skeletal muscle size and indirectly preventing IMF accumulation early after incomplete SCI.

show abstract

Section: Introductionmentioning

confidence: 99%

Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury

Gorgey

Dudley

2007

Spinal Cord

View full text Add to dashboard Cite

show abstract

“…Counting the intervertebral spaces before spinal block is an important way to evade damage to the spinal cord. The neurological structures at the level of the thoracolumbar spine are critical for lower-extremity motor, sensory function, as well as bowel, bladder and sexual functions [2]. Purpose of this study was to find relationship between the location of CM and spinal position in adult patients, with age, gender and body mass index (BMI).…”

Section: Dear Editormentioning

confidence: 99%

Variations in Position of Conus Medullaris in Adult Patients

Rostamzadeh

Naleini

Rostamzadeh

2016

Zahedan J Res Med Sci

View full text Add to dashboard Cite

Finding a safe location for spinal block during surgical procedures is a matter that requires attention. Conus medullaris (CM) is the most distal point of the spinal cord and dura that could be visualized on the sagittal sequence. CM location follows a normal distribution, from the lower third of L1 (ranging from the middle third of T12 to the upper third of L3) [1]. It is important to know the level of the lumbar spine to have a safe spinal block after an intervertebral injection. Counting the intervertebral spaces before spinal block is an important way to evade damage to the spinal cord. The neurological structures at the level of the thoracolumbar spine are critical for lower-extremity motor, sensory function, as well as bowel, bladder and sexual functions [2]. Purpose of this study was to find relationship between the location of CM and spinal position in adult patients, with age, gender and body mass index (BMI). This study was conducted on patients referring to Shahid Chamran MRI center in Sanandaj, West of Iran. For this study 350 patients (199 males and 151 females) were selected. T1-weighted sagittal spin echo MRI sequences of the lumbar spine with the patient in the supine position were studied to evaluate the location of CM. SPSS-20 was applied for the statistical analysis using χ 2 and ANOVA tests.The P values are at a significant level of P < 0.05. The position of the CM was between T12 upper third and L2 middle third with a mean of L1 upper third. The conus was located from T12 upper third to L2 upper third (mean: L1 upper third) in males and from T12 upper third to L2 middle third (mean: L1 middle third) in females. In different age groups, the mean position was variable ranging from T12 -L1 intervertebral disc to upper part of L1 middle third and did not seem to be clinically significant. Saifuddin et al. [3] in a study, with 504 adult cases without spinal deformity, found that the tip of the conus was between middle third of T12 and upper third of L3 with a mean position at the lower third of L1. They found that conus position was slightly lower in males than in females without statistical significance. The results of this study are congruent with our study. In contrast to the findings of Saifuddin et al. the results of our study did not show a significant difference between CM position in males and female [3]. The present study showed that it would be practical to know the CM position in the same patient population; since lumbar radiograph and MRI cannot be routinely recommended for all patients scheduled for spinal block. It is important to consider the possible range of CM level when performing lumbar puncture and avoid complications for lumbar surgery. Finally, the variation of the CM position could be a guidance that why neurological symptoms varies for different patients. References1. Demiryurek D, Aydingoz U, Aksit MD, Yener N, Geyik PO. MR imaging determination of the normal level of conus medullaris.

show abstract

“…The mortality after spinal cord injury is nearly 50% and about 15–20% of the patients surviving the initial trauma will die later in hospital [2]. The patients are often young and left with paralysis, spasticity and loss of sphincter control.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

et al. 2012

View full text Add to dashboard Cite

Following the initial acute stage of spinal cord injury, a cascade of cellular and inflammatory responses will lead to progressive secondary damage of the nerve tissue surrounding the primary injury site. The degeneration is manifested by loss of neurons and glial cells, demyelination and cyst formation. Injury to the mammalian spinal cord results in nearly complete failure of the severed axons to regenerate. We have previously demonstrated that the antioxidants N-acetyl-cysteine (NAC) and acetyl-L-carnitine (ALC) can attenuate retrograde neuronal degeneration after peripheral nerve and ventral root injury. The present study evaluates the effects of NAC and ALC on neuronal survival, axonal sprouting and glial cell reactions after spinal cord injury in adult rats. Tibial motoneurons in the spinal cord were pre-labeled with fluorescent tracer Fast Blue one week before lumbar L5 hemisection. Continuous intrathecal infusion of NAC (2.4 mg/day) or ALC (0.9 mg/day) was initiated immediately after spinal injury using Alzet 2002 osmotic minipumps. Neuroprotective effects of treatment were assessed by counting surviving motoneurons and by using quantitative immunohistochemistry and Western blotting for neuronal and glial cell markers 4 weeks after hemisection. Spinal cord injury induced significant loss of tibial motoneurons in L4–L6 segments. Neuronal degeneration was associated with decreased immunostaining for microtubular-associated protein-2 (MAP2) in dendritic branches, synaptophysin in presynaptic boutons and neurofilaments in nerve fibers. Immunostaining for the astroglial marker GFAP and microglial marker OX42 was increased. Treatment with NAC and ALC rescued approximately half of the motoneurons destined to die. In addition, antioxidants restored MAP2 and synaptophysin immunoreactivity. However, the perineuronal synaptophysin labeling was not recovered. Although both treatments promoted axonal sprouting, there was no effect on reactive astrocytes. In contrast, the microglial reaction was significantly attenuated. The results indicate a therapeutic potential for NAC and ALC in the early treatment of traumatic spinal cord injury.

show abstract

A clinician's view of spinal cord injury

Cited by 34 publications

References 31 publications

Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury

Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury

Variations in Position of Conus Medullaris in Adult Patients

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

Contact Info

Product

Resources

About