Slope analysis of somatosensory evoked potentials in spinal cord injury for detecting contusion injury and focal demyelination

Agrawal, Gracee; Sherman, David; Maybhate, Anil; Gorelik, Michael; Kerr, Douglas A.; Thakor, Nitish V.; All, Angelo H.

doi:10.1016/j.jocn.2010.02.005

Cited by 31 publications

(30 citation statements)

References 22 publications

(21 reference statements)

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“…We have previously reported that SSEPs recorded upon hindlimb stimulation after a thoracic SCI are significantly reduced in amplitude immediately following injury, then partially recover over several weeks post-injury [16][17][18][19]. As an internal control, we verified our current injury model by reporting SSEP amplitudes recorded during hindlimb stimulation (Fig.…”

Section: Resultssupporting

confidence: 57%

“…Five transcranial screw electrodes were implanted on the cranium of each rat for SSEP recordings, as previously described [16][17][18][19][20]. Briefly, an incision was made along the midline of the shaved head and a dental drill was used to drill five burr holes in the exposed part of the skull corresponding to the hindlimb and forelimb regions of the S1.…”

Section: A Contusion Injurymentioning

confidence: 99%

“…For SSEP recordings, rats were anesthetized with 1.5% isoflurane and intramuscular needle electrodes were used to electrically stimulate the median and tibial nerves of the left and right limbs, as previously described [16][17][18][19][20]. An isolated constant current stimulator (Digitimer, Welwyn Garden City, Hertfordshire, UK) was used to deliver positive current pulses of 3.5 mA with 200 µs duration at 0.5 Hz to one limb at a time while concurrently recording the evoked potential responses on the cortex.…”

Section: B Electrophysiologymentioning

confidence: 99%

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Plasticity associated changes in cortical somatosensory evoked potentials following spinal cord injury in rats

Bazley

All

Thakor

et al. 2011

2011 Annual International Conference of the IEEE Engineering in Medicine and Biology Society

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Spinal cord injury (SCI) causes a number of physiological and neurological changes resulting in loss of sensorimotor function. Recent work has shown that the central nervous system is capable of plastic behaviors post-injury, including axonal regrowth and cortical remapping. Functional integrity of afferent sensory pathways can be quantified using cortical somatosensory evoked potentials (SSEPs) recorded upon peripheral limb stimulation. We implanted 15 rats with transcranial screw electrodes and recorded SSEPs from cortical regions corresponding to each limb before and after a mild or moderate contusion injury. We report a post-injury increase in the mean amplitude of cortical SSEPs upon forelimb stimulation. SSEP amplitudes for mild and moderate SCI groups increased by 183% ± 95% and 107% ± 38% over baseline, respectively, while hindlimb SSEPs decreased by 58% ± 14% and 79% ± 4%. In addition, we report increased SSEP amplitude measured from the anatomically adjacent hindlimb region upon forelimb stimulation (increase of 90% ± 19%). Our results show that previously allocated hindlimb cortical regions are now activated by forelimb stimulation, suggesting an expansion in the area of cortical forelimb representation into hindlimb regions after an injury. This result is indicative of adaptive plasticity in undamaged areas of the CNS following SCI.

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Section: Resultssupporting

confidence: 57%

Section: A Contusion Injurymentioning

confidence: 99%

Section: B Electrophysiologymentioning

confidence: 99%

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Plasticity associated changes in cortical somatosensory evoked potentials following spinal cord injury in rats

Bazley

All

Thakor

et al. 2011

2011 Annual International Conference of the IEEE Engineering in Medicine and Biology Society

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“…It has been postulated that maximal amplitude improvement in SSEP is a function of the absolute number of axons that remain intact and that cavitation prevents the endogenous regrowth of axons across the lesion site [28]. Thus, the recovery in SSEP latency in OPC treated rats may indicate that this fraction of axons, which were non-functional due to demyelination, were successfully remyelinated and their conductivity was restored to pre-injury levels.…”

Section: Discussionmentioning

confidence: 99%

Human Embryonic Stem Cell-Derived Oligodendrocyte Progenitors Aid in Functional Recovery of Sensory Pathways following Contusive Spinal Cord Injury

et al. 2012

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BackgroundTransplantations of human stem cell derivatives have been widely investigated in rodent models for the potential restoration of function of neural pathways after spinal cord injury (SCI). Studies have already demonstrated cells survival following transplantation in SCI. We sought to evaluate survival and potential therapeutic effects of transplanted human embryonic stem (hES) cell-derived oligodendrocyte progenitor cells (OPCs) in a contusive injury in rats. Bioluminescence imaging was utilized to verify survivability of cells up to 4 weeks, and somatosensory evoked potential (SSEPs) were recorded at the cortex to monitor function of sensory pathways throughout the 6-week recovery period.Principal FindingshES cells were transduced with the firefly luciferase gene and differentiated into OPCs. OPCs were transplanted into the lesion epicenter of rat spinal cords 2 hours after inducing a moderate contusive SCI. The hES-treatment group showed improved SSEPs, including increased amplitude and decreased latencies, compared to the control group. The bioluminescence of transplanted OPCs decreased by 97% in the injured spinal cord compared to only 80% when injected into an uninjured spinal cord. Bioluminescence increased in both experimental groups such that by week 3, no statistical difference was detected, signifying that the cells survived and proliferated independent of injury. Post-mortem histology of the spinal cords showed integration of human cells expressing mature oligodendrocyte markers and myelin basic protein without the expression of markers for astrocytes (GFAP) or pluripotent cells (OCT4).ConclusionshES-derived OPCs transplanted 2 hours after contusive SCI survive and differentiate into OLs that produce MBP. Treated rats demonstrated functional improvements in SSEP amplitudes and latencies compared to controls as early as 1 week post-injury. Finally, the hostile injury microenvironment at 2 hours post-injury initially caused increased cell death but did not affect the long-term cell proliferation or survival, indicating that cells can be transplanted sooner than conventionally accepted.

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“…Our SCI model has been previously described (Agrawal et al, 2008(Agrawal et al, , 2010a(Agrawal et al, , 2010bAl-Nashash et al, 2009;All et al, 2009All et al, , 2010All et al, , 2012Iyer et al, 2010;Kerr et al, 2010;Bazley et al, 2011Bazley et al, , 2012aBazley et al, , 2012b. A laminectomy was performed by removing the T8 thoracic vertebra to expose the dorsal surface of the spinal cord without opening the dura mater.…”

Section: Laminectomy and Contusion Injurymentioning

confidence: 99%

The Effects of Local and General Hypothermia on Temperature Profiles of the Central Nervous System Following Spinal Cord Injury in Rats

Bazley

Pashai²,

Kerr

et al. 2014

Therapeutic Hypothermia and Temperature Management

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Local and general hypothermia are used to treat spinal cord injury (SCI), as well as other neurological traumas. While hypothermia is known to provide significant therapeutic benefits due to its neuroprotective nature, it is unclear how the treatment may affect healthy tissues or whether it may cause undesired temperature changes in areas of the body that are not the targets of treatment. We performed 2-hour moderate general hypothermia (32°C core) or local hypothermia (30°C spinal cord) on rats that had received either a moderate contusive SCI or laminectomy (control) while monitoring temperatures at three sites: the core, spinal cord, and cortex. First, we identified that injured rats that received general hypothermia exhibited larger temperature drops at the spinal cord (-3.65°C, 95% confidence intervals [CIs] -3.72, -3.58) and cortex ( -3.64°C, CIs -3.73, -3.55) than uninjured rats (spinal cord: -3.17°C, CIs -3.24, -3.10; cortex: -3.26°C, CIs -3.34, -3.17). This was found due to elevated baseline temperatures in the injured group, which could be due to inflammation. Second, both general hypothermia and local hypothermia caused a significant reduction in the cortical temperature (-3.64°C and -1.18°C, respectively), although local hypothermia caused a significantly lower drop in cortical temperature than general hypothermia ( p < 0.001). Lastly, the rates of rewarming of the cord were not significantly different among the methods or injury groups that were tested; the mean rate of rewarming was 0.13 -0.1°C/ min. In conclusion, local hypothermia may be more suitable for longer durations of hypothermia treatment for SCI to reduce temperature changes in healthy tissues, including the cortex.

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Slope analysis of somatosensory evoked potentials in spinal cord injury for detecting contusion injury and focal demyelination

Cited by 31 publications

References 22 publications

Plasticity associated changes in cortical somatosensory evoked potentials following spinal cord injury in rats

Plasticity associated changes in cortical somatosensory evoked potentials following spinal cord injury in rats

Human Embryonic Stem Cell-Derived Oligodendrocyte Progenitors Aid in Functional Recovery of Sensory Pathways following Contusive Spinal Cord Injury

The Effects of Local and General Hypothermia on Temperature Profiles of the Central Nervous System Following Spinal Cord Injury in Rats

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