Rats with chronic spinal cord transection as a possible model for the at-level pain of paraplegic patients

Scheifer, Caroline; Hoheisel, Ulrich; Trudrung, P.; Unger, Thomas; Mense, Siegfried

doi:10.1016/s0304-3940(02)00116-7

Cited by 20 publications

(14 citation statements)

References 15 publications

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“…In addition, changes in supraspinally mediated behaviors, such as activity levels and exploratory behaviors, have been linked with moderate contusion spinal injury [146] and are relevant to similar reports of decreased activity with pain after human SCI [147]. In an unusual animal model that combines both moderate contusion and complete spinal transection [41], electrophysiologic recording of dorsal neurons immediately rostral to the injury demonstrated that the SCI caused abnormal discharge frequency with mechanical stimulation, in addition and related to autotomy and excessive grooming, the onset of which was delayed.…”

Section: At-level Models Of Central Painmentioning

confidence: 76%

“…Without complete spinal transections, animals recover most motor function, a situation not seen in humans, where even partial spinal lesions often lead to chronic spasticity [38]. However, complete transection results in an animal that requires at least daily bowel and bladder expression, and often results in myriad postsurgical complications and morbidity, such as autonomic dysreflexia, cystitis, skin and gastric lesions, and autotomy [39][40][41][42]. Studies with the rat as the model animal have usually involved hemisections, partial transections [36], or contusion injuries [37], all injuries similar to those used in studies of spasticity in the cat [32][33][34]43].…”

Section: Animal Models For Spasticitymentioning

confidence: 99%

“…However, contusion injury and central cord lesions have demonstrated lowered thresholds for nocifensive behavior with stimulation of at-level dermatomes and tactile allodynia in skin responses [138,139], and in a few cases, use of paw withdrawal responses or vocalization to paw pressure in a moderate contusion [139][140][141]. Both contusion and transection have better used biochemical and electrophysiologic methods to assess markers of at-level neuropathic pain [41,[142][143][144][145]. In addition, changes in supraspinally mediated behaviors, such as activity levels and exploratory behaviors, have been linked with moderate contusion spinal injury [146] and are relevant to similar reports of decreased activity with pain after human SCI [147].…”

Section: At-level Models Of Central Painmentioning

confidence: 99%

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Common animal models for spasticity and pain

Eaton¹

2003

JRRD

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Abstract-Animal models of spasticity and pain have allowed for the elucidation of possible mechanisms and the evaluation of potential therapeutic interventions for these serious clinical problems. Each model mirrors the clinical appearance of many features of the syndrome, but few reproduce the myriad patient reports of either intensity or relevant contributing factors, especially in models of chronic neuropathic pain. Often these models have been used to predict the potency and efficacy of pharmacologic agents that work in human pain states. Pain models have relied on measurements of the shifts in behavioral hypersensitivity to tactile and thermal stimuli, tests that are not used quantitatively in human patients. Even with the multiple peripheral and central models of spasticity and pain used in animals, only a few actually test human conditions: namely, diabetic neuropathy, chemotherapy, and immunotherapy for tumors. However, all these models have allowed for the comparison of certain behavioral, cellular, biochemical, and molecular mechanisms with human patient populations. Here we review the few extant models of spasticity, nerve injury, and central injury models of pain, and describe their features and use.

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Section: At-level Models Of Central Painmentioning

confidence: 76%

Section: Animal Models For Spasticitymentioning

confidence: 99%

Section: At-level Models Of Central Painmentioning

confidence: 99%

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Common animal models for spasticity and pain

Eaton¹

2003

JRRD

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“…In vivo electrophysiological studies demonstrate that hyperexcitable neurons show enhanced response properties, including evoked and spontaneous activities and afterdischarges in spinal dorsal horn neurons following SCI [3][4][5]. Neuronal hyperexcitability triggers sensitizations of spinal dorsal horn neurons followed by the development and the maintenance of central neuropathic pain-like outcomes, such as mechanical allodynia and hyperalgesia [3,6].…”

Section: Introductionmentioning

confidence: 99%

Bilateral hyperexcitability of thalamic VPL neurons following unilateral spinal injury in rats

Gwak

Kim

et al. 2009

J Physiol Sci

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In the present study, we have examined whether spinal hemisection injury induces changes in the electrophysiological properties of thalamic ventral posteriorlateral (VPL) neurons in rats. Male Sprague-Dawley rats were subjected to unilateral spinal cord injury by transverse hemisection at the T13 spinal segment. Four weeks after the T13 spinal hemisection, the injured rats displayed robust allodynic behaviors on both sides of hindpaws compared to sham controls (P < 0.05). Extracellular recordings taken 4 weeks after the hemisection revealed that wide dynamic range (WDR) neurons had significantly increased spontaneous and brush-, pressure-, and pinch-evoked activities, respectively, on both sides of the thalamic VPL regions (P < 0.05). In contrast, low threshold (LT) neurons showed only an increase in the brush-evoked activity compared to sham controls (P < 0.05). However, afterdischarge activity in both types of neurons showed no changes. In addition, both sides of the thalamic VPL regions showed higher incidences of WDR neurons. In conclusion, our data demonstrate that spinal unilateral injury induces bilaterally increased evoked activity in thalamic VPL neurons.

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“…These spinal injuries are complex, often resulting in the tearing, or avulsion, of ventral and/or dorsal roots from the transitional zone interface between the central and peripheral nervous systems (CNS/PNS) (Moschilla et al, 2001, Hans et al, 2004. Neuropathic pain resulting from these types of injuries can extend one or two segments rostral to the level of injury, and is often referred to as at-level pain (Scheifer et al, 2002, Oatway et al, 2004, Siddall and Middleton, 2006.…”

Section: Introductionmentioning

confidence: 99%

At-level neuropathic pain is induced by lumbosacral ventral root avulsion injury and ameliorated by root reimplantation into the spinal cord

Bigbee

Hoang

Havton

2007

Experimental Neurology

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Neuropathic pain is common after traumatic injuries to the cauda equina/conus medullaris and brachial plexus. Clinically, this pain is difficult to treat and its mechanisms are not well understood. Lesions to the ventral roots are common in these injuries, but are rarely considered as potential contributors to pain. We examined whether a unilateral L6-S1 ventral root avulsion (VRA) injury in adult female rats might elicit pain within the dermatome projecting to the adjacent, uninjured L5 spinal segment. Additionally, a subset of subjects had the avulsed L6-S1 ventral roots reimplanted (VRA+Imp) into the lateral funiculus post-avulsion to determine whether this neural repair strategy elicits or ameliorates pain. Behavioral tests for mechanical allodynia and hyperalgesia were performed weekly over 7 weeks post-injury at the hind paw plantar surface. Allodynia developed early and persisted post-VRA, whereas VRA+Imp rats exhibited allodynia only at 1 week postoperatively. Hyperalgesia was not observed at any time in any experimental group. Quantitative immunohistochemistry showed increased levels of inflammatory markers in laminae III-V and in the dorsal funiculus of the L5 spinal cord of VRA, but not VRA+Imp rats, specific to areas that receive projections from mechanoreceptive, but not nociceptive, primary afferents. These data suggest that sustained at-level neuropathic pain can develop following a pure motor lesion, whereas the pain may be ameliorated by acute root reimplantation. We believe that our findings are of translational research interest, as root implantation surgery is emerging as a potentially useful strategy for the repair of cauda equina/conus medullaris injuries.

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Rats with chronic spinal cord transection as a possible model for the at-level pain of paraplegic patients

Cited by 20 publications

References 15 publications

Common animal models for spasticity and pain

Common animal models for spasticity and pain

Bilateral hyperexcitability of thalamic VPL neurons following unilateral spinal injury in rats

At-level neuropathic pain is induced by lumbosacral ventral root avulsion injury and ameliorated by root reimplantation into the spinal cord

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