The effect of glutamate receptor blockers on glutamate release following spinal cord injury. Lack of evidence for an ongoing feedback cascade of damage → glutamate release → damage → glutamate release → etc.

McAdoo, David J.; Hughes, Michael G.; Nie, Linghui; Shah, Bhavin; Clifton, Cannon; Fullwood, Steven D.; Hulsebosch, Claire E.

doi:10.1016/j.brainres.2005.01.024

Cited by 38 publications

(23 citation statements)

References 55 publications

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“…61,62 Several investigators have evaluated the systemic administration of riluzole in acute SCI models. [63][64][65][66][67][68][69] These studies report a significant reduction in secondary damage around the injury site, and improved functional recovery with riluzole-treated animals.…”

Section: Riluzolementioning

confidence: 84%

Emerging Repair, Regeneration, and Translational Research Advances for Spinal Cord Injury

Kwon¹,

Sekhon²,

Fehlings³

2010

Spine

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Section: Riluzolementioning

confidence: 84%

Emerging Repair, Regeneration, and Translational Research Advances for Spinal Cord Injury

Kwon¹,

Sekhon²,

Fehlings³

2010

Spine

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“…Spinal cord injury leads to increased tissue levels of excitatory amino acids and inflammatory mediators which alter dorsal horn neuron responses to cutaneous stimulation, as observed by prolonged activity following a brief stimulus and sensitivity to stimuli outside of the normal receptive field (Yezierski, 2000;McAdoo et al, 2005). These physiological changes are found in neurons distal to the injury site.…”

Section: Discussionmentioning

confidence: 99%

Expansion of formalin-evoked Fos-immunoreactivity in rats with a spinal cord injury

Castellanos

Daniels

Morales

et al. 2007

Neuroscience Research

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Peripheral tissue injury as well as spinal cord injury (SCI) may lead to sensitization of dorsal horn neurons and alterations in nociceptive processing. Thus, peripheral injuries experienced by SCI patients, even if not initially perceived, could result in a persistent and widespread activation of dorsal horn neurons and emerge as chronic pain with interventive repair or modest recovery from SCI. To visualize the spinal neuron response to peripheral tissue injury following complete SCI in rats, the neural transcription factor Fos was quantitated in the spinal cord. Two weeks following either a complete transection of the spinal cord at the level of T8 or a sham surgery (laminectomy), rats were injected with formalin into the left hind paw. Sham-operated rats demonstrated biphasic hind paw pain-related behavior following formalin injection, but transected rats displayed fewer behaviors in the second (tonic) phase. Stereological analysis of the sham group revealed that the extent of formalininduced Fos expression was within the lumbar dorsal horn, with numerous Fos-like immunoreactive profiles in the ipsilateral dorsal horn and some contralateral immunoreactive profiles. In contrast, the level of Fos-like immunoreactivity in the transected group was significantly elevated and expanded in range compared to the sham group, with increases observed in the normal laminar distribution regions, as well as multisegmentally through sacral levels and increases in the contralateral dorsal horn segments. The data demonstrate that widespread activation of spinal, especially dorsal horn, neurons following peripheral insult can occur in the injured spinal cord, despite reduced pain responsiveness, and suggests that exaggerated pain may emerge as spinal recovery or repair progresses.

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“…Stutzmann et al [56] report a combination of less white matter hemorrhage and improved somatosensory-evoked potentials in riluzole-treated animals over controls. The only negative study, reported by McAdoo et al [39], demonstrated that riluzole had no direct effect on glutamate release as measured by microdialysis. In terms of behavioral outcomes, five of eight studies reported this metric with mixed results [3,33,43,53,56].…”

Section: Questionmentioning

confidence: 95%

“…The neuroprotective agent riluzole, currently in use to treat patients with ALS, has been the focus of eight preclinical studies (Table 1) [3,33,39,43,44,53,55,56]. Its neuroprotective properties are the result of blocking voltage-sensitive sodium channels and antagonism of presynaptic calcium-dependent glutamate release.…”

Section: Questionmentioning

confidence: 99%

Spinal Cord Injury: A Systematic Review of Current Treatment Options

Cadotte

Fehlings

2011

Clinical Orthopaedics &Amp; Related Research

118

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Background Spinal cord injury (SCI) is a devastating event often resulting in permanent neurologic deficit. Research has revealed an understanding of mechanisms that occur after the primary injury and contribute to functional loss. By targeting these secondary mechanisms of injury, clinicians may be able to offer improved recovery after SCI. Questions/purposes In this review, we highlight advances in the field of SCI by framing three questions: (1) What is the preclinical evidence for the neuroprotective agent riluzole that has allowed this agent to move into clinical trials? (2) What is the preclinical evidence for Rho antagonists that have allowed this group of compounds to move into clinical trials? (3) What is the evidence for early surgical decompression after SCI?Methods We conducted a systematic review of MEDLINE and EMBASE-cited articles related to SCI to address these questions.

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The effect of glutamate receptor blockers on glutamate release following spinal cord injury. Lack of evidence for an ongoing feedback cascade of damage → glutamate release → damage → glutamate release → etc.

Cited by 38 publications

References 55 publications

Emerging Repair, Regeneration, and Translational Research Advances for Spinal Cord Injury

Emerging Repair, Regeneration, and Translational Research Advances for Spinal Cord Injury

Expansion of formalin-evoked Fos-immunoreactivity in rats with a spinal cord injury

Spinal Cord Injury: A Systematic Review of Current Treatment Options

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