Recovery of function after brain damage: Facilitation by the calcium entry blocker nimodipine.

LeVere, T. E.; Brugler, T.; Sandin, M.; Gray-Silva, Susan

doi:10.1037/0735-7044.103.3.561

Cited by 42 publications

(13 citation statements)

References 16 publications

(31 reference statements)

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“…Nimodipine administration has also been reported to reverse trauma-induced retrograde amnesia following bilateral aspiration of the visual neocortex in rats (LeVere et al, 1989) and to dilate pial arterioles and induce angiogenesis in rat cortex (Yuan et al, 1990). Dihydropyridine calcium channel blockers have recently been evaluated in a series of clinical trials in TBI.…”

Section: Calcium Channel Blockersmentioning

confidence: 98%

Novel Pharmacologic Strategies in the Treatment of Experimental Traumatic Brain Injury: 1998

McIntosh¹,

Juhler²,

Wieloch³

1998

Journal of Neurotrauma

291

143

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The mechanisms underlying secondary or delayed cell death following traumatic brain injury are poorly understood. Recent evidence from experimental models suggests that widespread neuronal loss is progressive and continues in selectively vulnerable brain regions for months to years after the initial insult. The mechanisms underlying delayed cell death are believed to result, in part, from the release or activation of endogenous "autodestructive" pathways induced by the traumatic injury. The development of sophisticated neurochemical, histopathological and molecular techniques to study animal models of TBI have enabled researchers to begin to explore the cellular and genomic pathways that mediate cell damage and death. This new knowledge has stimulated the development of novel therapeutic agents designed to modify gene expression, synthesis, release, receptor or functional activity of these pathological factors with subsequent attenuation of cellular damage and improvement in behavioral function. This article represents a compendium of recent studies suggesting that modification of post-traumatic neurochemical and cellular events with targeted pharmacotherapy can promote functional recovery following traumatic injury to the central nervous system.

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Section: Calcium Channel Blockersmentioning

confidence: 98%

Novel Pharmacologic Strategies in the Treatment of Experimental Traumatic Brain Injury: 1998

McIntosh¹,

Juhler²,

Wieloch³

1998

Journal of Neurotrauma

291

143

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“…Similar results were obtained when the hypoxic insult was replaced with a hypoglycemic one (Schurr et al, 1990;1991a). Other recent studies have shown partial success in protecting brain tissue in vivo against hypoxicischemic or other cell injury by calcium antagonists such as (S)-emopamil (Ginsberg et al, 1991) and nimodipine, nicardipine, or isradipine (Bunnell et al, 1987;Grotta et al, 1988;Hadani et al, 1988;LeVere et al, 1989;Sauter et al, 1988;Sauter and Rudin, 1990;Greenberg et al, 1991; see also a review by Horowitz and Powell, 1989). In an immunocytochemical study, Leranth and Ribak (1991) showed that calcium-binding proteins are concentrated in the hippocampal CA2 region, which may explain this region's high resistance to epileptic damage and other damage-causing insults such as hypoxia and ischemia.…”

Section: Calcium and Cerebral Hypoxic-ischemic Damagementioning

confidence: 55%

The mechanism of cerebral hypoxic‐ischemic damage

Schurr

Rigor

1992

Hippocampus

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The four most prominent hypotheses on the cellular processes leading to hypoxic-ischemic neuronal damage or death are (1) the lactacidosis hypothesis, (2) the calcium overload hypothesis, (3) the excitotoxic hypothesis, and (4) the oxygen-free radical hypothesis. The authors comment on the evidence in favor of and against each in an attempt to select the one hypothesis that best explains the mechanism of cerebral hypoxic-ischemic damage while withstanding the scrutiny of scientific testing. A major part of this inquiry is derived from in vitro studies that are suited to mechanistic exploration. They conclude that the calcium overload hypothesis is the best qualified in this respect. It is important to note, however, that some of the other hypothetical mechanisms may play a secondary role in exacerbating neuronal damage by accelerating calcium influx and overload.

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“…Clinical trials in TBI suggest that some benefit is seen in the subgroup of patients that are younger and those with traumatic subarachnoid hemorrhage (tSAH) [180]. In animal studies these agents have been shown to improve regional CBF, decrease cerebral edema, prevent injury related amnesia, improve recovery of passive learning and lessen motor deficits [181][182][183]. Unfortunately, a recent European multicenter clinical trial found no significant benefit in the use of nimodipine in TBI patients, but there was a trend towards benefit in the subgroup with tSAH [184].…”

Section: Receptor Channelsmentioning

confidence: 99%

Outcome from traumatic brain injury

Jallo¹,

Shutter²

1998

Trauma Quarterly

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Traumatic brain injury (TBI) continues to be a significant public health issue. Advances in acute medical care after brain injury have improved mortality, but the morbidity from residual neurological deficits remains high. Multiple variables have been shown to have an impact on the outcome from TBI and, although many of these factors are not modifiable, a number of them can be influenced by medical interventions. Multidimensional assessments of the early clinical findings can provide some predictions regarding the potential for recovery after TBI. In addition, an awareness of the modifiable factors may assist with the prevention of secondary injury and optimization of the long-term outcome. Certain neurodiagnostic studies can be used to supplement the patients' physical findings and help guide medical management. Finally, rehabilitation services have documented benefit in the TBI population and are being initiated earlier in the course of medical care. This article attempts to review many of these variables and provide information on the clinical outcomes following TBI.

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Recovery of function after brain damage: Facilitation by the calcium entry blocker nimodipine.

Cited by 42 publications

References 16 publications

Novel Pharmacologic Strategies in the Treatment of Experimental Traumatic Brain Injury: 1998

Novel Pharmacologic Strategies in the Treatment of Experimental Traumatic Brain Injury: 1998

The mechanism of cerebral hypoxic‐ischemic damage

Outcome from traumatic brain injury

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