The effects of PBN (phenyl-butyl-nitrone) on GLT-1 levels and on the extracellular levels of amino acids and energy metabolites in a model of iron-induced posttraumatic epilepsy

Samuelsson, Christina; Kumlien, Eva; Elfving, Åse; Lindholm, Dan; Ronne-Engström, Elisabeth

doi:10.1016/j.eplepsyres.2003.09.004

Cited by 20 publications

(14 citation statements)

References 36 publications

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“…However, administration of only the ROS scavenger and nitrone spin trap agent S-PBN, did not separately affect iNOS or eNOS/nNOS activity (-6.9%, non-significant and +9.8%, non-significant, respectively), nor did it influence iNOS immunoreactivity. This indicated that S-PBN, in contrast to PBN (Samuelsson et al 2003) was not an efficient NOSinhibitor. Accordingly, the NOS-activity inhibition demonstrated by the combined treatment was related to L-NAME.…”

Section: Nos Inhibition In Combination With a Ros-scavenger (Iii)mentioning

confidence: 92%

Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine

Gahm

Holmin

Rudehill

et al. 2005

Acta Neurochir (Wien)

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The findings underscored that an early neuroprotective effect does not necessarily lead to increased long-term neuronal survival. The absence of a significant long-term effect with nimodipine and dexamethasone agrees with clinical studies. Colchicine with an anti-macrophage/anti-inflammatory activity and the free radical scavenger tirilazad mesylate were effective for amelioration of experimental contusion with moderate energy transfer. Early neuroprotection may to some extent target iNOS via different pathways since all tested drugs affected both iNOS expression and neuronal degeneration.

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Section: Nos Inhibition In Combination With a Ros-scavenger (Iii)mentioning

confidence: 92%

Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine

Gahm

Holmin

Rudehill

et al. 2005

Acta Neurochir (Wien)

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“…This finding is not surprising. Epileptogenesis after TBI appears to be a very complex and still unclear process; a wide spectrum of factors possibly involved is under investigation at macroscopic, microscopic, and molecular levels (30)(31)(32)(33)(34)(35). Although the cohort studied was initially selected with regard to risk factors for epilepsy, individual factors that might play a role cannot be excluded.…”

Section: Discussionmentioning

confidence: 99%

Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

et al. 2005

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Summary:Purpose: Evaluation of morphologic risk factors for posttraumatic epilepsy (PTE) by using brain magnetic resonance imaging (MRI) in serial assessments ≤2 years after traumatic brain injury (TBI).Methods: Brain MRI hyperintense (gliosis) or hypointense (hemosiderin) areas or both were assessed in the images of 135 adult TBI inpatients who completed a 2-year clinical, EEG, and MRI study protocol. Overall clinical follow-up for the development of PTE was 5-10 years (median, 102 months). Morphologic risk factors for PTE were evaluated by using Kaplan-Meier curves and Cox regression analysis.Results: In 20 patients, PTE developed. Kaplan-Meier curves showed that gliomesenchymal sequelae of focal brain lesions (subdural hematomas/contusions) that required surgical treatment (sSDH-C) were a PTE risk factor (p < 0.001), as were sequelae of nonsurgical hemorrhagic contusions with gliosis wall incompletely surrounding hemosiderin dregs (IW) (p = 0.039) and mainly those with time-related changes from incomplete to complete gliosis wall around hemosiderin (I/CW) (p = 0.005); those with early hemosiderin completely surrounded by gliosis (CW) were not (p = 0.821). Cox regression analysis showed that for patients with sequelae of sSDH-C, the PTE risk was 4.38 (p = 0.023) times higher than for those who did not require surgical treatment or underwent surgery because of purely extradural hematoma; for those with IW and I/CW lesions, considered pooled, it was 6.61 times higher (p = 0.014) than for those with CW lesions.Conclusions: MRI follow-up examination in the early chronic stage can differentiate among low-, intermediate-, and high-risk sequelae of TBI. These findings yield new evidence for, but do not resolve, the debate on posttraumatic epileptogenesis. Key Words: Posttraumatic epilepsy-Brain MRI-HemosiderinGliosis.Risk factors for posttraumatic epilepsy (PTE) are still debated; however, the extensive use of computed tomography (CT) scanning in patients with traumatic brain injury (TBI) has confirmed the important role of documented focal brain lesions not only in military, but also in civilian TBI (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). This means that a precise neuroradiologic diagnosis is of paramount value in determining the individual PTE risk.Magnetic resonance imaging (MRI) has become the imaging method of choice for evaluation of TBI patients in the chronic stage because of its exquisite capability in showing posttraumatic brain abnormalities, provided that the appropriate pulse sequences are used. However, the relation between PTE and brain damage as revealed by MRI has not been established (18). A few years ago, our group participated in a joint prospective longitudinal study to evaluate risk factors for PTE in adults by using clini-

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“…Superoxide has been shown to increase the function of excitatory synapses as a messenger molecule in the neuronal processes of long-term potentiation (LTP) [48,49]. Melatonin, phenylbutylnitrone and edaravone, free radical scavengers, have protective effects against TBI via scavenging ROS and reactive nitrogen species (RNS) [29,[50][51][52]. It has been demonstrated that mild hypothermia (32-34°C) reduces post-traumatic neuronal disturbance by suppressing the production of superoxide and NMDA receptor-mediated nitric oxide (NO) production [53][54][55].…”

Section: Discussionmentioning

confidence: 99%

Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

et al. 2009

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The effects of PBN (phenyl-butyl-nitrone) on GLT-1 levels and on the extracellular levels of amino acids and energy metabolites in a model of iron-induced posttraumatic epilepsy

Cited by 20 publications

References 36 publications

Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine

Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine

Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

Mild Hypothermia Prevents Post-Traumatic Hyperactivity of Excitatory Synapses in Rat Hippocampal CA1 Pyramidal Neurons

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