Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies.

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Abstract Text:

Helen M Bramlett,W Dalton Dietrich,

The pathophysiology of brain and spinal cord injury (SCI) is complex and involves multiple injury mechanisms that are spatially and temporally specific. It is now appreciated that many of these injury mechanisms remain active days to weeks after a primary insult. Long-term survival studies in clinically relevant experimental studies have documented the structural changes that continue at the level of the insult as well as in remote brain structures. After traumatic brain injury (TBI), progressive atrophy of both gray and white matter structures continues up to 1 year post-trauma. Progressive changes may therefore underlie some of the long-term functional deficits observed in this patient population. After SCI, similar features of progressive injury are observed including delayed cell death of neurons and oligodendrocytes, axonal demyelination of intact fiber tracts and retrograde tract degeneration. SCI also leads to supraspinal changes in cell survival and remote brain circuitry. The progressive changes in multiple structures after brain and SCI are important because of their potential consequences on chronic or developing neurological deficits associated with these insults. In addition, the better understanding of these injury cascades may one day allow new treatments to be developed that can inhibit these responses to injury and hopefully promote recovery. This chapter summarizes some of the recent data regarding progressive damage after CNS trauma and mechanisms underlying these changes.

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Publishing Authors By Initials

HM Bramlett,WD Dietrich,

For similar nervous system diseases: central nervous system diseases: spinal cord diseases: spinal cord injuries research abstracts see: nervous system diseases: central nervous system diseases: spinal cord diseases: spinal cord injuries research

PUBMED ID PMID:

MEDLINE DATE:

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Journal Published:

PUBLICATION TYPE: Review

Journal: Progress in brain research

VOLUME: 161

Page Numbers: 125-41

Journal Abbreviation: Prog. Brain Res.

ISSN: 0079-6123

DAY: 3

MONTH: 12

YEAR: 2007

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Information

Number of References: 155

LANGUAGE: eng

NlmUniqueID: 376441

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Keywords Mesh Terms:

KEYWORDS: Spinal Cord Injuries

MESH TERMS: therapy

Chemical & Substance for Abstract: Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies.

AFFILIATION: Department of Neurological Surgery, Neurotrauma Research Center, The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 NW 14th Terrace, Miami, FL 33136, USA. hbramlett@miami.edu

Country: Netherlands

AGENCY: United States NINDS

GRANT: NS38665

ACRONYM: NS

MEDLINETA: Prog Brain Res

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies Related Publications

• Accident prevention in childhood is your problem, too.
• Activity of vitamin B12 in the growth of chicks.
• Analysis of neuroendocrine tumour metastases in the liver using contrast enhanced ultrasonography.
• Apolipoprotein E in hypercholesteremia and beyond.
• Can language-concordant prevention care managers improve cancer screening rates?
• Childhood maltreatment and revictimization:the role of affect dysregulation, interpersonal relatedness difficulties and posttraumatic stress disorder.
• Conceptual aspects of line tensions.
• Critical Casimir effect in superfluid wetting films.
• Early prediction of hypocalcemia after thyroidectomy using parathyroid hormone: an analysis of pooled individual patient data from nine observational studies.
• Effects of methylphenidate in ADHD adults on target evaluation processing reflected by event-related potentials.
• Extrinsic versus intrinsic cues in avian paraxial mesoderm patterning and differentiation.
• Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury.
• Impact of pain on the outcomes of depression treatment: Results from the RESPECT trial.
• Interplay of critical Casimir and dispersion forces.
• Motion of Nanodroplets near Edges and Wedges.
• Peptide mimotopes selected with HIV-1-blocking monoclonal antibodies against CCR5 represent motifs specific for HIV-1 entry.
• Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies.
• Restriction of Legionella pneumophila growth in macrophages requires the concerted action of cytokine and Naip5/Ipaf signalling pathways.
• Solvation of proteins: linking thermodynamics to geometry.
• Spreading in narrow channels.
• Subcellular stress response after traumatic brain injury.
• The Reacquisition of Biotin Prototrophy in Saccharomyces cerevisiae Involved Horizontal Gene Transfer, Gene Duplication and Gene Clustering.
• The p47 GTPases Igtp and Irgb10 map to the Chlamydia trachomatis susceptibility locus Ctrq-3 and mediate cellular resistance in mice.
• Therapeutic hypothermia modulates TNFR1 signaling in the traumatized brain via early transient activation of the JNK pathway and suppression of XIAP cleavage.
• Widespread cellular proliferation and focal neurogenesis after traumatic brain injury in the rat.
• [Crohn's disease and cancer risk. Incidence/prevalence, clinical characteristics, and potential prevention strategies]
• [Disability caused by affective disorders--what do the Federal German Health report data teach us?]
• [Not Available.]
• [Not Available.]
• [The depressive self, neurobiology and destiny: considerations regarding the theatre work "4.48 psychosis" by Sarah Kane]