Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Pharmacological treatment of traumatic brain injury - A review of agents in development
Autore:
Hatton, J;
Indirizzi:
Univ Kentucky, Dept Pharm, Coll Pharm, Div Pharm Practice & Sci, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 ctice & Sci, Lexington, KY 40536 USA
Titolo Testata:
CNS DRUGS
fascicolo: 7, volume: 15, anno: 2001,
pagine: 553 - 581
SICI:
1172-7047(2001)15:7<553:PTOTBI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
CLOSED-HEAD INJURY; TUMOR-NECROSIS-FACTOR; FREE MAGNESIUM CONCENTRATION; FOCAL CEREBRAL-ISCHEMIA; B-2 RECEPTOR ANTAGONIST; CORTICAL IMPACT INJURY; CENTRAL-NERVOUS-SYSTEM; ACUTE-PHASE RESPONSE; CYCLOSPORINE-A; TNF-ALPHA;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
163
Recensione:
Indirizzi per estratti:
Indirizzo: Hatton, J Univ Kentucky, Dept Pharm, Coll Pharm, Div Pharm Practice & Sci,800 Rose St,RmC117, Lexington, KY 40536 USA Univ Kentucky 800 Rose St,RmC117 Lexington KY USA 40536 0536 USA
Citazione:
J. Hatton, "Pharmacological treatment of traumatic brain injury - A review of agents in development", CNS DRUGS, 15(7), 2001, pp. 553-581

Abstract

Successful treatment strategies for patients with traumatic brain injury (TBI) remain elusive despite standardised clinical treatment guidelines, improved understanding of mechanisms of cellular response to trauma, and a decade of clinical trials aimed at identifying therapeutic agents targeted at mediators of secondary injury. The information explosion relative to mechanisms of secondary injury has identified several potential targets for intervention. Depending on the typeof injury to the brain and the intensity and the success of resuscitation,necrosis, apoptosis, inflammatory and excitotoxic cellular damage can be seen. These, same processes may continue postinjury, depending on the adequacy of clinical care. Each of these mechanisms of cellular damage can initiate a cascade of events mediated by endogenous signals that lead to secondary neurological injury. Several factors contributed to the failure of earlier clinical trials. Nowthat these have been recognised, a positive impact on future drug development in TBI has been realised. Both the US and Europe have organised brain injury consortiums where experts in the treatment of TBI provide insight into study design, implementation, conduct and oversight in conjunction with the pharmaceutical industry. Consequently, future clinical trials of new investigational treatments have greater potential for identifying therapies ofmerit in specific populations of patients with TBI. Pharmacological strategies under investigation are targeting sites involved in the secondary cascade that contribute to overall poor outcome following the primary injury. These treatments include ion channel antagonists including Calcium channel antagonists, growth factors, antioxidants, stem cells, apoptosis inhibitors, and inhibitors of other signal modulators. In conclusion, the complexity of TBI pathology and the mechanisms contributing to secondary injury present unique therapeutic challenges. Appropriateresearch targets for intervention continue to be investigated, however, the likelihood of improving outcomes with a single approach is extremely small. There is a need for collaborative efforts to investigate the optimal time for drug administration and the logical sequence or combination of treatments that will ultimately lead to improved neurological outcomes in this population.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:30:21