Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
VASCULAR MECHANISMS IN THE PATHOPHYSIOLOGY OF HUMAN SPINAL-CORD INJURY
Autore:
TATOR CH; KOYANAGI I;
Indirizzi:
TORONTO HOSP,WESTERN DIV,DIV NEUROSURG,CANADIAN PARAPLEG ASSOC SPINALCORD INJURY RES LAB TORONTO ON M5T 2S8 CANADA TORONTO HOSP,WESTERN DIV,PLAYFAIR NEUROSCI UNIT TORONTO ON M5T 2S8 CANADA UNIV TORONTO TORONTO ON CANADA
Titolo Testata:
Journal of neurosurgery
fascicolo: 3, volume: 86, anno: 1997,
pagine: 483 - 492
SICI:
0022-3085(1997)86:3<483:VMITPO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-FLOW PATTERNS; TRAUMATIC PARAPLEGIA; RAT; MICROANGIOGRAPHY; MICROVASCULATURE; ANGIOGRAPHY; TRANSITORY; MYELOPATHY; SECONDARY; EMPHASIS;
Keywords:
ACUTE SPINAL CORD INJURY; VASCULAR LESION; PATHOLOGY; HUMANS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
C.H. Tator e I. Koyanagi, "VASCULAR MECHANISMS IN THE PATHOPHYSIOLOGY OF HUMAN SPINAL-CORD INJURY", Journal of neurosurgery, 86(3), 1997, pp. 483-492

Abstract

Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3-5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was noevidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3-9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins bythe initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/07/20 alle ore 22:20:34