Lenticulostriate Artery and Lenticulostriate-artery Neural Complex: New Concept for Intracerebral Hemorrhage

Curr Pharm Des. 2017;23(15):2206-2211. doi: 10.2174/1381612823666170220163750.

Abstract

Background: Spontaneous intracerebral hemorrhage (ICH) is the poorest prognosis of all stroke subtypes with a high mortality and morbidity. Although considerable progress has been made, no intervention is currently available to alter the outcome of patients with ICH, suggesting a new concept directing ICH study is urgently needed.

Methods: Most ICH occurs in the deep area of the brain, the basal ganglion, whose blood supply is mainly from lenticulostriate arteries (LSAs). Thus, we focus on ICH occurring in this deep brain area. We summarize the structural and functional features of LSAs and the deep brain, and their interactions, which is essential for the pathogenesis, pathophysiology and management of ICH.

Results: Here, we review the microanatomy, histological characters, hemodynamics and hypertensive pathology of LSAs. Especially, we look into the interactions between LSAs and their surrounding nerve tissues. The unique microanatomic, histological and hemodynamic features of LSAs underpin its high risk of rupture. The interactions between LSAs and the deep brain determine the pathophysiological process of ICH.

Conclusion: LSAs and the circumferential deep brain are an interactive and mutually affected entity. We propose a new concept called lenticulostriate-artery neural complex (LNC) to integrate the structural, functional and pathological characteristics of this area, which would be a pragmatic paradigm in directing the future basic and clinical studies on ICH.

Keywords: Intracerebral hemorrhage; hemodynamics; lenticulostriate arteries; lenticulostriate-artery neural complex; microanatomy.

Publication types

  • Review

MeSH terms

  • Animals
  • Cerebral Hemorrhage* / metabolism
  • Cerebral Hemorrhage* / pathology
  • Humans
  • Middle Cerebral Artery* / metabolism
  • Middle Cerebral Artery* / pathology
  • Neurons* / metabolism
  • Neurons* / pathology