White Matter Injury and Recovery after Hypertensive Intracerebral Hemorrhage

Abstract

Hypertensive intracerebral hemorrhage (ICH) could very probably trigger white matter injury in patients. Through the continuous study of white matter injury after hypertensive ICH, we achieve a more profound understanding of the pathophysiological mechanism of its occurrence and development. At the same time, we found a series of drugs and treatment methods for the white matter repair. In the current reality, the research paradigm of white matter injury after hypertensive ICH is relatively obsolete or incomplete, and there are still lots of deficiencies in the research. In the face of the profound changes of stroke research perspective, we believe that the combination of the lenticulostriate artery, nerve nuclei of the hypothalamus-thalamus-basal ganglia, and the white matter fibers located within the capsula interna will be beneficial to the research of white matter injury and repair. This paper has classified and analyzed the study of white matter injury and repair after hypertensive ICH and also rethought the shortcomings of the current research. We hope that it could help researchers further explore and study white matter injury and repair after hypertensive ICH.

Minocycline reduces intracerebral hemorrhage–induced white matter injury in piglets

“…Brain neuroinflammation occurs after experimental ICH and causes secondary brain injury, including brain edema, neuronal death, brain atrophy, and poor neurological outcomes . WM injury, known to be a frequent complication of ICH, is one consequence of the inflammatory response induced by blood components and metabolites . The present study showed that minocycline confers protection against hemorrhagic WM injury in a mammal model and discovered a potential mechanism for this protection via the TGF‐β/MAPK signaling pathway.…”

“…Thus, WM injury reflects the brain's vulnerability to further insult and predicts poor outcomes after ICH. [4][5][6] Our previous work has shown that ICH-induced iron toxicity causes WM injury through c-Jun N-terminal kinase (JNK) and receptor-interacting protein kinase 1 (RIPK1) activation. 7 Because of white matter's critical role in neurotransmission, WM injury may also lead to severe sensorimotor dysfunction, neurobehavioral impairment, and cognitive disorders.…”

“…White matter fibers, including the corpus callosum, internal capsule, anterior commissure, and striatum bundles, are highly vulnerable to additional injury in ICH patients. Thus, WM injury reflects the brain's vulnerability to further insult and predicts poor outcomes after ICH . Our previous work has shown that ICH‐induced iron toxicity causes WM injury through c‐Jun N‐terminal kinase (JNK) and receptor‐interacting protein kinase 1 (RIPK1) activation .…”

Oligodendrocytes in intracerebral hemorrhage

“…As the cell type that contains a high level of iron in the CNS, oligodendrocytes are very sensitive to iron overload and thus particularly susceptible to ICH injury. It has been reported that ICH induces oligodendrocyte death and demyelination in white matter, where functional and morphological maintenance is highly dependent on oligodendrocytes and their myelin sheaths …”

“…It has been reported that ICH induces oligodendrocyte death and demyelination in white matter, 105,106 where functional and morphological maintenance is highly dependent on oligodendrocytes and their myelin sheaths. 107 How do oligodendrocytes die after ICH? On the one hand, there is evidence suggesting that apoptosis is responsible for oligodendrocyte death after ICH.…”