Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

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Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

Xufang Ru^1,2†, Ling Gao^3†, Jiru Zhou⁴, Qiang Li^1,2, Shilun Zuo⁵, Yujie Chen^1,2*, Zhi Liu^1,2* and Hua Feng^1,2

• ¹State Key Laboratory of Trauma, Burn and Combined Injury, Department of Neurosurgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China
• ²Chongqing Key Laboratory of Precision Neuromedicine and Neuroregenaration, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China
• ³Department of General Practice, Audio-Visual Education Center, Third Military Medical University (Army Medical University), Chongqing, China
• ⁴Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
• ⁵Department of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China

Aneurysmal subarachnoid hemorrhage (SAH) is one of the special stroke subtypes with high mortality and mobility. Although the mortality of SAH has decreased by 50% over the past two decades due to advances in neurosurgery and management of neurocritical care, more than 70% of survivors suffer from varying degrees of neurological deficits and cognitive impairments, leaving a heavy burden on individuals, families, and the society. Recent studies have shown that white matter is vulnerable to SAH, and white matter injuries may be one of the causes of long-term neurological deficits caused by SAH. Attention has recently focused on the pivotal role of white matter injury in the pathophysiological processes after SAH, mainly related to mechanical damage caused by increased intracerebral pressure and the metabolic damage induced by blood degradation and hypoxia. In the present review, we sought to summarize the pathophysiology processes and mechanisms of white matter injury after SAH, with a view to providing new strategies for the prevention and treatment of long-term cognitive dysfunction after SAH.

Introduction

Aneurysmal subarachnoid hemorrhage (SAH) is one of the special stroke subtypes with high mortality and mobility. Neurosurgical clipping or endovascular coiling is highly recommended for the early repair of ruptured aneurysms (1), focusing the medical management of SAH patients on early brain injury and delayed cerebral ischemia (2). However, more than 70% of survivors suffer from varying degrees of neurological deficits and cognitive impairments, leaving a heavy burden on individuals, families, and the society (3). Compared with cohorts with unruptured intracranial aneurysm, patients with aneurysmal SAH have higher mean diffusivity in white matter, leading to cognitive impartment 3 months after SAH onset (4). Apparently, the mammillothalamic tract is more vulnerable than the corticospinal tract in SAH patients with a good Glasgow Outcome Scale at 3 months after ictus (5), which demonstrates a correlation between early brain injury and long-term cognitive dysfunction after SAH.

White matter contains most of the volume of human brain and is made up of neural axons and myelin sheath. As early as 1989, the autopsy of six SAH cases had reported the remarkable hyperemia and edema in the deep frontal white matter, with microscopic axonal degeneration (6). Despite that enormous progresses have been made in the pathophysiology of early brain injury after SAH, the mechanisms of white matter injury are still a blur (7). Unlike intracerebral hemorrhage and traumatic brain injury, most SAH patients, especially those without obvious hematoma volume, do not usually fracture the nervous tract due to primary mechanical stress but suffer with remarkable secondary brain injury and neurological deficits. Mechanical pressure due to increased intracerebral pressure, glial response, and ischemia is considered as the pivotal mechanism of white matter injury after SAH but lacks high-quality clinical and basic research evidence (7).

In the present review, we sought to summarize the pathophysiology processes and mechanisms of white matter injury after SAH, with a view to providing new strategies for the prevention and treatment of long-term cognitive dysfunction after SAH.

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