Traumatic brain injury-induced cerebral microbleeds in the elderly
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REVIEW
Traumatic brain injury-induced cerebral microbleeds in the elderly Luca Toth & Andras Czigler & Peter Horvath & Balint Kornyei & Nikolett Szarka & Attila Schwarcz & Zoltan Ungvari & Andras Buki & Peter Toth
Received: 16 June 2020 / Accepted: 23 September 2020 # The Author(s) 2020
Abstract Traumatic brain injury (TBI) was shown to lead to the development of cerebral microbleeds (CMBs), which are associated with long term cognitive decline and gait disturbances in patients. The elderly is one of the most vulnerable parts of the population to suffer TBI. Importantly, ageing is known to exacerbate microvascular fragility and to promote the formation of CMBs. In this overview, the effect of ageing is L. Toth : A. Czigler : P. Horvath : A. Schwarcz : A. Buki : P. Toth (*) Department of Neurosurgery, University of Pecs, Medical School, 2 Ret Street, Pecs 7624, Hungary e-mail: [email protected] e-mail: [email protected] L. Toth : A. Czigler : N. Szarka : P. Toth Institute for Translational Medicine, University of Pecs, Medical School, Pecs, Hungary
discussed on the development and characteristics of TBI-related CMBs, with special emphasis on CMBs associated with mild TBI. Four cases of TBI-related CMBs are described to illustrate the concept that ageing exacerbates the deleterious microvascular effects of TBI and that similar brain trauma may induce more CMBs in old patients than in young ones. Recommendations are made for future prospective studies to establish the mechanistic effects of ageing on the formation of CMBs after TBI, and to determine long-term consequences of CMBs on clinically relevant outcome measures including cognitive performance, gait and balance function. Keywords Microbleed . Cerebral microhaemorrhage . Brain trauma . Mild traumatic brain injury . Ageing . Vascular changes
Introduction B. Kornyei Department of Radiology, University of Pecs, Medical School, Pecs, Hungary Z. Ungvari : P. Toth Reynolds Oklahoma Center on Aging, Department of Biochemistry, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA Z. Ungvari : P. Toth Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary P. Toth MTA-PTE Clinical Neuroscience MR Research Group, Pecs, Hungary
Traumatic brain injury (TBI) is a serious health problem worldwide [1, 2]. In addition to its acute clinical significance, TBI was shown to lead to chronic neurological dysfunction (including long-term impairment of gait and cognition) and to promote psychiatric disorders [3, 4]. After the direct neuronal damage caused by the impact, a divergent process is initiated resulting in secondary injury of neuroglial tissue [2, 3, 5–9]. Injury of cerebral vessels and cerebrovascular dysfunction play a central role in the pathological processes of secondary injury [7, 8, 10, 11]. After mild, moderate and severe TBI mitochondrial dysfunction, oxidative stress and
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redox-dependent activation of matrix metalloproteinases (MMP) are enhanced, contributing to the damage of the microvascular
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