Abstract
Lumbar spinal stenosis (LSS) is a common neurodegenerative condition. However, how neurogenic claudication develops with severe leg pain has not yet been clearly elucidated. Moreover, cerebrospinal fluid (CSF) physiology at the lumbosacral level is poorly understood because of the difficulties involved in quantification and visualization. Recent studies have suggested that assessment of mitochondrial function in CSF provides an indirect way to assess neurological disorders and an important feature of disease progression. In this study, we assessed the relevance of endogenous extracellular mitochondria in the CSF of rats after LSS. Mitochondrial changes within the CSF were analyzed following LSS at 1 week using flow cytometry. An increase in cell size and number was observed in CSF with LSS, and reactive oxygen species (ROS) levels were also increased within the CSF at 1 week in the LSS group. Elevated mitochondrial ROS and functional changes in the CSF are hallmarks of LSS. The present study is the first to demonstrate that elevated mitochondrial ROS within the CSF is a new index for the early detection of LSS. Moreover, it may represent a potential novel treatment target for LSS.
Highlights
Cerebrospinal fluid (CSF) can be used for the early diagnosis of changed pathophysiological states of various conditions and as a therapeutic indicator [1]
Existing clinical studies have reported a correlation between CSF dynamics and the pathogenesis of lumbar spinal stenosis (LSS)
dichlorofluorescin diacetate (DCFDA) with that in the sham group
Summary
Cerebrospinal fluid (CSF) can be used for the early diagnosis of changed pathophysiological states of various conditions and as a therapeutic indicator [1]. Existing clinical studies have reported a correlation between CSF dynamics and the pathogenesis of lumbar spinal stenosis (LSS). The sacral CSF flow after walking was barely detectable in LSS patients, and the peak flow velocity was slower in LSS patients than healthy controls. This change in CSF dynamics can be suggested as a test method for early diagnosis in the prediction of neurological signs of LSS, including claudication, but it is not specific enough to present a therapeutic target and is not sufficient as relevant evidence. Studies on neurological diseases related to CSF have mainly analyzed mitochondria [5,6,7,8]
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