Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, MI, USA.
Am J Physiol Endocrinol Metab. 2012 Nov 1;303(9):E1085-93. doi: 10.1152/ajpendo.00338.2012. Epub 2012 Aug 21.
Cerebral palsy (CP) is caused by an insult to or malformation of the developing brain which affects motor control centers and causes alterations in growth, development, and overall health throughout the life span. In addition to the disruption in development caused by the primary neurological insult, CP is associated with exaggerated sedentary behaviors and a hallmark accelerated progression of muscle pathology compared with typically developing children and adults. Factors such as excess adipose tissue deposition and altered partitioning, insulin resistance, and chronic inflammation may increase the severity of muscle pathology throughout adulthood and lead to cardiometabolic disease risk and/or early mortality. We describe a model of exaggerated health risk represented in adults with CP and discuss the mechanisms and secondary consequences associated with chronic sedentary behavior, obesity, aging, and muscle spasticity. Moreover, we highlight novel evidence that implicates aberrant inflammation in CP as a potential mechanism linking both metabolic and cognitive dysregulation in a cyclical pattern.
脑瘫(CP)是由发育中大脑的损伤或畸形引起的,它影响运动控制中心,并导致整个生命周期的生长、发育和整体健康的改变。除了原发性神经损伤引起的发育中断外,CP 还与过度的久坐行为以及与正常发育的儿童和成人相比标志性的肌肉病理进展加速有关。脂肪组织沉积过多和分布改变、胰岛素抵抗和慢性炎症等因素可能会增加整个成年期肌肉病理的严重程度,并导致心血管代谢疾病风险和/或早逝。我们描述了一个在 CP 成人中表现出的夸张健康风险模型,并讨论了与慢性久坐行为、肥胖、衰老和肌肉痉挛相关的机制和次要后果。此外,我们还强调了新的证据,表明 CP 中的异常炎症可能是一种潜在机制,将代谢和认知失调以循环模式联系起来。