Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI Scientific Reports volume 7, Article number: 3805 (2017) Huajun Tan, Weijian Yang, Chenggang Wu, Baolong Liu, Hao Lu, Hong Wang & Hua Yan
Abstract
In recent years, hypopituitarism caused by traumatic brain injury (TBI) has been explored in many clinical studies; however, few studies have focused on intracranial hypertension and stress caused by TBI. In this study, an intracranial hypertension model, with epidural hematoma as the cause, was used to explore the physiopathological and neuroendocrine changes in the hypothalamic–pituitary axis and hippocampus. The results demonstrated that intracranial hypertension increased the apoptosis rate, caspase-3 levels and proliferating cell nuclear antigen (PCNA) in the hippocampus, hypothalamus, pituitary gland and showed a consistent rate of apoptosis within each group. The apoptosis rates of hippocampus, hypothalamus and pituitary gland were further increased when intracranial pressure (ICP) at 24 hour (h) were still increased. The change rates of apoptosis in hypothalamus and pituitary gland were significantly higher than hippocampus. Moreover, the stress caused by surgery may be a crucial factor in apoptosis. To confirm stress leads to apoptosis in the hypothalamus and pituitary gland, we used rabbits to establish a standard stress model. The results confirmed that stress leads to apoptosis of neuroendocrine cells in the hypothalamus and pituitary gland, moreover, the higher the stress intensity, the higher the apoptosis rate in the hypothalamus and pituitary gland.
Hypercapnia can also lead to intracranial hypertension and suggests that a fairly rigid, unresponsive respiratory rate could also result in dysfunction and mechanical stress to parts of the hypothalamus and pituitary gland. Increased pressure causes physical stress, pushing on brain tissues located on the surface and in the centre of the brain, possibly in a fairly stereotypical manner, depending on the locations being squeezed.
It would be cool to make a computer program to simulate the effects of pressure mounting on brain tissues on the surfaces and in the folds.
Pressure from hypercapnia and pressure due to TBI are likely to be different. TBI’s are abrupt and violent in their effects where as hypercapnia will produce a gradual change to the brain as the pressure increases slowly.
Computer simulation of these effects should inform us about hormonal and behavioural responses to being physically prodded and pushed. Dr Penfield already taught us a lot about electrical stimulation of different parts of the brain, now would be a good time to look at how mechanical pressure might produce a response involving hormone release and possibly affecting motor behaviour.
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Of Sound Mind 