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Modeling Steady State Intracranial Pressures in Microgravity

This study explores the causes of Space Adaptation Sickness (SAS) by investigating the possible role of elevated intracranial pressure (ICP) in microgravity. Mathematical modeling is used to examine the relationship between ICP, blood-brain barrier function, and other physiological changes that occur during spaceflight. The results suggest that microgravity may not initiate intracranial hypertension, but potential alterations in the blood-brain barrier may contribute to SAS symptoms. Further research is needed to fully understand the mechanisms behind SAS.

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Modeling Steady State Intracranial Pressures in Microgravity

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  1. Modeling Steady State Intracranial Pressures in Microgravity • Scott A Stevens, PhD • Penn State Erie • William D Lakin, PhD • The University of Vermont • Paul L Penar, MD • The University of Vermont

  2. Motivation • Many astronauts experience symptoms of Space Adaptation Sickness during the first few hours or days of spaceflight. • The cause of all symptoms is not well understood. • We are investigating possible causes via mathematical modeling.Are some symptoms of SAS caused by elevated intracranial pressure (ICP)?

  3. Your Brain

  4. Cerebrospinal Fluid (CSF)

  5. A diagram of the lumped-parameter model

  6. Assumption 1: Fluid flow is driven by pressure

  7. Example: Flow from the capillaries to the veins

  8. Filtration across the blood-brain barrier (BBB) The Starling Landis Equation:

  9. The Starling Landis Equation: = Filtration across the blood-brain barrier = Hydrostatic pressure difference = Colloid osmotic pressure difference = Filtration Coefficient = Reflection Coefficient

  10. Colloid Osmotic Pressure

  11. Volume changes are accommodated via compliance terms

  12. Assumption 2: Volume changes are proportional to pressure difference changes

  13. Example:

  14. Conservation of Mass - Focus on Compartments I,C,S,F,T,B

  15. Example: Ventricular CSF Compartment (F) Rate of Volume Change = flow in – flow out

  16. Doing this in each compartment yields: where

  17. The resulting system; has a unique steady state P* defined by and all solutions tend to P*.

  18. Results • Intracranial pressures (PF and PB) change in parallel with the changes in central venous pressure (PV). • Intracranial pressures increase 0.37 mmHg for every one mmHg decrease in blood colloid osmotic pressure.

  19. Conclusions: • Microgravity probably does not initiate intracranial hypertension. • The intracranial pressure (ICP) in microgravity may be less than that experienced lying down on earth. • The sickness associated with microgravity is probably not due to intracranial hypertension unless microgravity alters additional physiology.

  20. Consider possible alterations in the blood-brain barrier (BBB) in space. Possible Causes: • The lack of orthostatic pressure in microgravity. • Radiation effects above low earth orbit

  21. CapillaryMembraneon Earth: Tight Proposed CapillaryMembranein Space: Leaky

  22. Radiation effects on the BBB • Leszczynski et al [1,2] (2002, 2004)- Cell phone radiation levels caused increases in the protein expression of hsp27 and p38MAPK in human endothelial cells.- It is hypothesized [1] that activation of hsp27 may cause an increase in blood-brain barrier permeability. • Radiation exposure in space appears capable of adversely impacting the integrity of the blood-brain barrier.

  23. A “leaky” blood-brain barrier is modeled in QCB by either • An increase in the filtration coefficientor • A decrease in the reflection coefficient

  24. More leaky With Normal BBB 6.3 mmHg drop in blood colloid osmotic pressure No change in central venous pressure

  25. Conclusions • If there is no alteration in the blood-brain barrier, it seems unlikely that ICP in microgravity is significantly higher than that experienced lying down on earth. • If the integrity of the barrier is reduced in microgravity then it is possible that intracranial hypertension causes some of the symptoms of Space Adaptation Sickness

  26. References • D. Leszczynski, S. Joenvaara, J. Reivinen, and R. Kuokka: Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer- and blood-brain barrier-related effects. Differentiation70: 120-129 (2002). • D. Leszczynski, R. Nylund, S. Joenvaara, and J. Reivinen: Applicability of discovery science approach to determine biological effects of mobile phone radiation.Proteomics4: 426-431 (2004). • S. Stevens, W. Lakin, and P. Penar: Modeling steady-state intracranial pressures in supine, head-down tilt, and microgravity conditions. Aviat Space Environ Med76:329-38 (2005)

  27. Extra Slides

  28. Another Example One-way

  29. Another Example

  30. Radiation Effects on BBB Recent experiments on Earth by Leszczynski et al. involving cell phone radiation demonstrate the potential effect that exposure to even small amounts of radiation in space can have on the blood-brain barrier [1,2]. As reported in these studies, the mobile phone radiation activated non-thermal transient changes in the protein expression levels of hsp27 and p38MAPK in human endothelial cells. It is hypothesized in [1] that activation of hsp27 may cause an increase in blood-brain barrier permeability through stabilization of endothelial cell stress fibers. Increased protein activity may even cause the endothelial cells themselves to shrink, lessening their volume, widening the junction gap, and reducing the overlap region. As a result, radiation exposure in space appears capable of adversely impacting the integrity of the blood brain barrier.

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