Old intracranial pathology , Respiratory Defects, and intracranial pressure*

Does Paula have subtle brain lesions from her anoxic birth? Is this the reason why she exchanges less air than others? Is a low minute volume and too slow breathing a compensation mechanism that we don’t know of? In health? What do others think?

Volume-Pressure Curve [(blood/CSF/brain tissue].

In the absence of pathology, normal homeostatic mechanisms maintain a normal intracranial pressure in response to small fluctuations in intracranial volume. Indeed, in the presence of pathology with a small volume, our compensatory mechanisms also ensure that the intracranial pressure remains maintained.

As the intracranial pathology increases in size, [perhaps due to the effects of increasing hypercapnia, for example, ] the patient will enter decompensated state, whereby small increases in intracranial volume result in a large increase in intracranial pressure* (Figure 6). If the intracranial pathology increases further in size, without intervention, the intracranial pressures rises even more rapidly, that can lead to brain herniation.

This is termed the volume-pressure relationship.

*Although this does mean that a neurosurgeon only has to remove a small volume (blood/CSF/brain tissue) in order to significantly reduce the intracranial pressure. By TeachMeSurgery (2020)

By TeachMeSurgery (2020)

Figure 5 – The intracranial volume-pressure curve (1) No pathology (2) Small volume pathology in a compensated state with normal ICP (3) Large volume pathology in a decompensated state with elevated ICP (4) Very large volume pathology with a significantly elevated ICP and brain herniation.

It seems that most of what we know about pressure inside the brain comes for neurosurgeons. I could not find much on pressure inside the brink outside clinical care or neurosurgical care patients; so we do not know a lot about this subject in people who have survived brain anoxia or major trauma [like being hit by a bus] or head injury.

I would guess that old childhood brain injuries would fade and leave little trace, even using our investigative imaging tools, especially if the person is healthy and was able to compensate through normal physiological mechanisms.

Maybe Paula’s and Kraepelin’s ventilatory defect is a compensatory mechanism to maintain inter-cranial pressure.

Maybe raising respiratory rate and minute volume is dangerous to maintaining proper inter cranial pressure in a brain that has been exposed to anoxia, early in life, as in the case of Paula. [we do not know of course, we are only guessing].

Does breathing less air [1.5 L] compensate and keep ICP more normal than breathing in 6-8 L of air?

This is too complicated.

And I think that no one really knows.

We have a lot to learn.

And we are wasting time……….[see earlier blogs on Manic Depressive Insanity].

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