** Intercranial Pressure

and bipolar attacks. It is possible that the changes in behaviour and mood may be autonomic reflex reactions to fixed abnormal minute ventilation and breathing rate at rest during some respiratory challenges. In Paula’s case, our prototype for bipolar depression, it is obvious that knowing that her minute ventilation is

Report minute ventilation results.

or “in extremis” by current standards does not explain how she is completely healthy most of the time, but it does explain how quickly she could have an increase in PCO2 and other bodily acids when her breathing is further challenged and cannot adjust normally in response. It would explain the response of sympathetic overdrive. the inner agitation, panic and distress, the disruption to thought and mood, the very high blood pressure [most likely to help maintain cerebral blood flow], the raise in heart rate, the heart arrhythmia’s and murmurs. A high intracranial pressure would explain the disinclination to move or eat [ or drink liquids] , to cough or sneeze, the disinclination to defecate or pee, the lowering of body temperature…all to keep bodily acids and PCO2 in check and avoid worsening of intracranial pressure/and/or acidosis. All this because Paula cannot raise her breathing rate adequately at rest or with locomotor activity to deal with a further rise in acids. The rest of the body must compensate instead.

It also seems logical that although this tactic can work for weeks, months, even years…because of the regularity of her respiratory defect/injury.- her continually depressed rate of breathing. .However this involuntary strategy may not work forever and the acid level of the blood can suddenly go up further, leading to the “in extremis” Cushing Response, suddenly changing breathing to an irregular pattern with apneas, difficulty maintaining as high a blood pressure, and intermittent bradycardia [heart rate that is lower than normal] and increased voluntary muscle activation [perhaps to help increase ventilation to eliminate more CO2 and lower intracranial pressure]. Behavioural and Postural adjustments include standing and moving a lot in order to maximize exhalation of CO2. Lying down increases intracranial pressure and so sleep is impossible in lieu of sitting and standing and remaining awake, to lower intracranial pressure. [Pressures in the skull are higher when patients are lying down than when sitting or standing…from .Intra-cranial pressure changes between supine and upright https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/intra-cranial-pressure-changes-between-supine-and-upright/%5D.

These are part of the reflex that Cushing named because they are necessary to avoid death . It seems that the Cushing “control of breathing ” mechanisms are intact and can be called into action if hypercapnia and intracranial pressures are increased enough to necessitate them. But function of mind and memory are worsened during such conditions.

Let us look at the issue of intracranial pressure a little more. From the point of view of the brain, it seems that control of intracranial pressure would be crucial, the brain being surrounded by bone and such.

Perhaps Paula’s low minute volume is necessary to maintain normal intracranial pressure for reasons we do not yet understand. This is only a hypothesis. Breathing less air in the correct ratio using much needed accessory muscles of the abdomen makes this possible. This would explain the sluggish respiratory response to exercise. . All to maintain and avoid sudden increases in PCO2 and intracranial pressure.

Reducing episodes of hypercapnia must become harder as a person grows taller and reaches reproductive maturity and perhaps needs more energy [oxygen] yet respiratory rate remains limited.

It seems from Kraepelin’s studies and from our knowledge of people like Paula and Jerry and others.[described in past blogposts] ..that respiratory rate and depth is abnormal during attacks and perhaps during periods of health. And that minute ventilation in illness, during different stages of attacks, may well indicate attacks of mild and more severe acidosis and PCO2 imbalance due to this motor injury affecting ventilation…

In keeping with our discussion in our last blog regarding Jerry and his visit to a biological clinic for his agitation and mania, let us imagine that in the 22nd century, they can image intercranial pressure in non invasive ways. . Let us imagine that a gradual rise in intracranial pressure is what was causing his agitation and mania, resulting in a shift in his breathing rate and pattern, explianing his irregular breathing and intermittent bradycardia and fall in blood pressure, still remaining high but which was even higher in the depressive stage. This would be consistent with what Jerry experienced or what people saw him experience and with what Kraepelin reports in depressed patients who suddenly become manic.



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