Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. Reanim. 1994;13(1):111-22. doi: 10.1016/s0750-7658(94)80194-0.Acid-base equilibrium and the brain. O Rabary 1 , M Boussofara, D Grimaud
One would think that checking the condition of the normal respiratory drive or motor mechanism of the skeletal muscles and nerves – as well as checking the health of the lungs would be an obvious way to check out cerebral metabolism, especially when a person exhibits changes of behaviour or mood or cognitive ability -[no yoga, no drugs] . The healthy body will alter minute volume [respiratory rate times tidal volume] in an attempt to maintain physiologic homeostasis, that is, if it can. Even at rest, rate and volume of breathing takes some effort, strength and coordination on the part of the respiratory muscles, more so if accessory muscles are enlisted to help under conditions of respiratory distress.
It is interesting that cerebral metabolism depends on involuntary and partially voluntary skeletal motor reflexes to regulate the acid base metabolism of the brain, especially since the throat, the neck and torso sensors, nerve fibres, and and muscles are vulnerable to injury and permanent damage, as is obvious in damage to the cervical spine after major physical trauma. Other, more subtle injuries and their consequences for breathing may be harder to spot. The patients may be unaware that their breathing is unusual in health and in illness.
Dr Emile Kraepelin found depressed rates of breathing at rest in thousands of non-medicated bipolar depressed patients. These patients exhibited psychomotor retardation.
“Psychomotor retardation has been characterized as a major feature of depression since antiquity. Hippocrates and Aretaeus of Cappadocia both described psychomotor retardation as a characteristic of depression (Sobin and Sackeim, 1997; Whitwell, 1936; Zilboorg, 1944). Darwin also discussed visible psychomotor symptoms and depressed patients who “no longer wish for action but remain motionless and passive, or may occasionally rock themselves to and fro” (Dantchev and Widlocher, 1998; Greden and Carroll, 1981). In the proceeding decades, authors such as Kraepelin expanded on psycho-motor retardation, building upon the knowledge of this noteworthy phenomenon by describing how it was more prominent than depressed mood and involved constrained speech, thought, and behavior (Greden and Carroll, 1981; Sobin and Sackeim, 1997).
Presently, psychomotor retardation is regarded as a key aspect of major depressive disorder (MDD) … ….
Table 1
Characteristics of psychomotor retardation.
Item | Presentation in psychomotor retardation | Assessed by | Reference |
---|---|---|---|
Speech | Increased pauses, decreased volume, reduced articulation, reduced tone and infection, delayed response | Subtle abnormalities — tape-recorder and oscilloscope Gross changes — observation by clinician | Greden et al. (1981a), Greden and Carroll (1981b), Greden (1993), Hardy et al. (1984), Sobin and Sackeim (1997), Szabadi et al. (1976) |
Eye movement | Fixed gaze, poor eye contact | Subtle abnormalities — EOG Gross changes — observation by clinician | Schmid-Priscoveanu and Allum (1999), Sobin et al. (1998), Widlocher (1983) |
Gross movement | Decreased and/or slowed movement of hands, legs, torso, head | Subtle abnormalities — reaction time, drawing times Gross changes — observation by clinician | Bezzi et al. (1981), Iverson (2004), Parker and Hadzi-Pavlovic (1996), Sobin et al. (1998), van Hoof et al. (1993), Widlocher (1983) |
Posture | Slumped while sitting or standing | Observation by clinician | Parker and Hadzi-Pavlovic (1996), Sobin et al. (1998), Widlocher (1983) |
Self-touching | Increased self-touching, especially face | Observation by clinician | Sobin and Sackeim (1997) |
Facial expression | Flat expression | Subtle abnormalities — EMG Gross changes — observation by clinician | Greden and Carroll (1981), Parker and Hadzi-Pavlovic (1996), Widlocher (1983) |
Despite its long observed prevalence in MDD, the characterization and clinical significance of psychomotor retardation are poorly understood.” (Greden and Carroll, 1981; Sobin and Sackeim, 1997).
Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30; 35(2): 395–409. Published online 2010 Oct 31. doi: 10.1016/j.pnpbp.2010.10.019 Psychomotor retardation in depression: Biological underpinnings, measurement, and treatment Jeylan S. Buyukdura,a,1Shawn M. McClintock,a,b,2 and Paul E. Croarkina,*
Paula and I think that psychomotor retardation in depression is due to abnormal and depressed breathing rate at rest. We think that all the characteristics described above are easily understood once we realize that the patients cannot ventilate adequately, do not realize it but instinctively minimize their speaking, their movements and their facial expressions in order to preserve their diminishing reserves of energy. It may not be obvious psychologically but it is perfectly clear once the vital signs are measured and found to be worrisome.
Any doctor, even a psychiatrist, even a layperson, will tell you that depressed breathing is very very bad and very unusual [without drugs or yoga].
Depressed rates of breathing more than explain the mental confusion and cognitive slowing experienced by these patients. It also explains the changes to speech.
Depressed breathing rates explains their discomfort, distress and anguish. There is nothing worse than being unable to breath sufficiently, except maybe not being aware that the anguish comes from being unable to breath adequately and being left like this for weeks and months on end.
Depressed breathing explains difficulty eating [this takes energy the patient does not have], difficulty sleeping, the involuntary loss of weight [being smaller requires less energy] and the mild hypothermia [hypothermia reduces total body metabolism and O2 requirements, as does not moving much].
But, outside death and dying and opioids and yoga, no one has ever seen spontaneously depressed breathing. No one sees Paula’s depressed breathing. No one sees her active exhaling, her use of the abdominal muscles to breathe every breath at rest with significant effort. Depressed breathing is invisible. This is why no one notices it. Paula’s shortness of breath and effort to breath in depressed breathing is only visible if her breathing rate is measured foe one minute with a stopwatch. When in respiratory distress, her external behavior becomes muted, more immobile, despite her internal terror. She does feel like she is suffocating but she does not recognize the feeling as suffocation, only terror.
It is extremely unpleasant!
One’s baseline breathing at rest is the key! Imagine if the range of your baseline respiratory rate is around 3-5 breaths per minute and does not rise easily with stimulation. Your depth of breathing would have to be bigger than normal to exchange enough air in your body per minute. This would take extra effort to accomplish, at rest. Exposure to CO2 [a respiratory stimulant] or congestion of the upper airways for a long enough period would eventually lead to a decrease tidal volume. If your respiratory rate still remained low, then you would not be getting enough air in and out of your body.
In this case depressed breathing with an increased respiratory challenge would lead to depressed behavior and horrible distress from not being able to breathe.
This is what Kraepelin suggested the depressive phase of bipolar illness to be.
All the signs and symptoms were a result of not being able to breath sufficiently due reduced ability to modulate one’s respiratory rate in the face of a respiratory challenge.
Kraepelin thought that these patients had a respiratory defect which caused their depressed and sluggish ventilatory drive. And their breathing began to fail them once they were full grown and in their reproductive years because their defect could not support their metabolism, especially when they got sick or weak from infection, blood loss, or further injury to the head, throat, neck or torso.
Kraepelin was intrigued by how well these patients survived in between attacks [lasting years of decades]. I think that he did not understand how they were even alive, given how important breathing is.
to be continued…..