[Research] Seizure Threshold Is Controlled by Breathing Pattern and Blood Gases

[Artour]

In normal conditions, all electrical signals that travel among nerve cells are related to objective and important processes, such as the work of the senses, memory, analysis, logic, decision making, voluntary and involuntary movements of muscles, etc. The electrical signal is transmitted from one nerve cell to another only when the voltage or strength of the signal is high enough. It should be no less than a certain threshold value: the threshold of excitability of the nerve cells that directly relates to seizure threshold. The normal value for the threshold of excitability is about 50 micro volts in mammals.

When this seizure threshold remains normal or high, the electrical signals are transmitted as in the normal computer. Adaptation and self-improvement are the normal final outcomes of these processes in living creatures. Hence, in order to have a positive effect on the biological system (learning, survival, self-defense, etc.), it is crucial that the transmission of these neuronal signals satisfies 2 criteria:
1) These (real or objective) signals are transmitted and facilitated through the network of the nerve cells so that no important information is lost.
2) Accidental or irrelevant signals get hampered so that they cannot interfere with the normal work of the senses, memory storage, memory retrieval, comparison of experiences, solution making, execution of solutions, feedback, etc.

If for some reason this threshold becomes too low, accidental signals can be amplified causing disruption or even suppression in the normal work of the central and peripheral nervous systems. Consider what happens during abnormal changes in breathing. When the breathing pattern is disturbed (less than 5% of modern people, according to tens of published studies - link removed, have normal breathing parameters these days), blood gases become abnormal. The most common abnormality is arterial hypocapnia (low CO2) and cell hypoxia (low O2 in tissues, the brain included), where overbreathing or hyperventilation (breathing more air than the medical norm) is the key cause for both effects. (For medical research visit Hyperventilation Syndrome in the Sick - 34 medical studies - link removed). Let us consider how the seizure threshold depends on carbon dioxide and oxygen.

How CO2 and O2 influence seizure threshold

This excitability threshold of the nerve cells is highly dependent on, and sensitive to, the CO2 concentration in nerve tissues. According to professional neurologists, hyperventilation or low CO2 in the brain "leads to spontaneous and asynchronous firing of neurons". Hence, when we overbreathe or hyperventilate, CO2 and O2 levels in cells becomes abnormally low. As a result, accidental or weak electrical signals can be strengthened and relayed through some parts of the brain interfering with the normal signals. This causes a reduction in the seizure threshold.

Overbreathing and irregular breathing patterns cause seizures

Depending on particular details of the hyperventilation procedure (many doctors use the light version that is based only on deeper breathing without changes in frequency and then claim that not all subjects had seizures) and individual health state, somewhere between 70 to 100% of epileptics can lower their seizure threshold and trigger their seizures by voluntary hyperventilation (see the abstracts below). Many studies found that hyperventilation could cause seizures in all patients. However, modern medical and physiological research have failed to find the exact CO2 threshold that can induce seizures in susceptible individuals. This is logical since, apart from the key role of brain CO2 concentration, there are many other factors that influence transmission of electrical signals in the brain, including surrounding neuronal activity, distribution of electrical firing within the brain, current metabolic rate (body position, posture, physical exercise, if any, thermoregulation, etc.), oxygen tension, availability and types of calcium and magnesium ions present in tissues, changes in glia cells, concentrations of neurotransmitters, amino acids, and many other substances. Therefore, while hypocapnia is the crucial necessary background for the lowered seizure threshold and appearance of seizures (the prime cause of seizures and epilepsy), many other factors play their roles in experienced symptoms and a clinical picture for some particular seizures.

Indeed, numerous medical studies have proven that hyperventilation reliably induces seizures in epileptics and patients suffering from seizures, as an additional indication that seizures threshold is controlled by breathing with some (limited) contribution from other factors (stress, sleep deprivation, low blood sugar, overheating, alcohol, etc.).

Other factors can influence the seizure threshold

It is known to many epileptics that seizures can be triggered, prolonged, and worsened by low blood glucose levels. There is even a special category of seizures which has a label "hypoglycemic seizure" or "low blood sugar seizures". Chronic hyperventilation worsens general blood sugar control increasing symptoms of reactive hypoglycemia and reactive hypoglycemia. In addition, hypocapnia-induced vasoconstriction (see CO2 vasodilation effect) causes stenosis or spasm of the carotid artery and is an essential aggravating factor. (Fainting due to voluntary hyperventilation is partially based on the same effect: overbreathing decreases glucose availability for the brain.) Whatever the case, low blood sugar level also lowers the seizure threshold.

What about the low brain oxygen effects? Reduced brain oxygenation (due to chest breathing, vasoconstriction, and suppressed Bohr effect) is an additional factor that increases acidity of brain cells (due to anaerobic cell respiration and elevated lactic acid production). This further intensifies abnormal electrical activity lowering the seizure threshold even more.

This web page (Cause of seizures- link removed) provides information about medical research or how western doctors treated seizures and epilepsy with application of carbon dioxide and breathing techniques.

(This is a part of the web page: "Seizure Threshold Is Controlled by Breathing Pattern and Blood Gases") from NormalBreathing.com (see Diseases Section)

Medical references for calming CO2 effects on brain cells

“Studies designed to determine the effects produced by hyperventilation on nerve and muscle have been consistent in their finding on increased irritability” Brown EB, Physiological effects of hyperventilation, Physiological Reviews 1953 October, Vol. 33 No. 4; p. 445-471.

"Conclusions. Many cells clearly reacted to even small changes in Pco2 (e.g. 4 mm Hg). Moderate doses of CO2 led to both excitation and depression; typically there was an initial phase of excitation during the rise in PCO2, a subsequent longer period of depression, and some sharp excitation during the fall of PCO2." Krnjevic K, Randic M and Siesjo B, Cortical CO2 tension and neuronal excitability, Journal of Physiology 1965, No. 176: p.105-122.

"Orthodromically evoked compound action potentials ('population spikes') were depressed in hypercapnia and increased in hypocapnia." Balestrino M, Somjen GG, Concentration of carbon dioxide, interstitial pH and synaptic transmission in hippocampal formation of the rat, Journal of Physiology, 1988, No. 396: p. 247-266.

"Hyperventilation leads to spontaneous and asynchronous firing of neurons" Huttunen J, Tolvanen H, Heinonen E, Voipio J, Wikstrom H, Ilmoniemi RJ, Hari R, Kaila K, Effects of voluntary hyperventilation on cortical sensory responses. Electroencephalographic and magnetoencephalographic studies, Experimental Brain Research 1999, Vol. 125 No. 3: p. 248-254.

Neuron. 2005 Dec 22;48(6):1011-23.
Adenosine and ATP link PCO2 to cortical excitability via pH.
Dulla CG, Dobelis P, Pearson T, Frenguelli BG, Staley KJ, Masino SA.
Neuroscience Program, Department of Neurology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
In addition to affecting respiration and vascular tone, deviations from normal CO(2) alter pH, consciousness, and seizure propensity. Outside the brainstem, however, the mechanisms by which CO(2) levels modify neuronal function are unknown. In the hippocampal slice preparation, increasing CO(2), and thus decreasing pH, increased the extracellular concentration of the endogenous neuromodulator adenosine and inhibited excitatory synaptic transmission. These effects involve adenosine A(1) and ATP receptors and depend on decreased extracellular pH. In contrast, decreasing CO(2) levels reduced extracellular adenosine concentration and increased neuronal excitability via adenosine A(1) receptors, ATP receptors, and ecto-ATPase. Based on these studies, we propose that CO(2)-induced changes in neuronal function arise from a pH-dependent modulation of adenosine and ATP levels. These findings demonstrate a mechanism for the bidirectional effects of CO(2) on neuronal excitability in the forebrain.

Br J Anaesth. 1972 Nov;44(11):1128-32.
Effects of acute hypocapnia and hypercapnia on neuromuscular transmission and on monosynaptic spinal reflex in wakeful man.
Higashi H, Kano T, Shimoji K, Morioka T, Sances A.
The effects of both acute hypocapnia and hypercapnia on neuromuscular transmission (NMT) and monosynaptic spinal reflex (MSR) in conscious subjects were studied by observing the averaged evoked electromyogram. The M-wave amplitude increased to 165 ± 25 % (mean ± standard error) during acute hypocapnia with an end expiratory carbon dioxide concentration of 2.5 ± 0.2 vol.% and decreased to 73 + 7% during acute hypercapnia with an expiratory concentration of 6.8 ± 0 . 1 vol.%, in comparison with the control value. The H-wave amplitude increased to 226 ± 8 2% during acute hypocapnia and decreased to 85 ± 9% during acute hypercapnia in comparison with the control value. These results indicate that both NMT and MSR in conscious man are facilitated by acute hypocapnia, and that NMT is inhibited by acute hypercapnia. However, the effect of acute hypercapnia on MSR could not be ascertained only by the observation of the H reflex in these conditions.

 

[Nakamova]

Artour -- Since unconscious breathing habits can be difficult to correct, do you think it would be helpful to have conscious sessions several times a day (perhaps first thing in the morning, in the afternoon, and before going to bed)? A bit like meditation, but with the breathing focused on the techniques you've mentioned elsewhere for increasing CO2.

Also, are there studies out there where individuals have reduced their seizure frequency overall, or arrested a seizure as it initiates, by practicing this technique?

 

[Artour]

Yes, in order to change the automatic breathing pattern, one should practice breath work (to gradually readjust the breathing centre to higher CO2) and take care of the lifetysle factors. Among the key parameters that cause hyperventilation in modern people are mouth breathing, sleeping on one's back (these 2 explain highest mortality during early morning hours for chronic diseases and and highest chances of seizures), chest breathing, overeating, exercise with mouth breathing, etc. The details of the program of breathing retraining are located in "Learn Here" Section of NormalBreathing.com.

As about doctors attempts to deal with seizures, they are on the Seizure Cause Web page. Here are some of these studies:

Do medical studies prove that CO2 can cause seizures to disappear?

Who were among the first doctors who probably knew the cause of epilepsy? The first medical study that proved the beneficial effects of CO2-enriched air (with the "The effect of epileptic seizures of varying the composition of the respired air") was published over 80 years ago by the Journal of Clinical Investigations (Lennox, 1929). The result was replicated in the 1956 article published in Science, as is clearly indicated in the title “Inhibition of audiogenic seizures by carbon dioxide” (Mitchell & Grubbs, 1956). In both studies, inhalation of CO2-rich air reduced duration and severity of seizures due to the known effects of carbon dioxide on nerve and muscle cells. More recently, in 2006, Finnish scientists, after studying febrile seizures in rat pups, stated that “Suppressing alkalosis with 5% ambient CO2 abolished seizures within 20 s” (Schuchmann et al, 2006).

Abstracts (Western doctors who treated absence spells and seizures with breathing techniques)

Magarian GJ, Olney RK, Absence spells. Hyperventilation syndrome as a previously unrecognized cause, Am J Med. 1984 May;76(5):905-9.
Absence spells in adults have been recognized in association with disorders of excessive somnolence, transient ischemia of the temporal lobes, and seizure disorders. A 66-year-old man who presented with a history of absence spells for more than 20 years is described. After diagnosis of a hyperventilation syndrome without an associated seizure disorder, educational and behavioral therapy without the use of medication has produced a long, continuing remission of these spells. The hyperventilation syndrome continues to present in many ways, often without recognition by physicians for prolonged periods. The case presented exemplifies this problem and may be the first report of absence spells caused by hyperventilation.

Bruno-Golden B, Holmes GL, Hyperventilation-induced seizures in mentally impaired children, Seizure. 1993 Sep;2(3):229-33.
Boston Neurobehavioral Institute, Harvard Medical School, Children's Hospital, MA 02115.
Two children with profound development delay and medically intractable seizures were found to have hyperventilation-induced seizures. Following detection of this precipitating factor the parents, teachers and caretakers were taught to modify the childrens' breathing when they began to hyperventilate. In both patients this technique resulted in a dramatic decrease in seizure frequency.

Fried R, Rubin SR, Carlton RM, Fox MC, Behavioral control of intractable idiopathic seizures: I. Self-regulation of end-tidal carbon dioxide, Psychosom Med. 1984 Jul-Aug;46(4):315-31.
Eleven women and seven men with moderate to severe chronic hyperventilation and idiopathic seizures refractory to therapeutic serum levels of anticonvulsant medication were given diaphragmatic respiration training with percent end-tidal CO2 biofeedback. The training had a rapid correcting effect on their respiration, making it comparable to that of 18 asymptomatic control subjects. Ten of the seizure-group subjects were in the study at least 7 months and following treatment, 8 showed EEG power spectrum "normalization", restoration of cardio-respiratory synchrony (RSA), and their seizure frequency and severity were significantly reduced.