The Origin and Function of the Cerebral Electric Wave

and Clinical Implications

By Zhiping Xie

Hunan University of P.R.China

zpingxie@public.cs.hn.cn

Abstract: The traditional hypothesis that is used to explain the electroencephalogram (EEG) is shown not to be valid and a more accurate theory is developed in this paper based upon a logical evaluation of current data. The cerebral electric wave obviously emerges from oscillation, and this oscillation is caused by the flowing K+ current and the variation in K+ concentration which is created from simultaneous depolarization of some certain neurogliocytes. This wave rhythm acts mainly on Cl- directly by the variation in its potential which drives the Cl- out of or into neurolemma thereby contributing to and even controlling the depolarization or hyperpolarization of certain neurons. This concept has the clinical application of using the EEG to predict which comatose patients have the potential for coming out of the coma.

Additionally, the metabolism and health of neurons is herein predicted to be influenced by it being depolarized under a certain amplitude of brain wave. Dreams may be the result of the depolarization of neurons that have been inactive for longer than usual time period. Finally, this paper may lead to the use of electrical stimulation of the brain in specific manners to enhance the recover of comatose or brain damaged patients.

Keywords: electroencephalogram (EEG), brain physiology, cerebral electric wave, depolarization, hyperpolarization, neuron, coma, brain injury.

 

A Brief introduction of Significance

Life science needs entire information of the living animal but we are stuck in the quandary where only certain experiments can be done on the living animal and though more intensive study can be done on the tissues of a dead animal, the information obtained is limited in how it applies to the living creature. So, we are left to deduce the absent information by various hypotheses. The situation with the EEG is such a situation where we can only study the wave patterns of the brain by placing electrodes on the head and then try to find some correlation between these waves and other objective findings by analyzing the data and using statistical analysis.

Therefore, one traditional hypothesis that is accepted by most scientists is that was presented to explain this cerebral wave. But now I have already proved this traditional hypothesis is wrong. Though it can explain some phenomenon in a farfetched way, it cannot help us to research life science deeply. Moreover, there is no way to check this hypothesis by experiment, and it even leads us into a wrong study direction. In this paper, a new strict hypothesis that is based on rigid logic inference is presented to explain the mechanism of creating cerebral electric wave and the function of this wave. Then I offer the ways to check my hypothesis. I think this wave is a key link of the nervous system controlling its own action, and this paper can offer a new idea to breach the recognition of life science.

 

Introduction

The cerebral electric wave is considered to be the macro-response of neuron depolarization in synchronization and desynchronization. These wave tracings can then be compared normal EEG patterns and those for specific disease entities with the correlation helping the doctor in his/her diagnosis. However, the EEG ought to be able to show us additional information.

For example, Prof. Xuan Jiaji, deputy principal of Hunan University, was once in a vegetative state because of a right frontal lobe problem for which two EEGs were done on January 20th and February 25th , 1998 and by comparing two EEGs, the doctors thought that he would most likely not regain consciousness. But when I reviewed the EEGs, I found that fast-waves had increased largely on second one. According to the theory that I have developed over the last decade, I predicted that he had already taken a turn for better and that if he continued on this trend, he would come to in the near future. Just as expected, he came around on March 25th,1998 and by further studying of this case for more than a year, I have been able to make a series of rigid logic inferences, and subsequently a systematic hypothesis which if it continues to be valid in future study will give us a new understanding of living matter.

For this thesis, I have done a careful analysis utilizing logical methodology to come to a better understanding of the logical correlation between the origin of the brain wave and the actions exerted by it on neurons. I propose that the in-cortex variation of K+ concentration serves as the source of the cerebral cortex’s electric rhythm and that this action directly affects the Cl- concentration between the outside and inside of the neurolemma thereby affecting the in-neurolemma’s initial electric potential and subsequent control of some neurons state.

 

The Clash between Physical Logic and Traditional Theory

Most neuro-biologists hold that the cerebral electric waves are the macro-manifestation of the depolarization potential of postsynaptic neurons. Nevertheless this assumption is rather awkward from physical perspective and can not stand up to rigorous verification. I have delineated these points below.

(1) The diameter of axons, compared with the distance between the excited neuron and cortical surface, is so small that it is virtually infinitesimal, and that the electric-field variation caused by the relatively small amount of ions flowing in and out of the axolemma during depolarization, is comparatively rather weak. This variation on the part of astral neurons in the cerebral cortex is even weaker while the depolarization-transmission direction of pyramidal cells’ axons and other large cells’ axons are almost vertical to cortex and the ions in depolarization run slightly vertical to the axon and parallel to cortex. As a result of the ions movement, there is the generation of an absolute slight electric field variation, instead of the electric-wave visible to us on the EEG.

(2) During depolarization every time and everywhere, ions enter and leave the axolemma evenly from every direction surrounding the same relevant axon cross-section wherein the depolarization is happening which as previously stated is a rather narrow space. Thus most of the electric-field variation that is generated by each moving ion and subsequently observed from a relatively far distance on the EEG, can counteract each other since each ion likely has another ion moving in the opposite direction.

(3) The axons of astral neuronal cells in cerebrum take diversified forms, and the electric-field variation that is generated by their relevant ions during depolarization can not have their action potential phase superimposed. Moreover, the movement direction of ions produced during depolarization by the axons of large neuronic cells whose axons are almost vertical to cortex, are less likely to be the same, and even less likely to have synchronously superimposed.

Moreover, in the case of Prof. Xuan Jiaji, his EEG on January 20th,1998, indicated that when the damaged portion of the brain (according to his cerebral computerized tomography scan) was most active, the EEG wave developed a large amplitude which would run counter to the traditional theory where the damaged neurons would be seriously inhibited and unable to depolarize normally. In all of the vegetative states that I have already seen, the same case has been found.

Thus the said synchronization and desynchronization theory that has been used to explain the traditional theory of EEG, doesn’t hold. It is therefore inconceivable that there is any point for neurons to have synchronized activity which would be a useless situation for living matter. In terms of evolution, living matter having once evolved along all directions with an initial equal probability, beneficial traits would be reproduced and those that were not advantageous would be eliminated. Such a function as synchronization could not have spontaneously arisen in all kinds of high grade mammal consistently unless the rhythm of cerebral electric wave is not pointless but rather an indispensable characteristic of animal brain function.

 

A Positive Logic Analysis of Cerebral Electric Rhythm Occurrence

I think the cerebral electric wave is obviously a phenomenon of oscillation. To find which physical quantities are always changing in an alternating way is the key. Many scientists have reached the conclusion that the electric action of cerebral cortex originates from the thalamus as the cerebral cortex itself can not complete the rhythmic activity as recorded by the EEG.

By inference there is therefore two possible ways of accounting for the generation of cerebral electric wave rhythm. The first is that there is some kind of projection fibers from thalamus or brainstem producing the rhythm. The second option is that within the cortex there is some kind of neurogliocyte activity influencing the flow of K+ causing it to move across the low-electric-resistance-couple-current slots formed by the neurogliocytes resulting in the variation of K+ current which then yields the wave rhythm and the previously mentioned projection neurofibrils could then control the parameters of variation.

We can not entirely exclude the first possibility, but we have reason to suspect that the second one is more likely. Guang Xingmin holds that inside the cerebral cortex there is a mechanism which causes the transmission of K+ concentration under certain condition.1 Some neurogliocytes are very sensitive and easily pervious to K+, and neuronic activity can influence the depolarization and neurolemma potential of neurogliocytes.

Here, Guang Xingmin thinks that the neurogliocyte’s action on K+ mainly serves the function of a buffer for communication between neurons, however, I think that it is not only able to act as a passive buffer but also to act as an initiator in creating a physical oscillator of the physical volumes between the local K+ concentrations and the local K+ current which forms the cerebral electric wave.

Analysis can be made in line with physical theory. The depolarization of the neurogliocyte is mainly affected by the K+ concentration’s rate of change between outside and inside of its neurolemma. When the K+ concentration in a section attains a certain level, the depolarization of the neurogliocytes in the adjacent area will all occur.1 All of the neurogliocytes can then release K+ simultaneously leading to a sharp increase in the K+ concentration and giving rise to two forces, one caused by the K+ concentration gradient while the other being caused by the potential difference at various regions, which then drive the K+ to move along the slots between neurogliocytes from high K+ concentration section to low K+ section thereby forming the K+ current. Where the K+ concentration was once high, the K+ is being driven away and being absorbed into the neurogliocytes again, causing the K+ concentration to decrease rapidly. However, in the low K+ concentration section, by collecting the K+ coming from various directions, the section is enabled to increase its K+ concentration causing depolarization effect on some of the neurogliocytes. When the K+ comes from these cells, there is an increase of the K+ concentration immediately followed by the simultaneous depolarization of all neurogliocytes there, and the K+ concentration therein will in turn increase dramatically. This process alternates in the cortex and leads to K+ concentration variation in a different section thus causing a drifting of K+ which results in a partial irregular electric pulse.

In the cortex, the neurotransmitters can not only modify the process of neuronic depolarization but can also control the depolarization of the neurogliocytes. On neurogliocytes, there are some receptors of neurotransmitters such as Ach (acetylcholine) receptors, NA (noradrenaline) receptors, and DA (dopamine) receptors, and more. The neurotransmitters can affect the K+ transmission scale by acting on these receptors to dominate the necessary level of K+ concentration for depolarization of neurogliocytes and then control the rhythmic state of cerebral electric wave. Under the action of certain transmitters accordingly, the K+ that is moved, with certain frequency and amplitude alterations, will have its current altered in a migratory way. The excitatory transmitter which makes depolarization easier, renders the neurogliocytes more apt to depolarize and lead to a decrease in the migratory scale of the K+ current and subsequently increase the frequency. This is because only a low level of K+ concentration is needed to cause the neurogliocytes’ depolarization which will prevent the K+ from rising during a low level of K+ concentration in that section, and therefore can only gather less K+ relatively. And vice versa in the case of inhibitory transmitter.

The absence of neurotransmitter action will cause a slowing in the frequency and an increase in the amplitude of the oscillation of the K+ concentration. Due to the diversity of neurofibrils which come from the thalamus, brainstem etc. that pass into each cortical section causing various neurotransmitters to be released by various neurons of the in-cortex or out-cortex, different styles of rhythm are then traced by the EEG simultaneously of different portions of cortex.

 

The Function of Cerebral Electric Rhythm

Many non-gated ion channels researchers have demonstrated that the Cl- channels on the membrane have a relatively high permeablity capacity in most cases.1 Thus in the resting state, the electric field produced by the variation of the K+ concentration oscillation with the variation of K+ current, mainly acting on the Cl- which then exerts a direct draw (during potential is high) or push (during potential is low) on the Cl-in the surrounding neurolemma changing the Cl- concentration’s rate between the inside and the outside of the membrane. When the external potential caused by the variation in the K+ concentration increases rapidly, Cl- will instantly flow from the neurolemma’s interior to its exterior. Hence the internal potential will be raised. In the event of rapid decrease of the potential outside, the case is the opposite. By inference, the electric field’s action on Cl- is subject to the relative potential (such as a -wave,b -wave,q -wave and d -wave that shown on EEG), because the balanced state of K+ and Na+ concentrations can be adjusted between the outside and inside of neurolemma via the non-gated ion channels. In the case of a higher average potential outside, the K+ and Na+ concentrations are being higher inside and vice versa, so as to balance the impact of this average potential. This process is similar to a boat on a river…when the river rises, the boat floats higher. Cl- can affect the interior potential when it is allowed to more easily traverse the non-gated ion channels and when it is under the action of relative potential outside, as the Cl- is quicker in its response than the K+ and Na+ as it passes through membrane. The quick flowing of Cl- to the exterior of neurolemma causes the inside potential to arise, contributing to the occurrence of depolarization in the similar manner to the trigger impulse of computer’s CPU (central processing unit). The quick flowing of Cl- into the interior of neurolemma would otherwise most likely cause hyperpolarization.

Neurons of different size possess different capacities thereby allowing for the negative potential for driving Cl-. The corresponding amount of Cl- entering the neurolemma of different size cells under the same driving potential, will yield different results. If the radius is equal to R and the number of Cl- channels per unit area of membrane is A, then the per unit cross-section area of dendrite or axon in unit length will have a number of channels that is equal to:

C   =       =  

When A is considered as a constant, C will be inversely proportional to R. (the radius). Therefore a small neuron is affected by Cl- more easily than larger one. If the neurons are small, such as in the case of the astral neuron, under the certain level of Cl- driven by the same outside potential, the hyperpolarization may be likely to occur. Meanwhile, since the large neurons, whose C is less than small cells, have a strong capacity of allowing for the negative potential driving Cl-, the hyperpolarization is unlikely to occur. Furthermore, the hyperpolarization’s action will likely continue (Inhibitory Postsynaptic Potential (IPSP) duration of neurons in cortex constantly exceeds 100ms).1 Hence, many small neurons in the cortex are more apt to be inhibited by the electric rhythm of large amplitude waves with their deep trough resulting in the potential being too low and thereby causing hyperpolarization. And on the other hand, they are more apt to be activated by the small amplitude of rhythm since the small wave’s crest will contribute to depolarization.

In terms of the structure of cerebral cortex, the communication between the entry axons which import messages and the dendrites which export messages from inside the vertical column of cortex, is achieved via the small neurons which work as an essential bridge (i.e. astral neurons). If a slow-wave arises in some sections of cortex and the wave amplitude increases, then the small neurons will be inhibited and the message will not pass properly.

Moreover, I think that the cerebral electric wave may be able to contribute to metabolism of neurons. During the resting state, the usual inside potential of the neuron is lower than outside and may result in some of the electrified material that is needed for the neuronic metabolism (or yielded from neuronic metabolism) is less able to pass in or out of the neurolemma. When depolarization occurs this polarization is eliminated and the aforementioned material is more able to pass through the neurolemma.2 However, it is unlikely that all cortical neurons can be used everyday (some neurons are not often excited by normal psychological message) and if they are not depolarized for long time, their normal metabolism may be irreversibly altered in a negative manner. Therefore it is necessary for such cortical neurons to depolarize under the action of opportune cerebral electric waves, and this may be the reason for the occurrence of dreams.

If there is not any fast-wave with small amplitude in one’s cortex, the whole cerebrum will not be able to work normally and the individual will be unable to wakeup. Such is the case of a patient in a vegetative state. The hypothesis ventured herein may be of some therapeutic value in the treatment of comatose patient. Finally, the experiment using the sleeping factors, which are discovered recently by U.S.A scientists, might be helpful in order to determine whether the results predicted above that occur during the depolarization of the neurogliocytes do indeed occur and thereby validating the theory presented.

 

Conclusion

The traditional hypothesis to explain the EEG does not still hold true as I have presented here. The cerebral electric wave emerges from oscillation that is caused by the flowing K+ current and the variation of K+ concentration from the simultaneous depolarization of a type of neurogliocytes in certain section. This wave rhythm acts mainly on Cl- directly by its potential variation driving the Cl- out of or into neurolemma thereby contribute to, or even controlling the depolarization or hyperpolarization process of certain neurons.

After I had compared many relevant experimental and clinical results released by other scientists, I have not found any significant evidence that would invalidate my theory. However, I would like to offer two ways to check my hypothesis directly. First, by using a micro-electrode which is sensitive to K+ into a cortex of a mammal such as a monkey or a cat, then the variation of the K+ concentration inside the vertical column of cortex could be measured as well as the variation of in the potential at the corresponding surface of the cortex, with subsequent comparison. If these two variations possess the same characteristics of frequency and amplitude at the same time, then my hypothesis of cerebral electric wave occurrence will be validated. Secondly, a relative electric wave could be induced with a large amplitude on a large neuron’s micro-environment (not only at one point, but over a broad space) in order to observe whether or not the large neuron will be inhibited to hyperpolarization. If it does then my hypothesis of cerebral electric rhythm’s function will be validated.

I also predict that we shall find some materials which are indispensable during neuronal metabolism, specifically during the period of new processes (including axons and dendrites) and synapses growing. These materials will possess a better permeability when they pass through the neurolemma during the depolarization state than during resting state. And if we can find such materials, it will validate my theory to explain the mechanism of memory, which I released in Chinese publication.2 Meanwhile if my theory in this paper is right, it can be deduced that the treatment of using electric Chinese acupuncture in a proper way must be able to stimulate the damaged neurons in a patients’ brain enough to promote the patients to recover. There has been much material presented and with exciting research yet to be done. Since I do not have the facilities to adequately follow through with such experiments, I look forward to such institutions assisting me in my research which has obvious scientific and clinical importance.

 

References

  1. Neuroscience Survey, Han Jisheng, United Press of Peking Medical University& China Xiehe Medical University,1993;125,161,194,241.
  2. Xie Zhiping, Process and Mechanism of Psychological Message’s Motion in the Nervous System. Journal of Hunan University(Natural Science Edition),1999,Vol.26,No.2,104~111.
  3. Xie Zhiping, A Logic Analysis of Cerebral Electric Rhythm Exerting Neuronic Excitation. Current Physician,1998;Vol.3,No.9:61-62.
  4. Central Nervous System Anatomy, Tang Zhuwu, Shanghai Sci-Tech Press,1986,133~156.
  5. Molecular Neurobiology, Chen Yichang, Chinese People’s Medical Officer Press,1995,70~125.
  6. Sykova E. Extracellular K+ accumulation in the CNS. Prog Biophs MolecBiol,1983,42:135-189.
  7. Rudy B. Diversity and ubiquity of K+ channeles.Neuroscienceh,1988,25:729-749.
  8. Walz W. Potassium channels and carriers in glial cell membranes. In:Grisar T, Franck G, Hertz L,et al. eds. Dynamic Properties of Glial Cells ; Cellular and Molecular Aspects. Pregamon Press,1986,145-154.
  9. Koester J. Membrane Potential. In:Kandel ER, Schwartz JH,eds. Principles of Neural Science 3rd ed.New York:Elsevier 1991;81-94.

Journal Home Page