Initial Summary
The Institutes for the Achievement of Human Potential present a unified concept of the cause and treatment of seizures. The concept proposes that anticonvulsant drugs impair both cortical control of the reflex mechanism for seizures and the maturational and developmental processes by which such cortical control is ultimately established. For these reasons IAHP treatment procedures now include the gradual reduction and ultimate discontinuation of anticonvulsant drugs in all IAHP children who are taking them.
The concept also proposes that the injured cerebral cortex may achieve and retain its controlling functional position in the central nervous system by means of enhanced maturation and development acquired through specially structured environments with sensory inputs of highly increased frequency, intensity and duration under the best possible physiological conditions.
According to this concept it is through its working relationships with the cerebellum and the reticular system that the cerebral cortex acts to prevent the release of the reflex mechanism for seizures. The concept proposes further that it is probable that conditions which establish such cortical control also decrease the tendency toward generation in the injured brain of abnormal electrical discharges, thereby reducing or abolishing the basis for seizures.
Among the procedures in the Human Development Treatment Programs of The Institutes for the Achievement of Human Potential there is now included the gradual reduction and ultimate discontinuation of the use of anticonvulsant drugs in all IAHP children who are taking them.
Because you, the parents, and we, the staff of IAHP, are partners in the treatment of your children, we feel that you should have the opportunity to learn the reasons for this decision. We believe, furthermore, that you should know and understand how the Human Development Treatment Programs, with which you are all familiar, provide a much better solution for your children's seizures than any drugs which they may now be taking for this purpose.
Like all other actions taken at IAHP on behalf of brain-injured children, the decision to remove anticonvulsant drugs gradually from our children's programs was made after long and careful study and observation, during discussions among the staff as to the wisdom and actual need for such a move, and by weighing the benefits and the problems which this action might generate.
The decision is the result of our experience with over 10,000 children seen by the IAHP staff during a period of more than 25 years. We have studied the effects of anticonvulsant drugs as well as of seizures themselves on Human Development Treatment Programs. We have closely watched the results of cautious, very gradual withdrawal of these drugs on our children's seizures and on the children's improved responses to our treatment programs.
In 1971 we brought our concerns about anticonvulsant drugs to the attention of the World Organization for Human Potential. We discovered that our colleagues in other countries had shared these concerns for a long time. At that meeting the membership of WOHP "issued a cautionary note to the medical world and to the parents of brain-injured children regarding the widespread and sometimes indiscriminate use of anticonvulsive drugs in the management of brain-injured children. The collective membership of the organization has been responsible for the lives of many thousands of brain-injured children. It has been their experience that anticonvulsant drugs frequently fail to help the child use his brain effectively and there is a danger that the drug itself further delays the child's neurological growth."
IAHP Experience with Seizures and Anticonvulsant Drugs in Children
It is important at this point to note that we are discussing seizures and their treatment in children only. The extent of IAHP's experience with seizures and the drugs employed to suppress them can be seen in a comparison of the number of children with seizures in our patient population and the number of people with seizures in the general population. This is usually called the prevalence rate. We do not include here children whose seizures occur only with fever. Neither do we include those children who have had only one seizure.
It is important to remember that seizures are a common symptom of brain injury and that they occur more frequently in children than in adults. Therefore, IAHP's patient population has a higher prevalence rate for seizures than the general population, for which the most reliable rate figure available seems to be 6.6 per 1,000. IAHP’s prevalence rate is 454 per 1,000 children with a history of seizures at some time in their lives, nearly 70 times the rate in the general population.
Of the children with histories positive for seizures 55 per cent were still actively having them when they first came to see us. The remaining 45 per cent had stopped having seizures by that time. Most of the children in that 45 per cent group had not taken anticonvulsants at any time. Therefore, it is obvious that their seizures had ceased spontaneously and without the use of anticonvulsant drugs.
Of the children continuing to have seizures at the time of their first evaluation at IAHP, 80.8 per cent were taking anticonvulsants. From this it is evident that these children's seizure problems had not been solved by these drugs. As we have followed the progress of our children who came to us with seizures, the obvious ineffectiveness of anticonvulsant drugs has become increasingly clear. The conclusion is inescapable that these drugs do not accomplish the purpose for which they are given, namely, the control and, as is sometimes implied, the cure of seizures.
Ineffectiveness of Anticonvulsants
Our conclusions have been confirmed. More recently, serious doubts about the effectiveness of these agents have also arisen in other quarters. This was clearly stated in an editorial in Epilepsia (17: xiii-xv, 1976), a medical journal devoted to articles on seizures. The editorial discussed a recent review of the previous medical literature on prognosis in epilepsy" which "emphasized that the widespread misconception that 70 to 8O% of epileptics are controlled by drugs does not agree with the published facts. A persistent finding in the studies reviewed is that the longer the duration of follow-up, the worse the prognosis in terms of seizure control. An overall picture that emerged from the literature is that complete seizure control is achieved for 2 years in 30 to 37% of patients; but that this figure falls to approximately 20% at 5 years and 10% at 10 years." The editorial said further that the picture revealed by this review "is a consistent one, which, surprisingly has not altered throughout this century, despite the introduction of drugs which are so widely used today".[ our emphasis]
A further factor emphasizing the lack of efficacy of anticonvulsant drugs and confirming our own observations at IAHP is seen in another paragraph of the Epilepsia editorial which said, "As a result of the poor control of seizures reflected in the prognostic studies referred to above, it is well known that epileptic patients are frequently treated with multiple drugs. This is illustrated in a recent survey of 11,720 patients randomly selected from in- and outpatient populations from 15 centers in four European countries who were found to be taking 3.2 drugs per patient, of which 84.3% were antiepileptic drugs."
Excluding the "nonepileptic" drugs, on the basis of these figures it is evident that the mean number of anticonvulsant drugs in that survey was 2.69 per patient. Our children have been relatively fortunate in that the mean number of anticonvulsant drugs each child was taking when first coming to us was 1.97. But of those IAHP children who were taking anticonvulsant drugs when initially seen by us 5.2 per cent were receiving as many as 4 different drugs per day.
Thus, the experience and conclusions of IAHP with regard to the ineffectiveness of anticonvulsants are confirmed by statements in the recent medical literature. For the remainder of this Bill of Particulars let it be understood that we recognize that anticonvulsant drugs have some measure of effectiveness in suppressing seizures but that this is not sufficiently large, consistent or reliable for these drugs to be of value in the purpose for which they are used. Because these drugs do not properly do what they were intended to do, IAHP can see no justification for their continued use.
Side Effects of Anticonvulsant Drugs
Although the ineffectiveness of anticonvulsants is in itself enough to warrant their discontinuation in children on IAHP programs, there are other problems connected with them which strongly reinforce this decision. It is serious enough when a medication does not fulfill its promise in dealing with human illness. But if, in addition to its ineffectiveness, taking the drug exposes the individual to undesirable effects, many of which are not readily detected but are none the less potentially dangerous, it would seem that its continued use is certainly inadvisable.
A wide range of such undesirable side effects is produced by the various anticonvulsants. The fact that some of these effects may seem to be less harmful than others does not in any way compensate for the demonstrated ineffectiveness of these drugs. A common troublesome result of some anticonvulsant therapy is excessive, disfiguring overgrowth (hypertrophy) of the gums. Another effect is excessive and often disfiguring hairiness. Both of these drug effects are generally considered to be reversible.
Of even greater importance are those side effects which are insidious in their manifestations. One such symptom is the result of the toxic effects of anticonvulsants on the coordinating mechanisms of the brain. A patient who has such a response to long-term anticonvulsant medication may be incoordinate to the point of staggering, tripping and falling, unable to use arms and hands effectively. Until it was recognized that these symptoms could be due to anticonvulsant medication, the tendency was to attribute their cause to the brain abnormality underlying the seizures. For the severely brain-injured children of IAHP who are incapable of movement, toxic effects of this sort pose special problems. Because they cannot move, they cannot show the incoordination which may result from the drugs they are taking for seizure control.
Even less apparent, yet seriously harmful, side effects of anticonvulsant drugs are those resulting from interference of these drugs in various metabolic and endocrine activities of the body such as vitamin D utilization, folic acid utilization, calcium metabolism and the regulation of the body's defenses against infections and foreign substances. There are many other side effects, some potentially fatal.
The Epilepsia editorial cited above sums up the matter very well: "Some patients suffer more from chronic toxicity–due to anticonvulsants–than from their seizure disorder and the modern management of epilepsy requires constant vigilance to strike a balance between the burdens of the disease and the complications of therapy."
Mind-Dulling Effects of Anticonvulsant Drugs
While all of the objections to the use of anticonvulsants discussed thus far are of importance to brain-injured children there are additional reasons against their use which are of particular relevance to IAHP children. One of these has to do with the chemical structure of many of these agents. The problem begins with phenobarbital, which continues to be the most commonly used anticonvulsant. Phenobarbital is a member of a large family of synthetic chemical substances, called barbiturates, which were introduced in 1903. Barbiturates belong to the class of drugs known as central nervous system depressants. They are used more to produce sleep than for any other purpose. Different barbiturates act at different rates of speed in depressing the central nervous system but otherwise they all do pretty much the same thing. A striking example of the sleep-making power of some barbiturates is that which the substance known as thiopental or Pentothal possesses. This drug is very often given by vein to initiate general anesthesia. Starting with the moment Pentothal begins to run into your vein, you will probably become unconscious before you can count to ten.
Some time after its introduction it was discovered that phenobarbital not only has a calming effect and causes sleep, depending on the size of the dose, but that, to a degree much greater than that of other barbiturates, it also suppresses seizures. Efforts were then begun to modify the chemical structure of phenobarbital so as to eliminate its sedative effect and enhance its anticonvulsant capability. In 1937 the first result of this effect was introduced for the treatment of seizures. Its simplified chemical name is diphenyl hydantoin. After phenobarbital this is the next most commonly prescribed anticonvulsant drug.
In English-speaking countries seizures are also known as epilepsy, convulsions, grand mal, petit mal, jerks, absences, spells, fits, turns and spasms and by various other designations. Each language has coined its own names for seizures. In a somewhat parallel procedure manufacturers devise many different names for the same drug. Many of our parents have given diphenyl hydantoin to our children under a trade name, Dilantin. Others of our children throughout the world are receiving diphenyl hydantoin under various other trade names, at least 47 of them, by which it is known in some 120 countries other than the United States.
The attempt to eliminate the sleep-making effect of phenobarbital was not entirely successful, as many IAHP parents have observed in the dullness of those children who are or were taking diphenyl hydantoin. Other efforts to accomplish alteration in the stupefying action of phenobarbital resulted in the appearance in the pharmaceutical market of several additional drugs closely related to diphenyl hydantoin. In one way or another and to some degree or another they share with diphenyl hydantoin its disadvantages. Through various other attempts to achieve effectiveness in seizure suppression and to deal more specifically with various forms and types of seizures, additional classes of drugs have been synthesized or chemically adapted. Their successes have been no more conspicuous than those of the various drugs developed before them.
Other Objections to the Use of Anticonvulsants
Thus far in this Bill of Particulars we have noted the following disadvantages attached to the use of anticonvulsant drugs:
- Ineffectiveness
- Disfiguring side effects
- Insidious and serious alterations of fundamental metabolic processes in the human body
- A capability for potential fatal reactions
- Ability to cause incoordination, among other neurological disorders
- Mind dulling and stupefying actions.
However, even this list is incomplete. Another reason, basic and fundamental, is that the concept on which the use of anticonvulsants is based violates a primary principle of medicine: Whenever possible treat the cause, not the symptoms. To use anticonvulsants in the treatment of seizures is to treat symptoms. It is, in effect, an inadequate effort to cover them up, to sweep them under the rug.
For IAHP the ultimate objection to the use of anticonvulsants is specifically related to IAHP concepts and treatment procedures which, for brain-injured children with or without seizures, are directed at the injury. Because brain injury is the reason underlying seizures in IAHP children as well as the cause of their impaired neurological functions and their slowed and distorted developmental processes, it is the brain injury itself that must be the target of treatment, not the symptoms of brain injury. Many of the adverse effects of these drugs stand in the way of effective Human Development Treatment Programs.
Another objection to the use of anticonvulsants is derived from our experience with the 80.8 per cent of children who were still taking these drugs at their first evaluation because of persistent seizure activity. In most of these children gradual withdrawal of this medication was associated with a progressive decrease in seizures, both in frequency and severity. There are two possible reasons for this observation. One factor is the maturational benefits (discussed below) derived from the children's Human Development Treatment Programs. While we believe that this is the basis for the continuing absence or infrequency of seizure activity, once it has ceased or decreased, the fact that withdrawal of drugs was accomplished very early in the course of treatment in many of these children points to a second reason: In these children the anticonvulsants were in themselves responsible for perpetuation of the seizures.
The Cerebellum
The basis for this conclusion is the manner in which certain anticonvulsants, especially diphenyl hydantoin and phenobarbital, act to suppress seizures. The main site of action of these drugs is the cerebellum, a prominent structure at the back and underside of the brain where it lies beneath the overlapping cerebral cortex*. The cerebellum has widespread and intimate connections with many other major structures and functional elements of the central nervous system, especially the cortex. In recent years the role of the cerebellum in monitoring and guiding the smoothness and coordination of motor functions initiated by the cerebral cortex–mobility, manual competence and speech–has become increasingly clear. In this connection the cerebellum may be regarded as a modulator for the cerebral cortex, adjusting the electrical signals which the cortex sends to arms, legs, fingers, tongue, lips and other motor apparatus as well as the feedback which they return.
*The term cerebral cortex refers to the highest functional and anatomical level of the brain, the so-called gray matter. The other levels, in descending order, are the functional midbrain, pons and medulla-spinal cord. Parents of IAHP children are familiar with these terms.
A cortex, meaning an outer layer, is also present in such other organs as the kidney and adrenal gland. The cerebellum has its own cortex. In each case the structure and function of that cortex is special and peculiar to the organ in which it exists.
It is in the process of keeping motor actions, initiated by the cerebral cortex, regulated and in order that the cerebellum plays its role in suppressing seizures. When it receives abnormal signals arising elsewhere in the brain, usually in the cortex, the cerebellum responds by intensifying its regulating and order-keeping electrical impulses which tend to prevent the abnormal signal from spreading and setting off disorderly seizure activity. If the regulating signals from the cerebellum are not sufficiently strong, the seizure will occur anyway.
Anticonvulsant Drugs in the Cerebellum: Pharmacological Action
Although phenobarbital and diphenyl hydantoin had been used for many years in the control of seizures, their mode of action was not understood until the effect of the regulatory function of the cerebellum in suppressing seizures was discovered. It was then found that these drugs, and Valium also, aid in seizure suppression by stimulating the cerebellum, thus strengthening its ability to block abnormal electrical signals after they have been generated elsewhere in the brain.
Diphenyl hydantoin, which has been most extensively studied, does not act selectively on the basis of need from moment to moment, hour to hour or day to day as each abnormal electrical signal reaches the cerebellum. On the contrary, the action of these anticonvulsant drugs on the cerebellum is constant and unremitting.**
**The stimulation of the cerebellum by means of electrodes (popularly misnamed "brain pacemaker") placed on its surface through an opening made in the back of the skull is a procedure devised by Dr. Irving S. Cooper. Like diphenyl hydantoin, its action is to strengthen the electrical signals generated by the cerebellum but the stimulus is electrical and not chemical as in the case of the drugs. Also, unlike the drugs it acts intermittently, at intervals, for periods and with stimulus strength determined by the neurosurgeon.
Anticonvulsant Drugs in the Cerebellum: Toxic Action
The toxic action of anticonvulsant drugs has its adverse effects on the cerebellar nerve cells. Adding to this is the potentially harmful effect of constant stimulation on these cells without opportunity for physiological rest required by living tissues. It is now well known that longtime treatment of seizures with diphenyl hydantoin in full doses may cause degeneration and loss of cerebellar nerve cells. Although fatigue of these cells, even before degeneration or loss, has not been described, there is no reason to believe that this does not result from uninterrupted, prolonged stimulation. Obviously, through such cellular loss or fatigue the seizure suppressing power of the cerebellum becomes impaired. The result is a continuation or resurgence of seizure activity.
It is our belief that the recession of seizures in children whose anticonvulsant medications have been removed is due to the combined effects of the Human Development Treatment Programs plus the recovery by the cerebellum of its normal regulatory function.
More than thirty years ago, well before the newer knowledge concerning cerebellar function was available, Dr. Temple Fay, commenting on the search for "an ideal and easy drug therapy program, said at a meeting of the Association for Research in Nervous and Mental Diseases, ". . . There is danger in this quest of the 'magic formula' that the profession may lose sight of the fact that the convulsive seizure is only a symptom and to prevent or deter a symptom does not remedy the basic cause. If the seizure is a symptom (a warning of danger to the brain organ or a prehistoric 'reaction of defense'), it makes little difference to a progressive or fixed pathological process just to remove the symptom because it is unpleasant to view or experience. This is not unlike poisoning the dog that barks at the burglar; we gain temporary satisfaction to our esthetic senses at great risk to our valued possessions."
Although not directed at the specific subject which we are discussing here, a more recent comment is equally pertinent. In the March 31, 1977 issue of the New England Journal of Medicine there was published a letter to the editor from Dr. Derrick Lonsdale, of the Cleveland Clinic. Among other comments Dr. Lonsdale said, "One has only to look at the massive therapy that is given to an epileptic patient and, perhaps, above all to have the courage to remove such medication to see what serious implications such therapy has for the well being of a patient. It seems to me that we have reached the point where we treat a patient with a given medication and assume that it is the progression of the disease that makes things worse rather than the medicine we prescribed." [our emphasis]
A Unified Concept of the Cause and Treatment of Seizures
In presenting a unified concept of the cause and treatment of seizures we emphasize again that we are considering the subject of seizures as it relates to children and their brain injury. The important difference, among others, between child, especially the younger child, and adult is that the child has a large margin of uncompleted maturational and functional development. To the extent that such a margin may exist in individuals beyond the stage of childhood, it is possible that this concept may apply to them as well.
In the past 250 years there has been remarkable progress in the exploration of the anatomy, the structural details, of the brain and spinal cord which together constitute the central nervous system. In the past 100 years, and especially in the last half century, the manner in which these structures work has also been intensively studied and many firmly founded facts have been established. However, although many neurological phenomena have been discovered and closely examined, the exact way in which these activities, and especially the electrical phenomena which initiate a seizure, fit into the total picture of brain function remains largely a matter of interpretation and conjecture.
There have been superb insights into the mechanisms of the brain. Some of these have ultimately been fully confirmed. Others have stood the test of time and use without actual scientific confirmation but also without scientific disproof. One such insight was that of the great English neurologist, J Hughlings Jackson, who about 90 years ago wrote, "Convulsions and other paroxysms are owing to (1) sudden, (2) excessive, and (3) temporary nervous discharges. This was the first recognition that seizures arise within the brain cells.
Another such great insight was that of Temple Fay who in 1942 described seizures as being part of the innate, defensive reflexes of the body. "From an evolutionary standpoint," wrote Dr. Fay, "we must abandon the irritative theory [of the mechanism of seizures], for one of release of higher levels. We must view the convulsive seizure as we do the patellar reflex [knee jerk]. The response becomes exaggerated and more violent as the higher motor levels of the brain are removed....***
***This quotation is from Dr. Fay’s classic article, The Other Side of a Fit
The Reticular System
This statement is all the more remarkable because the concept which it enunciated was prophetic. The identification of the reticular system, which is an integral part of the neurological mechanism essential for "release of higher levels," specifically the cortex of the brain, was imminent but had not yet occurred. Knowledge of the role of the cerebellum in connection with seizures did not exist. The understanding of the manner of action of these mechanisms, envisioned by Fay, was still further in the future. Even in 1977 these developments may well be characterized as being very recent.
Through the reticular system Fay's concept and that of Jackson complement each other. We have already discussed briefly the role of the cerebellum in seizures. The reticular system (or reticular formation) is an incredibly complex meshwork of nerve cells (neurons) which extends throughout the spinal cord, medulla and pons to the midbrain where it reaches its greatest complexity and from which it sends projections to the cortex. Although its existence and much of its function have been clearly established, the reticular system is anatomically poorly delineated. In rather oversimplified terms the reticular system may be described as the integrating and tuning mechanism which ties all levels of the brain and spinal cord into a functioning whole.
The reticular system has a finely adjusted reciprocal relationship with the cortex and the cortex with the cerebellum, partly by way of the reticular system. The reticular system tunes your cortex down when you go to sleep and tunes your cortex up so that you awake. It also tunes selectively so that at this very moment you are concentrating on the print on this page and tuning out the noises of traffic or of your humming refrigerator, the movement of the clock pendulum in the periphery of your vision, the touch of the clothes you are wearing and the pressure of your chair against your bottom. Now that I have distracted you (the child who is highly distractible has not yet acquired adequate tuning capability in his reticular system), please let your reticular system retune you to this page so that we may go on.
Actions of Fay's Reflex Defense Mechanism
In the intact brain, functioning under normal physiological conditions, everything goes well. The cortex is in command and the reticular system tunes according to those commands. But suppose we subject that intact brain to sudden deprivation of oxygen. In such an abnormal physiological circumstance the cortex quickly reacts. In keeping with Jackson's concept, it generates "sudden, excessive, and temporary nervous discharges." These are cortical signals of physiological distress. They are carried to the reticular system, in brain levels below the cortex, and to the cerebellum. The cerebellum responds with what may be thought of as electrical counter-signals which may suppress the threat of seizure. Perhaps this is nature's way of trying to keep things in order with the cortex in control. However, if the environmental threat to the cortex, created by oxygen deprivation, is sufficiently great and the cortical distress signals are beyond the ability of the cerebellum to restrain them, the cerebellum stops sending its signals for the duration of the seizure which ensues. The mechanism envisioned in Fay's concept of reflex defensive action, the "release of higher levels" now comes into play.
The reticular system in lower brain levels, responding to a signal of distress, initiates two simultaneous actions. One tunes the cortex down so that its activity is depressed. This is necessary in order to free deep-seated defensive reflexes which are normally submerged by cortical-cerebellar control acquired during the process of functional development and maturation of the brain. In keeping with Fay's postulation and according to the present concept of the cause and mechanism of seizure activity, a seizure cannot occur unless the reticular system first depresses the cortex and the cerebellum ceases its seizure suppressing signals, thereby releasing the action of the reflex seizure mechanism.
As it depresses cortical function in response to the distress signal, the reticular system's second action is to set in motion the rest of the defensive reflex mechanism inherited by man from his amphibian ancestors. With cortical and cerebellar influences abolished, the reticular system now facilitates the released actions of lower brain levels which produce the convulsive movements of limbs and body, interpreted by Fay as movements of defense and escape.
If the signal from the cortex is minimal and the cerebellar seizure-inhibiting response is effective, the response of the reticular system will also be minimal and brief. In such a case there may be no visible evidence of seizure activity in the child's behavior. Or all that may be seen is a momentary cessation of general activity accompanied by a blank stare, a so-called "absence". But with cortical and cerebellar control (abolished there may be a wide range of seizure patterns between this and the major convulsive seizure.
Loss of consciousness during seizures is a result of the action of the reticular system in depressing the cortex. When the body economy comes back into balance after the violent physical activities of a major convulsive seizure the reticular system retunes the cortex upward, allowing cortical function to resume and consciousness to return.
Cortical Control of Deep-Seated Reflexes
It is useful to see how other deep-seated reflexes are released when cortical function is depressed or lost through factors having their origin in various abnormal situations. For example, emptying of bowel and bladder depends primarily on reflex neurological mechanisms. "Toilet training is purely a matter of maturation of a child's cortex to the point of controlling the reflex so that bowel and bladder emptying become subject to the person's choice of time, place and opportunity. The reticular system participates in this control so that normal, mature neurological mechanisms wake the person from sleep if necessary. The maturational process through which the cortex acquires control of these reflexes is the same as that by which it achieves the functions of vision, hearing, tactility, mobility, speech and manual competence which characterize man.
The person who suffers a stroke often becomes incontinent of bladder or bowel or both because the mechanism for reflex emptying has been released from control of the cortex which is the site of injury. The gradual deterioration of older people is often accompanied by progressive loss of bowel and bladder control because the deterioration is primarily in the cortex. Loss of sphincter control, with wetting and soiling of the clothing, commonly accompanies major seizures because a large degree of cortical control has been lost temporarily through depression by the reticular system, with consequent release of reflex emptying of bowel and bladder.
Another example, although less obvious, is the Babinski sign which, present in early infancy, is submerged as cortical function advances during the process of development and maturation of the brain. Cortical injury due to any cause characteristically releases the Babinski sign so that in abnormal circumstances it reappears in persons in whom it has been submerged for many years. The startle response often behaves similarly. It is probable that the cerebellum participates in such modification of reflex mechanisms but this question requires further study and clarification.
As with other reflex actions which are subject to cortical control, it is often possible to abort an incipient seizure in a child by abruptly reversing the early depressing action of the reticular system on the cortex, probably with the support of the cerebellum in suppressing seizure distress signals. Such a change in the direction of tuning by the reticular system, which in an instant restores the controlling position of the cortex and cerebellum, may be accomplished by a sharp, strong sensory input. We often see parents who, recognizing that a seizure is impending, yet unaware of the neurological mechanisms they are enlisting, call loudly to the child, shake or slap him sharply or pinch him strongly. The result is frequently an almost instantaneous recovery of the previous state of consciousness and alertness.
A recent experimental development in seizure control in adults is the use of biofeedback mechanisms which emphasize the preservation of cortical control. The discovery that body functions, such as heart rate and blood pressure, previously thought to be exclusively under autonomic control, can be influenced voluntarily through cortical action, has opened this avenue as a potential alternative to anticonvulsant drugs for some adults. The sense of an impending seizure may, with training in some people, permit the cortex to maintain control sufficient to withstand the depressing action of the reticular system and probably to enlist the support of the cerebellum. This would prevent transmission of abnormal electrical discharges which activate the defensive reflex mechanism. In other words, the individual consciously corrects or compensates neurologically for the environmental condition which is predisposing him to a seizure and cortically submerges the action of his seizure reflex mechanism.
Effect of Maturation of the Brain or Seizure Activity
In the normal mature brain it takes huge, wrenching, life-threatening physiological changes to set off the chain of events leading to a major seizure. In the immature brain of an infant or very young child a less drastic disturbance of the physiological environment, such as high fever with its greater general body demand for oxygen, is often sufficient to trigger this entire phenomenon. In the child who has suffered brain injury, abnormal electrical discharges may be more readily generated in local areas of injury because of increased susceptibility to changes in the physiological environment which trigger the seizure mechanism. In such a child developmental processes leading to progressive maturation and resulting cortical control have been slowed or impaired and cortical-cerebellar communication and reticular system tuning are immature and erratic.
It is here that the fallacy of anticonvulsant drug therapy becomes most apparent. These drugs may to some degree suppress the spread, in the brain, of cortical signals of distress during the brief periods that these phenomena occur. But, although they augment the seizure suppressing action of the cerebellum, every second of every day that they are in a child's body and brain they also depress cortical function in general. We believe that adding cortical depression, caused by drugs, to inadequate cortical function due to developmental lags resulting from brain injury often leads to insufficient cortical action and cortical-cerebellar integration to hold the reflex defense mechanism for seizures in check. The deleterious physical effects of these drugs in full, long-term doses, on cerebellar cells have already been discussed. We believe that it is in this way that anticonvulsants often contribute to the seizure activity they are supposed to suppress. Proof of this paradox is the progressive decrease in severity and frequency of seizures in IAHP children from whom anticonvulsant drugs have been gradually removed, as we have already noted.
A simple observation which points to maturation as the ultimate basis for the prevention or control of seizures is the well-known fact that seizure prevalence in adults is very much lower than in children. This is because most children with seizures grow up to become adults without seizures. Growing up obliterates seizures because the growth process is associated with physiological maturation, neurological as well as physical and sexual.
The physiological key to the prevention and control of seizures is the attainment of the highest possible level of cortical function and control. IAHP Human Development Programs, with their goals of achieving Intellectual Superiority, Physical Superiority and Social Superiority, recognize and implement this fundamental principle through specially structured environments with sensory inputs of hugely increased frequency, intensity and duration. It is also reasonable to consider that a second factor contributing to the reduction or cessation of seizures in children on IAHP treatment programs is decreased tendency toward generation of abnormal electrical discharges in the area of the brain which earlier suffered injury. The result would be reduction or abolition of seizure activity.
Do Seizures in Themselves Cause Additional Brain Injury?
It is not unusual to encounter parents who are apprehensive about withdrawal of anticonvulsant medication from their children. In such situations we have usually found that the apparent reason for this is worry that stopping anticonvulsant drugs might be followed by an increase in seizure frequency and severity. However, in further discussion with parents we have also learned that the more cogent reason is that they have been told that seizures in themselves cause brain injury or are capable of adding to already existing brain injury and, moreover, that failure to take prescribed anticonvulsants could result in seizures which would be fatal to their children.
Neither in our own very considerable experience nor in our careful, extensive and continuing search of the medical literature have we been able to find any convincing evidence to support this dreadful idea which stems largely from those seizure situations known as status epilepticus. In status epilepticus there are prolonged episodes of recurrent seizures following each other closely. Anticonvulsants may be implicated even in those uncommon instances in which status epilepticus ends in death. Dr. Cesare Lombroso of Harvard Medical School speaks of the effects attributable to excessive treatment with anticonvulsant drugs in status epilepticus. Dr. Raymond D. Adams, of the same medical school, states, "The real hazard in treating resistant recurrent convulsions is that consciousness and vital functions may be suppressed [by anticonvulsants] to a degree incompatible with life. The risk of deep coma without convulsions is greater than semicoma or stupor with an occasional convulsion." With regard to the belief "that status epilepticus and temporal lobe seizures aggravate pre-existing foci of brain damage," Dr. Norman Geschwind, also of Harvard Medical School, said in a letter to us, "this is not at all a clear fact."
At no point have we found any statement in the medical literature which shows recognition of the possibility that the admitted depressing effects of anticonvulsants on the cortex and their role in causing cerebellar intoxication or fatigue may be responsible for the perpetuation of status epilepticus through their continuing release of reflex seizure mechanisms.
Laboratory studies do not support the belief that seizures in themselves add to existing brain injury. For example, it is obviously impossible to examine human brain tissue immediately following a seizure. Even if such a procedure were feasible and fresh tissue injury were found in such an examination, it would still be impossible to determine whether the injury caused the seizure or the seizure caused the injury. Where people die in situations which are often associated with seizures, such as strokes, trauma, acute lack of oxygen or poisoning, it is not reasonable to conclude that the seizure causes brain injury; it is rather that brain injury causes the seizure.
In other laboratory studies on animals, investigators have found that seizures can readily be induced by many different means. However, such means must of necessity and in themselves be damaging to the brain or capable of interfering seriously, even though temporarily, with brain cell physiology. Here again the injury or the serious physiological embarrassment of the brain precedes seizures.
Another argument offered in support of the notion that seizures cause brain injury is based on studies which purport to show that people who have had seizures for many years are inclined to be dull and of lower intelligence than their peers. There are two fallacies in this argument. First, we remind you that many brain-injured children, both with and without seizures, are labeled mentally retarded. Your children have demonstrated how bright and capable they really are when given the benefits and opportunities provided by Human Development Treatment Programs.
The second fallacy lies in the fact that, so far as we have been able to determine, no study of the intelligence of people with long seizure histories has taken pains to discover how many were taking anticonvulsants and how much at the time of the study; to stop the use of anticonvulsant drugs well before the testing; or to give equivalent doses of these drugs to the people, not subject to seizures, with whom they are being compared. The depressing effects of anticonvulsants on the intellectual capabilities of people taking them is such as to put them at a serious disadvantage in comparison with their non-medicated peers. Although the limited effectiveness of anticonvulsants in controlling seizures declines even further with continuing use, the ability of these drugs to dull and stupefy usually goes on unabated.
Physiological Safeguards against Cortical Injury During Seizures
As we have pointed out, 55 per cent of the children with positive seizure histories were still having seizures when they first came to IAHP. Of these children 80.8 per cent were still taking anticonvulsant drugs when we first saw them, an indication of the failure of these drugs to control seizures. These are the children whose anticonvulsant drugs we have discontinued. We are not aware of a single death among them. We have observed a flurry of increased seizure activity in some children. This has usually subsided as the children's Human Development Treatment Programs were pursued. We have seen nothing in any child to indicate the occurrence of additional brain injury.
As we have already stated, we believe that the idea that seizures in themselves cause brain injury and death has no clinical support. Moreover, such an idea ignores newer knowledge concerning existing mechanisms within the brain by means of which the brain defends itself from injury during the stress associated with seizures.
The nature and extent of the safeguards provided for the brain during its reflex defensive seizure response to unfavorable physiological conditions are remarkable. Blood flow to the brain as a whole varies from moment to moment according to need. Blood flow to any small region of the cortex, such as that segment which controls voluntary opening and closing of the left hand, for example, also varies according to need. Thus, when such a minor activity as voluntary opening and closing of a hand is going on, the blood vessels in that area of the brain dilate and blood flow increases. When the hand action ceases, blood flow returns to the resting level. Whether overall or regionally, the brain normally regulates its own blood supply.
Seizure activity is accompanied by a large increase in blood flow in the area of injury where the seizure focus exists. During a major convulsion the cortex relinquishes control of its blood flow to those lower levels of the brain which regulate the general circulation of the body as a whole. At the same time the cortical vessels become dilated and their filling is assured by a sharp rise in body blood pressure. This action provides the cortex with a blood supply well beyond its immediate needs, even during a major seizure.
Possible Beneficial Effects of Seizures
The entire process of modification of cortical blood flow may be regarded as part of the reflex defensive mechanism postulated by Temple Fay. It would be paradoxical and indeed absurd if the brain, in response to a situation of need or distress, caused itself further injury. On the contrary, at IAHP we have observed events which would indicate that benefit rather than harm may be the net effect of seizures. A striking example of this is often seen when, immediately following a seizure, a brain-injured child who has never before been able to do so, talks, creeps, uses his hands or performs other functions for the first time. The reason for this important phenomenon may well lie in the heightened blood flow, provided by seizure mechanisms, which result in a net gain in overall blood supply. Even though this gain may be brief and temporary, it is an indication of the brain's potential for recovery or resumed development of cortical function after injury.
A Non-Pharmaceutical Approach to the Management of Seizures
A primary principle in procedures for the preservation of health is the prevention of illness. In the case of seizures, as with many other human ills, the fulfillment of this principle remains an unattainable ideal. This is largely because seizures are, in a vast majority of instances, symptoms of brain injury. Very little progress or even effort has been made to eliminate the almost numberless causes of brain injury. We are left, then, with problems for which there are as yet no preventive measures.
In the view of IAHP seizure activity associated with brain injury in children is the result of three factors acting conjointly:
1. Injured brain cells, having survived brain injury, may not yet have fully recovered normal physiological activity. Their physiological imbalances lead more readily to situations of functional stress and to generation of distress signals which, because of inadequate cortical-cerebellar control, may release the reflex defense mechanism leading to seizures.
2. Influences in the brain's environment unfavorably affect physiological processes made unstable by injury. This increases the possibility of functional stress and the generation of distress signals leading to seizures. From our observations at IAHP we believe that providing the injured brain with optimal environmental conditions is fundamental to (1) recovery of normal function; (2) appropriate physiological interaction among cortex, cerebellum and reticular system; and (3) a decrease or cessation of seizures. To achieve an optimal environment for the brain means to eliminate unfavorable influences and to reinforce those which are favorable. This is a basic principle in the Human Development Treatment Program of every IAHP child.
More than 25 years ago IAHP were the first to recognize that among the various adverse environmental conditions which affect the brain-injured child the most important is chronically insufficient oxygen supply to the brain. It is our experience that this is almost universally present to some degree in brain-injured children, although not ordinarily in outspoken, obvious form. The shallow and erratic breathing patterns and small chests seen in the majority of our brain-injured children are primary indications that such subclinical oxygen deficiency exists.
To deal with this problem of oxygen insufficiency, which may be crucial to a child's progress and in the control of seizures where they exist, we have devised various effective measures, among which are masking and respiratory patterning. IAHP parents are thoroughly familiar with the benefits their children have derived from these procedures. Increased oxygen availability, provided by respiratory patterning and by intensifying masking programs, has been the most effective single action taken by IAHP in decreasing seizure activity and making possible the reduction and discontinuation of anticonvulsant drugs.
Associated with oxygen insufficiency in various combinations are other adverse environmental factors contributing to seizures as well as other problems of the brain-injured child. Among these factors are blood sugar levels too low or unresponsive to the brain's changing needs; nutritional imbalances or deficiencies, very common among IAHP children, most of whose diets are extremely poor both quantitatively and qualitatively when they are first seen by us; and increases in pressure within the skull due to intake of liquids and water-retaining substances, such as salt, in amounts beyond the child's needs or capabilities for handling.
3. The third and possibly most important factor contributing to seizure activity is the child's immature neurological organization and development involving especially the cortex, cerebellum and reticular system. Because of maturational delay due to brain-injury the cortex has not yet attained a sufficiently dominating role in its normal functional position at the top of the neurological chain of command. Neither have adequate functional relationships developed among cortex, cerebellum and reticular system.
As we have already reported, in most of the 80.8 per cent of children who were taking anticonvulsant drugs at their first IAHP evaluation, gradual withdrawal of medication was associated with progressive decrease of seizure frequency and severity. A flurry of increased seizure activity, usually subsiding as their Human Development Treatment Programs are pursued, is noted in some of these children. In uncommon instances seizures continue unabated on withdrawing anticonvulsants. In rare situations this is associated with indications of active pathology in the brain. Such children are referred for neurosurgical study which usually reveals that both the continuing seizures and the signs of active pathology are due to the same underlying cause, such as hydrocephalus, tumor or fresh trauma.
Persistence of seizure activity without signs of active brain pathology is usually an indication that the Human Development Treatment Program, particularly the correction of unfavorable environmental factors and especially the need for increased oxygen availability, is not being sufficiently vigorously pursued.
Thus, by means of the principles and procedures employed in IAHP Human Development Treatment Programs, which greatly advance the rate of neurological growth and maturation, the cortex acquires the controlling functional position and the working relationships with cerebellum and reticular system necessary to prevent the release of the reflex mechanism for seizures. This process is the same as that by which a child achieves bowel and bladder control and the submergence of other deep seated neurological responses such as the Babinski and the startle. These principles and procedures are also well known to IAHP parents.
Conclusion
Experience with modern anticonvulsant drugs over the 40 years since their introduction shows that:
1. Their use is not based on sound physiological rationale.
2. Their use in children causes intellectual dulling and stupefaction, often sufficient to interfere seriously with developmental processes already impaired by brain injury, among them those which normally lead to control of reflex seizure mechanisms.
3. Their use is often accompanied by many other undesirable side effects, some developing insidiously but nonetheless capable of serious impact on health.
4. Their effectiveness in controlling seizures, which is the only purpose for their use, is at best highly questionable.
5. Their present-day continuing use ignores the newer knowledge of neurophysiological mechanisms and of the effects of maturation and development on these mechanisms.
6. Their toxic or fatiguing actions on the cerebellum, combined with their depressing effects on the cerebral cortex, often tend to release seizure mechanisms with the result that instead of suppressing seizures these drugs may encourage their occurrence.
7. The physiological key to the prevention or control of seizures is the attainment of the highest possible level of cerebral cortical function in its relation with the cerebellum and the reticular system. By their action in interfering with such an attainment anticonvulsant drugs negate this fundamental conceptual principle.
