A Complementary Medicine Approach to Abdominal Epilepsy

A Complementary Medicine Approach to Abdominal Epilepsy


Historical and current medical literature on abdominal epilepsy, discuss the biological aspects of the syndrome, and explain the abdominal/visceral component as a plausible etiological factor.   Based on this discussion, the clinical and research implications of abdominal epilepsy will be presented from the perspective of a complementary medicine model based on the work of Edgar Cayce as developed by the Meridian Institute.


From a medical perspective, the term epilepsy refers not to a single disease, but to a group of symptoms with numerous causes.  The common factor in all forms of epilepsy is an excessive electrical excitability of the brain.  The increased excitation is called a seizure and may manifest as a partial or total loss of consciousness and muscle spasms or other involuntary movements.

Many conditions can produce epilepsy.  For example, a genetic predisposition is believed to be involved in some cases.  In others instances,  trauma to the head, brain tumors and stroke are known to be causative factors.  Yet, in approximately one half of all cases of epilepsy the cause is unknown (Pedley, 1985).  This predominant category of epilepsy is classified as ideopathic, which means “disease without recognizable cause.”  (Thomas, 1973)

Historically, ideopathic epilepsy has been called by several names.  “Cases of epilepsy in which no cerebral lesion can be demonstrated are labeled as ideopathic, cryptogenic, essential,
pure, primary or true.”   (Epilepsy Foundation of America, 1975, p. 17)   The earlier designation of  ideopathic epilepsy as “true” epilepsy will be relevant later in this paper as it was the term used by Edgar Cayce.

This paper will focus on a form of ideopathic epilepsy known as abdominal epilepsy.  Selections from the historical and current medical  literature will be cited which support the idea that abdominal epilepsy may account for a significant portion of ideopathic epilepsy.  A later section will discuss the research and clinical implications of abdominal epilepsy from a complementary medicine model.

Abdominal Epilepsy

The association of abdominal symptoms with epilepsy has been recognized for many years.  For example, “gastric and intestinal disturbances” were viewed as primary etiological factors by medical doctors during the late 19th and early twentieth century (Musser & Kelly, 1912).  The invention and clinical application of the electroencephalogram (EEG) during the 1920’s shifted the focus of medical attention from the abdomen to the brain where, for the most part, it has remained to this day.

Another example of the abdominal connection in epilepsy is the aura which is common in certain types of epilepsy.  For example, temporal lobe epileptic seizures frequently begin with an aura.  In neurological terms, an aura is actually a mild seizure which precedes the primary seizure.  It can be thought of as a warning that a seizure is about to happen.  Most often, auras manifest as an altered consciousness or peculiar sensation.  “The most common aura is of vague gastric distress, ascending up into the chest”   (Gordon, 1942, p. 610).

Modern medical science has rediscovered the abdominal connection in epilepsy.  Several papers published in the medical journals during the 1960s called attention to the abdominal connection in epilepsy.  Over the past forty years,  numerous researchers and clinicians have reported on various aspects of abdominal epilepsy.  Appendix A contained a representative sample of the abdominal epilepsy literature.

Common clinical features of abdominal epilepsy include abdominal pain, nausea, bloating,  and diarrhea with nervous system manifestations such as headache, confusion, and syncope (Peppercorn & Herzog, 1989).  “Although its abdominal symptoms may be similar to those of the irritable bowel syndrome, it may be distinguished from the latter condition by  the  presence  of  altered  consciousness during some of the attacks, a tendency  toward  tiredness  after  an  attack,  and  by  an  abnormal EEG”(Zarling, 1984, p.687). Mitchell, Green- wood and Messenheimer (1983) regard cyclic vomiting as a primary symptom of abdominal epilepsy manifesting as simple partial seizures (1983).

Although abdominal epilepsy is diagnosed most often in children, the research of Peppercorn and Herzog (1989) suggests that abdominal epilepsy may be much more common in adults than is generally recognized:

Abdominal epilepsy is well described among pediatric patients but is recognized only infrequently in adults.  Our experience over the past 15 years indicates that the disorder may not be as rare as is suggested by the paucity of literature on the subject.  Moreover, the variability of the clinical presentation indicates a spectrum to both the gastrointestinal (GI) and central nervous system (CNS) manifestations of abdominal epilepsy in adults.”  (Peppercorn & Herzog, 1989, p. 1294)

One of the primary problems in understanding abdominal epilepsy is clearly defining the relationship of the abdominal symptoms to the seizure activity in the brain.  In other words, what is the pathophysiology of abdominal epilepsy.  Is the essential pathology in certain areas of the brain which happen to be connected to the abdominal organs?  Or, is the primary pathology in the abdomen which is conveyed through connecting nerve fibers to the brain resulting in epileptic seizures?  Peppercorn and Herzog noted both possibilities in their attempt to understand the cause of abdominal epilepsy:

    The pathophysiology of abdominal epilepsy remains unclear.  Temporal lobe seizure activity usually arises in or involves the amygdala.  It is not surprising, therefore, that patients who have seizures involving the temporal lobe have GI symptoms, since discharges arising in the amygdala can be transmitted to the gut via dense direct projections to the dorsal motor nucleus of the vagus.  In addition, sympathetic pathways from the amygdala to the GI tract can be activated via the hypothalamus.
    On the other hand, it is not clear that the initial disturbance in abdominal epilepsy arises in the brain.  There are direct sensory pathways from the bowel via the vagus nerve to the solitary nucleus of the medulla which is heavily connected to the amygdala.  These can be activated during intestinal contractions.  (Peppercorn & Herzog, 1989, p. 1296).

At this time, there is no definitive model of abdominal epilepsy which explains the association of brain seizures and abdominal symptoms.  However, there is a growing body of medical information which may lead to a better understanding of this complex relationship.

The Abdominal Brain

Although Peppercorn and Herzog allow for the possibility that abdominal epilepsy may be caused by abdominal processes transferred to the brain via the vagus (tenth cranial nerve), the anatomical and physiological basis for such an abdominal connection in epilepsy requires further discussion.  In other words, what is it about the abdomen that could possibly produce such an extreme neurological reaction as to cause a seizure in the brain?  To answer this important question, it is helpful to review the medical literature of the early decades of this century.  For example, the work of Byron Robinson, M.D., a well respected physician and researcher of that era, exemplifies the position that the abdomen contains a secondary brain.

    In mammals there exist two brains of almost equal importance to the individual and race.  One is the cranial brain, the instrument of volitions, of mental progress and physical protection.  The other is the abdominal brain, the instrument of vascular and visceral function.  It is the automatic, vegetative, the subconscious brain of physical existence.  In the cranial brain resides the consciousness of right and wrong.  Here is the seat of all progress, mental and moral … However, in the abdomen there exists a brain of wonderful power maintaining eternal, restless vigilance over its viscera.  It presides over organic life.  It dominates the rhythmical function of viscera….The abdominal brain is a receiver, a reorganizer, an emitter of nerve forces.  It has the power of a brain.  It is a reflex center in health and disease….
    The abdominal brain is not a mere agent of the [cerebral] brain and cord; it receives and generates nerve forces itself; it presides over nutrition.  It is the center of life itself.  In it are repeated all the physiologic and pathologic manifestations of visceral function (rhythm, absorption, secretion, and nutrition).  The abdominal brain can live without the cranial brain, which is demonstrated by living children being born without cerebrospinal axis.  On the contrary the cranial brain can not live without the abdominal brain….   (Byron Robinson,  1907, 123 – 126)

Robinson was not alone in his fascination with the nervous system of the abdomen.  At about the same time that Robinson was discovering the abdominal brain, British physiologist Johannis Langley of Cambridge University recognized that:

 … the ganglia of the gut do more than simply relay and distribute information from the cephalic [cerebral] brain.  He was unable to reconcile conceptually the great disparity between the 2 X 10 (8) neurons in the gut and the few hundred vagus fibers from the big brain, other than to suggest that the nervous system of the gut was capable of integrative functions independent of the central nervous system.   (Wood, 1994, p. 424)

Langley labeled the brain in the gut the enteric nervous system (ENS).  Although for several decades Robinson and Langley’s work has been ignored, modern medical research has finally rediscovered the abdominal brain with its enteric nervous system.  In fact, research on the nerve connections in the abdomen is one of the “hot” areas of medical research.

    To a considerable extent, the new interest in exploring the ENS has come from the realization that both the ENS and the remainder of the autonomic nervous system are richly endowed with neurotransmitters and neuromodulators.  Many substances are found in both the bowel and the brain, a coincidence that strikes most observers as intrinsically interesting, if not immediately explicable.   (Gershon, Kirchgessner & Wade, 1994, p. 386)

    The similarity between the structure of the ENS and that of the brain, combined with the ability of the ENS to mediate relatively simple behaviors, suggests that general principles can be derived from studies of the ENS that will eventually be applicable to the CNS.  Given the unique position of the ENS as the only peripheral system capable of autonomous function, it seems more likely that such principles will emerge from investigations of the ENS than from studies of other aggregates of peripheral ganglia.  The parallel between the bowel and the brain also suggests that newly discovered principles of central neural function may find applicability in studies of the ENS, in a sort of reverse form of reductionism whereby the brain serves as a model for the gut.  (Gershon, Kirchgessner & Wade, 1994, p. 414)

In addition to the biochemical and structural similarities between the cerebral brain and the abdominal brain, contemporary researchers are drawing computer analogies and using information processing models to describe the relationship between the brains of the body.

    The cephalic [cerebral] brain communicates with the smaller brain in the gut in a manner analogous to that of interactive communication between networked computers.  Primary sensory afferents and extensions of intramural neurons in the gut carry information to the central nervous system.  Information is transmitted from the brain to the enteric nervous system over sympathetic and parasympathetic pathways.  This, however, represents only one kind of input of an integrative network that also contains microcircuitry for processing information from a variety of sensory receptors along the digestive tract, as well as synaptic circuits that generate programmed patterns of neural outflow to the effector systems.  Input to enteric ganglion cells is not exclusively from the central nervous system as once thought, and the old habit of referring to the neurons of the enteric nervous system as postganglionic neurons has become outmoded and abandoned.
    The current concept of the enteric nervous system is that of a minibrain placed in close proximity to the effector systems it controls.  Rather than crowding the hundred million neurons required for control of the gut into the cranial cavity as part of the cephalic brain, and transmitting signals over long-unreliable pathways, natural selection placed the integrative microcircuits at the site of the effectors.  The circuits at the effector sites have evolved as an organized network of different kinds of neurons interconnected by chemical synapses.  (Wood, 1994, p. 424)
To extend Wood’s computer analogy of the enteric nervous system to abdominal epilepsy, one might say that the nervous system network “crashes” during a seizure.  The linkage between the abdominal brain and cerebral brain is broken.  Depending upon the severity of the incoordination, much of the information processing and regulatory functioning of the entire nervous system may temporarily go “offline.”

Although these selections from the medical literature do not solve the problem of the cause of abdominal epilepsy, they do tend to support the plausibility of primary abdominal pathology in the pathophysiology of abdominal epilepsy.

A Complementary Medicine Approach to Abdominal Epilepsy

The possibility that abdominal epilepsy may be caused by pathology in the abdomen raises some intriguing questions in regards to clinical practice and basic research.  What is the nature of the pathology?  Can it be measured?  If pathology  is shown (or assumed) to exist, what type of treatment regimen is most effective?  Is there any evidence to support therapies which focus on abdominal pathology?  What is the role of regular medical treatment modalities for abdominal epilepsy (i.e., medication and surgery).  Can abdominal epilepsy be cured?

In seeking answers to these questions, the  Meridian Institute (a research organization located in Virginia Beach Virginia) has developed a therapeutic model based on the work of Edgar Cayce.  Cayce was an intuitive diagnostician who died in 1945.  He is widely regarded as the father of modern holistic medicine (Callen, 1979; Mein, 1989).  Almost 15,000 of his readings were stenographically transcribed and are now available at the Association of Research and Enlightenment (A.R.E.) Library in Virginia Beach, Virginia and are also available in a CD-ROM format (Cayce, 1993).

His views regarding epilepsy are highly consistent with the medical information presented above.  For example, he believed that there are various forms of epilepsy produced by numerous causes.  However, he consistently maintained that the primary cause of epilepsy can most often be found in the peripheral nervous systems, particularly the abdomen.

His perspective is consistent with the findings of Peppercorn and Herzog (1989)  which asserts that abdominal epilepsy is more common that is generally recognized, especially in adults.  Cayce provided explicit, detailed descriptions of anatomical and physiological pathology in epilepsy, often tracing the problem back to an area of the abdomen which he called the “lacteal duct plexus.”

Physiologically, lacteal ducts are part of the lymphatic system.  They absorb fats and proteins  from the small intestine.  Cayce stated that various etiological factors (e.g., high fever, abdominal injury, reflexes from other portions of the nervous system) could produce “adhesions” in the area of the lacteal ducts.  An adhesion is a:

… union of two surfaces that are normally separate; also, any fibrous band that connects them.  Surgery within the abdomen sometimes results in adhesions from scar tissue.  As an organ heals, fibrous scar tissue forms around the incision.  This scar tissue may cling to the surface of adjoining organs, causing them to kink.  Adhesions are usually painless and cause no difficulties, although occasionally they produce obstruction or malfunction by distorting the organ.  The can also occur following peritonitis and other inflammatory conditions.  They may occur in the pleura, in the pericardium and around the pelvic organ, in addition to the abdomen.  (Miller & Keane, 1972, p. 16)

Abdominal adhesions were a major etiological factor in Cayce’s model of epilepsy.  He noted that adhesions to the lacteal duct area could be produced by a variety of sources including high fever, abdominal injury, and nerve  reflexes from injured spinal centers.

Here are a couple of examples of Cayce’s description of the pathophysiology of abdominal epilepsy.  The first case involved an eighteen year old male. Cayce stated that there had been a spinal injury producing nerve reflexes to the abdomen which:

    … caused a slowing of the circulation through the areas of the lacteal ducts, thus producing a cold area there, that has produced a partial adherence of tissue.
    With the activity of the lymph through the area, we find that periodically, when there is the lack of proper eliminations through the alimentary canal, there occurs a reflex to the coordination between sympathetic [abdominal brain]  and cerebrospinal [central nervous] system area; that takes the governing of the impulse, as it were, to the brain reactions; or a form of spasmodic reaction that might be called epileptic in its nature.  (Cayce, 1939)

Note the reference to adhesion (“adherence of tissue”) and a slowing of circulation through this area.  Cayce believed that  restricted circulation produced coldness in the area of the lacteal ducts (on the right side of the abdomen).  According to Cayce, “From EVERY condition that is of true [ideopathic] epileptic nature there will be found a cold spot or area between the lacteal duct and the caecum.”  (Cayce, 1934)
These points will be discussed later in regards to therapeutic rationale and research implications.  Also note the reference to periodicity associated with “activity of the lymph through the area” and “proper eliminations through the alimentary canal.”  In other words, cycles of seizure activity were linked to activity of the gastrointestinal tract (i.e., digestion and eliminations).  Hence seizure activity may be associated with digestive problems with certain types of foods (e.g., carbohydrates and fats) and/or with improper eliminations (diarrhea or constipation).

Another important point is the importance of  “coordination” between the nervous system in the abdomen and the nerves of the brain.  Consistent with the growing body of medical information on the “abdominal brain” and enteric nervous system, Cayce referred to the abdominal brain as the “solar plexus brain,” (1921 & 1926),  the “secondary brain” (1944), and the “central brain in the solar plexus” (1927).  He noted that the brain in the abdomen with its nervous system (the “sympathetic” system) and the brain in the head with its nervous system (the “cerebrospinal system”) must coordinate to maintain physical and mental health.  When these two systems are out of harmony with each other, various forms of illness usually result.  Epileptic seizures might be regarded as the most severe form of incoordination between these two brains and nervous systems of the body.  Actually, the extent of nervous system incoordination might be described as almost a complete dissociation.

Here is another description of the basic nervous system incoordination by Edgar Cayce given for an adult suffering from epilepsy:

    As indicated, the lesions – or adhesions and lesions – in the lacteal ducts are the basic cause for the disturbance in the nervous system…. When there is an expression or activity from the sympathetic nervous system … we find there is movement or impulse to and from the brain centers themselves.  Then with a lesion or adhesion the impulse is cut off – or deflected…. Then this … connection with the solar plexus nerve centers [abdominal brain], making for an incoordination with the cerebrospinal nerve system, produces at the base of the brain – or through the medulla oblongata – an incoordinant reaction [seizure] …
Q.  Do you find any condition existing in the brain, or is it reflex?
A.  As we find, and as indicated, the accumulations that have been there [in the cerebral brain] are rather reflex – and are produced by the condition in the lacteal duct area.   (Cayce, 1935)

Note that the reflex from the abdomen produced “accumulations” in the cerebral brain .  Perhaps a modern brain scan or electro-encephalogram would have detected a focal lesion in the brain as the source of the seizure.  Yet, Cayce insisted that the source of the condition was in the abdomen.  Also note that the reflex from the abdomen was mediated through the medulla oblongata, a important nerve center  at the upper portion of the spinal cord where it enters the skull.  This is significant because Cayce sometimes recommended that a piece of ice be placed at this area during the aura or at the beginning of the seizure.  This simple technique has proven effective in several contemporary cases where Cayce’s therapeutic model has been utlilized.  Incidently, this technique for preventing seizures  was also used by osteopathic physicians during the early decades of this century and is included in the therapeutic model developed by the Meridian Institute.

Because Cayce’s perspective has been supported by numerous anecdotal cases reporting improvement or cure in cases of epilepsy and other major illnesses, the Meridian Institute was formed to research this information “in a modern, scientific manner that would provide data acceptable to all healthcare professionals and agencies.”  (Meridian Institute, 1994).

The research protocol developed to test Cayce’s perspective on  epilepsy has the following format:

Selection of Subjects

Edgar Cayce and the modern medical literature are in agreement that epilepsy is a heterogenous condition consisting of various forms produced by various causes.  Although Cayce provided information for individuals suffering from many forms of epilepsy, the most common form was linked to abdominal pathology.  In current medical terminology, this would be abdominal epilepsy or ideopathic epilepsy with abdominal features.  This subgroup of epilepsy will be the most appropriate to test Cayce’s statements about the pathophysiology and recommendations for treatment.  Thus the first step is to identify subjects suffering from abdominal epilepsy or at least, ideopathic epilepsy with abdominal features.

Assessment of Subjects

The initial assessment is intended to collect a  broad spectrum of data related to symptoms, quality of life and biological functioning.  The assessment procedure begins with a physical examination (with particular attention to possible somatic dysfunction such as spinal lesions and abdominal pathology).

Thermography is utilized to assess for temperature variations on the surface of the abdomen and along the spine.  The rationale for this assessment is to test Cayce’s assertion that a cold area is produced by decreased circulation on the right side of the abdomen in the area of the lacteal ducts.  Preliminary studies by the Meridian Institute suggest that there may also be variations in temperature along the spine which are segmentally correlated to abdominal variations.

Quality of life, symptomology, daily activities, and treatment side-effects are measured by a variety of psychometric instruments.  This dimension of assessment is intended to address the whole person.

Therapeutic Rationale

The therapeutic model is a complementary medicine approach intended to supplement standard medical practices for the treatment of epilepsy.  Therefore, the first provision of the model is that whatever medical treatment has been prescribed by the attending physician will be continued.  Complementary medicine can be thought of as treatment “in addition to” standard medical practice.  Complementary medicine emphasizes cooperation between health care professionals of conventional and alternative therapies.  (Budd, C., Fisher, B., Parrinder, D. & Price, L. ,1990;  LaValley,  J.W. & Verhoef, M. J.,  1995).

Several basic adjunct therapies are recommended to normalize abdominal function- ing and assist the nervous systems to coordinate with each other.  These modalities are relatively inexpensive and non-intrusive.  For the most part, the treatments can be done in the home by nonprofessional caregivers.
Hot castor oil packs applied to the abdomen are the primary treatment.  According to Cayce, these packs are intended to break up adhesions in the lacteal duct plexus and normalize circulation throughout this area of the abdomen.  A typical session lasts approximately one hour per day with three sessions per week.

Gentle masssage is recommended following the castor oil session.  Particular attention is paid to the abdomen (to assist in breaking up adhesions) and along the spine (to assist with nervous system coordination).

Basic dietary suggestions include a balanced diet with a prepondence of fruits and vegetables and low amounts of meats and refined carbohydrates.  In addition to the nutritional aspect of the diet, it is intended to produce normal bowel movements.  In other words, improved digestion and normal eliminations through the colon are viewed as beneficial to the treatment of this form of epilepsy.

In cases where constipation is a chronic problem, colonic irrigations are recommended to cleanse the colon.  The rationale for this treatment is that “pressure” on the colon from chronic constipation may be the source of the nervous system incoordination via pressures on the enteric nervous system.

Spinal manipulations by an osteopath or chiropractor may be helpful, particularly in cases where history or assessment indicate somatic dysfunction.  As noted above, Cayce often cited spinal injury as the origin of the nerve reflexes producing adhesions in the abdomen.

If the subject is currently experiencing seizures and can sense the beginning of the episode, they are encouraged to use a piece of ice at the base of the brain for one to two minutes.

The protocol includes opportunities for addressing psychological and spiritual issues associated with the illness.  Individual and group counseling and support is integrated into the therapeutic regimen.

Outcome Evaluation

The Meridian Institute research project on abdominal epilepsy should be viewed as a preliminary study designed to test the plausibility of Cayce’s information on abdominal epilepsy and provide a foundation for further study if deemed appropriate based on outcome evaluation.

Outcome evaluation will consist of a post-test repeat of the initial assessment procedures approximately three months after the beginning of the therapeutic regimen.  Particular attention will be paid to Cayce’s assertion that a “cold spot” will be found on the right side of the abdomen in cases of “true” or ideopathic epilepsy.  It is assumed that abdominal epilepsy as defined in the medical literature and described in this paper will be included in Cayce’s category of “true” epilepsy.  It is possible that many individuals suffering from idiopathic epilepsy may have abdominal epilepsy which goes undiagnosed because the abdominal symptoms are mild and subclinical.  This may be particularly true of temporal lobe epilepsy.  Thus one of the goals of our outcome evaluation is to try to get a sense of the prevalence of abdominal epilepsy (or ideopathic epilepsy with abdominal features).

Furthermore, if a cold spot is found in the initial assessment, post treatment assessment will determine whether use of castor oil packs have had an impact on decreasing the thermal abnormality.

Longer term outcome evaluation will depend upon the efficacy of the above procedures.  If the subject appears to fit the profile of abdominal epilepsy described above and seems to benefit from the adjunct therapies in  the treatment regimen, perhaps the attending physician will be willing to reconsider the lowest therapeutic dosage of medication on a trial basis.

Quality of life issues will be monitored in the follow-up assessment to determine whether the treatment regimen has had effects in this area.


This paper has discussed a particular form of epilepsy designated as abdominal epilepsy.  Abdominal epilepsy is recognized in the medical literature in children and adults.  Recent research indicates that this type of epilepsy may be more common than is generally realized.

The pathophysiology of abdominal epilepsy has been considered from the standpoint of a well  established research literature on the abdominal nervous system.  It appears that there is a relatively autonomous nervous system with its own brain situated in the abdomen.

It has been hypothesized that incoordination between the abdominal brain and the cerebral brain may  be involved in abdominal epilepsy.  This perspective was first advanced by Edgar Cayce, a 20th century intuitive diagnostician who  provided a considerable amount of  information on various aspects of epilepsy and other medical conditions.

A research protocol has been developed by the Meridian Institute to investigate Cayce’s assertions and test specific hypothesises derived from the Cayce material.  A brief overview of the assessment procedures, therapeutic modalities, and outcome evaluation has been included.


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 Appendix A

 References on Abdominal Epilepsy

The following references are representative of the abdominal epilepsy literature.  They are included in this appendix as an aid to readers interested in further pursuing the topic.

Agrawal, P., Dhar, N. K., Bhatia, M. S. & Malik,  S. C.  (1989).  Abdominal epilepsy.  Indian  Journal of  Pediatriacs, 56(4), 539-541.

Babb, R. R. & Eckman, P. B.  (1972).  Abdominal epilepsy.  Journal of the American Medical      Association, 222(1), 65-66.

Berdichevskii, M. (1965).  Meso-diencephalic epilepsy after abdominal injury.  Vopr Psikhiatr  Nevropatol, 11, 374-376.

Bondarenko, E. S., Shiretorova, D. Ch. & Miron, V. A.  (1986).  Abdominal  syndrome  in  the  structure of cerebral paroxysms in children and adolescents.  Soviet Medicine, (2), 39-44.

Douglas,  E. F. & White, P. T.  (1971).  Abdominal epilepsy–a reappraisal.  Journal of   Pediatrics, 78(1), 59-67.

Hotta, T. & Fujimoto, Y.  (1973).  A study on abdominal epilepsy.  Yonago Acta Medica,  17(3),   231-239.

Juillard, E.  (1967).  Abdominal pains and epilepsy.  Praxis, 56(3),  83-84.

Loar,  C. R.  (1979).  Abdominal epilepsy.  Journal of the American Medical Association,   241(13), 1327.

Matsuo,  F.  (1984).  Partial epileptic seizures beginning in the truncal muscles.  Acta Neurologica     Scandinavia, 69(5), 264-269.

Mitchell, W. G., Greenwood, R.S. & Messenheimer, J. A.  (1983).  Abdominal  epilepsy: Cyclic   vomiting  as  the  major  symptom of simple partial seizures.    Archives of  Neurology, 40(4) 251-252.

Moore, M. T.  (1972).  Abdominal epilepsy.  Journal of the American Medical Association, 222    (11), 1426.

Moore,  M. T.  (1979).  Abdominal epilepsy [letter].   Journal of the American Medical  Association, 241(13), 1327.

O’Donohoe,  N. V.  (1971).  Abdominal epilepsy.  Developmental Medicine of Child Neurology,  13(6), 798-800.

Peppercorn, M. A., Herzog, A. G., Dichter, M. A. & Mayman, C. I.  (1978).  Abdominal epilepsy: A cause of abdominal pain in adults.  Journal of the American Medical Association,40(22), 2450-2451.

Peppercorn, M. A. & Herzog, A. G.  (1989).  The spectrum of abdominal epilepsy in adults. American Journal of Gastroenterology, 84(10), 1294-1296.

Reimann, H. A.  (1973).   Abdominal epilepsy and migraine.  Journal of the American Medical  Association, 224(1), 128.

Singhi, P. D. & Kaur, S.  (1988).  Abdominal epilepsy misdiagnosed as psychogenic pain. Postgraduate Medical  Journal, 64(750), 281-282.

Solana de Lope, J., Alarcon, F. O., Aguilar, M.  J., Beltran, C. J., Barinagarrementeria,  F. &  Perez, M. J.  (1994).  Abdominal epilepsy in the adult.  Review of Gastroenterology, 59(4), 297-300.

Takei, T. & Nakajima, K. (1967).  Autonomic  abdominal epilepsy–clinico-encephalographic  evaluation of 24 cases.  Nippon Shonika Gakkai Zasshi, 71(5), 543-551.

Yingkun,  F.  (1980).  Abdominal epilepsy.  Chinese Medical Journal, 93(3), 135-148.

Zarling,  E. J.  Abdominal epilepsy: an unusual cause of recurrent abdominal pain.  (1984).  American Journal of Gastroenterology, 79(9), 687-688.