A Traditional Osteopathic Approach to Abdominal Epilepsy
Abdominal epilepsy is one of numerous forms of seizure disorder recognized in the medical literature. The purpose of this paper is to review the 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 traditional osteopathic concepts. This paper is one of a series of research projects designed to explore the potential of historical/traditional healing approaches as applied to incurable medical conditions of unknown causation.
Introduction
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)
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 contains 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, Greenwood 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 Traditional Osteopathic 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 traditional osteopathic concepts as found in the early literature of osteopathy. Although modern osteopathy is almost identical to allopathic medicine, traditional osteopathy as it was invented by A. T. Still during the late nineteenth century and practiced during the first half of the twentieth century, was much more oriented to physical medicine modalities for the diagnosis and treatment of illness. The emphasis on somatic dysfunction as a common etiological factor in a wide range of illnesses (including neurological syndromes such as epilepsy) was strongly advocated in the early osteopathic literature.
Traditional osteopathic concepts have a strong biological base built upon the work of researcher/clinicians such as Byron Robinson and his formulation of the abdominal brain model. Actually, Robinson’s 1907 classic work on peripheral nervous system anatomy and physiology is entitled The Abdominal And Pelvic Brain (Robinson, 1907). Robinson saw the nervous system as a complex interactive organization of nerve fibers and ganglia.
The sympathetic nerve consists of, viz.: (a) ganglia (lateral chain); (b) conducting cords; (c) three ganglionic plexuses located in the chest (thoracic plexus), abdomen (abdominal brain), and pelvis (pelvic brain); and (d) automatic visceral ganglia. The conducting cords are not sheathed; they are non-medullated. The ganglia, composed of nerve cells, are little brains. They are reorganizing centers, receiving sensations and sending out motion. The abdominal and pelvic brains and the ganglionic plexuses are simply large brains or aggregations of nerve cells. (Robinson, 1907, p. 287)
In other words, the organization of the nervous system may be regarded as a “hierarchy of brains” with the cerebral brain being the most complex and influential, but other brain centers in the body are also capable of information processing and autonomous activity. Furthermore, (and most importantly with regard to epilepsy), these “little brains” in the peripheral nervous system may be able to influence the cerebral brain via nerve reflexes and vegetative processes, resulting in epileptic seizures.
A. T. Still also recognized a hierarchy of brains in the body, including ganglia along the spinal column in his model of the nervous system:
The term “CERVICAL BRAIN” has been applied by Dr. Still to the region lying between the first cervical vertebra and the fourth dorsal vertebra. The term “ABDOMINAL BRAIN” has been applied by him to the region lying between the first dorsal and third lumbar vertebrae, “PELVIC BRAIN,” to that region lying between the tenth dorsal and fifth lumbar vertebrae. (Hazzard, 1899, p. 9 – 10)
Thus, traditional osteopathic concepts acknowledged the cerebral and abdominal brains, but went further to include other portions of the peripheral nervous systems as “little brains” in the body. Not surprisingly, the traditional osteopathic perspective on epilepsy was strongly influenced by this view. Peripheral pathology was diagnosed in many cases of epilepsy, including recognition that the abdomen and its nerve plexus was involved in the pathophysiology of certain forms of epilepsy (e.g., Riggs, 1901; Hazzard, 1905; Murray, 1925).
This approach paid considerable attention to nervous system interactions such as nerve reflexes whereby one part of the system can influence other parts. For example, a pressure on spinal nerves might cause pathology in the abdomen. Or, conversely, pathology in the abdomen might produce a lesion (somatic dysfunction) in a spinal center.
It seems that lesion along the neck and spine anywhere may cause epilepsy. Dr. A. T. Still is credited with the statement that there is usually lesion between the 2nd and 3rd cervical vertebrae. He also ascribes epilepsy to lesion causing prolapse of the diaphragm, and obstruction to the arterial and venous blood, and of the lymph, in the vessels perforating it. In this way the products of digestion are retained and decompose, the patient suffering from auto-intoxication. (Hazzard, 1905, p. 273)
The complex nerve reflex interactions might involve almost any portion of the spine or abdominal nerve plexus. For example, “In a case of epilepsy in a boy, removal of lesion to the coccyx [tailbone] cured a case after all other means had failed.” (Hazzard, 1905, p. 273) The osteopathic literature contains numerous examples of manual medicine used to effectively treat epilepsy (e.g., Barber, 1898; Hazzard, 1905).
The abdominal connection in epilepsy was well established in this model both in terms of causation and treatment. Furthermore, treatment of both the spinal centers and abdomen was standard procedure as noted in the following excerpts:
Many authorities regard chronic alimentary autointoxication as a cause of epilepsy and consider colonic kinks, dilatations, adhesions, ptoses, and stasis of therapeutic importance. (Downing, 1935, pp. 116-117)
McConnell calls attention to the fact that in [epileptic] cases where the exciting factor seems to be in the intestine and there is reverse peristalsis of the intestines, causing a reversion of the nerve current in the vagi [vagus nerve], thorough rapid abdominal treatment will normalize peristalsis and aid in preventing an impending attack. Stimulation of the solar plexus may lessen the attack by calling blood to the intestines and thus reducing pressure in the cranium.
A general course of treatment is depended upon to prevent recurrence of attacks and to cure the cause. This consists in the removal of lesion, whatever it may be, and all causes of reflex irritation … Attention should be given to upbuilding the general health, and to keeping bowels and stomach in good condition…. The food should be light and easily digested … (Hazzard, 1905, p. 275)
The best osteopathic authorities have found various lesions from the neck to the lumbar region, including rib lesions, which have been the cause of the disease. The neck lesions are the most frequent, and we should make diligent search for them for the cause of the disease. At the time of the attack [seizure] we need not expect to do much for the case. Strong treatment and pressure at the base of the skull, suboccipital fossae, helps some cases, while others are helped by treatment over the solar plexus. Give a thorough abdominal treatment … A thorough general treatment should be given at least three times per week. Lesions wherever found should be removed….
The cervical sympathetic nerves should be treated. The bowels and stomach should receive attention. Stomach and intestinal indigestion may act as a cause by allowing the food to ferment and poison the system, causing autointoxication. The diet should be light and nutritious and easily digested…. Should there be chronic constipation a dose of calomel [laxative] is recommended once per week, followed in a few hours by a dose of salts, an enema of salt water, a tablespoon of salt to a quart of water, to be given twice per week. (Murray, 1925, pp. 360-362)
In addition to osteopathic manipulation of the spine and abdomen, traditional osteopathy utilized various adjunct therapies such as packs, hydrotherapy, diet, massage, and therapeutic milieu to help the body to heal itself by natural means. (e.g., Goetz, 1909; Johnstone, 1927a, 1927b; Hildreth, 1929) One of the interesting therapeutic techniques used by the early osteopaths for the treatment of epilepsy was to place a piece of ice on the spine. (Hazzard, 1905) Presumably, this technique was intended to prevent nervous system incoordination in the peripheral systems from affecting the cerebral brain.
Osteopathy is distinguished by its early emphasis of holistic concepts in medical treatment. “This whole-person approach is as the heart of osteopathic medical care, its very essence….” (Korr, 1990, p. 829). All the various aspects of each individual’s life is considered important in the treatment of illness. Hence, psychological and interpersonal functioning play a role in the manifestation of illness and its treatment.
THERAPEUTIC IMPLICATIONS
Several basic adjunct therapies are recommended to normalize abdominal functioning 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.
Spinal manipulations are a primary treatment modality, particularly in cases where history or assessment indicate somatic dysfunction. As noted above, the traditional osteopathic literature often cited spinal injury as the origin of the aberrant nerve reflexes producing dysfunctions throughout the body resulting in seizures in the cerebral brain.
Hot castor oil packs applied to the abdomen are also recommended. These packs are intended to increase circulation in the abdomen. A typical session lasts approximately one hour per day with three sessions per week.
Gentle massage is recommended following the castor oil session. Particular attention is paid to the abdomen and along the spine (to assist with nervous system coordination).
Basic dietary suggestions include a balanced diet with a preponderance 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.
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 1st and 2nd cervical vertebrae (at the base of the skull) 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.
Summary
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 peripheral nervous system (and particularly that portion designated as the abdominal brain) and the cerebral brain may be involved in abdominal epilepsy. This view is consistent with traditional osteopathic concepts as well as the current medical research literature.
References
American College of Mechano-Therapy. (1910). Text-book of Osteopathy.
Barber, E. D. (1898). Osteopathy complete. (4th Ed.). Kansas City, MO: Hudson-Kimberly Publishing Company.
Davis, C. L. (Ed.). (1973). Tabor’s cyclopedic medical dictionary. Philadelphia: F.A. Davis Co.
Downing, C. H. (1935). Osteopathic principles in disease. San Francisco: Ricardo J. Orozco.
Epilepsy Foundation of America. (1975). Basic Statistics on the Epilepsies. Philadelphia: F.A. Davis Company.
Gershon, M. D., Kirchgessner, A. L., & Wade, P. R. (1994). Functional anatomy of the enteric nervous system. In L. R. Johnson, (Ed.), Physiology of the Gastrointestinal Tract (3rd ed.). (Vol.1). New York: Raven Press.
Goetz, E. W. (1909). A manual of osteopathy: With the application of physical culture, baths and diet. Cincinnati, Ohio: Nature’s Cure Company.
Gordon, B. (Ed.). (1942). Hughes’ practice of medicine (16th ed.). Philadelphia: The Blakiston Company.
Hazzard, C. (1899). Principles of osteopathy, (3rd Ed.). Kirksville, MO: Journal Printing Company.
Hazzard, C. (1905). The practice and applied therapeutics of osteopathy, (3rd Ed.). Kirksville, MO: Journal Printing Company.
Hildreth, A. G. (1929). Fifteen years at Still-Hildreth. The Journal of Osteopathy. (Vol. 36).
Johnstone, E. O. (1927). Hydrotherapy in its relation to osteopathy. The Journal of Osteopathy, (Vol. 34), 86-87.
Johnstone, E. O. (1927). Packs and their uses. The Journal of Osteopathy, (Vol. 34), 323-325.
Korr, I. (1990). Osteopathic medicine: The profession’s role in society. The Journal of the American Osteopathic Association, 90(9), 824-837.
Miller, B. F. & Keane, C. B. (1972). Encyclopedia and dictionary of medicine and nursing. Philadelphia: W. B. Saunders Co.
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.
Murray, C. H. (1925). Practice of osteopathy: Its practical application to the various diseases of the human body, (6th Ed.). Elgin, Illinois: Charles H. Murray.
Pedley, T. A. (1985). Brain, nerve, and muscle disorders. In D. F. Tapley, R. J. Weiss, & T. Q. Morris (Eds.), The Columbia University College of Physicians and Surgeons Complete Medical Guide. (pp. 594-595). Mt. Vernon, NY: Consumers Union.
Peppercorn & Herzog. (1989). The spectrum of abdominal epilepsy in adults. The American Journal of Gastroenterology, 84(10), 1294-1296.
Riggs, W. L. (1901). Osteopathic manipulations and treatment. Elkhart, Indiana: New Science Publishing Company.
Wood, J. D. (1994). Physiology of the enteric nervous system. In L.R.Johnson, (Ed.), Physiology of the gastrointestinal tract (3rd ed.). (Vol.1). New York: Raven Press.
Zarling, E. J. (1984). Abdominal epilepsy: an unusual cause of recurrent abdominal pain. American Journal of Gastroenterology, 79(9). 687-688.
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.