The Abdominal Brain and Enteric Nervous System
David L. McMillin, M.A., Douglas G. Richards, Ph.D.,
Eric A. Mein, M.D., Carl D. Nelson, D.C.
Meridian Institute
Virginia Beach, VA 23454
[NOTE: This article was published in The Journal of Alternative and
Complementary Medicine, Vol. 5, No. 6, 1999; see below for continuing
education credit for this article.]
Abstract
Conventional medical treatment for neurological disorders such as
epilepsy, migraine, and autism focuses on the brain. Although
standard medical treatment is often helpful, the underlying causes of
these disorders are not well understood. Furthermore, some
individuals respond poorly, or not all to regular medicine. Evidence
is ac***ulating in the medical literature that the enteric nervous
system (ENS) - that part of the nervous system associated with the
alimentary canal - also plays a role in these disorders.
Historically, the concept of an autonomous abdominal nervous system
was advocated by Byron Robinson, Johannis Langley, and Edgar Cayce.
The work of these three prominent historical figures is considered
along with modern viewpoints on the abdominal nervous system.
Complementary therapies that address the nervous system of the abdomen
hold potential as useful adjuncts to conventional treatment for
certain neurological disorders.
Introduction
It is evident both from the historical and modern literature that the
peripheral nervous system, and particularly that ****tion associated
with the alimentary canal, is a prominent element in certain
neurological disorders associated with the cerebral brain. For
example, abdominal epilepsy and abdominal migraine are well
established diagnostic entities in modern medicine in both children
and adults (Babb and Eckman, 1972; Loar, 1979; Mitchell et al., 1983;
Reimann, 1973; Santoro et al., 1990; Symon and Russell, 1986). Some
researchers regard the presence of abdominal features in these
illnesses as im****tant and of possible etiological significance (Amery
and Forget, 1989; Mavromichalis et al., 1995; Peppercorn and Herzog,
1989). Recently, autism has been added to the list of neurological
conditions with abdominal features (Horvath et al., 1998; Murch et
al., 1998; Wakefield et al., 1998;).
A possible explanation of the relation****p between abdominal symptoms
and neurological syndromes can be found in the influence that the
enteric nervous system (ENS) has on the CNS. The ENS is an extensive
network of neurons widely dispersed throughout the gut, that
coordinate together to regulate gastrointestinal events such as
peristalsis, blood flow, secretion, and absorption (Costa and
Brookes, 1994; Goyal and Hirano, 1996; Gershon et al., 1994). The ENS
can influence the CNS both through nerve reflexes and the production
of neuropeptides. It is estimated that 80% of vagal fibers are
visceral afferents (Daven****t, 1978). Recent work has also shown a
vast overlap of neuropeptide activity in the gut and the brain (Pert
et al., 1985). The ENS is an active area in physiological research
with over 600 articles on Medline since 1985.
The revival of interest in the ENS has strong historical roots.
Nearly one hundred years ago, American physician Byron Robinson, a
medical doctor, did extensive research and writing culminating in his
impressive work, "The Abdominal and Pelvic Brain" (Robinson, 1907).
The premise of Robinson's book is that the abdominal viscera contain a
vast and complex nervous system, which influences, and to a great
degree regulates, the vegetative process of the abdominal viscera.
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 nervous system of the gut was capable
of integrative functions independent of the central nervous
system" (Gershon et al., 1994, p. 424). It is now known that the
human GI system, deprived of CNS innervation, is capable of
coordinated digestion, mobility, secretion and absorption (Daven****t,
1978). Langley labeled the brain in the gut the enteric nervous
system, the term now used for this system.
Edgar Cayce, who has been called the father of modern holistic
medicine (Callan, 1979; Mein, 1989) was another strong advocate for
the abdominal nervous system. Cayce believed that the idiopathic
forms of certain neurological syndromes (such as epilepsy and
migraine) have an abdominal etiology. A wide variety of non-intrusive
therapies were recommended by Cayce for the treatment of these
syndromes.
The remainder of this article will focus on abdominal epilepsy,
abdominal migraine, and autism with colonic features with the aim of
understanding peripheral nervous system involvement in these
disorders. Theoretical and clinical implications of the re-discovery
of the abdominal nervous system will be explored.
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 (Der***,
1912, p. 917). Osteopaths noted that, ".in 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, thorough rapid abdominal treatment will normalize peristalsis
and aid in preventing an impending attack" (Hazzard, 1905, p. 275).
Edgar Cayce insisted that idiopathic epilepsy is produced by lacteal
duct adhesions along the right side of the abdomen that produce nerve
reflexes to the brain. "From every condition that is of true
[idiopathic] epileptic nature there will be found a cold spot or area
between the lacteal duct and the cae***" (Cayce, 1934). The invention
and clinical application of the electroencephalogram (EEG) during the
1920's ****fted 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, tem****al
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. A few papers published in the medical journals during the
1960s called attention to the abdominal features in epilepsy
(Berdichevskii, 1965; Takei and ****ajima, 1967; Juillard, 1967).
Over the past twenty-five years, numerous researchers and clinicians
have re****ted on various aspects of abdominal epilepsy (Agrawal et
al., 1989; Babb and Eckman, 1972; Bondarenko et al., 1986; Douglas and
White, 1971; Hotta and Fujimoto, 1973; Loar, 1979; Matsuo, 1984;
Mitchell et al., 1983; Moore, 1972; O'Donohoe, 1971; Peppercorn et
al., 1978; Peppercorn and Herzog, 1989; Reimann, 1973; Singhi and
Kaur, 1988; Solana de Lope et al., 1994; Yingkun, 1980; Zarling,
1984).
Common clinical features of abdominal epilepsy include abdominal pain,
nausea, bloating, and diarrhea with nervous system manifestations
such as headache, confusion, and syncope (Peppercorn and 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 et al., (1983)
regard cyclic vomiting as a primary symptom of abdominal epilepsy
manifesting as simple partial seizures. 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.
One of the primary problems in understanding abdominal epilepsy is
clearly defining the relation****p 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. Tem****al
lobe seizure activity usually arises in or involves the amygdala. It
is not surprising, therefore, that patients who have seizures
involving the tem****al 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).
The vagal link in epilepsy has also received attention with regard to
a surgical procedure in which a pacemaker is implanted on the vagus
nerve in the upper chest. Regular stimulation of the vagus has
reduced or eliminated seizure activity in some treatment-resistent
patients (Amar et al., 1998; Handforth et al., 1998; Lundgren et al.,
1998). The therapeutic effect is thought to be produced by calming
"hyperexcited" nerve cells and reverting brain activity to its normal
patterns (Snively et al., 1998).
If stimulation of the peripheral nervous system, in this case the
vagus, can reduce seizure activity in the brain, perhaps pathological
irritation of this or other peripheral nerves may also play a role in
the etiology of certain forms of epilepsy. At this time, there is no
definitive model of abdominal epilepsy which explains the association
of brain seizures and abdominal symptoms. The clinical (therapeutic)
implications of abdominal etiology in epilepsy will be discussed
below.
Abdominal Migraine
From a medical perspective, migraine presents as a complex systemic
illness with various combinations of neurologic, gastrointestional and
autonomic symptoms. Although the neurological components are a
primary focus in medical diagnosis and treatment, historical and
contem****ary viewpoints also attribute great significance to
gastrointestinal features. "In the majority of migraine patients
there is some fault in the gastro-duodenal-hepatic chain." (Hare,
1912, p. 382). "Gastrointestinal disturbances including nausea,
vomiting, abdominal cramps, or diarrhea are almost
universal" (Silberstein, 1995, p. 387).
Historical perspectives on syndromes such as migraine tend to take all
of the symptoms into consideration in a more systemic interpretation
of the illness. Thus, the significant gastrointestinal aspects of
migraine received much greater attention, both with regard to
causation and treatment. The medical treatments prescribed for
migraine in previous eras addressed the gastrointestinal features of
the illness directly with a spectrum of relatively natural therapies
intended to improve digestion, assimilation and elimination through
the bowel.
Diet was frequently emphasized. For example, Spear (1916) cautioned
that, "Heavy pastries, rich foods, and alcoholic drinks are best
avoided" (p. 626). Therapies for intestinal cleansing were also
commonly prescribed. "The bowels should be regulated, and under no
condition should constipation be allowed to occur.if the lower bowel
contains much fecal matter, a hot soapsuds enema should be
given" (Spear, 1916, p. 626). Der*** relied on a mild saline laxative
(such as Carlsbad salts) for intestinal cleansing, claiming that "It
is a not uncommon experience to find that a beginning migraine attack
is frequently aborted by a saline, taken as soon as prodromal symptoms
are noted" (Der***, 1912, p. 906).
Modern medical science has acknowledged the rediscovery of the
abdominal connection in migraine in various ways. The most obvious is
the recognition of a diagnostic entity called "abdominal
migraine" (Bentley et al. 1984; Mortimer and Good, 1990; Santoro et
al., 1990; Symon and Russell, 1986). Abdominal migraine is diagnosed
most often in children. For example Mavromichalis et al. studied a
consecutive series of 31 children (median age 12 years) suffering from
migraine. Endoscopic oesophageal, gastric and duodenal biopsy were
used to determine whether the complaints were of gastrointestinal
origin. Of these 31 children, 13 (41.9%) showed esophagitis, 16
(51.6%) gastritis of corpus, 12 (38.7%) antral gastritis and 27
(87.1%) duodenitis. Thus, 29 of the 31 children studied had an
underlying inflammatory lesion explaining their complaints. The
researchers concluded, "Our findings provide further evidence that
recurrent abdominal pain is an early expression of migraine and
strongly sup****t a causal link between recurrent abdominal pain and
migraine" (Mavromichalis et al., p. 406).
The gastrointestinal connection in migraine has also been rediscovered
with regard to food allergies (Bentley et al., 1984; Dalton, 1975;
Grant, 1979; Hanington, 1980; Hughes et al., 1985; Mansfield, 1987;
Mansfield, 1988; Mansfield et al.,1985; Monro et al., 1984; Peatfield,
1995; Peatfield et al., 1984; Trotsky, 1994; Vaughan, 1994; Wilson, et
al., 1980). The designation of dietary migraine is sometimes used in
such cases (Dalessio, 1972). The conceptualization of migraine as a
gastrointestinal allergic response has historical precedent:
"The allergists have much to say which warrants careful evaluation as
to the nature of the migraine episode as well as its etiology. They
believe that fatigue, nervous and emotional factors produce changes in
the motor activities of the gastrointestinal system which result in
duodenal stasis. This promotes the absorption of the allergens to
which the patient reacts in his inherent pattern of migraine. They
re****t that accurate allergy diets result in complete relief in 30 per
cent of migraine patients and partial relief in 45 per cent" (Gordon,
1942, p. 556).
One of the major problems in understanding the etiology and
pathophysiology of migraine is how to conceptualize both the nervous
and vascular aspects of the syndrome. Traditionally, migraine has
been regarded as a "vascular" headache due the obvious abnormalities
in circulation to the head (Agnoli and DeMarinis, 1985; Thomsen and
Olesen, 1995). More recently, nervous system involvement has been
emphasized, with particular emphasis on the trigeminal or fifth
cranial nerve (Buzzi et al., 1995). An integration of these two
models has culminated in a trigemino-vascular theory which integrates
nerve and circulatory processes (Buzzi and Moskowitz, 1992).
Interestingly, Edgar Cayce, an intuitive diagnostician practicing
during the first half of the twentieth century, also recognized the
abdominal connection in migraine. Cayce claimed that the
pathophysiology of idiopathic migraine involves allergic processes in
the intestinal tract which trigger nerve reflexes to the trigeminal
(fifth cranial nerve) resulting in migraine headaches. Consistent
with abdominal etiology, Cayce's therapeutic recommendations focused
on the intestinal tract and peripheral nervous system (i.e., diet,
colonic irrigation, manipulative therapy). As an example of Cayce's
unique views on the association between the abdominal brain and
neurological disease, the following excerpt describes the
pathophysiology of migraine in a child:
"As we find, while the body is in the developing stages, the sources
of the conditions to which the body becomes allergic in the digestive
system should be looked for - that deal with all migraine headaches.
So, this information might be used universally as to the sources of
such, if it would be accepted. For, here we find such in its
beginnings, and it is in the digestive system, causing - through a
state of circulation - an inflammation in the connections of the
intestinal tract through [the] blood and nerve supply ." (Cayce,
1943).
Thus, according to Cayce, the general pattern of pathology in
idiopathic migraine involves an allergic irritation in the intestines
which is transmitted to the trigeminal (fifth cranial nerve) and also
triggers an imbalance of circulation to the head. Cayce's model of
idiopathic migraine takes into consideration both the nerve and
vascular aspects of migraine.
Although Robinson did not directly address the topic of abdominal
migraine, he did devote a significant ****tion of a chapter of his book
(Ch. 7) to the abdominal and pelvic influence on the trigeminal nerve.
(Robinson, 1907) Thus, in addition to the well-known visceral
connections of the vagus (tenth cranial nerve), the abdominal
connections of the trigeminal provide another possible route for nerve
reflexes to the head in migraine.
The possibility that the abdominal features of migraine may have
etiological and therapeutic implications suggests that further
research is needed. The degree to which abdominal migraine exists as
a subgroup within the broader classification of migraine must be
determined. Abdominal migraine in children is well established. The
prevalence of abdominal migraine in adults is less well known. The
efficacy of traditional clinical interventions for migraine that focus
directly on the gastrointestinal system (i.e., diet and colonic
irrigation) deserves further study.
Autism with Intestinal Features
People with classical autism show three types of symptoms: impaired
social interaction, problems with verbal and nonverbal communication
and imagination, and unusual or severely limited activities and
interests. Symptoms of autism usually appear during the first three
years of childhood and continue throughout life. Although there is no
cure, appropriate management may foster relatively normal development
and reduce undesirable behaviors.
Recent medical research may add autism to the growing list of
neurological illnesses with abdominal features. Wakefield et al.
(1998) investigated a consecutive series of children with chronic
enterocolitis and regressive developmental disorder. The twelve
children (mean age 6 years) had a history of normal development
followed by loss of acquired skills, including language, together with
diarrhea and abdominal pain. Murch et al. (1998) re****t that 47 out
of 50 autistic children they studied showed significant bowel
pathology. When subjected to colon cleansing, these children showed
notable improvement in their autism symptoms. The researchers
conclude, "We re-emphasize the fact that there is a consistent pattern
of gut inflammation in a high pro****tion of children within the broad
autistic spectrum. Understanding the link between the bowel and the
brain in autism may allow new insights into this devastating
illness." (Murch et al., p. 908).
Further evidence of intestinal involvement in autism has surfaced when
a substance called secretin has been surprisingly effective in the
treatment of autism for some children. After Victoria and Gary Beck
successfully treated their autistic child with secretin and triggered
interest in this substance, Horvath et al. (1998) studied the
therapeutic effects of secretin on three autistic children and noted
significant clinical improvement, both gastrointestinal and
behavioral. Secretin is now being tested with more autistic children
to determine its potential.
Secretin is a natural substance, produced in the intestinal tract by
all mammals. While it is not a drug, and not harmful, the FDA
nevertheless requires that it be sold only by prescription.
Secretin is usually given by slow injection (infusion), but other
methods of administration are being considered. The only FDA-approved
use for secretin is in the diagnosis of gastrointestinal problems, not
as a treatment for any disorder.
The Abdominal Nervous System
Although many of the researchers cited above allow for the possibility
that abdominal factors have etiological significance in neurological
conditions, the anatomical and physiological basis for such a
connection is uncertain. What is there about the abdomen that could
possibly be linked to neurological conditions such as epilepsy,
migraine, and autism? To answer this im****tant question, it is
helpful to review the medical literature of the early decades of the
twentieth century. For example, the work of Robinson exemplifies the
position that the abdomen contains a secondary brain.
"In mammals there exist two brains of almost equal im****tance 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)" (Robinson, 1907, pp. 123 - 126).
For Robinson, the abdominal brain is centered in the solar plexus
(Figure 1). The abdominal brain is the primary control center of an
extensive peripheral nervous system containing a number of "little
brains." Anatomically, this peripheral system is roughly equivalent
to the autonomic nervous system. Physiologically, the comparison
breaks down because Robinson's perspective of the abdominal nervous
system is much more autonomous than modern opinions about this
system.
Working separately from Robinson, British physiologist Johannis
Langley also recognized the relative independence of the abdominal
nervous system. Focusing on the ganglia of the gut, he believed that
they do more than simply relay and distribute information from the
cerebral brain. He was unable to reconcile conceptually the great
disparity between the enormous numbers of neurons [2 X 10 (8)] in the
gut and the few hundred vagus fibers from the cerebral 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). Langley labeled the brain in the gut the enteric nervous
system (ENS).
Although for several decades Robinson and Langley's work was 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 represents one of the exciting areas of
physiological 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 et al., 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 et al., 1994, p.
414).
In addition to the biochemical and structural similarities between the
cerebral brain and the abdominal brain, contem****ary researchers are
drawing computer analogies and using information processing models to
describe the relation****p between the cephalic and enteric brains.
"The cephalic 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.. 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" (Wood, 1994, p. 424).
Langley regarded the ENS as a third division of the autonomic nervous
system (ANS) (Gershon et al., 1994). Considering the modern view of
the ANS, this classification does not adequately convey the scope and
independence of the ENS. In fact, if Langley and Robinson are to be
taken seriously, the modern concept of the ANS must be reconsidered.
Currently, the entire ANS is taken to be little more than a handmaiden
to the CNS. Langely and Robinson held the role of the ANS in much
higher esteem than their modern counterparts.
It should also be noted that Langley focused on the nerves lining the
gut in defining the ENS, whereas Robinson was interested in the entire
abdominal nervous system. Robinson's perspective includes the solar
plexus (abdominal brain) and its extensive network of plexuses and
connecting fibers. In Robinson's book consisting of 40 chapters, the
ENS is covered in one chapter. If Robinson is correct in his view of
the peripheral nervous system, the re-discovery of the ENS is only the
beginning of a new appreciation of the nervous system of the abdomen.
Although this paper has focused on neurological conditions with
intestinal features, the reverse relation****p has also been observed.
For example, irritable bowel syndrome (IBS), a common intestinal
disorder involving abdominal pain, disturbed defecation, and bloating,
often presents with significant neurological and psychiatric features.
Watson et al. (1978) and Jones and Lydeard (1992) do***ented a
significant co-morbidity of IBS and migraine. Fent et al. (1999)
described associations between colonic sensitivity in IBS and
hemispheric preference and cognitive style. Whorwell et al. (1986) and
Maxton et al. (1991) have noted the numerous non-colonic features of
IBS, such as headache, which may be indicative of a much more diffuse
disorder than has previously been appreciated.
Numerous authors have described a link between IBS and psychiatric
illness, particularly anxiety and depression. The review by Walker et
al. (1990) is noteworthy, as it provides a pathophysiological model
linking ENS dysfunction in IBS to the locus ceruleus (LC), a ****tion
of the brain that regulates vigilance and attention to fear provoking
stimuli. Commenting on the ENS/LC model, Lydiard (1997) observed:
"This model suggests that a potentially vicious positive feedback loop
may be initiated and maintained by pathologic anxiety and arousal.
Like IBS patients, individuals suffering from anxiety or depression
experience excessive autonomic symptoms, suggesting some common
pathophysiology, perhaps in part at the level of the LC..GI distress
could theoretically cause or worsen psychiatric symptoms such as
anxiety" (p. 55).
Thus the gut brain/cerebral brain interaction can manifest in a
variety of signs, symptoms and diagnostic categories. The abdominal
nervous system provides a plausible link between gastrointestinal and
central nervous system functioning regardless of the classification of
the dysfunction.
Clinical Implications
The possibility that neurological syndromes such as epilepsy, migraine
and autism may be caused by pathology in the gastrointestinal system
raises some intriguing questions with regard 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 sup****t
therapies which focus on abdominal pathology? Can these illnesses be
cured?
As noted above, from an historical perspective, the medical treatment
of epilepsy and migraine often included therapy for the abdominal
aspects of these diseases. Robinson's work in particular was very
influential with some of the developing "alternative medicine"
practitioners of the late 19th and early 20th centuries. For example,
the early osteopaths held Robinson's discoveries in high esteem,
citing his findings as sup****tive of the premise of manual therapy for
the treatment of a wide range of somatic and visceral disease. Spinal
and visceral manipulation techniques were used to treat almost every
illness including neurological disorders such as migraine and epilepsy
(American College of Mechano-Therapy, 1910; Barber, 1898; Downing,
1935; Hazzard, 1905; Murray, 1925). Figure 2 illustrates a
traditional osteopathic technique for regulating the pneumogastric
nerve (vagus), a primary neurological connection between the cerebral
and abdominal brains. To provide easy access to these historic works,
McMillin (1998) has created a website containing the text of
Robinson's book and several of the early osteopathic texts. A
comparison of Robinson's and Cayce's views of the peripheral nervous
system is also available (McMillin, 1997).
Although osteopathy has become well integrated into mainstream medical
practice, the principles and techniques utilized by traditional
osteopaths (e.g., manipulative therapy, diet and nutrition,
hydrotherapy) have also been employed by various alternative
practitioners such as chiropractors and naturopaths. These forms of
therapy have received increasing interest as complementary to
conventional medicine. Manipulative therapy has been used in the
treatment of migraine (Parker et al., 1978) and epilepsy (McGarey,
1968; Swink et al., 1997). Dietary therapy is used for migraine
(Diamond et al., 1986; Mansfield et al., 1985; Vaughan, 1994). The
ketogenic diet has seen increasing use for epilepsy (Kinsman et al.,
1992; Swink et al., 1997). Hydrotherapy and abdominal castor oil
packs have been used for epilepsy and migraine (McGarey, 1968; Mein et
al., 1999).
As noted, Edgar Cayce emphasized the role of the abdominal nervous
system with regard to causation and treatment of epilepsy and
migraine. 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" (1926, 1944), the
"secondary brain" (1944), and the "central brain in the solar
plexus" (1927). Of particular interest are Cayce's therapeutic
recommendations for epilepsy and migraine which included special
diets, abdominal castor oil packs, colonic irrigations, spinal
manipulation and massage, and herbal teas to heal the intestinal
tract. All these therapies were directed to improving digestive
system functioning, and thereby decreasing nervous system
incoordination between the abdominal and cerebral brains. Detailed
analysis of Cayce's approach to epilepsy (Pahnke, 1968) and migraine
(Bjork, 1983) have been published. Reilly and Brod (1975), McGarey
(1983), and Mein (1989) have described Cayce's approach to the
digestive system as it relates to systemic functioning.
Interestingly, one reading given for a child with mild autistic
features recommended a digestive supplement similar to secretin
(1937). A pilot study of 16 children with minimal brain dysfunction
(including autism) based on Cayce's concepts of intestinal etiology,
showed promising results (Pecci, 1977). The Meridian Institute has
investigated Cayce's therapeutic recommendations for migraine in a
small pilot study (n=5). Participants who followed Cayce's
suggestions showed notable improvement (Meridian Institute, 1997).
Conclusion
Neurological diseases with systemic features (particularly with
significant gastrointestinal symptoms) may be approached from a
complementary medicine model that recognizes the role of the abdominal
nervous system with regard to etiology and treatment. By linking the
historical, systems-oriented clinical approaches to the modern
research literature on the enteric nervous system, a complementary
approach may be created which integrates the best of standard medical
practice with traditional and alternative modalities and systems that
are consistent with established anatomy and physiology.
Although epilepsy and migraine are common illnesses, the abdominal
form of each is generally regarded as rare. Based on the sources
described in this paper, we are suggesting that idiopathic epilepsy
and migraine may be better understood if the abdominal features were
more thoroughly investigated. Abdominal epilepsy and migraine may not
actually be rare. Modern medicine considers them rare because little
attention has been given to the meaning of abdominal symptoms
associated with these conditions. Perhaps the idiopathic forms of
both illnesses involve intestinal etiology. Similarly, the intestinal
aspects of autism may be clues to an im****tant subgroup of this
disorder.
Further research into the etiology and treatment of these conditions
should consider possible abdominal nervous system involvement.
Clinically, the presence of significant abdominal features may
indicate that the treatment plan include traditional features (i.e.,
diet, colon hydrotherapy, and manipulative therapy) which may
favorably influence the abdominal brain and enteric nervous system.
References
American College of Mechano-Therapy. Textbook of Osteopathy. Chicago:
American College of Mechanotherapy, 1910.
Agnoli A, De Marinis M. Vascular headaches and cerebral circulation:
An overview. Cephalalgia 1985;5 Suppl 2:9-15.
Agrawal P, Dhar NK, Bhatia MS, Malik SC. Abdominal epilepsy. Indian
J Pediatr 1989;56:539-541.
Amar AP, Heck CN, Levy ML, Smith T, DeGiorgio CM, Oviedo S, Apuzzo
ML. An institutional experience with cervical vagus nerve trunk
stimulation for medically refractory epilepsy: Rationale, technique,
and outcome. Neurosurgery 1998;43:1265-1276.
Amery WK, Forget PP. The role of the gut in migraine: The oral 51-Cr
EDTA test in recurrent abdominal pain. Cephalalgia 1989;9:227-229.
Babb RR, Eckman PB. Abdominal epilepsy. JAMA 1972;222:65-66.
Barber ED. Osteopathy complete. 4th Ed. Kansas City, MO: Hudson-
Kimberly Publi****ng Company, 1898.
Bentley D, Katchburian A, Brostoff J. Abdominal migraine and food
sensitivity in children. Clinical Allergy 1984;14:499-500.
Berdichevskii M. Meso-diencephalic epilepsy after abdominal injury.
Vopr Psikhiatr Nevropatol 1965;11:374-376.
Bjork RO. Migraine headaches. In W.A. McGarey (Ed.) Physicians
Reference Notebook. Virginia Beach, VA: A.R.E. Press, 1983.
Bondarenko ES, ****retorova DC, Miron VA. Abdominal syndrome in the
structure of cerebral paroxysms in children and adolescents. Soviet
Medicine 1986;2:39-44.
Buzzi MG, Moskowitz MA. The trigemino-vascular system and migraine.
Pathol Biol 1992; 40:313-317.
Buzzi MG, Bonamini M, Moskowitz MA. Neurogenic model of migraine.
Cephalalgia 1995;15:277-80.
Callan JP. Editorial. JAMA 1979;241:1156.
Cayce E. Edgar Cayce reading 2259-1; 1921.
Cayce E. Edgar Cayce reading 1800-15; 1926.
Cayce E. Edgar Cayce reading 4613-1; 1927.
Cayce E. Edgar Cayce reading 567-4; 1934.
Cayce E. Edgar Cayce reading 1179-4; 1937.
Cayce E. Edgar Cayce reading 3326-1; 1943.
Cayce E. Edgar Cayce reading 294-212; 1944.
Costa M, Brookes SJ. The enteric nervous system. Am J Gastroenterol
1994;89:S29-137.
Dalessio DJ. Dietary migraine. Am Fam Physician 1972;6:60-65.
Dalton K. Food intake prior to a migraine attack -- study of 2,313
spontaneous attacks. Headache 1975;15:188-193.
Daven****t WW. A digest of digestion. Chicago: Year Book Medical
Publishers, 1978.
Der*** FX. Treatment of the so-called functional disorders. In J.H.
Musser and A.O. Kelly (Eds.) A Handbook of Practical Treatment.
Philadelphia, PA: W. B. Saunders Co. 1912.
Diamond S, Prager J, Freitag FG. Diet and headache. Is there a link?
Postgrad Med 1986;79:279-286.
Douglas EF, White PT. Abdominal epilepsy - a reappraisal. J Pediatr
1971;78:59-67.
Downing CH. Osteopathic principles in disease. San Francisco: Ricardo
J. Orozco, 1935.
Egger J, Carter CM, Wilson J, Turner MW, Soothill JF. Is migraine food
allergy? A double-blind controlled trial of oligoantigenic diet
treatment. Lancet 1983;8355:865-869.
Fent J, Balazs L, Buzas G, Erasmus LP, Holzl R, Kovacs, A, Weisz J,
Adam G. Colonic sensitivity in irritable bowel syndrome and normal
subjects according to their hemispheric preference and cognitive
style. Integr Physiol Behav Sci 1999;34(1):54-62.
Gershon MD, Kirchgessner AL, Wade PR. Functional anatomy of the
enteric nervous system. In: Johnson LR, ed. Physiology of the
gastrointestinal tract. 3rd ed. (Vol.1). New York: Raven Press, 1994.
Gordon, B, ed. Hughes' Practice of Medicine. 16th ed. Philadelphia:
The Blakiston Company, 1942.
Goyal RK, Hirano I. The enteric nervous system. N Engl J Med
1996;334:1106-1115.
Grant EC. Food allergies and migraine. Lancet 1979;1:966-969.
Handforth A, DeGiorgio CM, Schachter SC, Uthman BM, Naritoku DK,
Tecoma ES, Henry TR, Collins SD, Vaughn BV, Gilmartin RC, Labar DR,
Morris GL, Salinsky MC, Osorio I, Ristanovic RK, Labiner DM, Jones JC,
Murphy JV, Ney GC, Wheless JW. Vagus nerve stimulation therapy for
partial-onset seizures: a randomized active-control trial. Neurology
1998;51:48-55.
Hanington E. Diet and migraine. Journal of Human Nutrition
1980;34:175-180.
Hare HA. A Text-Book of Practical Therapeutics, with Especial
Reference to the Application of Remedial Measures to Disease and Their
Employment upon a Rational Basis. 14th ed. Philadelphia: Lea &
Febiger, 1912:805-806.
Hazzard C. The practice and applied therapeutics of osteopathy. 3rd
ed. Kirksville, MO: Journal Printing Company, 1905.
Horvath K, Stefanatos G, Sokolski KN, Wachtel R, Nabors L, Tildon JT.
Improved social and language skills after secretin administration in
patients with autistic spectrum disorders. J Assoc Acad Minor Phys
1998;9:9-15.
Hotta T, Fujimoto Y. A study on abdominal epilepsy. Yonago Acta
Medica 1973;17:231-239.
Hughes EC, Gott PS, Weinstein RC, Binggeli R. Migraine: A diagnostic
test for etiology of food sensitivity by a nutritionally sup****ted
fast and confirmed by longterm re****t. Ann Allergy 1985;55:28-32.
Jones R, Lydeard S. Irritable bowel syndrome in the general
population. Br Med J 1992;304:87-90.
Juillard E. Abdominal pains and epilepsy. Praxis 1967;56:83-84.
Kinsman SL, Vining EP, Quaskey SA, Mellits D, Freeman JM. Efficacy of
the ketogenic diet for intractable seizure disorders: review of 58
cases. Epilepsia 1992;33:1132-1136.
Loar CR. Abdominal epilepsy. JAMA. 1979;241:1327.
Lundgren J, Amark P, Blennow G, Stromblad LG, Wallstedt L. Vagus
nerve stimulation in 16 children with refractory epilepsy. Epilepsia
1998;39:809-813.
Lydiard RB. Anxiety and the irritable bowel syndrome: psychiatric,
medical, or both? J Clin Psychiatry 1997;58 Suppl 3:51-8;59-61.
Mansfield LE. The role of food allergy in migraine: A review. Ann
Allergy 1987;58:313-317.
Mansfield LE. Food allergy and headache. Whom to evaluate and how to
treat. Postgraduate Medicine 1988;83:46-51.
Mansfield LE, Vaughan TR, Waller SF, Haverly RW, Ting S. Food allergy
and adult migraine: double-blind and mediator confirmation of an
allergic etiology. Ann Allergy 1985;55:126-129.
Matsuo F. Partial epileptic seizures beginning in the truncal
muscles. Acta Neurol Scand 1984;69:264-269.
Mavromichalis I, Zaramboukas T, Giala MM. Migraine of gastrointestinal
origin. Eur J Pediatr 1995;154:406-410.
Maxton DG, Morris J, Whorwell PJ. More accurate diagnosis of
irritable bowel syndrome by the use of "non-colonic" symptomatology.
Gut 1991;32:784-786.
McGarey WM. Physician's reference notebook. Virginia Beach, VA: A.R.E.
Press, 1968.
McGarey WA. The Edgar Cayce Remedies. New York: Bantam Books, 1983.
McMillin DL. The Early American Manual Therapy website located at:
http://members.visi.net/~mcmillin
1998.
McMillin DL. Selections from the abdominal and pelvic brain with
commentary by David McMillin. Virginia Beach, VA: Lifeline Press,
1997.
Mein EA. Keys to health: The promise and challenge of holism. San
Francisco, CA: Harper & Row Publishers, 1989.
Meridian Institute. Migraine re****t do***ents improvement. Meridian
Institute News, 1997:1(1)1-2.
Mitchell WG, Greenwood RS, Messenheimer JA. Abdominal epilepsy. Cyclic
vomiting as the major symptom of simple partial seizures. Arch Neurol
1983;40:251-252.
Monro J, Carini C, Brostoff J. Migraine is a food allergic disease.
Lancet 1984;2:719-721.
Moore MT. Abdominal epilepsy. JAMA 1972;222:1426.
Mortimer, MJ, Good PA. The VER as a diagnostic marker for childhood
abdominal migraine. Headache 1990; 30:642 - 645.
Murch SH, Thomson MA, Walker-Smith JA. Author's reply. Lancet
1998;351:908.
Murray CH. Practice of osteopathy: Its practical application to the
various diseases of the human body. 6th Ed. Elgin, IL: Charles H.
Murray, 1925.
Musser JH, Kelly AO. A handbook of practical treatment.
Philadelphia, PA: W. B. Saunders Co. 1912.
O'Donohoe NV. Abdominal epilepsy. Dev Med Child Neurol
1971;13:798-800.
Pahnke WN. Epilepsy. In W.A. McGarey (Ed.) Physicians Reference
Notebook. Virginia Beach, VA: A.R.E. Press, 1968.
Parker GB, Tupling H, Pryor DS. A controlled trial of cervical
manipulation of migraine. Aust N Z J Med 1978;8:589-593.
Peatfield RC, Glover V, Littlewood JT, Sandler M, Clifford RF. The
prevalence of diet induced migraine. Cephalalgia 1984;4:179-183.
Peatfield RC. Relation****ps between food, wine, and beer precipitated
migrainous headaches. Headache 1995;35:355-357.
Pecci EF. Minimal brain dysfunction in children. Lecture delivered at
the 10th Annual A.R.E. Clinic Medical Symposium. Scottsdale, Arizona,
January 1977.
Peppercorn MA, Herzog AG, Dichter, MA, Mayman CI. Abdominal epilepsy:
A cause of abdominal pain in adults. JAMA 1978;40:2450-2451.
Peppercorn MA, Herzog AG. The spectrum of abdominal epilepsy in
adults. Am J Gastroenterol 1989;84:1294-1296.
Pert CB, Ruff MR, Weber RJ, Herkenham M. Neuropeptides and their
receptors: A psychosomatic network. J Immunol.1985;135:820S-826S.
Reilly H., Brod R. The Edgar Cayce Handbook for Health Through
Drugless Therapy. Virginia Beach, VA: A.R.E. Press, 1975.
Reimann HA. Abdominal epilepsy and migraine. JAMA 1973;224:128.
Robinson B. The abdominal and pelvic brain. Hammond, IN: Frank S.
Betz, 1907.
Santoro G, Curzio M, Venco A. Abdominal migraine in adults. Case
re****ts. Funct Neurol 1990;5:61-64.
Silberstein SD. Migraine symptoms: results of a survey of self-
re****ted migraineurs. Headache 1995;35:387-396.
Singh PD, Kaur S. Abdominal epilepsy misdiagnosed as psychogenic
pain. Postgrad Med J 1988;64:281-282.
Snively C, Counsell C, Lilly D. Vagus nerve stimulator as a treatment
for intractable epilepsy. J Neurosci Nurs 1998;30:286-289.
Solana de Lope J, Alarcon FO, Aguilar MJ, Beltran CJ,
Barinagarrementeria F, Perez MJ. Abdominal epilepsy in the adult.
Review of Gastroenterology, 1994; 59:297-300.
Spear IJ. A Manual of Nervous Diseases. Philadelphia, PA: W. B.
Saunders Company, 1916:620-627.
Swink TD, Vining EP, Freeman JM. The ketogenic diet: 1997. Adv Pediatr
1997;44:297-329.
Symon DN & Russell G. Abdominal migraine: a childhood syndrome
defined. Cephalalgia 1986;6:223-228.
Takei T, ****ajima K. Autonomic abdominal epilepsy - clinico-
encephalographic evaluation of 24 cases. Nippon Shonika Gakkai
Zas**** 1967;71:543-551.
Thomsen LL, Olesen J. The autonomic nervous system and the regulation
of arterial tone in migraine. Clin Auton Res 1995;5:243-250.
Trotsky MB. Neurogenic vascular headaches, food and chemical
triggers. Ear Nose Throat J 1994;73:228-236.
Vaughan TR. The role of food in the pathogenesis of migraine headache.
Clin Rev Allergy 1994;12:167-180.
Wakefield AJ, Murch SH, Anthony A, Linnell J, Casson DM, Malik M,
Berelowitz M, Dhillon AP, Thomson MA, Harvey P, Valentine A, Davies
SE, Walker-Smith JA. Ileal-lymphoid-nodular hyperplasia, non-specific
colitis, and pervasive developmental disorder in children. Lancet
1998; 351:637-641.
Walker EA; Roy-Byrne PP; Katon WJ. Irritable bowel syndrome and
psychiatric illness. Am J Psychiatry 1990;147(5):565-72.
Watson WC, Sullivan SN, Corke M, Rush D. Globus and headache: common
symptoms of the irritable bowel syndrome. Can Med Assoc J 1978;118
(4):387-8.
Whorwell PJ, McCallum M, Creed FH, Roberts CT. Non-colonic features
of irritable bowel syndrome. Gut 1986;27(1):37-40.
Wilson CW, Kirker JG, Warnes H, O'Malley M. The clinical features of
migraine as a manifestation of allergic disease. Postgrad Med J
1980;56:617-621.
Wood J D. Physiology of the enteric nervous system. In: Johnson LR,
ed. Physiology of the gastrointestinal tract. 3rd ed. (Vol.1). New
York: Raven Press, 1994.
Yingkun F. Abdominal epilepsy. Chin Med J 1980;93(3), 135-148.
Zarling EJ. Abdominal epilepsy: an unusual cause of recurrent
abdominal pain. Am J Gastroenterol 1984;79:687-688.
Address reprint requests to: David L. McMillin, M.A., Meridian
Institute, 1853 Old Donation Parkway, Suite 1, Virginia Beach, VA
23454.
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