AN INTEGRATIVE MODEL OF MIGRAINE
BASED ON INTESTINAL ETIOLOGY
(c) Copyright 1999, all rights reserved
Current perspectives of migraine emphasize a multifactorical
approach which include neurological, vascular and gastrointestinal factors.
In this context, a systemic model based on intestinal etiology is proposed
to integrate the varied research and clinical findings in the migraine
Migraine is a complex, systemic disorder of unknown
causation. Typically, migraine presents with various neurologic, vascular,
and gastrointestional symptoms. 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 (Thomsen and Olesen, 1995; Agnoli and Marinis,
1985). 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,
Although the neurovascular components are a primary
focus in medical diagnosis and treatment, historical and contemporary viewpoints
also attribute great significance to gastrointestinal features. "Gastrointestinal
disturbances including nausea, vomiting, abdominal cramps, or diarrhea
are almost universal." (Silberstein, 1995, p. 387)
This article explores the
concept of intestinal pathology as a significant etiological factor in
migraine. The conceptual basis of the integrative approach advocated in
this article is derived from the systems approach of Edgar Cayce as described
by Mein et al. (1998). In essence, the model emphasizes that migraine is
often a consequence of problems in the intestinal system and enteric
nervous system, rather than the brain or central nervous system. According
to this theory, dietary or other irritations to the bowel are common causes
of migraine. Therapeutically, a variety of natural
remedies are utilized to reduce intestinal irritation, heal the gut, and
improve neurovascular functioning. These treatments are a complement to
standard medical treatments which are directed toward symptomatic relief.
Migraine is a general classification
which probably encompasses various etiological subgroups. Designations
such as abdominal migraine, dietary migraine, cervical migraine, menstrual
migraine, etc. suggest that a multifactorical approach is needed to understand
migraine. This article considers the role of intestinal pathology as one
subgroup, perhaps a major subgroup. Or alteratively, intestinal pathology
may represent a common pattern which ties together various other subgroups
into a more integrated model of migraine etiology.
INTESTINAL PATHOLOGY IN MIGRAINE
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 (Musser and Kelly, 1912;
Hare, 1912; Spear, 1916).
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; Symon and Russell, 1986; Mortimer and Good, 1990; Santoro
et al., 1990). 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 support a causal link between
recurrent abdominal pain and migraine." (Mavromichalis et al., p. 406)
The pathogenesis of abdominal migraine is unclear.
One obvious factor in causation of this form of migraine is diet. In fact,
diet (and associated allergic and inflammatory processes) have been implicated
as primary causal factors in the full spectrum of migraine manifestations.
This aspect of intestinal etiology in migraine will be discussed in the
Irritable bowel syndrome (IBS)
is common disorder of the intestines characterized by abdominal pain, bloating,
contipation and/or diarrhea. An association between migraine and IBS has
been noted. Watson et al. (1978) observed that persons with the
irritable bowel syndrome (IBS) have a significantly higher prevalence of
migraine-like headache than age-matched control subjects. The researchers
believed that the dispersed pattern of symptoms in IBS suggests that some
agent, such as a hormone, may be acting systemically. In a postal questionnaire
study involving 1620 participants, Jones and Lydeard (1992) found that
migraine and related systemic symptoms were significantly more common in
individuals with irritable bowel (IBS) than in persons without IBS. An
earlier epidemiological study by Bommelaer et al. (1990) also indicated
a strong association between migraine and IBS.
Using the 13C-urea breath test, Gasbarrini et al.
(1998) found that in 225 consecutive migraine patients, helicobacter pylori
was detected in 40% of the patients. In 83% of the patients who underwent
therapy for eradication of the H. pylori there was a significant reduction
in the intensity, duration and frequency of migraine attacks. The researchers
concluded that H. pylori is common in patients with migraine; bacterium
eradication decreases migraine; and the reduction of vasoactive substances
produced during infection may be an important pathogenetic mechanism in
Rousset et al. (1985) studied two hundred hospital
patients with gallstones who had been cholecystectomized on account of
typical biliary colics. The patients were shown to have a high rate of
migraine and other systemic symptoms which are characteristic of migraine
and intestinal illness including malaise, vertigo, flatulence, diarrhoea
and/or constipation. The researchers concluded that the symptoms
were indicative of real functional disorder.
DIET AND MIGRAINE
"An observed association between food consumption
and migraine is of respectable antiquity" (Glover et al., 1983, p. 53).
Fothergill observed that migraine-type headache is usually caused by inattention
to diet, with specific foods (such as milk, butter, fat meats, spices,
rich puddings) being especially potent in provoking the condition (Hanington,
1974). In 1885, Brunton linked the consumption of eggs and milk to migraine
(Mansfield, 1987). Early in this century, Brown reported that migraine
can be caused by foods. Accordingly, Brown claimed therapeutic efficacy
in the use of diet in the prevention and treatment of migraine (Brown,
The conceptualization of migraine as a gastrointestinal
allergic response also 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 report 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).
More recently, Unger and Unger (1952) advocated a
multifactorial etiology of migraine in which food and stress combined to
cause the syndrome. In a study by Grant (1979), 60 migraine patients used
an elimination diet to determine food intolerances. The commonest foods
causing reactions were wheat (78%), orange (65%), eggs (45%), tea and coffee
(40% each), chocolate and milk (37%) each), beef (35%), and corn, cane
sugar, and yeast (33% each). When an average of ten common foods were avoided
there was a dramatic fall in the number of headaches per month, 85% of
patients becoming headache-free. Grant concluded that both immunological
and non-immunological mechanisms may play a part in the pathogenesis of
migraine caused by food intolerance.
In 1980, Monro et al. reported that 75% of severe
migraine patients have raised levels of food-specific IgE antibodies. Wilson
et al. (1980) reported that migraine patients challenged with food antigens
by skin-prick test showed a significant correlation between specific food
allergens, the development of migraine headaches, and the appearance of
abdominal symptoms. They concluded that the clinical features of migraine
can be explained as a result of chemical mediators following antigen-antibody
reactions in the brain and other tissues were specific antibodies are localized.
However, a study by Merrett et al. (1983) failed to find a conventional
allergic mechanism associated with food intolerance in migraine patients.
In a double-blind controlled trial of oligoantigenic
(limited food) diet, Egger et al. (1983) reported the recovery of 93% of
88 children with severe frequent migraine. The oligoantigenic diet consisted
of one meat (lamb or chicken), one carbohydrate (rice or potato), one fruit
(banana or apple), one vegetable (brassica), water and vitamin supplements.
An optional diet consisting of none of the foods in the first diet was
offered to patients who did not respond to the first diet. After 3 or 4
weeks, patients who had no headaches or only one during the last 2 weeks
of the diet were reintroduced to excluded foods one at a time in a double-blind
format to verify that the foods were causing the migraine. 26 (70%) of
40 patients experienced migraine challenges to the reintroduction of provocative
foods. Interestingly, in most of the patients in whom migraine was provoked
by non-specific triggers (such as flashing lights), the provocation no
longer occurred while they were on the diet. Also, associated symptoms
(such as abdominal pain, behavior disorder, asthma, eczema) improved in
In attempting to identify biochemical markers which
distinguish dietary migraine from other forms of the illness, Glover et
al. (1983) noted a deficiency of the enzyme phenolsulphotransferase. Phenolsulphotransferase
is particularly active in the intestine where it probably serves to detoxify
phenols which may be present in migraine triggers such as chocolate, cheese
and citrus fruits. Ratner et al. (1983; 1984) demonstrated that some migraine
patients suffer from lactase deficiency and milk allergy.
Monro et al. (1984) identified foods which provoked
migraine in 9 patients. The patients were then given either sodium cromoglycate
or placebo orally in a double-blind format, with foods previously identified
as provocants. Patients given sodium cromoglycate experienced significantly
less migraine symptoms than the placebo group, supporting the hypothesis
of food-allergic etiology in migraine.
Mansfield et al. (1985) studied food allergy as a
cause of migraine. Skin testing, elimination diets, double-blind challenges,
and measurement of plasma histamine were performed on 43 adults with recurrent
migraine. Thirteen subjects experienced 66% or greater reduction in headache
frequency while on a diet free of milk, egg, corn and wheat. Double-blind
challenges in 5 of 7 patients provoked migraine whereas placebo challenges
produced none. The authors concluded, "In patients with chronic recurrent
migraine, evaluation of the role of foods in causing their disease appears
a worthwhile undertaking." (p. 129)
Hughes et al. (1985) utilized a nutritionally supported
fast (NSF) and nutritional supportive diet (NSD) in the assessment and
treatment of migraine. All 19 patients in the study showed exacerbation
of symptoms during the fast followed by nearly complete relief of symptoms
which the researchers interpreted as indicative of addictive withdrawal
associated with food sensitivities. Longitudinal results (3 to 18 months)
continued to show improvement in all 19 patients.
In seeking to understand how dietary etiology is
related to the obvious central nervous system manifestations of migraine,
the immune system has been cited as a possible pathophysiological link.
The work of Martelletti et al. (1993) supports the hypothesis of an altered
immune status in migraine without aura. Migraine may be due to a dysregulation
of the bidirectional homeostasis actively operating between the immune
system and central nervous system.
As an overview, Mansfield's (1987) excellent review
of food allergy in migraine is highly recommended for anyone seeking an
historical and conceptual overview of diet and migraine. A more general
overview which reviews the role of food allergies, chemical components
of foods, hypoglycemia, and taste aversion in migraine pathophysiology
is provided by Perkin and Hartje (1983).
NEUROVASCULAR ASPECTS OF MIGRAINE
As inviting as the dietary migraine hypothesis is,
it still does adequately explain the obvious neurovascular aspects of migraine.
In other words, what is the connection between the gut and the head in
migraine? Usually, gastrointestinal features of migraine are simply regarded
as side-effects of a primary central nervous system pathology.
There are two basic approaches to making the connection
between intestinal causes (such as food allergies) and neurovascular symptoms.
The chemical theory postulates that circulating substances produced in
the gut trigger neurological reactions. "In simplest terms, the interaction
of an allergen with IgE-specific antibody on a MAST cell leads to a cascade
of events directed by a series of released mediators. A possible role for
some of these mediators in the pathogenesis of the vasoconstriction and
vasodilation of migraine is likely" ( Mansfield, 1987, p. 315).
Another theoretical option involves nerve reflex
from the peripheral nervous system to the trigeminovascular complex. Autonomic
abnormalities in migraine are well known (Rubin et al., 1985; Havanka-Kanniainen
et al., 1986). The vascular abnormalities in migraine may result from excessive
sympathetic drive. From this perspective, neurological symptoms of the
prodromal phase of classic migraine result from vasoconstriction, which
is followed by vasodilation in later stages (Johnson, 1978). In addition
to the vascular disturbance, other autonomic aberrations including emotional
upset, increased irritability, sleep disturbance, appetite change, thirst,
nausea, and temperature dysregulation are associated with migraine (Appel
et al, 1992). Given the intimate relations between the autonomic and cranial
nerves, perhaps autonomic dysfunction is carried over into the trigeminal
Apart from the standard view of how the autonomic
(sympathetic/parasympathetic) nervous system functions, a new model is
developing which acknowledges the presence of a third division to the autonomic
system. Labeled the enteric nervous system (ENS), this extensive network
of neurons widely dispersed throughout the gut, regulates 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 central nervous system (CNS) both through nerve reflexes
and the production of neuropeptides. It is estimated that 80% of vagal
fibers are visceral afferents (Davenport, 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 ENS received its name from British physiologist
Johannis Langley who 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 Langley's work was ignored,
modern medical research has finally rediscovered the 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 gut brain, contemporary researchers
are drawing computer analogies and using information processing models
to describe the relationship between the brains of the body.
"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)
In summary, their are a variety of possible pathways
by which intestinal irritation can be transmitted to the CNS. In particular,
the enteric nervous system is a plausible link between intestinal and cerebral
SOMATIC DYSFUNCTION AND MIGRAINE
According to the Glossary of Osteopathic Terminology,
somatic dysfunction refers to "impaired or altered function of related
components of the somatic (body framework) system" (Kirksville College
of Osteopathic Medicine, 1990). Somatic dysfunction covers a wide variety
of musculoskeletal pathologies commonly referred to as subluxations, osteopathic
In reviewing the historical and modern perspective
on the causes and treatment of migraine, it must be noted that considerable
attention has been given to the role of somatic dysfunction. Somewhat like
the diet/migraine connection, there are numerous historical and modern
adherents of somatic dysfunction as a significant factor in migraine. The
point of this section is not to attribute migraine to "pinched nerves"
or imply that spinal manipulation is necessarily a primary treatment of
migraine. Rather it is to briefly review the literature and note its relevance
to an intestinal etiology of migraine.
Historically, numerous sources in the manual therapy
literature (primarily osteopathic and chiropractic) state that structure
does affect function and that physical manipulation is efficacious in the
treatment of migraine (Barber, 1898; Hazzard, 1905; American College of
Mechano-Therapy, 1910). More recent examples of this sort of thinking are
also in the literature (Parker et al., 1978; Vernon, 1995; Nelson et al.,
The obvious explanations of somatic dysfunction as
an etiological factor focuses on nerves which either directly affect the
trigeminal (fifth cranial nerve) or disturb the vasomotor regulation of
circulation. Presumably, relieving pressures on the relevant nerve centers
addresses the causes of migraine in some cases. In particular, temporomandibular
joint dysfunction (Clifford et al., 1996; Knutson, 1999) and cervical spine
dysfunction (Vernon et al., 1992; Blau and MacGregor, 1994) have been shown
to contribute to migraine.
A less conspicuous pathophysiological pattern associated
with somatic dysfunction is the effects of disturbed nerve reflexes on
the vegetative functions of the digestive system and intestinal tract.
The vagal parasympathetic nerves which innervate the abdominal viscera
parallel the spine along the cervical vertebrae. Disruption of vagal impulses
can adversely affect intestinal functioning. Notably, the splanchnic sympathetics
along the thoracic vertebrae also contribute to intestinal functioning.
Both aspects (sympathetic and parasympathetic) of autonomic functioning
coordinate closely with the ENS as described above.
Charles Hazzard, a well known and respected early
osteopathic physician, recognized the various possibilities of somatic
dysfunction in the etiology of migraine:
"Lesions act by disturbing sympathetic relations,
reflexly causing the headaches, just as may be the case in reflex headache
from uterine prolapsus. They all act by stoppage of blood flow. This may
occur in several ways. The vertebral arteries may be occluded by pressure
from the displaced cervical vertebra; the clavicle may hinder venous flow
in the external and internal jugulars, the sympathetic irritation may set
up vaso-motor reflexes and prevent proper circulation. A lesion may cause
headache by direct pressure of the luxated vertebra upon a nerve fiber.
A very common place for this to occur is at the atlas which impinges branches
of the suboccipital nerve sent to supply the occipito-atlantal articulation.
The same thing is apt to occur at any of the upper three cervical vertebra,
the corresponding nerves sending branches to supply sensation to the scalp.
Contraction of tissues over branches of the fifth nerve, or at their foramina
of exit may cause headache. Reflexes or direct irritation of the fifth
nerve may cause it. Lesion in the splanchnic area is often responsible
for migraine." (Hazzard, 1905, p. 278-279)
The premise that somatic dysfunction is a cause of
migraine and that manual therapy is a suitable treatment is certainly controversial.
To be sure, more research is needed in this area. With regard to the systemic
model presented in this article, somatic dysfunction and its treatment
should be considered as a possible factor in migraine, either directly
with regard to effects via the trigemino-vascular system, or indirectly
via abdominal visceral etiology. Assessment for somatic dysfunction and
appropriate spinal manipulation with special attention to the cervical
vertebrae and thoracic splanchnics are recommended as reasonable adjuncts
to the explicitly intestinal therapies described elsewhere in this article.
Given the significant literature linking migraine
to intestinal pathology and diet, it is reasonable to provide an initial
assessment to determine whether the migraine patient fits the profile for
intestinal etiology. A food/symptom diary is a simple tool for evaluating
the role of diet in migraine. The patient is instructed to record food
and beverage consumption which is compared to migraine episodes. The patient
may already be aware of food triggers which can be easily documented in
a clinical interview.
An elimination diet is another valuable assessment
tool. Raskin and Appenzeller recommend that a strict diet be adhered to
for two weeks. The diet consists solely of distilled water, lettuce, cauliflower,
carrots, boiled or baked potatoes, cottage cheese, chicken, olive oil,
and distilled white vinegar. Similar elimination diets have been advocated
by many of the authors cited in the earlier diet section. Most have in
common the elimination of highly suspect foods such as milk, wheat, corn,
soybean, peanut, chocolate, alcoholic beverages. Carter (1985), Diamond
et al. (1986), and Mansfield (1988) provide clear and practical guidelines
for assessment and application of dietary principles for migraine in a
Manual therapy to address somatic dysfunction is
also recommended. In addition to standard evaluation for cervical and temporomandibular
joint dysfunction, assessment should focus on the autonomic centers in
the cervical and thoracic splanchnic. Standard osteopathic or chiropractic
treatment is provided depending upon assessment of these areas.
Other physiotherapies may also assist with improving
intestinal and nervous system functioning. For example, Bjork (1983) recommended
colonic irrigation to decrease irritation in the large bowel. This may
be indicated in cases presenting with chronic constipation or an x-ray
of the colon showing fecal cakes or intestinal blockage.
Thus, diet, manual therapy, and physiotherapy are
complementary treatments. They are components of an integrative model in
which relatively natural therapies address the underlying causes of the
illness, in addition to standard medical treatment for symptomatic relief.
The etiology of migraine involves varied factors,
both specific and nonspecific. Based on the literature, the intestinal
etiology model described in this article provides a conceptual framework
for understanding certain systemic features of migraine. Clearly, intestinal
etiology in migraine does not account for all the varied manifestations
of the illness. Yet it does provide a plausible approach for integration
of some of the diverse research and clinical information in the literature.
A complementary medicine model, in which standard medical treatments (which
can often provide temporary symptomatic relief) are integrated with natural
therapeutics (intended to address more fundamental causes), is proposed
as a plausible next step in the treatment of migraine. Additional research
is needed to further document the clinical effectiveness of this model,
to evaluate the role of intestinal pathology in migraine, and to determine
which elements of the treatment protocol contribute to positive outcomes.
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