A Traditional Osteopathic
Approach
to Abdominal Epilepsy
Abstract
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
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Appendix A
References on Abdominal Epilepsy
The following references are representative of
the abdominal epilepsy literature. They are included in this
appendix as an aid to readers interested in further pursuing the topic.
Agrawal, P., Dhar, N. K., Bhatia, M. S. &
Malik, S. C. (1989). Abdominal epilepsy. Indian
Journal of Pediatriacs, 56(4), 539-541.
Babb, R. R. & Eckman, P. B. (1972).
Abdominal epilepsy. Journal of the American Medical
Association, 222(1), 65-66.
Berdichevskii, M. (1965). Meso-diencephalic
epilepsy after abdominal injury. Vopr Psikhiatr Nevropatol,
11, 374-376.
Bondarenko, E. S., Shiretorova, D. Ch. & Miron,
V. A. (1986). Abdominal syndrome in the
structure of cerebral paroxysms in children and adolescents. Soviet
Medicine, (2), 39-44.
Douglas, E. F. & White, P. T.
(1971). Abdominal epilepsy--a reappraisal. Journal of
Pediatrics, 78(1), 59-67.
Hotta, T. & Fujimoto, Y. (1973).
A study on abdominal epilepsy. Yonago Acta Medica, 17(3),
231-239.
Juillard, E. (1967). Abdominal pains
and epilepsy. Praxis, 56(3), 83-84.
Loar, C. R. (1979). Abdominal
epilepsy. Journal of the American Medical Association,
241(13), 1327.
Matsuo, F. (1984). Partial epileptic
seizures beginning in the truncal muscles. Acta Neurologica
Scandinavia, 69(5), 264-269.
Mitchell, W. G., Greenwood, R.S. & Messenheimer,
J. A. (1983). Abdominal epilepsy: Cyclic
vomiting as the major symptom of simple partial
seizures. Archives of Neurology, 40(4) 251-252.
Moore, M. T. (1972). Abdominal epilepsy.
Journal of the American Medical Association, 222 (11),
1426.
Moore, M. T. (1979). Abdominal
epilepsy [letter]. Journal of the American Medical Association,
241(13), 1327.
O'Donohoe, N. V. (1971). Abdominal
epilepsy. Developmental Medicine of Child Neurology, 13(6),
798-800.
Peppercorn, M. A., Herzog, A. G., Dichter, M.
A. & Mayman, C. I. (1978). Abdominal epilepsy: A cause
of abdominal pain in adults. Journal of the American Medical Association,40(22),
2450-2451.
Peppercorn, M. A. & Herzog, A. G. (1989).
The spectrum of abdominal epilepsy in adults. American Journal of Gastroenterology,
84(10), 1294-1296.
Reimann, H. A. (1973). Abdominal
epilepsy and migraine. Journal of the American Medical Association,
224(1), 128.
Singhi, P. D. & Kaur, S. (1988).
Abdominal epilepsy misdiagnosed as psychogenic pain. Postgraduate Medical
Journal, 64(750), 281-282.
Solana de Lope, J., Alarcon, F. O., Aguilar, M.
J., Beltran, C. J., Barinagarrementeria, F. & Perez, M.
J. (1994). Abdominal epilepsy in the adult. Review of
Gastroenterology, 59(4), 297-300.
Takei, T. & Nakajima, K. (1967). Autonomic
abdominal epilepsy--clinico-encephalographic evaluation of 24 cases.
Nippon Shonika Gakkai Zasshi, 71(5), 543-551.
Yingkun, F. (1980). Abdominal
epilepsy. Chinese Medical Journal, 93(3), 135-148.
Zarling, E. J. Abdominal epilepsy:
an unusual cause of recurrent abdominal pain. (1984). American
Journal of Gastroenterology, 79(9), 687-688.
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