Appendix F
Conceptual Issues
    Edgar Cayce, a prominent figure in the development of the holistic medicine movement in America, insisted that the etiology of most cases of idiopathic epilepsy could be traced to the peripheral nervous system, usually to the nerves of the abdomen. He also noted that abdominal thermal anomalies (especially a cold area on the right side of the abdomen) could be found in such cases (Cayce, 1934). On the face of it, such a model might seem ridiculous given the mainstream medical emphasis on the brain as the source of epileptic seizure disorders. Thus it has become important to look carefully at Cayce model in light of the historic and modern literature to determine if Cayce’s approach is even worthy of consideration. The discussion that follows explores several key conceptual issues relating to the plausibility of an abdominal etiology and pathophysiology for idiopathic epilepsy. In particular, increasing recognition of the diagnostic entities called reflex epilepsy and abdominal epilepsy are supportive of the Cayce model. 
Reflex Epilepsy 
    Reflex epilepsy includes a group of epileptic syndromes in which seizures are induced by a stimulus. The stimulus may be simple (e.g., visual, somatosensory, olfactory, auditory) or complex (e.g., eating, thinking, reading). Most cases of documented reflex epilepsy are diagnosed because the triggering stimulus is easily identified. The Cayce approach to epilepsy can be characterized as a broader conceptualization of reflex epilepsy to include visceral stimuli that are not as obvious as typical reflex seizure precipitants (i.e., visceral reflex epilepsy). 
    Visceral symptoms that precede seizures (premonitions) or occur during the early stages of the seizure itself (aura) are common and suggest autonomic nervous system (ANS) involvement at some level. Although it is usually assumed that ANS involvement is an effect of primary central nervous system (CNS) pathology, some researchers have suggested that ANS involvement may have etiological significance. Thus, visceral symptoms may be associated with underlying visceral processes that act as precipitating factors in some cases of 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 and Kelly, 1912). “The most common aura is of vague gastric distress, ascending up into the chest” (Gordon, 1942, p. 610). Thus, visceral symptoms may be associated with underlying visceral processes that act as precipitating factors in some cases of epilepsy. 
Abdominal Epilepsy 
    Abdominal epilepsy is diagnosed when the visceral symptoms predominate. A few papers published in the medical journals during the 1960s called attention to the abdominal features in epilepsy (Berdichevskii, 1965; Takei and Nakajima, 1967; Juillard, 1967). Over the past twenty-five years, numerous researchers and clinicians have reported 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. 
Vagus Nerve Involvement in Epilepsy 
    The vagal link in epilepsy has 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-resistant patients (Amar et al., 1998; Lundgren et al., 1998; Handforth 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). 
    The vagus nerve is a primary neural pathway between the viscera and the brain. It is estimated that 80% of vagal fibers are visceral afferents carrying impulses from the abdomen to the brain (Davenport, 1978). The effectiveness of vagus nerve stimulation treatment for epilepsy may be indicative of an interruption of such a reflex pathway between the viscera and brain. 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. Vagal nerve stimulation via visceral pathophysiology could be a significant factor in some cases of epilepsy. This nerve pathway between the abdomen and brain is fits the description of the abdominal nerve reflexes that produce seizures as documented in the Cayce readings in Appendix A. 
Enteric Nervous System 
    The gastrointestinal tract is richly innervated. Labeled the enteric nervous system (ENS or “gut brain”), this branch of the ANS constitutes about one-third of the body’s total nervous system. British physiologist Johannis Langley is credited with naming the ENS and recognizing the its relative independence from the CNS. Focusing on the ganglia of the gut, Langley 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). The relationship between the ENS and CNS has been compared to a computer network with each portion of the network acting as a computer in constant linkage with the other (Wood, 1994). Disruption or extreme synchronization of impulses between the ENS and CNS could play a role in the pathophysiology of one or more subgroups of epilepsy (e.g., abdominal epilepsy or visceral reflex epilepsy). 
Thermographic Assessment of ANS Functioning 
    Whereas noninvasive assessment of the brain cortex with EEG is relatively simple, evaluation of the visceral component of the ANS is problematic. In many respects, assessment of visceral ENS functioning is comparable to measuring deep structures within the brain that are not accessible via EEG. A possible solution to the problem of measuring ENS functioning is the use of surface thermography as a measure of sympathetic nervous system vasomotor activity. 
    Conceptually, assessment with cutaneous thermography is regarded as a noninvasive window into sympathetic nervous system (SNS) functioning. SNS functioning is an important division of autonomic nervous system (ANS) physiology that is known to be involved in many disease syndromes. Thermographic measurement of the ANS through its two branches (vasomotor ANS and visceral ENS) represents a promising means of quantifying this important division of the peripheral nervous system. 
ANS Vasomotor Physiology Implications Of Abdominal Thermographic Anomalies 
    One of the primary problems in researching the Cayce cold spot hypothesis is how to explain the underlying physiology that can link abdominal thermal variations to the etiology or pathophysiology of epilepsy. As discussed above, the ANS vasomotor system (SNS) represents the leading candidate for connecting cutaneous thermography to neurologic illness. The following information may help to elaborate this association: 
  • Physiology of Systemic Thermal Regulation – Thermography of biological systems assesses the status of dermal thermoregulatory function. The hypothalamus is believed to be the primary regulator of core temperature for body-heat maintenance (Bentzinger, 1969). This is essentially a systemic process by which the organism coordinates body temperature with internal (e.g., fever) and external (e.g., room temperature) factors and conditions.
  • Vasomotor Physiology – More precise local thermoregulation within each spinal dermatome may account for changes in dermal temperatures along the torso and extremities (Simon, 1975). This is generally described as a vasomotor process by which the sympathetic (SNS) division of the ANS regulates blood flow by dilating or constricting arterioles and capillaries within the innervated dermatome. Vasodilation tends to increase dermal temperature while vasoconstriction has the opposite effect. Thus the hypothalamic systemic regulation of temperature serves as a background against which location variations in ANS vasomotor function are manifested. We may have detected such local ANS vasomotor variations in our epilepsy patients.
  • Pathophysiological Implications of ANS Vasomotor Anomalies – Normal body surface temperatures are essentially symmetrical. Bilateral cutaneous thermal asymmetries and anomalies are suggestive of ANS vasomotor dysfunction, unless an identifiable surface feature (such as scar tissue or adhesion) is present to account for the variation. Likewise thermal anomalies in adjacent dermatomes are regarded as suggestive of sympathetic neuronal dysfunction (Korr, 1962). Some theorists maintain that SNS vasomotor function is closely associated with ANS visceromotor functioning (ENS). Thus thermographic anomalies may represent a “window on the sympathetic system” (Abernathy, 1988). An inherent ANS dysfunction could help account for the common abdominal/visceral symptoms within one or more subgroups of epilepsy.
Abdominal Symptomatology As A Window Into the Brain 
    The concept of using abdominal physiology and symptomatology as a window into brain pathophysiology in epilepsy has been used by Henkel et. al. (2002) who quantified the prevalence of abdominal aura in focal epilepsies (involving specific areas of the brain). The seizures of 491 consecutive patients with focal epilepsies were prospectively classified using prolonged EEG video monitoring and MRI scan. Two hundred twenty-three patients (45%) had temporal lobe epilepsy (TLE); 113 patients (23%) had extratemporal epilepsies; and for 155 (32%) patients, the epilepsy could not be localized to one lobe. Abdominal auras were more frequent with TLE (117 of 223 patients, 52%) than in extratemporal epilepsy (13 of 113 patients, 12%, p < 0.0001) and more frequent in mesial TLE (70 of 110 patients, 64%) than in neocortical TLE (16 of 41 patients, 39%, p = 0.007). Abdominal auras were followed by ictal oral and manual automatisms (automotor seizure) in at least one seizure evolution in all patients with TLE (117 patients, 100%). In contrast, only two patients with extratemporal epilepsy (2 of 13 patients, 15%, p < 0.0001) had abdominal auras evolving into automotor seizures. An abdominal aura is associated with TLE with a probability of 73.6%. The evolution of an abdominal aura into an automotor seizure, however, increases the probability of TLE to 98.3%. This study is a good example of one of the positive outcomes that we may be able to achieve by monitoring abdominal symptoms and physiology for comparison with seizure manifestations. 
Treatment Implications 
    If abdominal/visceral ANS reflexes in epilepsy can be consistently identified via noninvasive assessment, innovative treatments may be developed to address this specific pathophysiological pattern. Here are some possibilities: 
  • Medication – For epilepsy patients with significant abdominal/visceral features (including vasomotor anomalies) medications that selectively target the enteric nervous system could play a role in seizure prevention.
  • Nonsurgical Vagus Stimulation – Osteopathic physicians have developed specific techniques to manually stimulate the vagus nerve along its course in the neck. Such a technique (or a similar effect produced by an electric vibrator) should be researched to see if such nonsurgical vagus stimulation could be efficacious in epilepsy. This could be could be especially helpful in medication-resistant cases where surgical implantation of a vagus stimulator is being considered. Patients that respond to some extent to nonsurgical vagus stimulation may be good candidates for the surgical procedure if seizures are not entirely controlled.
  • Ketogenic Diet – Used initially in the 1920's as a treatment option for patients with intractable epilepsy, the ketogenic diet has seen increasing use for epilepsy (Kinsman et al., 1992; Swink et al., 1997). The diet is essentially an extremely high fat diet that is low in carbohydrate and protein. When consumed on a regular basis the diet produces ketosis that exerts an anti-epileptic effect. Though the precise mechanism of action is not completely understood, it is interesting that the location on the abdomen where Cayce described thermal anomalies is also an area of concentration for lacteals (lymphatics) that absorb fats from the intestinal tract. Dysfunction in this process could result in thermal anomalies and reduction of absorption of fats required for optimal nervous system operation.
  • Physiotherapy – Interestingly, Hughlings Jackson described an epilepsy patient who could sometimes prevent the “march” of a seizure from the extremities of a limb to the torso by vigorously rubbing the affected limb above the area manifesting the seizure (Jackson, 1931). If abdominal/visceral reflexes play a role in the etiology and/or pathophysiology of some cases of epilepsy, simple, noninvasive forms of physiotherapy may be helpful in decreasing the frequency and/or severity of seizures. Osteopathic physicians have claimed success in using OMT (osteopathic manipulative treatment) in epilepsy by giving spinal and visceral manipulations intended to improve ANS dysfunction (Hazzard, 1905). Early osteopathic physicians suggested placing a piece of ice at the base of the skull during the premonition or aura of a seizure to stop the seizure or lessen its impact (Hazzard, 1905). The Cayce readings recommend hot abdominal packs and visceral massage to reduce the frequency of seizures. Conceptually, direct alteration of visceral afferent input to the CNS may be helpful as a preventative or when visceral premonitions are noted.
     The point of this extended discussion of the conceptual basis of the Cayce abdominal hypothesis of epilepsy is to suggest that the model is plausible and worthy of research. The variable thermographic findings that we have documented in this report require a detailed discussion of Cayce’s abdominal cold spot hypothesis and our thermographic research results. 
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