Abstract -- delayed gastric emptying is called gastroparesis (associated with Irritable Bowel Syndrome -constipation). The following procedure was developed to produce gastric emptying. Drinking coffee is a pre-requisite for the anti-gastro paretic effects of the procedure. The procedure, in a nutshell, is this: for one hour after taking coffee and rocking on one’s side, gastric emptying of coffee is induced (and palpable). The above steps are necessary for the cervical traction device (TD) to function. During application of TD, one lies on one’s side while performing neck pulls. The following analysis of the inputs of the procedure uses known research about how the steps of the procedure work.

There are differences in Ghrelin in patients with irritable bowel syndrome (c-constipation predominant) and controls. After an overnight fast, biopsies were taken from mucosa and duodenum. The density of ghrelin-immunoreactive cells in the mucosa was significantly lower in IBS-c, than in healthy controls. In order to compensate for the decrease in the ghrelin cell density, the synthesis of ghrelin may be increased in IBS-c patients, (causing fatigue).(1) Plasma ghrelin levels and their relationship with gastric emptying time was investigated in dysmotility-like FD (functional dyspepsia) patients. Preprandial ghrelin levels were significantly lower in FD patients than in controls. Delayed gastric emptying was observed in patients with abnormally low ghrelin levels. (2)

Ghrelin improves small intestinal transit; therefore, decreased ghrelin in the duodenum would decrease transit time causing duodenal distension (DD) until it stops gastric emptying, (discussed later).
The carbohydrate metabolism of runners can influence gastric emptying (GE) . T(50) (½ emptying time) was 47 min. for clear carbohydrate drink. Running-induced hypoglycemia is one of the essential factors leading to enhanced liquid GE. (3)

Increased cytosolic Ca(2+) is necessary and sufficient for astrocytes to exocytotically release the transmitter glutamate. The source of Ca(2+) for the exocytotic release of glutamate from astrocytes predominately comes from endoplasmic reticulum stores with some ryanodine/caffeine-sensitive stores. Caffeine is a ryanodine receptor agonist. The basic mechanism in neurometabolic coupling is the glutamate-stimulated aerobic glycolysis in astrocytes, such that the sodium-coupled reuptake of glutamate by astrocytes and the ensuing activation of the Na(+)-K(+) ATPase triggers glucose uptake and its glycolytic processing, which results in the release of lactate from astrocytes. Lactate can then contribute to the activity-dependent fueling of the neuronal energy demands associated with synaptic transmission. That is the role of glutamate signaling on astrocytes in neurometabolic coupling. (4)

Glial cells take up a significant fraction of glucose (50% or more) from the blood and provide neurons with glucose-derived energy substrates. Furthermore, the amplitude of this transfer is correlated to the activity level of the brain; the larger the activity, the more metabolites are shuttled from glia to neurons. This is the “astrocyte-neuron lactate shuttle.” (5)

The glucose-sensing mechanism in the VMH (ventromedial hypothalamus-- a measuring center for blood glucose) responds to lactate and, thus, is not specific for glucose. Local lactate perfusion of the VMH suppresses hypoglycemic counter regulation.(6) Glucose sensing by neurons of the VMH hyperpolarize and inhibit the VMH when physiological rises in extra-cellular glucose levels rise. Glucose induced activation of K(+)-selective currents are of sufficient size to cause complete inhibition of whole-cell electrical activity. These K (+) currents contribute to suppression of firing in the VMH.(7)

Delayed gastric emptying is induced by duodenal distension (DD). Intestinal electrical stimulation (IES) has been shown to produce inhibitory effects on gastric emptying. IES at the duodenum activated 70% of the DD-responsive neurons in the VMH. Therefore, DD causes VMH activation, and increased lactate, equivalent to increased glucose, causes decreased VMH activation, reversing DD signaling at VMH and activating GE. (8)

Patients with subarachnoid hemorrhage were micro dialyzed and the relationship between ICP (intracranial pressure) and markers of energy metabolism were analysed. Levels of glutamate and lactate were lower during periods of decreased ICP, as compared with elevated ICP. When CSF (cerebro-spinal fluid) drainage was increased and the ICP was lowered, there was an instantaneous sharp increase in interstial glutamate. (9) (Remember--glutamate causes lactate causes decreased VMH activation, negatively associated with DD that causes decreased GE). How does one cause CSF drainage and decrease ICP?

Traction Device hypothesis. It would seem implausible that gentle external compression would compress deep internal spaces without significant damage to the brain. It does, however, provide gentle deep pressure to the sub-occipital muscles which will lead to a functional relaxation which allows for the occipito-atlantoid joint to extend more comfortably. It also dramatically reduces the tension holding the occipital bone in a flexed position, allowing the cranial base to flatten into expansion (the “bowl” becoming a “saucer”). The new hypothesis makes certain assumptions: (1) that the cavernous sinuses control venous outflow through the spinal venous network, (2) the ivvp/evvp (internal/external venous plexus) system allows for a controlled release of venous blood out of the internal spinal/skull vault but can facilitate a dramatic reversible flow of blood back into the sealed system when there is a sharp drop in intracranial pressure, and (3) a ball valve system operates in the great cerebral vein and the cavernous sinus where the csf filled arachnoid granulations swell to reduce venous blood flow. A suitable starting point will be when the venous blood flow through the cavernous sinus is at its maximum. Large volumes of blood enter the ivvp, the cuff surrounding the spinal cord. The valves in the veins exiting the ivvp restrict the exiting blood to the extent that the ivvp has more blood is entering the cuff than is able to leave. In normal posture, like any vessel, it fills from the bottom upwards so the csf is forced upwards as the arachnoid space is pressurized. Eventually, the pressure wave reaches the level of the skull, where the raised intracranial pressure directly affects the brain. The increased csf pressure backs up to the base of the brain and swells the arachnoid granulations in the cavernous sinus. The swelling reduces the venous flow through the sinus, redirecting the blood to the internal jugular vein and safely out of the skull. (Pressure also engorges the granulation at the level of the great cerebral vein and straight sinus, reducing blood flow to the site of csf filtration). The greater csf pressure in the arachnoid granulations around the superior saggital sinus then promotes re-absorption back into the venous blood stream. Reduced blood flow to the plexus ivvp allows it to drain faster than it can be refilled so the blood volume shrinks. The resulting drop in local pressure allows the csf to drain down the cord, relieving pressure on the arachnoid granulations in the cavernous sinus, therefore returning to the start of the cycle. (10)

The traction device, causing the skull bones not to take a spherical shape (the maximum volume per surface area), such that the intra-cranial volume is reduced, causes a cavernous sinus ball valve opening that would decrease intracranial pressure via jugular vein flow. This allows CSF drainage and lactate production such that decreased VMH activation blocks DD’s delay of GE.

ACC (anterior cingulate cortex) nociceptive transmissions are mediated by glutamate receptors. ACC responses to CRD (colorectal distension) are enhanced in viscerally hypersensitive rats and causes increased global brain activity. Although some lamina I spinal afferents terminate directly in the LC, the main source of nociceptive excitation of LC neurons appears to be noxious spinal inputs, and from there drive the ACC. (11)

An increase in brain activity producing glutamate above a 1 Mm concentration causes this toxic neurotransmitter to be absorbed by astrocytitic EAAT2. Now EAAT2 has been found on the somata themselves and has a high and low affinity state. High affinity causes decreased brain glutamate causing decreased brain lactate by the astrocytitic shuttle. An increase in excitatory axon terminals causes a low affinity state that causes a decrease in transport coupling due to causing increased brain glutamate and decreased uptake at astrocytes causing increased lactate (desirable in deactivating VMH). (12)

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Lee KJ, et al, “Plasma ghrelin levels and their relationship with gastric emptying in patients with dysmotility-like functional dyspepsia.” Digestion, 2009; 80(1): 58-63.

Chang FY, et al, “Interaction of carbohydrate metabolism and rat liquid gastric emptying in sustained running.” J Gastroenterol Hepatol, 2006; 21(5):831-6.

Reyes RC, Parpura V, “The trinity of Ca(2+) sources for the exocytotic release from astrocytes.” Neurochem Int, 2009;55(1-3):2-8.

Jolivet R, Magistretti PJ, Weber B, “Deciphering neuron-glia compartmentalization in cortical energy metabolism.” Front Neuroenergetics, 2009; 1:4.

Borg MA, et al, “Local lactate perfusion of the ventromedial hypothalamus suppresses hypoglycemic counter regulation.” Diabetes, 2003;52(3):663-6.

Williams RH, Burdakov D., “Silencing of ventromedial hypothalamic neurons by glucose-stimulated K(+) currents.” Pflugers Arch, 2009; 484(4): 777-83.

Zhang J, Zhu H, Chen JD, “Central neuronal mechanisms of intestinal electrical stimulation: effects on duodenum distention-responsive (DD-R) neurons in the VMH of rats.” Neurosci Lett. 2009; 457(1):27-31.

Samuelsson C, et al, “Relationship between intracranial hemodynamics and micro dialysis markers of energy metabolism and glutamate-glutamine turnover in patients with subarachnoid hemorrhage.” J Neurosurg. 2009 May 8. [E-pub ahead of print]

Gard G., “An investigation into the regulation of intra-cranial pressure and its influence upon the surrounding cranial bones.” J Bodyw Mov Ther. 2009; 13(3): 246-54.

Wu X et al., Role for NMDA receptors in visceral nociceptive transmission in the anterior cingulate cortex of viscerally hypersensitive rats, Am J Physiol Gastro Liver Physiol :2008;294(4) p.g918-27.
Kabakov AY, Rosenberg PA, Evidence for change in current flux coupling of GLT-1 at high glutamate concentrations in rat primary forebrain neurons and GLT1a-expressing COS-7 cells. Eur J Neurosci 2009:30(2): 186-195.

By: screeb