A Personal Experience with Diverticulitis of the Sigmoid: A Study in Visceral Neurology

My apology for detailing this personal experience is that it has furnished an unusual opportunity to apply the facts of visceral neurology to the study of the various symptoms, particularly the reflexes which may be caused by an inflammatory lesion in the colon and sigmoid. I did not have to take the indefinite answers of patients which often fail to convey the correct impression and which are difficult for the physician to interpret, but furnished the answers myself, as they were manifested in my own body and perceived by myself. 

When I came home from work in the evening of November 8, 1927, I noticed that I was somewhat more fatigued than usual. After eating dinner I did not feel quite comfortable. At ten o’clock I went to bed, but awakened at midnight with feelings of illness. I had a general discomfort through the lower half of the chest and upper portion of the abdomen, particularly the thoracic cutaneous zones Vth to IXth on both sides, as shown in fig. 1A, which lasted for eighteen hours. lt was not a severe pain but a very depressing sensation, much as though I were held in a vice. Nausea and vomiting were present. The stomach contents expelled at midnight showed that the food was still undigested. Vomiting occurred twice later in the night. A diarrhea also followed. The temperature was elevated to 101°, and the pulse was slow. Coincident with this attack frequent eructations of small amounts of gas occurred, which became very annoying and persisted thereafter for months. This indication of a relaxed cardia increased in severity whenever the symptoms of acute diverticulitis were present, and has persisted until the present time. 

A physician was called next morning who considered the possibility of the presence of an ulcer of the stomach, an appendicitis, or a diseased gallbladder. Food and drink were withheld until later in the day, when the acute symptoms had subsided; then a dose of castor oil was taken. Following this the acute symptoms disappeared and three days later I resumed work as usual. 

Fig. 1. Diagram showing the localization of various sensory phenomena as expressed in Head’s sensory zones in a case of diverticulitis of the sigmoid.

1. Vertical lines including thoracic zones 5 to 12, area of pain from pylorospasm.

2. Stippled area sensory zones thoracic, 9 to 12, area of hyperalgesia from diverticulum.

3. Solid black area in first lumbar and third sacral zones area, in which recurrent pain was experienced.

4. Horizontal lines in lumbar zones 1 and 2, area in which anesthesia was expressed.

 

On November 13th, I came home at five o’clock in the afternoon, again feeling very uncomfortable. I was tired, somewhat nauseated, yet hungry. I ate an apple and lay down on a couch for a few minutes, and fell asleep. When I awakened the nausea was more marked. I vomited several times. I again experienced discomfort in the lower half of the thorax and upper abdomen, similar to that on the previous occasion, feeling as though I were held in a vice. The temperature was elevated and the pulse was slow. A physician was called, who gave me codeine hypodermically to relieve the pain. I slept some, but awakened in the night with nausea, vomiting and diarrhea. 

The situation appeared so serious next morning that I was taken to the hospital. Both food and drink were withheld because of fear of a perforated gastric ulcer. Temperature was 101°, pulse in the fifties, and appeared severely ill; leucocytes were about 20,000. Aside from the distress previously mentioned an area of hyperalgesia developed about two and one-half inches to the left of the umbilicus, the upper limit being a little above the level of the umbilicus, the lower border being about two and one half inches below, thoracic cutaneous zones IX to XII, fig. B. The area was about two inches wide. 

The temperature remained elevated at 100-101° for about one week. Neither food nor water was allowed during the first few days. The leucocytes remained high, from 20,000 to 30,000, part of which during the latter period was due to the concentration of the blood due to dehydration from lack of fluid intake. The red corpuscles were about 7,000,000, for the same reason. After a week the acute symptoms had subsided sufficiently to permit giving me a barium meal and making a study of the gastrointestinal canal. Before the study was made a probable diagnosis of diverticulitis was made. 

The x-rays revealed a single diverticulum of the sigmoid, and a marked spasticity of the entire colon above. 

All symptoms subsided and I left the hospital on the twelfth day. After a two weeks’ convalescence I returned to work. On several occasions during the next six months I had feelings similar to those noticed when the original attack came on, with distress in the lower thoracic and upper abdominal areas. These were accompanied by nausea and preceded by a mild constipation. The symptoms were promptly relieved by colon irrigations. The area of hyperalgesia over the left side of the abdomen, while continuously present except when I would forget it during my busy hours, was always more pronounced during these periods of mild activity. 

In June 1928, seven months after the initial illness, I was suddenly seized with elevation of temperature, nausea, vomiting, distress in the upper abdomen and lower thoracic areas, and severe diarrhea. The diarrhea continued for three days, after which all acute symptoms disappeared except the hyperalgesia, which became very much lessened. The relief from acute symptoms lasted for about six months. 

In December 1928, I was suddenly seized with an acute pain like the stab of a knife, in the lower left quadrant of the abdomen which was accompanied by a cramping of the muscles. This passed off and has never since been felt. About once in every four or five weeks, from December 928 to January 1930 , some evidence of gastrointestinal symptoms, nausea, discomfort after eating, and constipation appeared.

In May of 1929 a very severe diarrhea was brought on apparently from eating some food at a banquet, for others who had eaten of the same food suffered likewise. The diarrhea continued for several days until the diverticulum or diverticuli were apparently emptied of toxic substances, for thereafter marked relief was experienced. Following the diarrhea in May, however, discomfort in the area of hyperalgesia on taking food was often noted, the pain coming on as soon as the food entered the stomach. This was similar to the gastro-colic reflex complained of by many patients, only it was always felt in the area of hyperalgesia. 

Before classifying the symptoms manifested during and since the first acute onset I wish to record other symptoms which I had noticed over a period of three or four years prior to the time of the acute attack, and which I, not knowing of the diverticulum, had interpreted as being probably connected with the ureter. On one occasion I.had noticed an area of anesthesia over the upper, front and inner aspect of the left thigh in the areas of the 1st and 2d lumbar cutaneous zones, fig. 1D, which lasted for a period of two or three days. Another symptom which had been noticed on many occasions during the previous three or four years, and which at times would come on six or eight times a day, was a very acute pain in a small area on the upper inner aspect of the thigh in the 1st lumbar cutaneous zone, and at the same time in the scrotum in the area supplied by the 3d sacral nerve (fig. 1C). This pain would come on suddenly and last only a second or two, but often was repeated several times in quick succession like a series of electric shocks. It was so severe at times that it made me make a sudden audible gasp which would cause those near me to ask what was the matter. This symptom disappeared after the first acute attack and has been noticed only at rare intervals since. These areas are shown in fig. 1.

 

The Toxic Syndrome of Diverticulitis

The toxic syndrome present during the acute attack consisted. of most of the usual symptoms which accompany severe toxemia; slight chilliness, cutaneous vasoconstriction, followed by elevation of temperature, tiredness, aching, nervousness, prostration, insomnia, lack of appetite, coated tongue, inhibition of digestion, nausea and vomiting, loss of taste noted when I began to take food, and leucocytosis. Instead of the pulse showing the accustomed rapidity which accompanies toxic states, it was slow. The reflex stimulation through the vagus was able to overcome the central stimulation of the sympathetics; or, possibly some vagotropic substance which acted upon the heart was released from the inflamed diverticulum.

It will be noted that this toxic syndrome, in its peripheral expression produced effects similar to the body’s reaction to fear, anger, pain and rage, as described by Cannon, which is expressive of widespread sympathetic stimulation and parasympathetic inhibition. The effects are expressed in every tissue of the body because the sympathetics are distributed to all, as may be understood from fig. 2. The sympathetico-adrenal-thyroid mechanism which speeds up metabolism is stimulated both by the major emotions and by toxemia. Any marked toxemia causes prolonged action during which time not only is more than the normal amount of heat produced but its dissipation is minimized to the point of causing an abnormal heat retention, causing elevation of temperature while the major emotions are of short duration and usually accompanied by sweating and rapid loss of heat. Purely emotional reactions sometimes show an elevation in temperature amounting to a few tenths of a degree but rarely more than a degree.

Fig. 2. Schematic illustration of the distribution of the two components of the vegetative nervous system, showing its division into sympathetic and parasympathetic and their branches to the various organs.

 

The thoracolumbar portion of the cord, which gives origin to the sympathetic nervous system, is represented by lines. The portions of the midbrain and medulla, and sacral segments of the cord, which give origin to the parasympathetic system, are represented in black. The peripheral nerves belonging to the parasympathetics, are shown as solid black lines, while those belonging to the sympathetic system are shown as broken lines. This chart shows the double innervation of the structures of the head, heart, and the entire enteral system, and likewise indicates the single innervation for the blood vessels, pilomotor muscles and sweat glands of the body. (From Symptoms of Visceral Disease)

 

While the x-rays revealed a single diverticulum filled with barium, and that in the sigmoid, from the study of the pathology and from usual clinical experience in diverticulitis, we are justified in assuming that there was probably more than one.

 

Reflex Symptoms of Diverticulitis

Reflex symptoms were evident in the stomach, the colon, the rectum, the heart and in those sensory cutaneous zones which are in reflex connection with the stomach, colon and sigmoid. 

The reflex symptoms noticed in this study are many, but can probably best be presented according to the afferent and efferent neurons over which the impulses were carried. 

Precedent to the discussion of reflexes which either arise in or are manifested in the gastrointestinal canal, it is necessary to disabuse our minds of any idea that we may possess of the necessity of juxtaposition, in the cord, of the entering and outgoing neurons which form the receptor and effector elements of the reflex arc. 

While Sherrington’s law that each afferent neuron finds in the segment of the cord which it enters an efferent neuron with which it will combine most readily in the formation of reflexes holds true for visceral reflexes as usually met, it does not include combinations of other neurons which belong to different segments of the cord, in the formation of reflexes. Such variation is found in many diseases of viscera. The segments in which reflexes from the important viscera are most apt to occur may be judged from fig. 3; which shows the connector neurons to each of the more important viscera.

It has been shown by Carlson and his coworkers that each and every portion of the gastrointestinal canal may be influenced by irritants applied to each and every other portion of the gastrointestinal canal.

Physiologic evidence points to the possibility of a single afferent impulse being transferred to practically all efferent neurons, as is illustrated in strychnia poisoning, in which a stimulus, whether of sight, sound or touch, may produce generalized spasm of the musculature of the whole body.

Referred pain follows laws similar to true reflexes and bears out the segmental nature of all such effects.

Response on the Part of the Stomach. The stomach manifested motor, secretory and sensory reflexes in response to the acute diverticulitis. The effects which predominated were those recognized as being produced when sympathetic action predominates over the parasympathetic. There was nausea, vomiting and a delayed or rather almost complete absence of digestion, for the vomitus ejected at twelve o’clock, six hours after eating, showed the food to be little changed by its residence in the stomach. Eructations of gas were also frequent. We assume, therefore, that gastric peristalsis was not only deficient but reversed, that the pyloric sphincter was contracted or closed and the cardia relaxed. The distress felt in the thoracic sensory zones Vth to IXth, fig. 1A, was bilateral and corresponded to the pain of pylorospasm. Impulses can cross in the cord and produce bilateral reflexes according to well established physiologic laws. This is not uncommon in severe anginal attacks.

FIG. 3. The connector neurons for the important thoracic abdominal, and pelvic viscera. 

In the figure the connecting neurons are those which belong to the thoracolumbar outflow; except those going to the diaphragm, which are spinal nerves (phrenics). The motor cells for the viscera are found in the various collateral ganglia.
The figure shows that the innervation of the various viscera may be divided into groups. The heart and lungs are innervated from practically the same segments, the upper Ist to VIth thoracic. The stomach, liver, pancreas, and small intestine from the same segments, Vth to IXth thoracic. The colon, kidney, and pelvic viscera from practically the same segments, IXth and Xth thoracic to IIId and IV lumbar.
This figure shows the colon as receiving innervation from the upper three lumbar segments, as well as the lower four thoracic segments, although this is not generally accepted by physiologists. In spite of this grouping in innervation, each organ is brought in reflex connection with efferent neurons, both sensory and motor, which are more or less definite, in such a way that the motor and sensory reflexes do not overlap as much as might be indicated. (From Symptoms of Visceral Disease)

If we disregard the possibility of impulses being transferred from one segment of the gastrointestinal tract to another through the nerve plexuses found in its walls, we may account for the transference of the stimuli from the inflamed diverticulum to the stomach by central intersegmental paths. Such stimuli may pass from the inflamed areas in the gut to the cord through the afferent neurons which course with the sympathetics of the lumbar and the lower thoracic segments (in case the lower thoracic segments also supply the colon), whence they may be transferred upward in the cord until brought into reflex connection with the connector neurons (thoracic Vth to IXth) of the sympathetic system, which supply the stomach and pyloric sphincter. The course which such stimuli would follow may be understood from figs. 2 and 3. 

In this connection it is necessary to inject a few observations on the moot question of the sympathetic and vagus control of the stomach and pylorus. In order to understand the various activities of the stomach it must be understood that peristaltic effects and opening and closure of the pylorus may be carried on autonomously, independent of extrinsic nerves. How efficiently it could be carried on if the intrinsic nerves, as represented by the plexuses of Auerbach and Meissner were removed, is a question. At the same time we must recognize that smooth muscle, regardless of nervous effects, possesses the property of tonus and rhythmic action. 

The question of the control of the pylorus has not been definitely established by experiment. It seems certain from experiments from Carlson’s laboratory that both sympathetic and vagal stimulation are able to cause its closure. Nevertheless, reasoning from analogy, in case of other sphincters, the innervation of which is not disputed, we must ascribe to the sympathetic nerves the preponderance of activating control, and to the vagus an inhibiting action for both the sphincter and the antrum. 

It seems but natural that every organ whose exit is guarded by a sphincter should possess a nervous mechanism so arranged that a stimulus which closes the sphincter will at the same time relax the musculature of the body of the organ; and that a stimulus which relaxes the sphincter will at the same time increase the tension of the muscle of the body of the organ, so as to aid in its emptying, as is found in the urinary bladder. This reciprocal innervation, according to the idea of Meltzer, seems essential to physiologic efficiency of action. 

There is also considerable discussion as to the exact part played by the sympathetic nerves in the innervation of the fundus, cardiac sphincter and esophagus. It seems that the sympathetic nerves are represented by few fibers in these structures; in fact, some authors claim that the entire nerve control, both activating and inhibiting, depends upon the vagus; and that contraction and relaxation is due to stimulation of different fibers of the nerve. It is at least safe to say that a preponderance of vagus control is proved for the cardiac sphincter and esophagus, and that possibly the same is true for the fundus, although the sympathetic fibers that are present probably aid in producing inhibitory effects. 

During the acute phase of the diverticulitis, if the aforementioned innervation is correct, gastric and pyloric effects were noticed which may be explained as representing a preponderance of sympathetic stimulation while the effects in the cardiac sphincter and the structures on both sides of it represented vagal inhibition, probably largely due to the stimulation of vagal inhibitory fibers. Such were pylorospasm, relaxed cardia, cessation of peristalsis and secretion, dilatation of the fundus and esophagus, and the reversed peristalsis associated with vomiting. It is not entirely clear how these effects were produced. The stimuli may have arisen in either the diverticulum or stomach. If they were caused reflexly by the diverticulum, the stimulus must have been transferred to intrasegmental paths in the cord either through the afferent fibers of the sympathetic system or through the sacral nerves of the parasympathetic system. But no matter over which system the afferent impulses were transferred, on entering the cord the stimuli must have been carried upward to some central cerebral station from which they were distributed. It is assumed, however, that the parasympathetics usually carry the visceral afferent impulses which cause vomiting. 

It is further possible that some or even all of the impulses which caused the vomiting might have arisen in the stomach itself, for the pylorus was closed, the musculature of the antrum was probably contracted, the fundus, cardia, and the lower portion of the esophagus were relaxed, and the food was not digested; therefore, it was natural that the stomach should have attempted to empty itself. 

The act of vomiting is released from some common nerve station in the brain, probably in the medulla from which stimuli must be sent out to produce three distinct effects which are necessary to accomplish it as follows: (1) efferent impulses must be sent over the sympathetics to the pylorus and pyloric end of the stomach, contracting them; and opposing vagal action in all areas innervated by both systems resulting in inhibition of peristaltic action and gastric secretion; (2) over the inhibitory fibers of the vagus to the cardiac sphincter, the fundus of the stomach and the lower portion of the esophagus, supplementing the antagonistic action of the sympathetics and relaxing them; the total nerve effect being to check and reverse the peristaltic waves; and (3) over skeletal nerves to the diaphragm and the abdominal muscles, causing them to contract and expel the contents from the stomach. The mechanism of emptying would be the same whether the stimuli arose in the stomach itself or in the inflamed diverticulum, or in both the stomach and the diverticulum. 

The vomiting mechanism may be stimulated to activity by all kinds of sensory disturbances–sight, smell, sound, touch, intracranial pressure; or sensory impulses from various organs, such as the eye, heart, lungs, stomach itself, liver and gall-bladder, pancreas, or any other portion of the gastrointestinal canal, the kidney, bladder and the genital organs; or by psychical impulses, such as fear, disgust worry, pain and so forth. 

Response in other Parts of the Intestinal Tract. According to the law of the intestine, when a stimulus is applied to any portion of the gastrointestinal tract the motility of that portion of the gastrointestinal tract above the stimulus is slowed and that below is increased. True to this law hyperactivity beyond the point of inflammation was shown by the diarrhea. Inhibition of activity above the point of irritation was shown in the stomach as above mentioned, and we assume that the same inhibition was probably present in the small intestine. In the colon it was shown by a persistent tendency to constipation after the acute attacks were over, something that had never shown before. 

Reflexes in the Skeletal Structures. Several different reflexes were noted in the skeletal structures, most of which were of a sensory nature, if I may be permitted to speak of the referred pain, the hyperalgesia and other sensory phenomena as though they were reflexes. Motor and trophic phenomena were also present. 

The phenomena described above in connection with the stomach were only partly directly due to the diverticulitis. The stomach was so thoroughly thrown off its normal course of action, that we may assume that a local condition might well have been set up in it which was accompanied by symptoms which almost dominated the picture. 

The muscles on the left half of the abdomen, in the area marked by the hyperalgesia, fig. 1B, showed a motor reflex during the acuteness of the attack and at one time, as previously mentioned, there was a spasm of the muscles in the lower left quadrant which was so severe that I was obliged to stop my work for a few minutes. In this connection, it must be borne in mind that broad muscles contract reflexly in segments and not as a whole. In this they differ from the long muscles of the extremities. 

The persistence of the hyperalgesia was indicative of marked and probably permanent injury to the neurons, if we may judge from the fact that it still persists more than two and one half years after its beginning. Any stimulation continuing over such a period of time would be expected to cause permanent effects in the way of trophic reflexes. These are recognized as an atrophy of the skin, subcutaneous tissue and muscles in an area coextensive with the area of hyperalgesia, fig. 1B. The tissues here have lost their normal texture and give an impression of loss of elasticity and firmness, similar to the trophic reflexes which I have described in the dermal tissues which receive stimuli from the lung over a long period of time, as seen to best advantage in chronic pulmonary tuberculosis. 

Sensory Reflexes. The sensory impulses which were referred to different skin areas require special consideration. 

The thoracic localization of hyperalgesia in the IXth to XIIth thoracic segments is irregular for sigmoid involvement, if the sympathetic innervation is, as usually given, from the lumbar segments through the inferior mesenteric ganglion. Nevertheless, the most constant and most evident sensory phenomenon experienced by me from the time of the appearance of the first symptom of active disease until the present time has been the hyperalgesia in these sensory zones to the left of the umbilicus. 

In accounting for the localization of hyperalgesia, three possibilities must be considered. (1) Assuming that the entire colon receives its innervation through the inferior mesenteric ganglion from the lumbar segments alone, which is in accordance with the teachings of most physiologists, we must account for the hyperalgesia in the IXth to XIIth thoracic segments by the transference of the impulses from the sigmoid upward in the cord, through intrasegmental paths. (2) Assuming that the colon receives innervation through both the superior mesenteric ganglion from the lower thoracic segments, and the inferior mesenteric ganglion from the lumbar segments, which is in accordance with the teachings of some physiologists, and which is followed in the illustration (fig. 3) which shows the connecting neurons for the important viscera, then the area of hyperalgesia could be caused perfectly regularly by inflammation in the sigmoid, according to the usual law which governs segmental reflexes. (3) Assuming that the small intestine is innervated through the superior mesenteric ganglion from the lower thoracic segments only, and that the large intestine receives innervation through the inferior mesenteric ganglion from the lumbar segments only, then, if the area of hyperalgesia was produced regularly according to the law which governs segmental reflexes, it would be necessary for the lesion causing the hyperalgesia to be in the small intestine. There was no evidence of this found, however, on physical and x-ray examination. 

This is the only clinical observation connected with the case that offers particular difficulty in explanation on the basis of the sigmoid receiving its sympathetic innervation alone from the lumbar segments of the cord. 

The area of anesthesia in the upper inner aspects of the left thigh in front, in the areas supplied by the Ist, IId and IIId lumbar (fig. 1D) nerves, and the acute pains in the area supplied by the first lumbar nerve, together with the scrotal pain in the areas supplied by the IIId sacral nerve were perfectly regular in their localization if the sigmoid is innervated by the lumbar segments alone. These pains, strange to say, almost totally disappeared after the second acute attack of inflammation in June of 1928.

The area of hyperalgesia has been most interesting because of its localization, its varying quality, and its constancy. It always has been present when I have looked for it. It was not noticed previously to the acute attack of November 1927. It lessened for a time after the acute attack in June 1928, to return fully a little later. At times it was so pronounced that I would find myself lifting my clothes off it, for their pressure was sufficient to cause discomfort. 

Reflex from Stomach to Diverticulum. A very interesting phenomenon which appeared months after the acute onset was what might be called a reversed reflex from the stomach to the diverticulum. Just as I had a reflex stimulus from the inflamed area to the stomach and pylorus causing the pain of pylorospasm in the thoracic sensory zones Vth to IXth, so I noticed at certain periods that when food was taken into the stomach there was an increase in the sensation in the area of hyperalgesia. This symptom did not come on during the first year. It was possibly connected in some way with the chronic irritation of the neurons. The stimulus must have been conveyed downward in the cord from the gastric neurons to those connected with the sigmoid. It is probably the same type of abdominal distress as is so often complained of when patients who have had irritative lesions in the gastrointestinal tract take food into the stomach. 

 

The Cause of Recurrent Sensory Phenomena (Pain)

After my own experience I can well understand those complaints of recurrent pain or discomfort on the part of patients who have previously suffered from inflammation of some abdominal viscus, although no definite symptoms of active disease can be elicited at the time. I am sure if I had not been a student of visceral neurology that I would have urged and probably forced my surgeon to operate to relieve me, particularly because the discomfort always recurred in the same place–in the area of hyperalgesia. Then later, when it again manifested itself, following eating, this would have had a tendency to remove all doubt and make certain that there must be some serious trouble which probably called for operative procedure. 

As physicians, we do not sufficiently appreciate the fact that whenever a viscus has been chronically inflamed, recurrent sensory disturbances may appear in the areas on the surface of the body to which pain from that viscus is referred, without there being present any active inflammatory process at the time. These referred sensory disturbances on the surface of the body are usually accepted as meaning active disease of internal viscera when in reality they very often mean instead that the threshold of response on the part of the sensory neurons has been lowered somewhere in the pathway from the viscus to the area of expression on the surface of the body, or to the areas of consciousness in the cerebrum, rendering the transference of sensory phenomena abnormally easy. 

There is the same connection between afferent nerves and the sensory nerves on the surface of the body during conditions of visceral health that exists in conditions of visceral disease; but it is only in conditions of disease that sensation or pain is manifested, because under normal conditions the threshold of reaction in the sensory paths and the central inhibition by which normal stimuli are prevented from reaching consciousness and are held to their vegetative levels, are both normal; but when, through disease of some internal viscus, afferent impulses have been repeatedly carried centralward, over a long period of time, the sensory mechanism becomes hypersensitive so that impulses are transmitted more readily than under normal conditions; and the central inhibition is broken down so that the irritation which is responsible for the pain or discomfort registers in the brain, although it is a lesser stimulus than that which would be necessary to overcome the threshold of response and register in the brain if the sensory mechanism had not been previously injured. 

This situation is met frequently in our practice, but usually goes unrecognized. A patient who has had such diseases as tuberculosis pleurisy, inflammation of the gastrointestinal tract, inflammation of some pelvic viscus, arthritis or neuritis, suffers from recurrent pain under many conditions of stress, such as acute or chronic fatigue, worry, discontent, unhappiness, ill health, at the time of menstruation, and with changes in weather or seasons, which are in no way directly related to the diseased viscus. These, however, are all conditions which call for considerable physiologic adjustment, and the neurons injured by preceding disease fail to make the adjustment and so show pain or discomfort. 

Reflex in Heart. The bradycardia noted, unless due to chemical stimulation as mentioned above, was a reflex through the vagus, the impulse being transferred to it in the medulla by intersegmental nerves which picked up the stimuli in the lower segments of the cord and carried them upward from either the sacral or from the lower thoracic and upper lumbar sympathetic nerves. Reflex bradycardia is not infrequently found in tuberculosis, in gastric ulcer and in infections of the bowel, liver and gallbladder.

 

Summary 

1. An attempt is made to explain in terms of vegetative neurology the major symptoms personally experienced in recurrent attacks of diverticulitis. 
2. I have attempted to show by this analysis how the vegetative nervous system integrates and correlates action in different parts of the body, and how the normally submerged reflexes which are present but not in the field of consciousness in conditions of health may disturb function and produce symptoms when they are exaggerated by the inflammatory process of disease. 
3. The various reflexes and referred sensory changes which manifested themselves during the illness are described and as far as possible ascribed to the afferent and efferent neurons which were responsible for their production. 
4. The method by which a chronically inflamed viscus may produce recurrent pain when no active inflammation is present is discussed in connection with the subject of recurrent sensory phenomena. It is pointed out that whenever a viscus is chronically inflamed there is more or less permanent injury produced in the path of sensory expression leading from that viscus, as a result of which pain or other sensory phenomena are thereafter produced upon a minimum of irritation. Such sensations are apt to occur whenever an extra amount of strain is thrown on the patient’s physiologic adaptive mechanism. They come with tiring, worry, other illness, seasonal changes, changes in weather, and in women they are often associated with the menstrual period. 
5. The reflex in the hyperalgesic area noticed on taking of food explains the complaints of patients which are met so often when there is some inflammatory reaction in the intestinal tract, such as appendicitis, ulcer of stomach or intestine, and tuberculosis of the bowel. As soon as food enters the stomach pain is felt in the area in which it is referred from the inflamed organ.