Symptomatic abdominal epilepsy

SYMPTOMATIC

ABDOMINAL T.

MATTHEW Assistant

Professor

of NeuropathoIogy,

University

M.D.

of PennsyIvania

PHILADELPHIA,

I

MOORE,

EPILEPSY * Graduate

School of Medicine

PENNSYLVANIA

T is not a too infrequent experience for the surgeon or chnician to be confronted with a diagnostic dilemma and the decision whether to operate or not, when abdomina1 pain is the presenting symptom. In tht majority of cares the symptom of abdomina1 pain is surrounded by other signs and symptoms with a recognizabIe sequence of events and an overa11 pattern which permit of the anatomic, etioIogic and pathoIogic diagnosis. When these are partIy wanting special Iaboratory or diagnostic procedures may be utilized to definiteIy estabIish the presence of intraabdomina1 organic disease in its many forms. On the other hand many surgeons have feIt the warm ffush of embarrassment when faced with the reaIization of their diagnostic faIIibiIity or impotence in certain cases, after removing an innocuous appendix or retreating empty-handed after an expIoratory Iaparotomy. This situation usuaIIy arises in those cases in which abdomina1 pain has been a chronic symptom and which has eIuded correct diagnosis after empIoying the numerous generaIIy accepted diagnostic methods and which has not yieIded to varied attempts at treatment. In this percentiIe smaI1 group is numericaIIy Iarge which, however, enough to justify and indeed require careful anaIysis before resorting to surgery or other ineffectua1 measures, there is to be considered the disorder known as symptomatic abdomina1 epiIepsy. * The true cIinician wiI1 not make this diagnosis by excIusion but wiI1 require some criteria which are at Ieast suffIcientIy cIear to draw this condition into the paIe of a recognizabIe entity. However, thus far, the consideration of symptomatic abdomina1 epiIepsy, as a cause of abdomina1 pain has

been a Iast resort measure, the usua1 story being one of proIonged, assiduous, extensive, futiIe studies of the gastrointestina1 tract, other abdomins1 viscera, thoracic viscera, genitourinary tract, vertebrae, and spina cord and its roots, with the final chapter often ending with a fruitless abdomina1 exploration or the patient being stigmatized with the appeIIation of psychoneurotic. Definition. Symptomatic abdomina1 epiIepsy is a disorder characterized by bouts of paroxysma abdomina1 pain, the Iatter being due to hypermotiIity of the bowel, provoked by ahnorma discharges of certain neurones in the vicinity of biochemicaIIy or structuraIIy aItered cerebral tissue, presumabIy situated in the premotor, and postmotor cerebra1 cortex and/or the diencephaIon. The attack of abdomina1 pain at times may be single and proIonged onIy when the symptom occurs as the result of a vascuIar jctus, or a neopIasm invoIving the fronta and parieta1 Iobe and/or diencephaIon. Experimental and Clinical Data. The most definitive recent work reIating abnorma gastrointestina1 motiIity with cortica inffuence has been by FuIton and his co-workers,* SpiegeI, Weston and Oppenheimer,3 PenfieId and Gage,4 and PenfieId and Erickson.5 In a briIIiant series of anima1 experiments FuIton et a1. * demonstrated that stimuIation of area six (Brodmann) produced disturbances in gastrointestina1 motility; abIation of the fronta Iobes foIlowed by hypermotility of the stomach and pyIoric spasm enduring severa days; and acute intussusception with fata obstruction foIIowing biIatera1 abIation of the fronta Iobes or its parts. These investigators were of the opinion that areas three

* From the services of the Jewish and Doctors HospitaIs, Philadelphia, Pa. The histopathoIogic sections are from the John L. Eckel L.aboratory of Neuropathology and were used through the courtesy of Dr. N. W. Winkeiman.

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EpiIepsy

DECEMBER,1946

understood. However, Watts and FuIto+ have produced experimenta diencephaIic Iesions resuIting in disturbed gastrointestina1 activity. Gushing’ caIIed attention to the probabIe r&e pIayed by the diencephaon in disturbances of gastrointestina1 motiIity and the production of peptic uIcer foIlowing brain trauma when there was invoIvement of the diencephalon. CIinicaIIy, it has been known for some time that abdomina1 distress or even pain may constitute part of the preconvuIsive aura of epiIepsy and FuItor? has stated that this pain usuaIIy coincides with vigorous abnorma1 gastrointestina1 movements. AbdominaI pain Iikewise has been reported as a symptom of gross cerebra1 disease. WechsIer9 has seen patients who were treated for some time and even operated upon for abdomina1 syndromes in whom abdominal pain was the symptom of a cerebra1 Iesion. This pain can cIoseIy reFIG. I. Location of foci from which the gastrosembIe the pain of gaIIbIadder disease, intestinal system couId be influenced. The foci gastric or duodena1 uIcer, appendicitis or are indicated by the cruciate suIcus by (cortica1 areas in the dog according to KeImpin) renaI coIic. WinkeImanlO cited the case of (SPIEGEL, E. A., WESTON, K. and OPPENa forty-five year oId man who experienced HEIMER, M. J. Courtesy of authors and J. intense abdominal pain as the initia1 sympNeuropath. CYExper. Neurol.) tom of a cerebra1 hemorrhage invoIving the frontoparieta1 areas. AbdominaI pain in and five of Brodmann were aIso concerned chiIdren frequentIy is an extremeIy diffIcuIt with gastrointestina1 activity. PenfieId and Gage4 stimuIated eIectricaIIy area five-a of symptom to evaIuate and recent studies by KIingman, Langford, GreeIey and Hoefer,l’ the exposed brain of a patient, resuIting and aIso by Lambert12 have shown that in pain in the Iower right quadrant of the abdomen which then was foIIowed by a formerIy unexpIained attacks of paroxysma abdomina1 pain were a manifestation of the convuIsive seizure. It was shown quite convuIsive state. These workers were abIe cIearIy in experiments on dogs by SpiegeI, to observe cerebra1 dysrhythmias in the Weston and Oppenheimer” that the whoIe eIectroencephaIographic studies of their gastrointestina1 tract couId be inff uenced patients of the petit-ma1 and psychomotor by stimuIation of areas six, five and three. equivaIent varieties. Some of the chiIdren (Fig. I.) They observed that stimuIation of these areas may produce effects in a11 had associated symptoms of the convuIsive state accompanying the paroxysma abparts of the gastrointestina1 tract synergicdomina1 pain. aIIy, increase of activity in one part may In his very succinct and inclusive way, be associated with inhibition in other parts HughJings Jackson said, “ EpiIepsy is the of the gastrointestina1 system, or occasionname for occasiona1, sudden, excessive, aIIy onIy a Iimited part of the bowe1 may rapid and IocaI discharge of gray matter.“lY be inff uenced. The expression of subjective or objective The exact manner in which the manifestations in the patient depends upon diencephaIon exerts its influence upon the locus of discharge. The commonIy seen gastrointestina1 motiIity is not entireIy

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motor Jacksonian convuIsive seizure is often the symptomatic expression of a foca1 discharge in the motor area resuIting from a discrete Iesion, be it tumor, traumatic scar or other morphoIogic structura1 change. ShouId the Iesion which initiates paroxysma1 cerebra1 dysrhythmias be situated eIsewhere in the brain, the symptoms wouId reflect the function of that part. It is, therefore, not an exercise of the imagination to conceive of foca1 Iesions invoIving any one or a11 of areas six, five and three of the cerebra1 cortex or of the diencephaIon which couId produce, under appropriate abnorma1 discharges which conditions, wouId Iead to disturbed gast.rointestinaI activity and consequent abdomina1 pain. These Iesions couId very we11 be of varying magnitude in size and of different histopathoIogic appearance. In order to demonstrate the reIationship existing between abdomina1 pain as a symptomatic expression of cerebral disease, the representative cases cited here wiI1 take into account those Iesions which are gross and demonstrabIe, those in which a history of pre-existing disease or trauma wouId conceivabIy Iead to a cortica1 Iesion, and finaIIy those in which there may be some question as to a specific causa1 factor producing a foca1 Iesion with subsequent abnorma cortica1 discharges. CASE I. (Brain tumor-singIe focal Iesion). H. P., was a sixty-three year oId maIe whose chief compIaints consisted of periodic attacks of severe epigastric pain and headache. He w&s first seen by me on ApriI 21, 1946. For six to eight weeks prior to this he had complained of recurrent attacks of intense abdomina1 pain which led to complete x-ray study of the gastrointestinal tract by his attending physician. These proved negative. Loss of weight directed attention to possible malignancy, but none couId be unearthed. About five weeks prior to examination he developed headaches situated over the frontal and suboccipita1 regions. ShortIy thereafter a pronounced menta1 change occurred which was interpreted as a depression and the diagnosis of invoIutiona1 depression was made by several physicians. He was to he transferred to a mental institution

Epilepsy

American

Journal

of Surgery

8%

to receive eIectroshock

treatment when I was requested to see him. On the day of examination he showed the foIlowing; menta1 hebetude, spontaneous, brief outbursts of unprovoked crying, miId Ieft hemiparesis, suggestive hesitancy of the Ieft leg in waIking, wavering of the outstretched Ieft hand, increase of the deep tendon reflexes of the Ieft arm and Ieg as compared with the right side, characteristic grasp reflex in the Ieft hand, suggestive Babinski phenomenon on the Ieft, mild weakness of the Ieft corner of the mouth and biIatera1 choked discs. When questioned as to the most distressing symptom he pointed to the “pit of his stomach.” Spinal puncture revealed a pressure of 320 mm. C.S.F. X-ray examination of the skuI1 was negative. A diagnosis of tumor of the right fronta lobe Iying rostra1 to the motor gyrus impinging on area six was made. In view of the rapid progress of symptoms it was believed that the Iesion probabIy was a glioma. On ApriI 30, 1946, a craniotomy was performed by Dr. Robert A. Groff at the Graduate Hospital of the University of Pennsylvania. DirectIy beneath area six at a depth of about 2 to 255 cm. beIow the pia surface a discrete spherical tumor mass was encountered and removed. (Fig. 2.) The overlying and surrounding brain tissue was soft and appeared swolIen. The tumor mass was firm, showed a smooth pseudocapsuIe and measured 2.1 cm. in diameter. HistoIogic study reveaIed the cytoIogic appearance of a metastatic maIignant growth with some characteristics resembIing spongiobIastoma muItiforme. The surrounding white matter and overIying cortex showed a pronounced glia1 proIiferation. Postoperatively the symptoms of headache and abdomina1 pain disappeared. The pronounced forced grasping quickly diminished within three days after operation. This case paroxysma

illustrates abdomina1

the occurrence pain which

of

had been interpreted as a form of intrinsic disease of the gastrointestina1 tract. The early phase of this patient’s SymptomatoIogy was excIusiveIy gastrointestina1. The subsequent headache apparentIy had been dismissed in its significance and Iater even the gastrointestina1 symptoms, after the x-ray findings had been negative, were likewise dismissed as a somatic complaint

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FIG. 2. Sketch of right side of brain indicating the position of the tumor found in Case I, soIid circIes motor area 4; open circIes pre-motor area 6.

part of the picture of an invoIutiona1 depression. The menta1 status of the patient shouId have been considered, as it was Iater, as a symptom of organic brain invoIvement. Had this been done and the headache properIy evaIuated, the symptom of abdomina1 pain wouId have compieted the pattern estabIishing the diagnosis of a brain tumor invoIving the right fronta Iobe. The abdomina1 pain, therefore, was the symptomatic expression of a bnorma1 discharges arising in the premotor area secondary to the “irritation” or stimuIation by a IocaIized space-taking Iesion subjacent to area six. CASE 11.l~ (Tuberous scIerosis--disseminated Iesions in the brain.) A. D., femaIe, aged three years, was admitted to the Jewish Hospital with a diagnosis of rickets. At the age of five months she had recurrent attacks of abdomina1 pain which caused her to “double-up” and cry out. These seizures were of reIativeIy short duration and occurred both during the day and at night. The attacks: of abdomina1 pain were folIowed by excessive urination and sIeep. Studies of the gastrointestinal tract reveaIed nothing abnormal. The attacks of abdomina1 pain endured unti1 the patient was eleven months of age. A tentative diagnosis of intestinal tetany was made and the patient treated on this basis. SubsequentIy the child faiIed to deveIop in a normaI manner and was unabIe to taIk, had no control of bowel or bIadder function and showed abnorma1 behavior with periodic, abrupt attacks of crying, screaming and thrashing about. These attacks

EpiIepsy

DECEMBER,1946

FIG. 3. Section of brain showing disseminated Iesions of tuberous scIerosis. (Weil stain X

2.)

were unpredictabIe and occurred at irreguIar intervaIs during the day. When examined nemologically the positive lindings were pronounced menta1 deficiency, partia1 atrophy of both optic discs, defective hearing, nevus muItipIex of BourneviIIe (sebaceum adenoma of Pringle) over the nose and maxillary region. CompIete Iaboratory studies consisting of x-ray examinations and chemica1 studies of the bIood and spinal fluid proved negative. The paroxysmal nature of the abdomina1 pain from the age of five months to seventeen months was interpreted as an epileptoid manifestation since these were repIaced by recurrent bouts of behavior disorder having the pattern of the convuIsive state.15 The triad of menta1 deficiency, nevus muItipIex of Bourneville and epiIeptic phenomena aIIowed the diagnosis of tuberous scIerosis. The noduIes of tuberous scIerosis are irreguIarIy scattered throughout the brain and not onIy can they invoIve the motor area producing the usua1 epiIeptic motor seizures observed in tuberous scIerosis but they undoubtedIy aIso invoIve premotor area six and the postcentra1 areas five and three. In the case cited here the Iesions provoked abdomina1 pain as part of the total picture of an epileptic dispIay. Figure 3 shows the irreguIar distribution of the Iesions of tuberous scIerosis and how they impIicate the cerebra1 cortex producing abnormal discharges from “ irritated ” cortica1 gangIion ceIIs. (Cerebral trauma.) N. T., maIe, CASE III.~~ age eIeven years, gave the history of having had three attacks of unconsciousness during the four years prior to examination on December

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FIG. 4. (Case III). Electroencephalographic

American Journal of Surgery

EpiIepsy

tracing prior to treatment.

(Courtesy

887

J. A. M. A.1

RikhtFrontalto Right

ear

-----------~--_--_---._______--~

__----------_~

-------_____

1944. There were numerous interva1 II, seizures of abdomina1 pain, nausea, occasional vomiting and diarrhea. The abdomina1 pain came on intermittentIy and consisted of “waves” of abdomina1 pain occurring about twice weekly. The individua1 attacks of abdomina1 pain would Iast from two to three minutes and appeared at intervaIs of from two to ten minutes, the entire “wave” Iasting approximateIy one hour. These “waves” of pain appeared either in the early morning or at

--------mm-_____

--------_

night and were not associated with unconsciousness or diarrhea. He had one severe attack of abdomina1 pain in JuIy, 1944, which endured ten minutes and which was foIIowed by vomiting and diarrhea. During the year preceding examination he had frequent nightmares and taIked in his sIeep. This patient had sustained a severe head injury five vears before. WhiIe sledding down ai incline he struck his head and was unconscious for twenty-four hours. The outstanding symptoms which for-

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of Surgery

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Epilepsy

FIG. 6. CorticaI damage due to craniocerebra1 x

Iowed the head injury were recurrent episodes of abdominal pain interspersed with occasiona convuIsive seizures and unconsciousness. It was believed that the entire constellation was a form of epiIepsy resuIting from injury to the cerebra1 cortex. EIectroencephaIographic studies as shown in the iIIustration (Fig. 4) reveaIed SIOW waves which couId be seen in a11 leads. These slow waves seemed to predominate and were more persistent in the frontal areas. It was concIuded by Dr. DonaId Scott, the encephaIographist, that “the record most cIoseIy approximated the pattern seen in idiopathic epiIepsy.” This patient was subsequentIy pIaced on an anti-convuIsant therapeutic regimen consisting of dietary contro1, supervision of activities, and medication in the form of diphenylhydantoin sodium (dilantin sodium) gr. I $4 twice daiIy and caIcium-bromido-gaIactogIuconate (Calci2 Gm. dissoIved in water bronat-Sandoz) three times daiIy. ImmediateIy after being pIaced on this form of therapy the attacks of abdominal pain ceased and to the present writing, one year and five months after treatment was started, this patient has had no abdominal pain and no grand ma1 seizures. Subsequent eIectroencephaIographic tests (Fig. 5) with the patient on medication showed the usua1 IeveI of normal activity with groups of sIow waves both with and without spikes. The Iatter occurred most prominentIy in the fronta and occipita1 regions. This record showed 30 per cent Iess abnorma1 activity than the previous study.

trauma.

DECEMBER.

(ToIuidin

1946

blue stain

100.)

This patient had had three attacks of incompIete convuIsive seizures during a five-year period foIIowing severe head injury. The predominant feature during that interval had been recurrent attacks of abdomina1 pain coming on at frequent intervaIs. These had been mis-

interpreted compIeteIy and eIuded treatment unti1 anti-convuIsant therapy was instituted, since which time there has been a complete cessation of symptoms. This case iIIustrates the reIationship between cerebra1 injury producing cortica1 damage and the resuItant abnorma1 discharges from the adjacent cortica1 neurones, as graphicaIIy demonstrated by the eIectroencephaIographic studies, resuIting in paroxysma abdomina1 pain (due to invoIvement of the fronta and/or parieta1 Iobes) or convuIsive seizures (due to impIication of the motor cortex). The photomicrograph (Fig. 6) shows the degree of cortica1 damage which may resuIt from cerebra1 trauma, and the gangIion ceIIs in the immediate periphery of such Iesions may be the origin of abnorma1 discharges capabIe of being picked up by the eIectroencephaIograph. CASE 1v.l’ (Angioneurotic edema of the brain with foca1 cortica1 damage.) P. P., maIe, aged thirty-seven, was first seen by me in June, 1941. The chief compIaint was the singIe

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symptom of periodic attacks of severe cramplike pain invoIving the entire abdomen. The pain often started in the lower right quadrant and then invoIved the whole abdomen. Individua1 attacks of pain endured up to two hours or more and were intense and unremitting. During the attack there was a “rumbling” sensation in the abdomen. When the attack of pain subsided, he was exhausted and feIt “achey all over.” The bouts of pain began at the age of nine months and occurred at irreguIar intervals, appearing every seven or eight days for months preceding my origina examination, and during the week preceding the examination four seizures had occurred. The first attack came on shortly after the patient had received diphtheria antitoxin, which had made him quite III. When eight years of age an appendectomy was performed during one of the seizures and a norma appendix was removed. At the age of sixteen he injured himself and anti-tetanus serum was given. He became extremeIy iI and experienced one of his usua1 attacks of intense abdomina1 pain. He aIso had urticaria and a high degree of fever for two days thereafter. There was a history of deveIopment of hives after eating certain foods. This patient had been studied thoroughIy in many institutions over a period of practicaIIy the entire range of his illness. The types of treatment were many, but at no time did he obtain Iasting reIief. The longest attack free interva1 was fourteen months. An objective neuroIogica1 examination faiied to revea1 any evidence of overt disturbance of the nervous system. Complete studies with respect to cytoIogy, bIood and spinal fluid chemistry, x-ray studies of the gastrointestinal tract, gaIIbIadder and urinary tract, a11 proved negative. The bIood pressure was 102 systolic, 68 diastolic, pulse rate 76, weight 13935 pounds. During the study of this patient it occurred to the examiner that the symptom of abdomina1 pain, in view of its irreguIar occurrence, paroxysma nature, duration of the seizure, and the post-seizure statement by the patient that he was “exhausted and felt achey a11 over,” a frequentIy observed phenomenon in the postconvuIsive phase of epilepsy, represented a form of epileptic disturbance. In order to ascertain the correctness of this point of view, two steps were pursued; the first consisted of having eIectro-encephalographic studies performed, and the other to place the

Epilepsy

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patient upon an anti-convuIsant regimen. These studies reveaIed the presence of abnorma Iow voItage waves seen mainIy in the right and Ieft fronta regions. They were aIso present in the parieta1 and occipita1 lobes. HyperventiIation increased this abnorma1 activity. (Fig. 7.) AnticonvuIsant medication was begun during the middle of June, 1941. This consisted of phenytoin sodium (dilantin sodium) I $5 gr. (0.1 Gm.) twice daiIy and a bromide mixture, I fIuid dr. (4 cc.) four times daily. For a period of over seven and one-haIf months he remained attack free, foIIowing which he was requested to stop medication in order to determine whether the seizures would return. Within a period of Iess than a month, he developed a severe attack. Medication was resumed and he remained attack-free for seven and one-haIf months, at which time the diIantin sodium was repIaced by Iactose in the white and red ringed capsule and the bromides repIaced by sodium chIoride. This was done without the patient’s knowIedge in order to eliminate the eIement of suggestion. Fifteen days Iater he deveIoped the characteristic seizure. He was informed about the experiment after his extreme aIarm at the reappearance of the attack. This patient has remained attack free from July, 1942, to the present writing, ApriI, 1946, with onIy two exceptions which occurred during the Iatter part of 1945 when the patient had grippe and stopped taking the anti-convulsant medication, and during the early part of 1946 when he had again lapsed in the use of dilantin sodium and the bromide mixture. During the period of three and onehaIf years between JuIy, 1942, and December, 1945, he was entirely free of seizures and took the diIantin sodium faithfuIIy and the bromide mixture somewhat irreguIarIy. Electro-encephaIographic studies performed during the time he was on active treatment (Fig. 8) showed that the cerebra1 potentiaIs in both hemispheres were within normal limits. There was an occasional abnormal sharp wave. Large, slow, abnorma1 waves couId be brought out in both fronta lobes after hyperventilation. This patient had an exquisitely defined symptom of abdominal pain without any preceding phenomena and foIIowing an attack onIy the experience of exhaustion and achiness. The question as to whether this might be abdomina1 migraine had been eliminated diagnosticaIIy, first because this diagnosis had been made rn

FIG. 7. r&se IV). EIectroenceohaIographic. tracing ‘prior to treaiment, showing Iow vokage three per second abnormal waves in the right and left fronta cortex. They are present to a Iesser extent in the parieta1 and occipita1 areas. (Courtesy J. A. M. A.)

FIG. 8. (Case IV). EIectroenceohaIoeraDhic tracing during treatment with akiconvulsants. The cerebra1 potentiaIs throughout both hemispheres are within norma Iimits as to ampIitude and rhythm. After hyperventiIation, denoted by arrow, Iarge sIow abnorma1 waves are detected in both frontal Iobes. (Courtesy J. A. M. A.)

one of the hospitaIs where he had been examined and the use of ergotamine tartrate faiIed to prevent attacks or abort one in progress. Furthermore, the usua1 history of abdominal migraine was absent. That is, other migranious phenomena failed to appear such as hemicrania preceding or fohowing the attack of abdomina1 pain, visua1 disturbance, nausea, vomiting or diarrhea. The pattern of the occurrence of abdomina1 pain coming on suddenly, at irregular intervaIs, and presenting a stereotyped form, suggested the epiIeptic nature of the disorder. It was believed that the disturbance probabIy arose in those cortica1 areas of the brain subserving gastrointestina1 function and that the origina use of serum, when the patient was nine months of age, probabIy had produced angioneurotic edema of the brain with some aIteration of structure in the areas stated. That such a point of vie* is justifiable is based upon the experimental and clinical observations of Dechaume and Croizat18 and Bassoe,lg and the objective eIectroencephaIographic findings of abnorma1 activity in the fronta and parieta1 lobes. Dechaume and Croizat18 experimentaIIy produced congestive, hemorrhagic and degenerative changes in the brain following serum shock in animaIs. The case reported by Bassoelg of a woman who deveIoped aphasia, hemiplegia, hemianopsia and convulsive seizures following the injection of serum, showed upon expIoratory craniotomy an area of dark, hyperemic softened brain tissue, which was regarded as the effect of a foca1 angioneurotic edema of the brain. This

case

iIIustrates

the

deveIopment

of

the symptom of paloxysma1 abdomina1 pain in an individua1 in whose brain changes had occurred foIIowing the use of an antiserum. SpecificaIIy, angioneurotic edema is postuIated to have occurred with subsequent damage to the cortica1 neurones of the cerebra1 cortex, mainIy in the frontal Iobes and to a Iesser degree in the parietal Iobe. These areas of aItered tissue have provoked a cerebra1 dysrhythmia as seen in the eIectro-encephaIographic studies, and when the appropriate factor or factors were present, such as the reaction set up by certain foods to which he had been shown to be aIIergic, the process of cummation in the irritated gangIion ceIIs was invoked eventuating in the expIosive discharge producing hypermotiIity of the bowe1 and abdomina1 pain. CASE v.~O (Isolated symptom of paroxysmal abdominal pain without demonstrabIe etioIogy.) P. P., a married female, aged fortyfour, complained of bouts of abdomina1 pain, beginning twelve years prior to the date of examination on May 4, 1944. Two years after the onset of her repeated abdomina1 pain, she had her appendix removed. The Iatter showed no morbid process. The attacks began with a pecuIiar sensation of “gnawing in the abdomen” which was then followed by generalized pain. The latter was accompanied by a “rumbling noise in the intestine.” The abdomina1 pain at times was associated with a “funny, dazed feeIing” and at such times she

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feared that she was going to “pass out.” The attacks of abdomina1 pain appeared for the most part at night. She aIways maintained consciousness throughout these seizures. During the tweIve-year span there were three occasions, al1 of which occurred while in bed, in which the abdomina1 pain was associated with a “shaking” of her limbs and jaw, which she was unabIe to contro1 voluntarily. The latter episodes Iasted from ten to fifteen minutes and wouId awaken her from sleep. There were no premonitory symptoms other than the “gnawing” sensation cited above. The seizures occurred about twice weekly for the fourmonth period preceding examination. Her attack free intervaIs usualIy Iasted no longer than one week. She had been married nineteen years and the past medical history revealed no data which would throw any light on the possible etioIogic cause. From the time of her appendectomy, she had consuIted numerous physicians and was uItimateIy labelled a A review of her personaIity psychoneurotic. deveIopment and the psychiatric examination showed no disturbance in her emotional or menta1 spheres. There was no evidence of organic disturbance of the nervous system foIIowing a detaiIed neuroIogica1 examination. X-ray studies of the gastrointestina1 tract and laboratory studies showed norma findings during the attack free intervals. PhysicaI examination of the chest and abdomen Iikewise was negative. EIectroencephaIographic studies reveaIed no abnormal cerebral discharges. Despite the fact that this patient presented no previous history of cerebra1 in jury or disease predisposing to changes in the brain or meninges, it was beIieved, because of the several facts, such as the periodicity of the attacks, their sudden explosive onset, the occasional aura-Iike introduction by a “gnawing” sensation in the abdomen, the “funny, dazed feeIing” and the pseudoconvuIsive movements which had occurred in a few of the seizures, that when pieced together, these fitted into the pattern of an epileptic dispIay. This patient was put on an anti-convuIsant regimen, the medication consisting of hydantoin sodium I 44 gr. (0.1 Cm.) twice daily and phenobarbita1 gr. s/4 (16 mg.) three times daily. Within one week after the institution of treatment on ApriI 24, 1944, the attacks of abdomina1 pain disappeared and she has remained attack free since that time.

EpiIepsy

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891

The onIy eIements in this case which appear to warrant and justify the diagnosis of abdomina1 epiIepsy are (I ) the epiIeptic pattern of the aura-Iike manifestations, the manner of occurrence of the abdomina1 pain and the accompanying epiIeptoid symptoms; (2) the immediate and continued response to anti-convuIsants. COMMENTS

The five cases which have been summarized in brief fashion represent a variety of causes which may produce the symptom of abdomina1 pain as an expression of aItered changes of gastrointestina1 motiIity effected by the remote disturbances occurring in the cerebra1 cortex, mainIy in areas six, five and three. They aIso represent the iIIustrative cases of a Iarger series in which the most frequent cause appears to be craniocerebra1 injury.21 Case I demonstrates perhaps most cIearIy a specific IocaIe as to the origin of abnorma1 discharges provoking the symptom of abdomina1 pain. In this case the abdominal pain was first thought to be of intrinsic gastrointestinal origin. The surrounding historica data, such as headache, menta1 change, and the neuroIogica1 findings of increased intracranial pressure, hemiparesis, grasp reflex, aItered tendon reflex activity, etc., Ied to the consideration of a cerebra1 neopIasm. The operative finding of a discrete tumor Iying directIy beneath area six in the cortex, wouId seem to be ampIe indication of a causa1 reIationship between “ irritation ” of the neurones in this area and the symptom of abdomina1 pain. The expIanation for the other fronta lobe signs and symptoms, such as miId motor weakness, grasp reflex, occasiona hebetude and tendon refJex phenomena, may be based on the gIia1 reaction and sweIIing of the tissue surrounding the discrete tumor mass. The topographica situation of the tumor in this case cIinicaIIy bears out the experimenta findings of FuIton and his co-worker? and of SpiegeI et a1.3 UnfortunateIv, time and Jack of faciIities did not permjt of electro-encephaIographic studies

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being performed in this case. Had they been done, however, it is not at a11 unIikeIy that foca1 abnorma1 discharges wouId have been picked up at the periphery of the Iesion in area six.22 It is onIy a step, therefore, beyond this to interpret positive, abnorma eIectroencephaIographic findings from the fronta Iobes and/or the parieta1 area in cases in which abdomina1 epiIepsy exists as evidence of an intrinsic disorder of,. or morphoIogicalIy aItered, cerebral cortex in areas six, five, or three. The sIterations of structure in these regions may be due to one of numerous conditions, most of which have aIready been we11 outIined by Cobb.23 For purposes of i!Iustrating the mode of study in this type of disorder I shaI1 cite mereIy a few conditions which may be predisposing factors in the syndrome of abdomina1 epiIepsy. The existence of a gross Iesion such as tumor, abscess, intracerebra1 hemorrhage, thrombosis of a cerebra1 vesse1, are both cIinicaIIy and pathoIogicaIIy demonstrabIe as invoIving either the fronta or parieta1 Iobes. When the symptom of abdomina1 pain occurs under such circumstances, it can be attributed to stimuIation of cortica1 areas six, five or three. At times the abdomina1 pain is the direct resuIt of massive stimuIation of the neurones in these areas a.s in an ictus due to hemorrhage or thrombosis. However, in brain tumor, as in the case reported here and in cases in which the pain was paroxysma1, there must, therefore, be an expIanation other than continuous “irritation” which provokes the “seizures of pain,” just as there must be some expIanation for the periodic fits in the cIassica1 form of grandma1 epiIepsy. An effort at expIanation of this wiI1 be offered Iater. Brain tumor is a notabIe cause of epiIeptic fits as has been shown by an extensive Iiterature on the subject.24 The cases of crania-cerebra1 injury previousfy reported by me’ in which the symptom of paroxysmaJ abdomina1 pain was an outstanding feature, I beIieve to be a demonstration of cortica1 scars occurring in areas six, five, or three. The

EpiIepsy

DECEMBER. 1946

iIIustration of the cerebra1 cortex (Fig. 6) of an individua1 who sustained a craniocerebra1 injury, shows the damage to the functioning cortex and the definite morphoIogic changes which occur. The functioning neurones at the periphery or in the vicinity of such a Iesion may and do give off abnorma1 discharges, which under appropriate conditions may be of such magnitude as to constitute an adequate stimuIus to an effector structure. The scars consequent to brain injury can be seen directly at operative expIoration.5 They aIso frequentIy can be demonstrated by eIectroencephaIographic studies after a definite history of brain injury is in evidence. It is we11 estabIished both cIinicaIIy and neurohistopathoIogicaJIy that infections of the brain and the meninges, especiaIIy the Iatter, mzy produce fixed tissue changes which may uItimateIy manifest themseIves in disturbed function of the affected brain in the form of convulsive seizures. Here then, is another cause which, if the Iesion or Iesions occur in areas six, five or three, may produce the symptom of abdomina1 pain either singIy if the Iesion is exquisiteIy pIaced, or in association with other manifestations of the epiIeptic state. Disseminated Iesions of the brain offer by mathematica1 chance a greater Iikelihood of one or more of the lesions being pIaced in areas six, five or three, producing the symptom of abdominal pain. Case II iIIustrates this. Other conditions such as muItipIe scIerosis in which the brain has become invoIved, SchiIder’s disease, toxopIasmosis, muItipIe cerebra1 arterioscIerotic scars and the Iike, may aIso invoIve areas six, five or three, producing the symptom of abdomina1 pain, usuaIIy in conjunction with other symptoms reflecting the function of the invoIved brain. Figure 9 illustrates the nature and extent of a cortical arterioscIerotic scar which conceivably couId be a singIe scar involving one of the cortica1 areas under discussion. Under such circumstances a patient could have the isoIated symptom of paroxysma abdomina1 pain, and cIinicaIIy one can imagine the

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many conditions which probably wouId be considered first in the way of intrinsic abdominal disease before reIating the symptom of abdomina1 pain to a possibIe cerebra1 cause. Other conditions provocative of structura1 cerebra1 change may be toxins of various types. SpecificaIIy metaIIic poisonings, the main offender being lead, may produce changes either of a minimal degree or more extensive disseminated changes in the brain. The form of Iead encephaIopathy encountered in infancy or chiIdhood producing miId symptoms, may ensue in recovery, because of the reIativeIy minimal damage to the brain. Figure IO shows an area of the cerebral cortex of a case of Iead encephaIopathy in which there is a smaI1 foca1 aIteration with destruction of neurones, and changes in the gangIion ceIIs in the immediate vicinity of the focal devastation. It wiI1 be seen that the endotheIia1 nucIei of the capiIIaries are swoIIen and where they oppose each other cause a sIowing up or stoppage of blood ffow with resuItant dropping out of ceIIs, and ischemic ceil changes of other neurones in the area suppIied by the vesseIs.2” It is from such Iesions which may or may not uItimateIy cause electroencephaIographic abnormaIities and which may not be surmised unIess an extremeIy carefu1 history is obtained, that the symptom of abdomina1 pain may occur either singIy or in association with other IarvaI or aberrant dispIays of epiII5 This together with other noxious ePsY* agents, such as the cerebra1 reactions to sera, vaccines, high fever and the secondary encephaIopathies incident to measIes, scarlet fever and other infections26 constitute a group of causes which may occur at any time after the birth of the individuai, and which if the Iesion or Iesions be situated as already mentioned, the symptom of abdomina1 pain can and does occur. Intrauterine existence does not protect the fetus from contracting some type of cerebra1 affection which may uItimateIy produce a form of epiIeptic disorder. It has been shown that the cerebra1 Iesions of toxopIasmosis begin in utero27 and cIinicaIIy

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FIG. 9. ArterioscIerotic scar producing “puckering” of the cerebra1 cortex. (Klarfeld stain x 65.)

this condition is characterized, among other things, by convuIsive seizures. ShouId Iesions in this condition affect onIy cortical areas six, five and three, one can see the causa1 reIationship with abdomina1 pain. Other conditions of ante-nata originzx are Iikewise known to resuIt in epiIeptic seizures. A Iess easiIy demonstrable, but equaIIy important consideration of what may be a factor in unexpIained paroxysma abdomina1 pain occurring both in chiIdren and in adoIescents may be the minima1 neurohistoIogica1 changes which are produced in the brain of the fetus secondary to febriIe or toxic conditions occurring in the mother during the period of gestation. Figure I I shows a foca1 area, one of many, which occurs in the brain of an individua1 suffering from toxemia of pregnancy. There are changes in the smaI1 vesseIs, particuIarIy the capiIIaries, in which there is endotheIia1 thickening, resuIting in foca1 areas of ceIIuIar devastation and severe ceII disease. Other areas may show ischemic ceI1

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EpiIepsy

DECEMBER, 1946

IO.

FIG..II.

FIG. IO. Lead encephalopathy, showing focal cortica1 area of ceIIuIar devastation, intima1 changes in the capiIIaries and ceI1 disease of the adjacent ganglion ceIIs. (Toluidine bIue stain X 210.) FIG. I I. Toxemia of pregnancy, showing foca1 cortical damage, with an aceIIuIar area, capiIIary proliferation and gIiosis. (Toluidine bIue stain x

210.)

disease secondary to the disturbance of circuIation in the smaI1 vesseIs. The biochemical disturbances which constitute the condition known as toxemia of pregnancy are operative not onIy on the cerebra1 tissues of the mother, but certainIy must affect the more vuInerabIe brain of the fetus aIso. In those individuaIs in whom toxemia of pregnancy subsides under proper treatment and where the deIivered infant survives, it is not taxing creduIity to visuaIize at Ieast a few such areas, as

shown in the iIIustration, in the brain of the surviving offspring. Again, braving the criticism of repetition, a Iesion of this sort in areas six, five or three presumabIy couId eventuate in disturbance of gastrointestina1 motiIity, giving the cIinica1 picture of abdomina1 epiIepsy, or perhaps in other forms of gastrointestina1 syndromes, which to the present have escaped acceptable expIanation. Further study aIong the Iines of eIectroencephaIographic findings in various gastrointestina1

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disorders, characterized by changes in motility, may yield fruitful information with respect to cerebral disorders. This tenuous hypothesis may be borne out somewhat by the case previously reported by me,’ in which the forty-three year old patient, over a period of many years, had had abdominal symptoms consisting of paroxysmal abdominal pain, “rumbling” of the bowel and diarrhea. These gastrointestinal manifestations were at times associated with vasomotor phenomena and occasional unconsciousness and muscular twitchings. He had been considered at various times as having enterocolitis, duodenitis, spastic colon and the like. Treatment with an anti-convulsant regimen provided relief for the first time since the age of twelve when the attacks were initiated. MECHANISM

OF

ABDOMINAL

EPILEPSY

The various factors concerned in the initiation and discharge of an adequate stimulus from cerebral neurones to effector structures resulting in paroxysmal abdominal pain are in no way different from those operative in the generally accepted forms of symptomatic epilepsy. A discussion of the literature and theoretical aspects of the mechanism of the epileptic discharge would lead too far afield and hnally would reveal only the open question as to the ultimate nature of the “trigger” factor or factors. Electroencephalographic abnormalities as a graphic reflection of underlying cortical disturbances have been reported in conditions too numerous to mention here and range from the gross space-taking Iesion to the finer lesions of microscopic size.2g In an electroencephalographic study of four cases of encephalitis and meningoencephalitis, Ross30 showed non-specific electroencephalographic abnormalities in the acute phase of the disease. He also indicated that the abnormal discharges may persist and be the harbinger of epilepsy.

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ln 1924, Harri$l reported live cases of spontaneous hypoglycemia wherein the symptoms of excessive hunger, weakness, nervousness and anxiety were predominant, and in several patients abdominal distress was an added outstanding feature. Bulatao and Carlson, in experimentally insulin-induced hypoglycemia in man and animals, observed an increase in gastric tone and in the height and frequency of contractions gradually developing into tetany. The abdominal pain thus induced could be either generalized or localized depending on the extent of bowe1 stimulated. Hoefer et al.33 studied a group of twenty-seven patients having verihed islet cell adenoma of the pancreas, with respect to the neuropsychiatric manifestations of “convulsions, coma, and related states of impaired consciousness.” Among twentytwo of these patients having “autonomic, visceral symptoms,” four had abdominal pain. Eleven of these had electroencephalographic studies and eight records taken during the fasting state showed abnormal discharges, among which were synchronous bursts diffusely scattered of the spike-andwave variety, and others of the slow activity. Extensive studies by Gellhorn34 have indicated that an “anoxidative state” in the brain is induced by hypoglycemia, metrazol convulsions, injections of sodium cyanide and inhalation of high concentrations of carbon dioxide. Gibbs, et aL3” stated, “nitrogen breathing, standing with a lowered blood pressure and over-ventilation, all of which produced large, slow waves in normal subjects, also tend to precipitate seizures in epileptic persons.” Putnam and Hoefer36 have shown, by means of the electroencephalograph, abnormal cerebral discharges in conditions associated with lowered metabolism of the cerebral neurones with special reference to anoxia, and disturbances of carbohydrate metabolism. They made the significant observation “that depression of metabohc function may precipitate an increase in cerebral activity under a variety of con-

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ditions and that impaired consciousness and increased neurona activity are compatibIe.” Thus any of the numerous physioIogic and organic disorders, which disturb carbohydrate metabolism, or which induce cerebra1 anoxia, may Iead to abnormaldischarges from cerebra1 neurones. It wiI1 be seen from the foregoing briefly submitted data that two groups of conditions can provide a miIieu conducive to setting off abnorma1 eIectrica1 discharges from cerebra1 tissue, capabIe of being perceived eIectro-encephaIographicaIIy. The first is concerned with definite structura1 alterations of brain tissue of varying types and causes which may, under “appropriate ” conditions, “ fire off” and provide an epiIeptic dispIay. The second group deaIs with biophysiochemica1 disturbances which, in the fina anaIysis, produce a deficient oxygen up-take and impoverished carbohydrate suppIy to the functioning neurone. It is believed, therefore, that in those fixed morbid tissue changes of the brain the gangIion ceIIs in the vicinity of the Iesion may give off a continuous subIimina1 discharge; and when bodiIy disorders, whatever their origin, provoke the second factor of disturbed oxygen and carbohydrate metaboIism of the brain, which Iikewise may induce a subIimina1 discharge, the Iatter thereby constitutes the “appropriate ” condition which by “summation” provides the “adequate” stimuIus to an effector organ. In the present case the effector organ is the terminal motor-sweIIing in the smooth muscIe of the boweI. The pain is due to the disordered motiIity of the gastrointestina1 tract and is transmitted by the afferent projection pathways. Method of Study. I. Anamnesis: This shouId be painstaking, detaiIed and exhaustive, and shouId incIude a11 historica data pertaining to the progenitors, physica state of the mother during gestation, evidence of birth trauma, aIIergic phenomena during and subsequent to infancy, infectious diseases of chiIdhood and a11 other

Epilepsy

DECEMBER, 19.46

infections, craniocerebra1 injury, endocrine and metaboIic disturbances, and a11 other organic conditions which required medical or surgica1 treatment. The symptom of abdomina1 pain shouId be considered with respect to age of onset, frequency and rapidity of appearance, time of day (preor post-prandiaI), duration, association of pre- or post-seizure sensory phenomena, accompanying symptoms usuaIIy associated with the epileptic state, or epiIeptic phenomena antedating the presenting episodes of abdomina1 pain, and symptoms referabIe to increased intracranial pressure or active cerebra1 disease or dysfunction. I cannot emphasize too strongIy the vaIue of an adequate history, which in most instances shouId often suffice to indicate the proper direction toward correct diagnosis. 2. Each patient shouId be examined intensiveIy, by the indicated avaiIabIe methods, to ruIe out the existence of (I) intrinsic disease of the abdomina1, peIvic and thoracic viscera, (2) metaboIic or endocrine disorders, (3) morbid invoIvement of the spina cord or periphera1 nerves, and (4) psychosomatic projection mechanisms. 3. Thorough neuroIogica1 examination and compIete Iaboratory investigation, shouId, when indicated, incIude cytoIogic and chemica1 studies, roentgenoIogic studies of the skuII,-both direct and contrast (pneumo-encephaIography and thorotrast cerebra1 angiography) and eIectro-encephaIographic studies, shouId be empIoyed to discIose the presence of some structura1 or physioIogic disorder of the brain residing in cortica1 areas six, five or three and/or the diencephaIon. 4. FinaIIy, resort to the empirical method of the therapeutic test may be the onIy or corroborative evidence of the existence of abdomina1 epiIepsy. ShouId the symptom of paroxysma abdomina1 pain disappear or be radicaIIy aItered by an anti-convufsant regimen, recur upon cessation of treatment and again yieId to active therapy, the requirements of an ac-

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ceptabIe therapeutic test wiII have been met. Treatment. When the collective data reveaI the presence of an intracrania1 space-taking Iesion, surgica1 intervention, in operabIe cases, is indicated. FocaI traumatic scars Iikewise shouId be excised, when the symptom of paroxysma abdomina1 pain and any attendant phenomena cannot be controlled by an anti-convulsant regimen. Those conditions which may disturb carbohydrate metaboIism and/or oxygen suppIy of the cerebra1 neurones thus providing the biochemica1 “trigger factor” in the production of abdomina1 pain, such hyperthyroidism, conas hyperinsulinism, gestive heart failure, Adams-Stokes disease, intoxications, allergies, blood dyscrasias and the Iike, shouId receive treatment specificaIIy directed. If cerebra1 syphiIis is uncovered during the study for the cause of abdomina1 pain the obvious treatment is anti-Iuetic. Foci of infection shouId be eradicated and attention shouId be directed to factors which might precipitate reflex afferent stimuli. The fixed morphoIogic cerebra1 changes and the biochemicaIIy aItered cortica1 cells, already alluded to and not amenabIe to surgica1 treatment, which act as the sources of abnorma1 eIectrica1 discharges producing paroxysma abdomina1 pain shouId be treated by the foIIowing anti-convulsant regimen: (I) The use singIy or preferabIy in combination of (a) diphenyIhydantoin sodium (diIantin sodium), (b) phenobarbital, (c) bromides-aIkaIine or calcium (calcibronat). bromido-galactogluconate These drugs are to be used in adequate dosage depending upon age, weight and habitus of the patient; (2) high vitamin, high protein, moderate fat, moderate carbohydrate diet; (3)controIIed Iiquid intake, adequate to meet the daiIy needs of a baIanced water metabolism. This means neither dehydration nor water intoxication; (4) supervised social, physical and emotional activities within reasonabIe Iimits, designed to estabIish an even tenor of living.

EpiIepsy SUMMARY

American

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897

CONCLUSION

Attention has been directed to a form of abdomina1 pain which represents the symptomatic projection of distant cerebra1 disease or dysfunction. Experimenta and clinica data are presented indicating the reIationship of abnormal gastrointestina1 motiIity and abdomina1 pain, with Iesions affecting cortica areas six, five and three and/or the diencephaIon. AIIusion is made to some of the various morbid organic changes, and other disorders which may resuIt in Iess easiIy demonstrabIe neuropathoIogic conditions, which may provoke abnorma1 eIectrica1 discharges in those areas subserving gastrothus providing the intestinal function, stimuIus for aItered motiIity of the bowel ending in the symptom of abdomina1 pain. Representative cases are cited to iIIustrate the location of definabIe gross cerebra1 Iesions capabIe of visua1 observation, and others, due to a variety of causes, demonstrable by eIectro-encephaIography, which are believed to be the origin for the symptom of paroxysma abdominal pain. An effort is made to describe and define, with sufficient incIusiveness, a syndrome which provides the essentiars for definitive diagnosis without resorting to a diagnosis by excIusion; and a tentative expIanation of the mechanism of symptomatic abdomina1 epiIepsy is submitted. The method of study and treatment are outIined. The symptom of paroxysma abdominal pain, when properIy fitted into the pattern of historica events and symptoms, in the Iight of the foregoing presented data, may be considered not onIy as a form of symptomatic abdomina1 epiIepsy but aIso may serve as a guide-post in the topographical IocaIization of cerebral Iesions. REFERENCES I. MOORE, M. T. Paroxysmal

abdominal pain: a form of focaI symptomatic epilepsy II. J. A. M. A., 129: 1233-‘23g. 1945. 2. WATTS, J. W. and FULTON, J. F. Intussusception: the relation of the cerebra1 cortex to intestinal

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in the monkey. New England J. Med., 1934. WATTS, J. W. Inffuence of the cerebra1 cortex on gastrointestinal movements. J. A. M. A., 104: 335, 1935. SHEEHAN, D. Effect of cortical stimulation on gastric movements in the monkey. J. Pbysiol., 83: 177, 1935. SPIEGEL. E. A.. WESTON. K. and OPPENHEIMER. M. J: Postmotor foci’ influencing the gastro: intestinal tract and their descending pathways. J. Neuropatb. EdExper. New& 2: 45, 1943. _ PENFIELD. W. and GAGE. L. Cerebral IocaIization of epileptic manifestations. Arch. Neural. Ed Psycbiat., 30: 709, 1933. PENFIELD, W. and ERICKSON, T. C. EpiIepsy and Cerebral Locahzation, SpringfieId, III., 1941. CharIes C. Thomas. WATTS, J. W. and FULTON, J. F. The effect of Iesion of the hypothaIamus on the gastrointestina tract and heart in monkeys. Ann. Surg., IO, : 363, 1935. (a) CUSHING, H. Peptic uIcers and the interbrain. Surfi., Gynec. @ Obst., 55: I, 1932; (b) CUSHING,H. ‘Papers ReIating to the Pituitary Body, Hypothalamus and Parasympathetic Nervous System, Springfield, Ill., 1932. CharIes C. Thomas. FULTON, J. F. Physiology of the Nervous System. New York, 1943. Oxford University Press. (a) WECHSLER, I. S. Abdominal pain as a symptom of disease of the brain. J. A. M. A., 105: 647, 1935. (b) WECHSLER, I. S. Text Book of CIinicaI Neurology, 5th ed., p. 494. PhiIadelphia, 1943. W. B. Saunders Company. WINKELMAN, N. W. Discussion: paroxysmal abdomina1 pain, a form of focal symptomatic epilepsy II. J. A. M. A., 129: 1233-1239, x945. KLINGMAN, W. O., LANGFORD, W. S., GREELEY, D. M. and HOEFER, P. F. A. Paroxysmal attacks of abdomina1 pain, an epileptic equivalent in children. Tr. Am. Neurol. A., 67: 228, 1941. LAMBERT, J. P. Psychiatric observations on children with abdominal pain. Am. J. Psycbiat., 98: 451, motility

210: 883,

2.

d

A.

5.

6.

7.

8. g.

to.

II.

12.

‘94’. 13. JACKSON, J. H. Selected Writings of John Hughlings Jackson, VoI. I, on Epilepsy and Epileptiform ConvuIsions. Edited bv James TavIor. ” London, 1931. Hodder and Houghton. 14. Reported in full.’ 15. MOORE, M. T. Aberrant forms of epiIepsy-their disguise in somatosensory, psychic, and unusual motor displays. Pennsylvania M. J., 48: 569-572, ‘945.

16. Reported in fu1I.r I 7. MOORE, M. T. Paroxysmal abdomina1 pain: a form of focal symptomatic epilepsy. J. A. M. A., 124: 561-563, 1944. 18. DECHAUME, J. and CROIZAT, P. Lesions nerveuses dans I’anaphylaxie chronique experimentaIe, Compt. rend. Sot. de biol., IOI: 1145, 1929; Systeme nerveux et anaphylaxie: Faits experimentaux; documents anatomocliniques. Paris med., 2: 262, 1932. rg. BASSOE, P. Angioneurotic edema of the brain. M. Clin. Nortb America, 16: 409, 1932. 20. Reported in ful1.r z I. MOORE, M. T. Some usual and unusual mechanisms of abdominal pain. Soutb. Med. c~.Surg., 108: 135146. 1946.

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22. WALTER, W. G. The Iocation of cerebra1 tumours by

electro-encephaIography. Lancet, 2: 305-308, 1936; The electro-encephaIogram in cases of cerebral tumour. Proc. Roy. Sot. Med., 30: 57g598, 1937. 23. COBB, S. Causes of epiIepsy. Arch. Neural. u Psycbiat., 27: 1245, 1932. 24. (a) OPPENHEIM, H. Textbook of Nervous Diseases. Edinburgh, rgr I. 0. Schulze & Co. (b) WILSON, S. A. K. Neurology. Edited by A. N. Bruce, BaItimore, 1940. WiIIiams & WiIkins Company. 25. (a) WINKELMAN, N. W. and ECKEL, J. L. Productive endarteritis of the smaI1 cortica1 vessels in severe toxemias. Brain, 50: parts 3 and 4, 1927. (b) WINKELMAN, N. W. and ECKEL, J. L. Endarteritis of the smaII cortica1 vesseIs in severe and toxemias. Arch. Neural. e’p infections Psycbiat., 21: 863, rg2g. (c) WINKELMAN, N. W. and ECKEL. J. L. The brain in acute rheumatic fever. Arch: Neurol. @ Psycbiat., 28: 844, 1932. 26. FERRARO, A. and SCHEFFER, I. H. Toxic encephaIopathy in measIes. Arch. Neurol. @ Psych&., 27: 1209, 1932. 27. PAIGE, B. H., COWEN, D. and WOLF, A. ToxoencephaIomyelitis: v further obserpIasmic vations of infantile toxoplasmosis; intrauterine inception of the disease; viscera1 manifestations. Am. J. Dis. Cbild., 63: 474-514, 1942. 28. WINKELMAN, N. W. and MOORE, M. T. Progressive degenerative encephaIopathg; occurrence in infancy, with antenatal onset-simulating “swayback” of lambs. reoort of a case. Arch. Neurol. PP Psycbiat., 48: 54-7;. 1942. 29. (a) COBB, W. A. The electro-encephaIographic Iocalization of intracranial neopIasms. J. Neural., Neurosurg. ti Psycbiat., 7: &-102, 1944. (b) WALTER. W. G. and DOVEY. V. J. Electroencephalography in cases of sub-cortica1 tumor. J. Neurol., Neurosurg. @ Psycbiat., 7: 57-65, 1944. (c) YEAGER, C. I... and LUSE, A. Electroencephalographic IocaIization and differentiation of Iesions of fronta lobes; pathoIogic confrrmation. Arch. Neurol. Ed Psycbiat., 54: rg7-201, 1945. (d) GIBBS, F. A., WEGNER, W. R. and GIBBS, ERNA L. The eIectroencephaIogram in post-traumatic epiIepsy. Am. J. Psycbiat., IOO: 738, ,944. (e) LIBERSON,W. T. and SEGUIN, C. A. Brain waves and clinica features in arterioscIerotic and seniIe menta1 patients. Psycbosom. Med., 7: 30-35, 1945. (f) CASE, T. J. and BUCY, P. C. LocaIization of cerebral lesions by eIectroencephaIography. J. Neuro-pbysiol., I : 245-261, 1938. (g) GREENBLATT, M. and LEVIN, S. Factors affecting the eIectro-encephalogram of patients with neurosyphilis. Am. J. Psycbiat., 102: 40-48, 1945. 30. Ross, I. S. EIectroencephaIographic findings during and after acute encephaIitis and meningoencephaIitis. J. Nerv. TV Men. Dis., 102: 172-182, 1945. 3 I. HARRIS, S. Hyperinsulinism and dysinsulinism. J. A. M. A., 83: 729. 1924. 32. BULATAO, E. and CARLSON, H. J. Influence of experimenta changes in bIood sugar level on the gastric hunger contractions. Am. J. Pbysiol., 69: 107, 1924.

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33. HOEFER, P. F., GUTTMAN,S. A. and SANDS, I. J. ConvuIsive states and coma in cases of islet ceil adenoma of the pancreas. A. J. P., 102: 486-495, 1946. 34. GELLHORN, E. Effects of hypogIycemia and anoxia on the central nervous system. Arch. Neural CY Psych&., 40: 125, 1938. GELLHORN, E. and KESSLER, M. The effect of hypogIycemia on the eIectroencephaIogram at varying degrees of

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oxygenation of the bIood. Am. J. Pbysiol.,

899 136:

1, 1942. 35. GIBBS, F. A., DAVIS, H. and LENNOX, W. G. The electroencephalogram in epiIepsy and in conditions of impaired consciousness. Axb. Neurol. HPsycbiat., 34: 1133, 1935. 36. PUTNAM, T. J. and HOEFER, P. F. Physiologic and clinica aspects of the eIectroencephaIogram. Arch. Neurol. ti Psycbiat., 5 I : 581, 1944.

DISRUPTION or eventration of abdomina1 wounds usually occurs between the seventh and eleventh days after operation, after the use of vertical incisions cIosed with catgut. Wound infection, drainage, cough or other strain favors the disruption. After a secondary cIosure, a secondary eventration may occur. From “PrincipIes and Practice of Surgery” by W. Wayne Babcock (Lea & Febiger).