Digestion 13: 49 -55 (1975)

EEC in Ulcerative Colitis J. Eshchar, A. Arlazoroff, M. Kleinhaus, A. Mera, T. Gilat and I. Weissman Institute of Gastroenterology, Department of Neurology, Psychiatric Service and Institute of Electroencephalography, Asaf Harofe Government Hospital, Zerifin, Department of Gastroenterology, Ichilov Government-Municipal Hospital, Sackler School of Medicine, and Department of Statistics, Tel-Aviv University, Tel-Aviv

Key Words. Colectomy • Colitis, ulcerative - Diarrhea • Electroencephalography Abstract. Electroencephalographic tracings of 50 patients with ulcerative colitis (UC) were compared with those of 75 controls. In the UC patients a 24 % incidence of abnormal tracings was found as compared with an 8 % incidence in the controls. A higher incidence of abnormal electroencephalograms was found among active cases of UC than among those in remission. The meaning of these results is not yet clear.

The etiology of ulcerative colitis is unknown (4) and the relevance of psy­ chogenic factors is still under debate (3). In the literature we noted only one report on the electroencephalogram (EEG) in patients with UC (7). Sprachez et al. (7) described transitory nonspecific changes during periods of activity of the disease (increased amplitude, unstable frequency of alpha waves, peaked waves over the vertex and sensitivity to hyperventilation) as well as permanent abnor­ malities which persisted during remissions of UC and even after colectomy (rapid localized beta rhythm, theta waves and discrete, isolated, slow occipital waves). This report deals with abnormalities found in the EEG tracings of a group of UC patients in Israel.

Materials and Methods

Received: February 18, 1975; accepted: June 4. 1975.

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Ulcerative colitis. This group consisted of 50 unselected and consecutive patients with UC seen in the outpatient clinics. They were diagnosed according to the criteria of Mendeloff et al. (6) for 'definite UC’ and ‘definite ulcerative proctitis’.

Eshchar/Arlazoroff/Kleinhaus/Mera/Gilat/Weissman

50

'Remission' and "activity’ were defined according to the criteria of Binder (1) with some modifications. A patient was considered to be in remission if he had no more than two normal appearing bowel movements per day and was without symptoms of systemic distur­ bances. Activity of UC was defined as more than two daily bowel movements and/or blood in the stools, and/or systemic symptoms and complications. All UC patients underwent a neurologic examination. Control group (C). 50 patients and volunteers without neurological diseases and with­ out diarrhea were matched for age, sex and ethnic origin with the UC patients. Diarrhea group (D). An EHG was performed on 25 consecutive patients with diarrhea, mostly due to acute gastroenteritis or irritable bowel syndrome. They had no known neuro­ logic disease. This group was not matched with the UC patients. Electroencephalogram. Tracings were obtained according to the 10-20 international system (5). Reference and bipolar montages were used. Recording was performed on a 12-channel Alvar machine. The first tracing of each patient was evaluated by one of us (A.A.) without knowledge of the diagnosis (UC, C, D). The EEG was graded as follows: 0, no pathological activity; 1, diffuse occasional theta waves; 2, diffuse theta and delta activity without focal accentuation; 3, diffuse theta and delta activity with focal accentuation, 4, paroxysmal, generalized bursts of theta and delta waves; 5, paroxysmal, generalized bursts of spikes and waves; 6, paroxysmal and nonparoxysmal pathology with focal accentuation. UC patients having a pathologic EEG were asked to have a repeat examination under identical conditions in 1.5-3 years time. Statistical methods, x3 tests for homogeneity of distributions were used.

The results of the EEG evaluation are shown in table 1. It is obvious that the two control groups (C and D) are very similar with respect to their EEG. Combining the pathologic EEG (grades 1—6) makes groups C and D identical (table II a) so it is legitimate to combine them to one control group. This makes the results even more significant (table IIb). Electroencephalographic pathology was found three times more frequently in UC patients (24 %) than in both groups of controls (8 %). The results are statistically significant (table II a, b). Even if only obviously pathological tracings (grades 2—6) are considered with respect to normal and borderline tracings (grades 0 -1 ), the results are similar and statistically significant (table III). When findings in the UC group were related to the activity of the disease (table IV), twice as many pathologic tracings (grades 1-6) were encountered in patients with active disease as compared with those in remission (30 vs. 15 %). However, these results are not statistically significant. Obviously pathologic tracings (grades 2 -6 ) are more common in patients with active UC than in quiescent cases (13 vs. 5 %). Associations between electroencephalographic pathology and other variables (sex, age, ethnic origin, duration of disease, treatment) were not found. No

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Results

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HEG in Ulcerative Colitis

Table I. The EEG in the study and control groups graded 0 - 6 ' Group

UC C D

EEG 0

1

2

38 46 23

7 3 1

1

3

4

5

6

1

_

31 —

-

1 1

-

_

' For details see text. 2 One patient had two spells of grand mal. x2 test is meaningless due to many empty cells.

Table Ha. Normal versus pathologic EEG in UC and the two control groups Group

EEG

Total

normal

UC C D

pathologic

n

%

n

%

38 46 23

76 92 92

12 4 2

24 8 8

50 50 25

X ! test = 6.23 with 2 d.f. (degrees of freedom). p < 0 05.

Table I/b. Normal and pathologic EEG in UC and combined controls Group

EEG

Total

normal

UC Controls

pathologic

n

%

n

%

38 69

76 92

12 6

24 8

50 75

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xJ test = 6.23 with 1 d.f. 0.01 < p < 0.015 (significant at the 1.5 % level).

h'slichar/Arlazoroff/Kleinhaus/Mera/GUat/Weissman

52

Table III. Normal and almost normal versus marked EEG pathology in UC and controls Group

EEG

Total

normal and almost normal -------------------------------------0 1

UC Controls

marked pathology 2-6

n

%

n

%

n

%

38 69

76 92

7 4

14 5.3

5 2

10 2.7

50 75

test = 6.34 with 2 d.f. p < 0.05.

X5

neurological abnormalities were found in the UC patients. One patient, however, had two spells of grand mal. Out of 12 UC patients with an abnormal EEG, nine were available for a repeat examination. Six of these had active disease at the time of the first EEG, but all nine were either in remission (8 patients) or after total proctocolectomy (1 patient) at reexamination. The results are shown in table V. The EEG had improved in seven and did not change in two of the patients. Of the four tracings initially graded as 1, three became normal (grade 0) and of the five graded 2 -6 , four reverted to normal or almost normal (grades 0—1). Only one tracing, that of the patient with the grand mal seizures, did not change.

The grouping of the electroencephalographic findings made analysis of the data feasible. This grouping was neither meant to grade exactly the severity of pathology nor to describe fully the nature of the abnormalities in each case. It was, however, made to include as many variants of electroencephalographic findings as possible. Special attention was paid to the possibility of diffuse versus focal changes, and to paroxysmal activity of varying degrees of severity. The electroencephalographic changes described in this paper are by no means specific for UC and they occur in a multitude of neurologic and other diseases. Nevertheless, these abnormalities appear in a significant number of our patients with UC, as compared to controls and to patients with diarrhea, thereby raising the question of their particular meaning in this disorder. In view of the links between the gastrointestinal tract and the limbic system (also called the visceral brain), are the EEG changes a manifestation of some limbic system pathology?

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Discussion

53

EEG in Ulcerative Colitis

Table IV. The EEG in UC patients with respect to activity of disease Activity

EEG

Total

normal almost normal marked ------------------- ------------------- pathology 0 1 2 -6

Active Remission

n

%

n

%

n

%

21 17

70 85

5 2

17 10

4 1

13 5

30 20

test = 1.57 with 2 d.f. p > 0.45. XJ

Table V. Data on UC patients with repeat EEGs Activity of UC

EEG grading

1st EEG repeat EEG

1st EEG repeat EEG

S.C. Z.H. M.L. F.S. Z.Y. A.S.

A1 A R R A A

C‘ R' R R R R

1 1 1 2 3 5

0 0 0 0 1 1

G.F. B.Y. A.M.

A R A

R R R

5 1 5

1 1 5

Patient

Accompanying diseases

— -

diabetes mellitus repeated fetal loss -

bronchial asthma grand mal

The present data are insufficient for discerning any possible correlation between UC and various patterns of pathologic EEGs. However, one patient only (table I; Z.Y. in table V) had focal pathologic accentuations (grade 3). This paucity of focal changes was expected as it is not logical to assume localized focal brain pathology in conjunction with UC. It seems to us that this isolated case is coincidental. Five patients, however, had abnormal EEGs in groups 2 - 6 and three of these showed a paroxysmal pattern (grade 5). One of these three had clinical overt epilepsy and the EEG did not change with the improvement in colitic activity. In the other two patients the paroxysmal disorder disappeared

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1 A = Active disease; C = state after total proctocolectomy; R = remission

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54

during remission of the UC. The electroencephalographic changes might thus be connected with UC, permitting one to speculate on a possible relationship between UC and paroxysmal disorders. The significant difference between UC patients and controls might be related also to a neuropsychiatric (3) or other etiology of the disease. However, this might not necessarily be so, since there is also some association with the activity of UC (table IV, V). This latter association might mean that the electro­ encephalographic pathology could be the result or a complication of some subtle aspects of disturbed metabolism (2, 3) in UC. We were unable to find a gross metabolic derangement. All the patients were in a relatively good general condi­ tion, no one was bedridden at the time the EEC was performed, and no marked pathology was present in blood counts, serum total proteins, albumin and elec­ trolytes. Also, it has to be pointed out that in the group of patients with diarrhea (D), some had more severe diarrhea than that seen in most UC patients, but significantly fewer changes in the EEC. In addition, an association with drug administration had to be considered. This, however, was not supported by the data in this study. The tendency of the electroencephalographic changes to improve during remission of UC might be due to the fact that the EEG changes result from the activity of the disease. This speculation is, by no means, necessarily right and the reverse could still be true, meaning that the changes seen on the EEG represent some etiologic factor(s). The results reported here may be a special, local feature of UC which have to be reconfirmed by other centers. We are, however, unable to compare our data with those from Rumania (7). Also, the association with the state of activ­ ity of UC should be further investigated. Computor analysis of the EEG might bring out more significant details for further statistical analysis. When all these data become available from larger groups of patients a better understanding of this phenomenon might evolve. Until that time we are quite uncertain regarding the significance of these findings, whether they are due to the disease process of UC itself or to some consequences thereof. A cknowledgment The help of the technical staff of the EEG Institute at the Asaf Harofe Hospital and that of Dr. S. Korenblit and Dr. L. Cohen is greatly appreciated.

1

Binder, V.: A comparison between clinical state, macroscopic and microscopic appear­ ances of rectal mucosa and cytologic picture of mucosal exudate in ulcerative colitis. Scand. J. Gastroent. 5: 627-632 (1970).

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References

LEG in Ulcerative Colitis

3 4 5 6

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Coursin, D.S.: Central nervous system hypersensitivity to tryptophane. Am. J. clin. Nutr. 24: 821-825 (1971). Engel. G.L.: Psychological factors in ulcerative colitis in man and gibbon. Gastro­ enterology 57: 362-365 (1969). Goligher. J.C.; deDombal. F.T.: Watts. J.McK.. and Watkinson. G.: Ulcerative colitis (Bailliere, Tindall & Cassell, London 1968). Jasper. M.: The ten twenty electrode system of the International Federation. Electroenccph. clin. Neurophysiol. 10: 371-375 (1958). Mendeloff. A.I.; Monk. M.: Siegel, C.I., and Lilienfeld. A.: Some epidemiological features of ulcerative colitis and regional enteritis. A preliminary report. Gastroenterol­ ogy 51: 748-752 (1966). Sprachez. T.: Brosteanu. E.: Oproiu. A.; Almasanu, E., and Boicescu, L.: Research on clectroencephalographic changes caused by ulcero-hemorrhagic rectocolitis. Stud. Cercet. Med. Int. 9: 271-278 (1960).

J. Eshchar, MD, Chief, Institute of Gastroenterology, Asaf Harofe Government Hospital, Zerifin (Israel)

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EEG in ulcerative colitis.

Electroencephalographic tracings of 50 patients with ulcerative colitis (UC) were compared with those of 75 controls. In the UC patients a 24% inciden...
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