I
[
II
I
Electroencephalographic study in acute rheumatic carditis Ali Ertugrul, M.D. Yavuz Renda, M.D. Muhsin Saraciar, M.D. Mine Oner, M.D. Sezer Akay, M.D. Ankara, Turkey
In the last century, various authors have written about the presence of vascular and cerebral changes due to endarteritis found during the autopsy of rheumatic cases? In all these autopsies, rheumatic patients who had endarteritis also had some lesions of rheumatic carditis. Electroencephalographic (EEG) studies of rheumatic fever were done in cases of Sydenham's chorea in 1941, and later in other types of rheumatic disease. Nyman, 13 Lavy and associates, 3 Oner, ~ Ozturk, ~ Sezer, 7 and Renda and associates ~ showed that EEG changes can be seen in rheumatic fever patients without neurologic symptoms. Our preliminary studies gave the impression that EEG changes were consistent with active carditis and that the EEG returned to normal when the disease subsided2 ,7 This study has been planned in order to answer the following questions. (1) How often can EEG changes be seen in rheumatic fever patients who do not have neurologic findings? (2) W h a t is the frequency of EEG changes in acute polyarticular rheumatic fever without carditis? (3) W h a t is the frequency of EEG changes in rheumatic carditis? (4) Are the EEG changes related to rheumatic activity? (5) What is the correlation, if any, between the sedimentation rate and tachycardia From the Pediatric Cardiology Unit, Children's Hospital, Hacettepe Medical School, Hacettepe University, Ankara, Turkey. Preliminary study supported in part by T.B.T.A.K. (The Scientific And Technical Research Council of Turkey). Received for publication Jan. 9, 1975. Reprint requests: A. Ertugrnll M.D., Professor of Pediatrics aad Head of the Pediatrics Cardiology Unit, Hacettepe Medical School Children's Hospital, Ankara, Turkey.
February, 1976, Vol. 91, No. 2, pp. 163-167
in EEG changes? (6) How long do the EEG changes continue? (7) Finally, can the EEG changes be a criterion for the determination of the activity in rheumatic carditis? Material and methods
Cases in this study were selected from patients who were admitted to the Pediatric Cardiology Unit of the Hacettepe University Children's Hospital between 1971 and 1973. There were 1,243 rheumatic fever patients and 60 per cent of these were our regular follow-up cases. The age range was between 7 and 16 years; the sex distribution was almost identical. Of these cases we selected 30 patients with acute polyarticular rheumatic fever without carditis, 25 with inactive rheumatic heart disease, 25 with acute active rheumatic carditis, and 85 with Sydenham's chorea. The last 25 acute active r h e u m a t i c carditis cases were followed until EEG changes returned to normal. The history of the present disease and the past history of rheumatic fever were carefully noted. Complete physical (including neurologic) examinations were done. Patients with neurologic findings were excluded from this study and also patients with a definite or suspected history of epilepsy. Another 43 children from the outpatient clinic, with no signs of rheumatic, collagen, or neurologic disease, were matched for age and sex and used as a control group (Table I); 85 patients with definite findings of Sydenham's chorea were also chosen as a second control group. Only those patients with all the following findings were considered as having active rheumatic carditis: tachycardia in sleep, joint symptoms, significant murmurs, increased heart size,
American Heart Journal
163
Ertugrul et al.
Fig. 1. First EEG tracing of an active rheumatic carditis patient, showing definite slow and sharp wave abnormalities over all brain regions.
Fig. 2. Fourth EEG (same patient as in Fig. 1) after 9 weeks shows complete normalization of the tracing. fever of 37 ~ C. and over, elevated s e d i m e n t a t i o n rate, and increased ASO titer. {Only t h r e e of these patients had a t e m p e r a t u r e u n d e r 37 ~ C., and only one patient's ASO titer was less t h a n 300 U.; there was only one p a t i e n t with h e a r t failure who had a normal sedimentation rate on admission). Eleven of 25 patients had h e a r t failure; 10 patients had pure MI; five had MS + MI; six h a d MI § AI; two had M I § MS + AI; one had M S § TI; one had M S + AI § TI. Patients with active carditis had been hospitalized for 4 weeks or more. All hospitalized patients were kept at bed rest, Corticosteroids, penicillin, and, if necessary, anticongestive t r e a t m e n t for h e a r t failure were given. T h e first E E G ' s were obtained on the first day of admission and the second E E G ' s 7 to 10 days later. F u r t h e r E E G ' s were t a k e n every 15 to 20 days while the p a t i e n t was in hospital, and every
164
30 days after discharge, until the E E G r e m a i n e d normal in two consecutive readings. In the inactive r h e u m a t i c h e a r t disease group (25 cases) only those patients with definite rheumatic valvular disease (but who did not show a n y changes other t h a n n o r m a l variation, at least during the last year, in their s e d i m e n t a t i o n rate, ASO titer, pulse rate, h e a r t size, m u r m u r s , E E G , and x-rays) were included. There was no significant difference in the severity of heart lesions in the two groups, although there were a few more h e a r t failure patients in the active r h e u m a t i c h e a r t disease group. T h r e e of the 25 n o n a c t i v e r h e u m a t i c carditis patients had h e a r t failure; 11 had MI; one had MS; three had AI; five h a d M I + MS; two had MS + AI; one had M I + MS + AI. T h e E E G ' s were obtained by Grass V1. Eightchannel a p p a r a t u s and 19-20 i n t e r n a t i o n a l electrode system was used. T w o interpreters a n a l y z e d the recordings by the double-blind m e t h o d , without knowing from which groups the patients came or their diagnoses. Abnormalities were classified as follows: 1. Changes in the b a c k g r o u n d activity were grouped as: Focal slow and sharp waves in 4 to 6 c.p.s. frequency. Localization of these waves was inconsistent in each tracing. Diffuse slow waves in 3 to 7 c.p.s, frequency. These were more p r o n o u n c e d on the posterior head regions and quite irregular. Paroxysmal sharp waves in 3 to c.p.s. frequency.There were no definite foci for these. Loss (or paucity) of alpha r h y t h m in m a n y tracings. 2. T h e r e was diffuse voltage suppression in most of the recordings, b u t this finding was t h o u g h t to be inconclusive. T h e abnormalities were continuous and not consistent with the eye opening or closing. Hyperventilation and photic s t i m u l a t i o n did not induce m a r k e d changes in any of these tracings. None of the patients showed m a r k e d drowsiness or slept during the recordings.
Findings There were 137 tracings of 25 patients with active acute rheumatic carditis. Each p a t i e n t had
February, 1976, Vol. 91, No: 2
E E G in a c u t e r h e u m a t i c c a r d i t i s
9 E.E.G. o Sedimentation x Tachycardia
Rate
O0
o o 84 o
O0 O0
X K x XX XX
u I
0
lXll X X X X yx
x
XX
X
X
'1:" 'l:
9
Weeks
9
i 3
~
! 4,
,,
9
~
9
~
9
"~
oo
i 8
! 9
I
110
11
9
1'Z
9
113 I~
I'5
I'6
I'7
I'8
9
119 2'0
9
2'I
2'2
213 2 I/'
2'5
1,
3. Comparative durations of abnormalities of EEG, high sedimentation rate, and tachycardia. All these patients were under corticosteroid treatment in the hospital. The mean duration for returning to normal was about 16 days for sedimentation rate, 4 weeks for tachycardia, and 8 weeks for EEG abnormality. Fig.
T a b l e I. E E G studies in 208 cases of r h e u m a t i c fever
Acute active rheumatic carditis No.
Inactive rheumatic valvular heart disease No.
Polyarticular rheumatic fever No.
of cases
Abnormal EEG
of cases
Abnormal EEG
25
24 96%
25
3 12%
of cases
30
a m i n i m u m of two and a m a x i m u m of nine tracings. These p a t i e n t s were followed for a period which r a n g e d f r o m 2 to 22 weeks (see Figs. 1 and 2). O u t of 25 p a t i e n t s with active a c u t e r h e u m a t i c carditis, 24 h a d a b n o r m a l E E G ' s (94 per cent). All showed r h y t h m a b n o r m a l i t i e s a n d 10 h a d a m a r k e d voltage suppression ( T a b l e I). T h e r a t e of E E G a b n o r m a l i t y f r o m t h e 43 control p a t i e n t s was 14 per cent, c o m p a r e d w i t h 27 per cent found in 23 of t h e 85 p a t i e n t s with S y d e n h a m ' s chorea. Only two of 30 a c u t e r h e u m a t i c p o l y a r t h r i t i s p a t i e n t s h a d a b n o r m a l E E G changes (6.6 per cent). As shown in Fig. 3, E E G tracings r e t u r n e d to n o r m a l after a p p r o x i m a t e l y 8 weeks, whereas t h e s e d i m e n t a t i o n r a t e r e t u r n e d to n o r m a l within 289 weeks a n d t a c h y c a r d i a within 4 weeks. Of the 25 active carditis p a t i e n t s with r h y t h m
American Heart Journal
Sydenham' s chorea No.
Abnormal EEG
2 6.6%
of cases
85
Abnormal EEG
23 27%
Control group No. of cases
43
Abnormal EEG
6 14%
abnormalities of E E G , 21 r e t u r n e d to normal. T h r e e patients did not a p p e a r for E E G controls. Four of 10 patients w h o h a d diffuse voltage suppression h a d c o m p l e t e l y n o r m a l voltage on the last tracing. Of the 25 patients with inactive r h e u m a t i c heart disease, there was only one w h o h a d r h y t h m disturbance in his E E G . Of 30 p a t i e n t s with a c u t e polyarticular r h e u m a t i c fever w i t h o u t carditis, there were only two with r h y t h m a b n o r m a l i t i e s and one with low voltage. Discussion and c o n c l u s i o n
E E G abnormalities h a v e been n o t e d in p a t i e n t s with S y d e n h a m ' s chorea since 1941. During the last t h r e e decades E E G a b n o r m a l i t i e s h a v e been found in r h e u m a t i c fever p a t i e n t s w i t h o u t Sydenh a m ' s chorea and w i t h o u t a n y neurologic findings. On t h e other hand, D i a m o n d 2 f o u n d no E E G abnormalities in r h e u m a t i c p a t i e n t s w i t h o u t
165
Ertugrul et al.
chorea. N y m a n 13 noticed t h a t E E G abnormalities in active r h e u m a t i c fever r e t u r n e d to n o r m a l after the signs of activity disappeared. In this study we divided our r h e u m a t i c fever patients into three groups: (1) acute p o l y a r t h r i t i s without carditis, (2) acute active carditis, and (3) nonactive old r h e u m a t i c valvular h e a r t disease.' An earlier s t u d y concerned with E E G findings in S y d e n h a m ' s chorea cases 12 in this institution showed an a b n o r m a l i t y r a t e of 27 per cent. This study d e m o n s t r a t e d t h a t i n v o l v e m e n t of the central nervous system in a c u t e r h e u m a t i c carditis is more c o m m o n t h a n is generally believed. Although clinical e x a m i n a t i o n of patients did not show a n y neurologic deficit, the E E G ' s almost always d e m o n s t r a t e d abnormalities in acute carditis. T h e incidence of a b n o r m a l E E G ' s in n o n a c t i v e r h e u m a t i c valvular h e a r t disease and polyarticular rheumatic fever w i t h o u t carditis is not higher t h a n the abnormal E E G ' s found in n o r m a l persons. In this study, patients with d e f i n i t e active carditis and nonactive old r h e u m a t i c h e a r t disease were selected from several h u n d r e d rheumatic patients. T h e E E G ' s of 21 follow-up cases with active r h e u m a t i c carditis r e t u r n e d to n o r m a l within 3 to 23 weeks. We can assume t h a t a n a t o m i c a l changes of the central nervous system could be the cause of E E G changes, and normalization of the E E G findings can be a t t r i b u t e d to the i m p r o v e m e n t of the original lesion in the central nervous system. When the E E G abnormalities are c o m p a r e d with the other signs of activity of r h e u m a t i c fever, such as sedimentation rate and pulse rate, E E G abnormalities would seem to be a m o r e persistent indication of activity of r h e u m a t i c fever. Fig. 3 shows t h a t the s e d i m e n t a t i o n rate returns to normal within 4 weeks and the E E G returns to n o r m a l within 8 weeks in all the patients under corticosteroid t r e a t m e n t . We have not tried to determine the d u r a t i o n of E E G abnormalities in a c u t e active carditis patients who did not have corticosteroid t r e a t m e n t . One could assume from the above findings t h a t corticosteroid t r e a t m e n t is not effective enough to change the E E G abnormalities. If the E E G abnormality is an i m p o r t a n t indicator of the rheumatic activity, it is conceivable t h a t the normalization of the E E G could be a more
166
reliable l a b o r a t o r y finding in determining the long-range recovery process of active r h e u m a t i c carditis. A n o t h e r study in our d e p a r t m e n t revealed t h a t Australia antigen was also positive in 40 per cent of acute r h e u m a t i c cases2 All these observations suggest t h a t the p a t h o genesis m a y be different in two clinical types of r h e u m a t i c fever. Migratory p o l y a r t i c u l a r rheumatic fever w i t h o u t carditis m a y be due to only poststreptococcal reaction, whereas for rheumatic carditis an additional cofactor seems to be necessary. In active carditis the presence of Australia antigen and a b n o r m a l i t y of the E E G are strongly suggestive of the presence of such a cofactor in r h e u m a t i c cases. This cofactor might be a viral infection during or prior to streptococcal infection, as was suggested by B u r c h and his colleagues. TM It is obvious t h a t this problem requires f u r t h e r investigation. Summary Electroencephalographic studies were done in rheumatic fever patients in order to d e t e r m i n e the distribution of n o r m a l and a b n o r m a l E E G patterns in different clinical forms. T h e d u r a t i o n of E E G abnormalities related to r h e u m a t i c activity was compared with the d u r a t i o n of increased sedimentation rate and tachycardia. Rheumatic fever cases were divided into four groups: ( 1 ) a c u t e active r h e u m a t i c carditis, (2) acute polyarthritis without carditis, (3) n o n a c t i v e old rheumatic valvular h e a r t disease, and (4) Sydenham's chorea. E E G findings were within n o r m a l limits in acute polyarthritis and in nonactive r h e u m a t i c valvular heart disease, b u t there were a b n o r m a l E E G findings in 29 per cent of chorea and in 94 per cent of active carditis cases. In active carditis all E E G changes r e t u r n e d to normal approximately within 8 weeks, whereas the sedimentation rate and t a c h y c a r d i a r e t u r n e d to normal within a shorter period. REFERENCES 1. Huxtable, B. G.: Cerebral rheumatism, Med. J. Aust. 48:220, 1961. 2. Diamond,E. F.: The encephalogram in rheumatic fever, J. A. M. A. 182:685, 1962. 3. Lavy, S., Lavy, R., and Brand: Neurological and electroencephalographic abnormalities in rheumatic fever, Acta Neurol. Scand. 40-76, 1964. 4. Oner,M.: E.EiG. changes in rheumatic patients without neurological findings, Ankara, 1972, Hacettepe University Press.
February, 1976, Vol. 91, No. 2
E E G in acute rheumatic carditis
5. Ozturk, N.: E. E. G. changes in systemiclupus erythematosus and rheumatoid arthritis in children, Ankara, 1973. 6. Johnston, D. A.: Electroencephalogram in Sydenham's chorea, Arch. Neurol, 21:27, 1964. 7. Sezer, A.: E.E.G. changes in rheumatic carditis (thesis) 1973. 8. U . K . and U. S. Joint Report: The natural history of rheumatic fever and rheumatic heart disease: Cooperative clinical trial of ACTH, cortisone and aspirin, Circulation 32:457, 1965.
American Heart Journal
9. Ertugrul, M.: Rheumatic fever and Australia antigen, Lancet 1:507, 1973. 10. Burch, G. E., Giles, T. D , and Colcolough, H. L.: Pathogenesis of "rheumatic heart disease"-Critique and theory, AM. HEART J. 80"556, 1970. 11. Markowitz, M., and Gordis, L.: Rheumatic fever, ed. 2, Philadelphia, 1972, W. B. Saunders Company, p. 71. 12. Renda, Y., Aksoy, M., and Yalaz, K.: Sydenham's chorea and E.E.G. findings, Turk. J. Pediatr. 15:153, 1972. 13. Nyman, G. E.: E.E.G. in rheumatic fever, Acta Med. Scand. 149:126, 1954.
167
[
II
I
Electroencephalographic study in acute rheumatic carditis Ali Ertugrul, M.D. Yavuz Renda, M.D. Muhsin Saraciar, M.D. Mine Oner, M.D. Sezer Akay, M.D. Ankara, Turkey
In the last century, various authors have written about the presence of vascular and cerebral changes due to endarteritis found during the autopsy of rheumatic cases? In all these autopsies, rheumatic patients who had endarteritis also had some lesions of rheumatic carditis. Electroencephalographic (EEG) studies of rheumatic fever were done in cases of Sydenham's chorea in 1941, and later in other types of rheumatic disease. Nyman, 13 Lavy and associates, 3 Oner, ~ Ozturk, ~ Sezer, 7 and Renda and associates ~ showed that EEG changes can be seen in rheumatic fever patients without neurologic symptoms. Our preliminary studies gave the impression that EEG changes were consistent with active carditis and that the EEG returned to normal when the disease subsided2 ,7 This study has been planned in order to answer the following questions. (1) How often can EEG changes be seen in rheumatic fever patients who do not have neurologic findings? (2) W h a t is the frequency of EEG changes in acute polyarticular rheumatic fever without carditis? (3) W h a t is the frequency of EEG changes in rheumatic carditis? (4) Are the EEG changes related to rheumatic activity? (5) What is the correlation, if any, between the sedimentation rate and tachycardia From the Pediatric Cardiology Unit, Children's Hospital, Hacettepe Medical School, Hacettepe University, Ankara, Turkey. Preliminary study supported in part by T.B.T.A.K. (The Scientific And Technical Research Council of Turkey). Received for publication Jan. 9, 1975. Reprint requests: A. Ertugrnll M.D., Professor of Pediatrics aad Head of the Pediatrics Cardiology Unit, Hacettepe Medical School Children's Hospital, Ankara, Turkey.
February, 1976, Vol. 91, No. 2, pp. 163-167
in EEG changes? (6) How long do the EEG changes continue? (7) Finally, can the EEG changes be a criterion for the determination of the activity in rheumatic carditis? Material and methods
Cases in this study were selected from patients who were admitted to the Pediatric Cardiology Unit of the Hacettepe University Children's Hospital between 1971 and 1973. There were 1,243 rheumatic fever patients and 60 per cent of these were our regular follow-up cases. The age range was between 7 and 16 years; the sex distribution was almost identical. Of these cases we selected 30 patients with acute polyarticular rheumatic fever without carditis, 25 with inactive rheumatic heart disease, 25 with acute active rheumatic carditis, and 85 with Sydenham's chorea. The last 25 acute active r h e u m a t i c carditis cases were followed until EEG changes returned to normal. The history of the present disease and the past history of rheumatic fever were carefully noted. Complete physical (including neurologic) examinations were done. Patients with neurologic findings were excluded from this study and also patients with a definite or suspected history of epilepsy. Another 43 children from the outpatient clinic, with no signs of rheumatic, collagen, or neurologic disease, were matched for age and sex and used as a control group (Table I); 85 patients with definite findings of Sydenham's chorea were also chosen as a second control group. Only those patients with all the following findings were considered as having active rheumatic carditis: tachycardia in sleep, joint symptoms, significant murmurs, increased heart size,
American Heart Journal
163
Ertugrul et al.
Fig. 1. First EEG tracing of an active rheumatic carditis patient, showing definite slow and sharp wave abnormalities over all brain regions.
Fig. 2. Fourth EEG (same patient as in Fig. 1) after 9 weeks shows complete normalization of the tracing. fever of 37 ~ C. and over, elevated s e d i m e n t a t i o n rate, and increased ASO titer. {Only t h r e e of these patients had a t e m p e r a t u r e u n d e r 37 ~ C., and only one patient's ASO titer was less t h a n 300 U.; there was only one p a t i e n t with h e a r t failure who had a normal sedimentation rate on admission). Eleven of 25 patients had h e a r t failure; 10 patients had pure MI; five had MS + MI; six h a d MI § AI; two had M I § MS + AI; one had M S § TI; one had M S + AI § TI. Patients with active carditis had been hospitalized for 4 weeks or more. All hospitalized patients were kept at bed rest, Corticosteroids, penicillin, and, if necessary, anticongestive t r e a t m e n t for h e a r t failure were given. T h e first E E G ' s were obtained on the first day of admission and the second E E G ' s 7 to 10 days later. F u r t h e r E E G ' s were t a k e n every 15 to 20 days while the p a t i e n t was in hospital, and every
164
30 days after discharge, until the E E G r e m a i n e d normal in two consecutive readings. In the inactive r h e u m a t i c h e a r t disease group (25 cases) only those patients with definite rheumatic valvular disease (but who did not show a n y changes other t h a n n o r m a l variation, at least during the last year, in their s e d i m e n t a t i o n rate, ASO titer, pulse rate, h e a r t size, m u r m u r s , E E G , and x-rays) were included. There was no significant difference in the severity of heart lesions in the two groups, although there were a few more h e a r t failure patients in the active r h e u m a t i c h e a r t disease group. T h r e e of the 25 n o n a c t i v e r h e u m a t i c carditis patients had h e a r t failure; 11 had MI; one had MS; three had AI; five h a d M I + MS; two had MS + AI; one had M I + MS + AI. T h e E E G ' s were obtained by Grass V1. Eightchannel a p p a r a t u s and 19-20 i n t e r n a t i o n a l electrode system was used. T w o interpreters a n a l y z e d the recordings by the double-blind m e t h o d , without knowing from which groups the patients came or their diagnoses. Abnormalities were classified as follows: 1. Changes in the b a c k g r o u n d activity were grouped as: Focal slow and sharp waves in 4 to 6 c.p.s. frequency. Localization of these waves was inconsistent in each tracing. Diffuse slow waves in 3 to 7 c.p.s, frequency. These were more p r o n o u n c e d on the posterior head regions and quite irregular. Paroxysmal sharp waves in 3 to c.p.s. frequency.There were no definite foci for these. Loss (or paucity) of alpha r h y t h m in m a n y tracings. 2. T h e r e was diffuse voltage suppression in most of the recordings, b u t this finding was t h o u g h t to be inconclusive. T h e abnormalities were continuous and not consistent with the eye opening or closing. Hyperventilation and photic s t i m u l a t i o n did not induce m a r k e d changes in any of these tracings. None of the patients showed m a r k e d drowsiness or slept during the recordings.
Findings There were 137 tracings of 25 patients with active acute rheumatic carditis. Each p a t i e n t had
February, 1976, Vol. 91, No: 2
E E G in a c u t e r h e u m a t i c c a r d i t i s
9 E.E.G. o Sedimentation x Tachycardia
Rate
O0
o o 84 o
O0 O0
X K x XX XX
u I
0
lXll X X X X yx
x
XX
X
X
'1:" 'l:
9
Weeks
9
i 3
~
! 4,
,,
9
~
9
~
9
"~
oo
i 8
! 9
I
110
11
9
1'Z
9
113 I~
I'5
I'6
I'7
I'8
9
119 2'0
9
2'I
2'2
213 2 I/'
2'5
1,
3. Comparative durations of abnormalities of EEG, high sedimentation rate, and tachycardia. All these patients were under corticosteroid treatment in the hospital. The mean duration for returning to normal was about 16 days for sedimentation rate, 4 weeks for tachycardia, and 8 weeks for EEG abnormality. Fig.
T a b l e I. E E G studies in 208 cases of r h e u m a t i c fever
Acute active rheumatic carditis No.
Inactive rheumatic valvular heart disease No.
Polyarticular rheumatic fever No.
of cases
Abnormal EEG
of cases
Abnormal EEG
25
24 96%
25
3 12%
of cases
30
a m i n i m u m of two and a m a x i m u m of nine tracings. These p a t i e n t s were followed for a period which r a n g e d f r o m 2 to 22 weeks (see Figs. 1 and 2). O u t of 25 p a t i e n t s with active a c u t e r h e u m a t i c carditis, 24 h a d a b n o r m a l E E G ' s (94 per cent). All showed r h y t h m a b n o r m a l i t i e s a n d 10 h a d a m a r k e d voltage suppression ( T a b l e I). T h e r a t e of E E G a b n o r m a l i t y f r o m t h e 43 control p a t i e n t s was 14 per cent, c o m p a r e d w i t h 27 per cent found in 23 of t h e 85 p a t i e n t s with S y d e n h a m ' s chorea. Only two of 30 a c u t e r h e u m a t i c p o l y a r t h r i t i s p a t i e n t s h a d a b n o r m a l E E G changes (6.6 per cent). As shown in Fig. 3, E E G tracings r e t u r n e d to n o r m a l after a p p r o x i m a t e l y 8 weeks, whereas t h e s e d i m e n t a t i o n r a t e r e t u r n e d to n o r m a l within 289 weeks a n d t a c h y c a r d i a within 4 weeks. Of the 25 active carditis p a t i e n t s with r h y t h m
American Heart Journal
Sydenham' s chorea No.
Abnormal EEG
2 6.6%
of cases
85
Abnormal EEG
23 27%
Control group No. of cases
43
Abnormal EEG
6 14%
abnormalities of E E G , 21 r e t u r n e d to normal. T h r e e patients did not a p p e a r for E E G controls. Four of 10 patients w h o h a d diffuse voltage suppression h a d c o m p l e t e l y n o r m a l voltage on the last tracing. Of the 25 patients with inactive r h e u m a t i c heart disease, there was only one w h o h a d r h y t h m disturbance in his E E G . Of 30 p a t i e n t s with a c u t e polyarticular r h e u m a t i c fever w i t h o u t carditis, there were only two with r h y t h m a b n o r m a l i t i e s and one with low voltage. Discussion and c o n c l u s i o n
E E G abnormalities h a v e been n o t e d in p a t i e n t s with S y d e n h a m ' s chorea since 1941. During the last t h r e e decades E E G a b n o r m a l i t i e s h a v e been found in r h e u m a t i c fever p a t i e n t s w i t h o u t Sydenh a m ' s chorea and w i t h o u t a n y neurologic findings. On t h e other hand, D i a m o n d 2 f o u n d no E E G abnormalities in r h e u m a t i c p a t i e n t s w i t h o u t
165
Ertugrul et al.
chorea. N y m a n 13 noticed t h a t E E G abnormalities in active r h e u m a t i c fever r e t u r n e d to n o r m a l after the signs of activity disappeared. In this study we divided our r h e u m a t i c fever patients into three groups: (1) acute p o l y a r t h r i t i s without carditis, (2) acute active carditis, and (3) nonactive old r h e u m a t i c valvular h e a r t disease.' An earlier s t u d y concerned with E E G findings in S y d e n h a m ' s chorea cases 12 in this institution showed an a b n o r m a l i t y r a t e of 27 per cent. This study d e m o n s t r a t e d t h a t i n v o l v e m e n t of the central nervous system in a c u t e r h e u m a t i c carditis is more c o m m o n t h a n is generally believed. Although clinical e x a m i n a t i o n of patients did not show a n y neurologic deficit, the E E G ' s almost always d e m o n s t r a t e d abnormalities in acute carditis. T h e incidence of a b n o r m a l E E G ' s in n o n a c t i v e r h e u m a t i c valvular h e a r t disease and polyarticular rheumatic fever w i t h o u t carditis is not higher t h a n the abnormal E E G ' s found in n o r m a l persons. In this study, patients with d e f i n i t e active carditis and nonactive old r h e u m a t i c h e a r t disease were selected from several h u n d r e d rheumatic patients. T h e E E G ' s of 21 follow-up cases with active r h e u m a t i c carditis r e t u r n e d to n o r m a l within 3 to 23 weeks. We can assume t h a t a n a t o m i c a l changes of the central nervous system could be the cause of E E G changes, and normalization of the E E G findings can be a t t r i b u t e d to the i m p r o v e m e n t of the original lesion in the central nervous system. When the E E G abnormalities are c o m p a r e d with the other signs of activity of r h e u m a t i c fever, such as sedimentation rate and pulse rate, E E G abnormalities would seem to be a m o r e persistent indication of activity of r h e u m a t i c fever. Fig. 3 shows t h a t the s e d i m e n t a t i o n rate returns to normal within 4 weeks and the E E G returns to n o r m a l within 8 weeks in all the patients under corticosteroid t r e a t m e n t . We have not tried to determine the d u r a t i o n of E E G abnormalities in a c u t e active carditis patients who did not have corticosteroid t r e a t m e n t . One could assume from the above findings t h a t corticosteroid t r e a t m e n t is not effective enough to change the E E G abnormalities. If the E E G abnormality is an i m p o r t a n t indicator of the rheumatic activity, it is conceivable t h a t the normalization of the E E G could be a more
166
reliable l a b o r a t o r y finding in determining the long-range recovery process of active r h e u m a t i c carditis. A n o t h e r study in our d e p a r t m e n t revealed t h a t Australia antigen was also positive in 40 per cent of acute r h e u m a t i c cases2 All these observations suggest t h a t the p a t h o genesis m a y be different in two clinical types of r h e u m a t i c fever. Migratory p o l y a r t i c u l a r rheumatic fever w i t h o u t carditis m a y be due to only poststreptococcal reaction, whereas for rheumatic carditis an additional cofactor seems to be necessary. In active carditis the presence of Australia antigen and a b n o r m a l i t y of the E E G are strongly suggestive of the presence of such a cofactor in r h e u m a t i c cases. This cofactor might be a viral infection during or prior to streptococcal infection, as was suggested by B u r c h and his colleagues. TM It is obvious t h a t this problem requires f u r t h e r investigation. Summary Electroencephalographic studies were done in rheumatic fever patients in order to d e t e r m i n e the distribution of n o r m a l and a b n o r m a l E E G patterns in different clinical forms. T h e d u r a t i o n of E E G abnormalities related to r h e u m a t i c activity was compared with the d u r a t i o n of increased sedimentation rate and tachycardia. Rheumatic fever cases were divided into four groups: ( 1 ) a c u t e active r h e u m a t i c carditis, (2) acute polyarthritis without carditis, (3) n o n a c t i v e old rheumatic valvular h e a r t disease, and (4) Sydenham's chorea. E E G findings were within n o r m a l limits in acute polyarthritis and in nonactive r h e u m a t i c valvular heart disease, b u t there were a b n o r m a l E E G findings in 29 per cent of chorea and in 94 per cent of active carditis cases. In active carditis all E E G changes r e t u r n e d to normal approximately within 8 weeks, whereas the sedimentation rate and t a c h y c a r d i a r e t u r n e d to normal within a shorter period. REFERENCES 1. Huxtable, B. G.: Cerebral rheumatism, Med. J. Aust. 48:220, 1961. 2. Diamond,E. F.: The encephalogram in rheumatic fever, J. A. M. A. 182:685, 1962. 3. Lavy, S., Lavy, R., and Brand: Neurological and electroencephalographic abnormalities in rheumatic fever, Acta Neurol. Scand. 40-76, 1964. 4. Oner,M.: E.EiG. changes in rheumatic patients without neurological findings, Ankara, 1972, Hacettepe University Press.
February, 1976, Vol. 91, No. 2
E E G in acute rheumatic carditis
5. Ozturk, N.: E. E. G. changes in systemiclupus erythematosus and rheumatoid arthritis in children, Ankara, 1973. 6. Johnston, D. A.: Electroencephalogram in Sydenham's chorea, Arch. Neurol, 21:27, 1964. 7. Sezer, A.: E.E.G. changes in rheumatic carditis (thesis) 1973. 8. U . K . and U. S. Joint Report: The natural history of rheumatic fever and rheumatic heart disease: Cooperative clinical trial of ACTH, cortisone and aspirin, Circulation 32:457, 1965.
American Heart Journal
9. Ertugrul, M.: Rheumatic fever and Australia antigen, Lancet 1:507, 1973. 10. Burch, G. E., Giles, T. D , and Colcolough, H. L.: Pathogenesis of "rheumatic heart disease"-Critique and theory, AM. HEART J. 80"556, 1970. 11. Markowitz, M., and Gordis, L.: Rheumatic fever, ed. 2, Philadelphia, 1972, W. B. Saunders Company, p. 71. 12. Renda, Y., Aksoy, M., and Yalaz, K.: Sydenham's chorea and E.E.G. findings, Turk. J. Pediatr. 15:153, 1972. 13. Nyman, G. E.: E.E.G. in rheumatic fever, Acta Med. Scand. 149:126, 1954.
167
