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Electroencephalographic changes in siblings with hypocalcemia due to hypoparathyroidism
CLINICAL A N D
LABORATORY
ELECTROENCEPHALOGRAPHIC WITH
CHANGES
NOTES IN
SIBLINGS
HYPOCALCEMIA DUE TO HYPOPARATHYROIDISM CHR. H~,NSTED, M.D. and S. BaAND'r, M.D.
Electroencephalographieal
Laboratory, Dronning Copenhagen, D e n m a r k
The electroencephalographic changes in patients with idiopathic or postoperative hypoparathyroidism (h.p.) have been studied by Odoriz et al. (1944) and by Gotta and Odoriz (1948). Such changes have also been mentioned by Sutphin et al. (1943), Taubenhaus and Engle (1945) and Mortell (1946). Similar electroencephalographic changes were observed in patients with pseudo-hypoparathyroidism by Albright et al. (1942), Peterman and Garvey (1949) and Eirick et al. (1950). I t has been suggested by Gotta and Odoriz that the changes in the electrical activity of the brain arc caused by alterations in the calcium level. The most common change has been the occurrence of high voltage 2 to 5 per see. potentials, appearing singly or in a series, sometimes interspersed with spikes. The occurrence of pathological potentials is more frequent during hyperpnoea. I f hypoparathyroidism is accompanied by epileptic fits paroxysmal discharges may be found in the record. The changes disappear or considerably diminish when normal serum calcium level has been reestablished. We have made the following clectroencephalographic observations in two siblings with h.p. before and after treatment. TECIINIQUE A six-channel Kaiser electroencephalograph was employed for registration. The placement of electrodes was according to the scheme advocated by Jasper. Electrodes were made as recommended by Gibbs. In unipolar derivations either left or right ear was used for reference. Bipolar leads were also used. Sleep was induced by Persedon (Roche). RESULTS The first patient - - a 19 year old girl - - had been subject to frequent attacks of a tetanic nature since she was 5 or 6 years of age. At the age of 15 these symptoms became complicated by fits which were thought to be petit real and a diagnosis of eryptogenic epilepsy was made. An electroenceph.Mogram ~ s taken at that time, which
Louises Boernehospital,
showed changes similar to those found b) this study. H e r petit real disappeared on phenobarbital medication but the tetanic symptoms remained unchanged. In 1950 she was admitted for further observation to Dronning Louises Boernehospital (Queen Louise's Hospital for Sick Children) where her baby sister had been treated for tetanic symptoms. .k diagnosis of idiopathic hypoparathyroidism was made based ell typical tetanie symptoms, blood chemistry and a negative Howard-Ellsworth's test. (For details see Hansted 1952). She was treated with A.T. 10 and has been free from seizures on maintenance d o s e s now for one year without administration of phenoba rbital. The first electroencephalogram from this patient (EEG no. 187) was taken on a serum ~aleium level between 5.7 and 7.2 rag. per cent. A 6 to 8 per sec. occipital activity was found while awake with moderate shift in frequency and amphtude (fig. 1A, first part). This activity was frequently interrupted or distorted by long runs of 5 per so.:~. waves of medium voltage (100 to ]50 ~tV.). In derivations with right or left ear as a common reference this slow activity appeared in central, parietal and occipital areas only (fig. 1B to 1D). In bipolar longitudinal derivations (1F) this abnormal activity appeared in the fronto-central leads, but was less marked in the rear leads. In transverse runs (1E), on the other hand, temporo-central derivations showed this slow activity synchronously on both sides. Circular runs (1G) showed this abnormal activity most nmrked in the temporo-occipital areas, here distorting the alpha-frequency. Short generalized paroxysmal discharges of even higher and slower potentials appeared occasionally overlapping the abnormal activity and such discharges were also been interrupting the more regular dominant 6 to 8 per see. activity (fig. 1A, last part). Sleep and hyperpnoca added no further information of significance. After treatment with A.T. 1O two new EEGs were taken (no. 205 and 2 1 1 ) , o n e on a serum calcium level of 8.8 rag. per cent, the other on a calcium level between 9.4 and 10,2 rag. per cent. As
[ lOl ]
102
CItR. I I A N S T E I )
a n d S. B R A N D T
these two E E G s were practically identical only tile l a t t e r will be described in detail. T h i s record showed a f a i r l y r e g u l a r 9 to 10 p e r see. a c t i v i t y in all leads ( f i g . 2 A ) . I n a few places very s h o r t periods of m e d i u m - - rarely h i g h - a m p l i t u d e 5 to 6 p e r sec. waves were seen. D u r i n g h y p e r p n o e a some s h o r t p a r o x y s m a l generalized disc h a r g e s a n d slow p o t e n t i a l s were induced ( f i g . 2 B ) . Sleep s t u d i e s a d d e d no f u r t h e r i n f o r m a t i o n . T h e seco~Ld p a t i e z ~ t - - s i s t e r to the f i r s t one - w:is a 2t,~ y e a r old girl, one of a l):dr of m o n o z y g o t i e
r e - a d m i t t e d two m o n t h s later with s y m p t o m s of t e t a n y b u t w i t h o u t s i g n s of ricketts. T h i s t i m e blood c h e m i s t r y c o n f i r m e d tile d i a g n o s i s : idiopathic h y p o p a r a t h y r o i d i s m . She h a s been free of s y m p t o m s for one y e a r on t r e a t m e n t with A.T. 10. E E G f r o m t h i s child (no. 1 1 9 - - t a k e n on a s e r u m calcium level of 5.5 m g . p,*r cent - - while awake showed a n a c t i v i t y e o n s i s t i ~ g m a i n l y of irr e g u l a r 4 to 5 per sec. w a v e s of m e d i u m to h i g h voltage a n d with several 2 till 3 per sec. p o t e n t i a l s of high a m p l i t u d e in the occipita a r e a s ( f i g . 3). '~ 5
LC,
L-
"i C
LR
RO.- Rf~L £~
~ -~-~~D
RT,,~L E~
~E
LF," LC,
Lr~o~.LT~ LT~-. LC~
LC,-~L P~
RC~'*RT~ RT, ~ R E ~
~t2/( t:::-~¢J~,fV,t~t:/,
LT~*LF,
4G
LF, ~RF~
LP~" LO~
LC ~RC~
L -~ R E ~
4F
RF~-~RC~
RT~-~RO~
RC~,"~RP~
RO:",LO, LO, " LT~
~,---,---'~~'-
Fig. 1 ( h - G) E E G f r o m B.C., ]9 y e a r s old, t a k e n on a s e r u m caleimn level between 5.7 a n d 7.2 rag. per cent. A : Generalized p a r o x y s a m l d i s c h a r g e of h i g h v o l t a g e 2 to 3 per sec. w a v e s i n t e r r u p t i n g an occipital r h y t h m of 6 to 8 per see. waves. ( N o t e : T h e p e n of t h e ~econd c h a n n e l is n o t q u i t e in line, b e i n g a p p r o x i m a t e l y 50 msee. behind)'. B - G : L o n g periods of 5 per see. m e d i u m voltage waves of h i g h e s t a m p l i t u d e in either f r o n t o - t e m p o r a l a r e a s or in p a r i e t o - e e n t r a l areas.
twins. She w a s a d m i t t e d in t h e S p r i n g of 1950 to D r o n n i n g L o u i s e ' s B e e r n e h o s p i t a l because of r i e k e t t s a n d t e t a n y . Blood c h e m i s t r y , i n c l u d i n g blood phosp h a t a s e w a s in accordance w i t h t h i s diagnosis. J u s t b e f o r e a d m i s s i o n t h i s child h a d f i t s w i t h tonie-elonie convulsions followed b y uneonscioumaese l a s t i n g f r o m 5 to 10 m i n . She w a s c u r e d a f t e r t r e a t m e n t with calcium a u d a t o t a l of 200.000 u n i t s o f V i t a m i n D. A f t e r d i s c h a r g e she received 1.000 t m l t s V i t a m i n D daily. I n s p i t e o f t h i s t r e a t m e n t t h e child was
D u r i n g sleep no distinct a b n o r m a l i t i e s a p p e a r e d p a r t i c u l a r l y no a b n o r m a l p a r o x y s m a l discharges. A f t e r t r e a t m e n t a new E E G w a s t a k e n on a s e r u m calcium level b e t w e e n 8.3 a n d 9.7 rag. p e r cent. T h i s w a s a b o u t t h r e e weeks l a t e r ( E E G no. 192). T h e curve h a d c h a n g e d r e m a r k a b l y ( f i g . 4 ) . A n a c t i v i t y of a b o u t 5 to 6 p e r see. w a s f o u n d of h i g h e s t v o l t a g e in the c e n t r a l leads. T h e p r e d o m i n a n t a n d v e r y slow occipital w a v e s seen at t h e f i r e t e x a m i n a t i o n were no l o n g e r evident.
103
THE EEG I N I I Y P O P A R A T H Y R O I D I S M For comparison an EEG was taken on the p a t i e n t ' s twin sister who was completely well and had shown normal blood chemistry. This record - taken on a calcium level of 10.4 rag. per cent - demonstrated an activity of 5 to 6 per see. with the highest voltage in the central areas. This EEG was regarded as normal for a 2]/., year old child and showed a remarkably similarity to the sister's EEG taken after treatment, illustrated in figure 4.
alographic observations as to the question which of these two possibilities may be the right one. The abnormality disappeared after the re-establishment of a normal serum calcium level. In this patient the EEG too showed short paroxysmal discharges, which L.F. - R.E~*,
A L£
-
..,.
~..c. ~
g.£,,',-.
,,t [. - P. ~,.+
Lr.. - It.Eo,..+ R.¢. - R E ~ LO,
- R.E--..
R O
- R.~,~.
_
$ l~,
^
-
_
_
_ _ , + +
B
D " ~
A
+4+=
o
Fig. 3 EEG from M.C., 21/: years old, on a serum calcium level of 5.5 mg. per cent, showing irreg~flar activity of mainly 4 to 5 per sec. waves with a ~reat deal of high voltage 2 to 3 per sec. potentials.
L P. - R ~ - .
R.F'. -
g~
+
did not disappear completely when the serum calcium had returned to normal. These latter changes may be symptomatic of an epileptic disposition, since petit mal seizures had been rcport,~d. None of the EEGs from this patient were, how:.ver, typical
8.1~" R. [,ffi',..
4 .tcr_
Fig. 2 ( A - B ) EEG from B.C., 19 years old, taken on a serum calcium level between 9.4 and 10.2 rag. per cent. Regular 9 to 10 per s~c. activity. A f t e r 50 sec. hyperpnoea short generalized paroxysmal discharge (B). DISCUSSION In two patients with idiopathic hypoparathyroidism the EEO showed abnormal slow activity. The slow activity in an adult patient appeared in long periods interrupting a normal rhythm. Although bilateral synchronous, this abnormal 5 per see. activity has a certain focal character. The placement of the generator must be either anteriorly, projecting to the frontal and temporal areas, making also ears active, or posteriorly, projeeting to the central, parietal and oecipit~al areas. We do not feel that any further conclusions m a y be drawn from the electroenceph-
L.O "R.e~-.
/
I+.c~ - R . E ~
L
~
+. + . .
Fig. 4 EEG from M.C., 2 ~ years old, on a serum calcium level between 8.3 and 9.7 rag. per cent, showing normal 5 to 6 per see. activity of maximum voltage in central leads. for petit mal (i.e. contained long bursts of 3 per see. spikes and waves). In the other patient, 2 ~ y e a r of age, the EEG showed diffuse slowing with a low calcium blood level but normal frequencies for the age after treatment with A.T. 10.
104
CHR. H A N S T E D and S. BRANDT
SUMMARY In two siblings with idiopathic hypoparathyroidism - - aged 19 and 21/.2 years - - the EEG showed widespread slow activity, which disappeared a f t e r the serum calcium level had returned to normal values. I n the adult patient who had had attacks suggestive of petit real paroxysmal discharges persisted even after treatment. Both patients have been free from tetanic symptoms after treatment with A.T. 10. No antiepileptic medication has been neeessary. REFERENCES ALBRIGHT, F., BURNETT, C. H., S:~ITH, P. I]~. and PARSON, W. Pseudo-hypoparathyroidism - - an example of L, Seabright-Bantam's ' ' syndrome. Endocrinology/, 1942, 30: 922-932. EIRICK~ H.~ ALBRIGIIT, F., BARTTER, F. (]., FORBES, A. P. and REEVES, J. D. Further studies on pseudo-hypoparathyroidism: Report of four new cases. Acta Endovrinologica, 1950, 5: ]99225.
GOTTA, H. and ODORIZ,J. B. The electroencephalogram in hypoparathyroidism with tetany and epilepsy. J. Clin. Endocrinology, 1948, 8: 674686. HA•STED, CHE. Fejldiagnoser ved idiopatisk hypoparathyreoidisme. Ugeskrift for Lewger, 19§2, 114: 840-844. MORTELL, E. J. Idiopatie hypoparathyroidism with mental deterioration: E f f e c t of treatment on intellectual function. J. C l i n Endocrinology, 1946, 6: 266-274. ODORIZ, J. B., MANFREDI, J. Po and DE LA BALZE, J. F. Parathyroid insufficiency and the human electroencephalogram. J. C l i n Endocrinology~ 1944, 4: 493-499. PETERMAN, M. G. and GARVEY, M. ]). Pseudohyperparathyroiclism. Pediatrics, 1949, 4: 790-797. SUTPmN, A., ALBRmHT, F. and McCuNE, D. J. Five cases (three in siblings) of idiopatic bypoparathyroidism associated with moniliasis. J. Clin. Endocrinology, 1943, 3: 625-634. TAURENHAUS, M. and ENGLE, H. :M. Clinical observations on a case of idiopatie tetany and epilepsy. J. C$in. Endocrinology, 1945, 5: 147-150.
Refercnw: H.~STlm, CHR. and BRANIr$, S. Electroeneephalographic changes in siblings with hypoealcemia due to hypoparathyroidism. EEG Clan. Neltrophysiol., 1963, 5: 101-104.
LABORATORY
ELECTROENCEPHALOGRAPHIC WITH
CHANGES
NOTES IN
SIBLINGS
HYPOCALCEMIA DUE TO HYPOPARATHYROIDISM CHR. H~,NSTED, M.D. and S. BaAND'r, M.D.
Electroencephalographieal
Laboratory, Dronning Copenhagen, D e n m a r k
The electroencephalographic changes in patients with idiopathic or postoperative hypoparathyroidism (h.p.) have been studied by Odoriz et al. (1944) and by Gotta and Odoriz (1948). Such changes have also been mentioned by Sutphin et al. (1943), Taubenhaus and Engle (1945) and Mortell (1946). Similar electroencephalographic changes were observed in patients with pseudo-hypoparathyroidism by Albright et al. (1942), Peterman and Garvey (1949) and Eirick et al. (1950). I t has been suggested by Gotta and Odoriz that the changes in the electrical activity of the brain arc caused by alterations in the calcium level. The most common change has been the occurrence of high voltage 2 to 5 per see. potentials, appearing singly or in a series, sometimes interspersed with spikes. The occurrence of pathological potentials is more frequent during hyperpnoea. I f hypoparathyroidism is accompanied by epileptic fits paroxysmal discharges may be found in the record. The changes disappear or considerably diminish when normal serum calcium level has been reestablished. We have made the following clectroencephalographic observations in two siblings with h.p. before and after treatment. TECIINIQUE A six-channel Kaiser electroencephalograph was employed for registration. The placement of electrodes was according to the scheme advocated by Jasper. Electrodes were made as recommended by Gibbs. In unipolar derivations either left or right ear was used for reference. Bipolar leads were also used. Sleep was induced by Persedon (Roche). RESULTS The first patient - - a 19 year old girl - - had been subject to frequent attacks of a tetanic nature since she was 5 or 6 years of age. At the age of 15 these symptoms became complicated by fits which were thought to be petit real and a diagnosis of eryptogenic epilepsy was made. An electroenceph.Mogram ~ s taken at that time, which
Louises Boernehospital,
showed changes similar to those found b) this study. H e r petit real disappeared on phenobarbital medication but the tetanic symptoms remained unchanged. In 1950 she was admitted for further observation to Dronning Louises Boernehospital (Queen Louise's Hospital for Sick Children) where her baby sister had been treated for tetanic symptoms. .k diagnosis of idiopathic hypoparathyroidism was made based ell typical tetanie symptoms, blood chemistry and a negative Howard-Ellsworth's test. (For details see Hansted 1952). She was treated with A.T. 10 and has been free from seizures on maintenance d o s e s now for one year without administration of phenoba rbital. The first electroencephalogram from this patient (EEG no. 187) was taken on a serum ~aleium level between 5.7 and 7.2 rag. per cent. A 6 to 8 per sec. occipital activity was found while awake with moderate shift in frequency and amphtude (fig. 1A, first part). This activity was frequently interrupted or distorted by long runs of 5 per so.:~. waves of medium voltage (100 to ]50 ~tV.). In derivations with right or left ear as a common reference this slow activity appeared in central, parietal and occipital areas only (fig. 1B to 1D). In bipolar longitudinal derivations (1F) this abnormal activity appeared in the fronto-central leads, but was less marked in the rear leads. In transverse runs (1E), on the other hand, temporo-central derivations showed this slow activity synchronously on both sides. Circular runs (1G) showed this abnormal activity most nmrked in the temporo-occipital areas, here distorting the alpha-frequency. Short generalized paroxysmal discharges of even higher and slower potentials appeared occasionally overlapping the abnormal activity and such discharges were also been interrupting the more regular dominant 6 to 8 per see. activity (fig. 1A, last part). Sleep and hyperpnoca added no further information of significance. After treatment with A.T. 1O two new EEGs were taken (no. 205 and 2 1 1 ) , o n e on a serum calcium level of 8.8 rag. per cent, the other on a calcium level between 9.4 and 10,2 rag. per cent. As
[ lOl ]
102
CItR. I I A N S T E I )
a n d S. B R A N D T
these two E E G s were practically identical only tile l a t t e r will be described in detail. T h i s record showed a f a i r l y r e g u l a r 9 to 10 p e r see. a c t i v i t y in all leads ( f i g . 2 A ) . I n a few places very s h o r t periods of m e d i u m - - rarely h i g h - a m p l i t u d e 5 to 6 p e r sec. waves were seen. D u r i n g h y p e r p n o e a some s h o r t p a r o x y s m a l generalized disc h a r g e s a n d slow p o t e n t i a l s were induced ( f i g . 2 B ) . Sleep s t u d i e s a d d e d no f u r t h e r i n f o r m a t i o n . T h e seco~Ld p a t i e z ~ t - - s i s t e r to the f i r s t one - w:is a 2t,~ y e a r old girl, one of a l):dr of m o n o z y g o t i e
r e - a d m i t t e d two m o n t h s later with s y m p t o m s of t e t a n y b u t w i t h o u t s i g n s of ricketts. T h i s t i m e blood c h e m i s t r y c o n f i r m e d tile d i a g n o s i s : idiopathic h y p o p a r a t h y r o i d i s m . She h a s been free of s y m p t o m s for one y e a r on t r e a t m e n t with A.T. 10. E E G f r o m t h i s child (no. 1 1 9 - - t a k e n on a s e r u m calcium level of 5.5 m g . p,*r cent - - while awake showed a n a c t i v i t y e o n s i s t i ~ g m a i n l y of irr e g u l a r 4 to 5 per sec. w a v e s of m e d i u m to h i g h voltage a n d with several 2 till 3 per sec. p o t e n t i a l s of high a m p l i t u d e in the occipita a r e a s ( f i g . 3). '~ 5
LC,
L-
"i C
LR
RO.- Rf~L £~
~ -~-~~D
RT,,~L E~
~E
LF," LC,
Lr~o~.LT~ LT~-. LC~
LC,-~L P~
RC~'*RT~ RT, ~ R E ~
~t2/( t:::-~¢J~,fV,t~t:/,
LT~*LF,
4G
LF, ~RF~
LP~" LO~
LC ~RC~
L -~ R E ~
4F
RF~-~RC~
RT~-~RO~
RC~,"~RP~
RO:",LO, LO, " LT~
~,---,---'~~'-
Fig. 1 ( h - G) E E G f r o m B.C., ]9 y e a r s old, t a k e n on a s e r u m caleimn level between 5.7 a n d 7.2 rag. per cent. A : Generalized p a r o x y s a m l d i s c h a r g e of h i g h v o l t a g e 2 to 3 per sec. w a v e s i n t e r r u p t i n g an occipital r h y t h m of 6 to 8 per see. waves. ( N o t e : T h e p e n of t h e ~econd c h a n n e l is n o t q u i t e in line, b e i n g a p p r o x i m a t e l y 50 msee. behind)'. B - G : L o n g periods of 5 per see. m e d i u m voltage waves of h i g h e s t a m p l i t u d e in either f r o n t o - t e m p o r a l a r e a s or in p a r i e t o - e e n t r a l areas.
twins. She w a s a d m i t t e d in t h e S p r i n g of 1950 to D r o n n i n g L o u i s e ' s B e e r n e h o s p i t a l because of r i e k e t t s a n d t e t a n y . Blood c h e m i s t r y , i n c l u d i n g blood phosp h a t a s e w a s in accordance w i t h t h i s diagnosis. J u s t b e f o r e a d m i s s i o n t h i s child h a d f i t s w i t h tonie-elonie convulsions followed b y uneonscioumaese l a s t i n g f r o m 5 to 10 m i n . She w a s c u r e d a f t e r t r e a t m e n t with calcium a u d a t o t a l of 200.000 u n i t s o f V i t a m i n D. A f t e r d i s c h a r g e she received 1.000 t m l t s V i t a m i n D daily. I n s p i t e o f t h i s t r e a t m e n t t h e child was
D u r i n g sleep no distinct a b n o r m a l i t i e s a p p e a r e d p a r t i c u l a r l y no a b n o r m a l p a r o x y s m a l discharges. A f t e r t r e a t m e n t a new E E G w a s t a k e n on a s e r u m calcium level b e t w e e n 8.3 a n d 9.7 rag. p e r cent. T h i s w a s a b o u t t h r e e weeks l a t e r ( E E G no. 192). T h e curve h a d c h a n g e d r e m a r k a b l y ( f i g . 4 ) . A n a c t i v i t y of a b o u t 5 to 6 p e r see. w a s f o u n d of h i g h e s t v o l t a g e in the c e n t r a l leads. T h e p r e d o m i n a n t a n d v e r y slow occipital w a v e s seen at t h e f i r e t e x a m i n a t i o n were no l o n g e r evident.
103
THE EEG I N I I Y P O P A R A T H Y R O I D I S M For comparison an EEG was taken on the p a t i e n t ' s twin sister who was completely well and had shown normal blood chemistry. This record - taken on a calcium level of 10.4 rag. per cent - demonstrated an activity of 5 to 6 per see. with the highest voltage in the central areas. This EEG was regarded as normal for a 2]/., year old child and showed a remarkably similarity to the sister's EEG taken after treatment, illustrated in figure 4.
alographic observations as to the question which of these two possibilities may be the right one. The abnormality disappeared after the re-establishment of a normal serum calcium level. In this patient the EEG too showed short paroxysmal discharges, which L.F. - R.E~*,
A L£
-
..,.
~..c. ~
g.£,,',-.
,,t [. - P. ~,.+
Lr.. - It.Eo,..+ R.¢. - R E ~ LO,
- R.E--..
R O
- R.~,~.
_
$ l~,
^
-
_
_
_ _ , + +
B
D " ~
A
+4+=
o
Fig. 3 EEG from M.C., 21/: years old, on a serum calcium level of 5.5 mg. per cent, showing irreg~flar activity of mainly 4 to 5 per sec. waves with a ~reat deal of high voltage 2 to 3 per sec. potentials.
L P. - R ~ - .
R.F'. -
g~
+
did not disappear completely when the serum calcium had returned to normal. These latter changes may be symptomatic of an epileptic disposition, since petit mal seizures had been rcport,~d. None of the EEGs from this patient were, how:.ver, typical
8.1~" R. [,ffi',..
4 .tcr_
Fig. 2 ( A - B ) EEG from B.C., 19 years old, taken on a serum calcium level between 9.4 and 10.2 rag. per cent. Regular 9 to 10 per s~c. activity. A f t e r 50 sec. hyperpnoea short generalized paroxysmal discharge (B). DISCUSSION In two patients with idiopathic hypoparathyroidism the EEO showed abnormal slow activity. The slow activity in an adult patient appeared in long periods interrupting a normal rhythm. Although bilateral synchronous, this abnormal 5 per see. activity has a certain focal character. The placement of the generator must be either anteriorly, projecting to the frontal and temporal areas, making also ears active, or posteriorly, projeeting to the central, parietal and oecipit~al areas. We do not feel that any further conclusions m a y be drawn from the electroenceph-
L.O "R.e~-.
/
I+.c~ - R . E ~
L
~
+. + . .
Fig. 4 EEG from M.C., 2 ~ years old, on a serum calcium level between 8.3 and 9.7 rag. per cent, showing normal 5 to 6 per see. activity of maximum voltage in central leads. for petit mal (i.e. contained long bursts of 3 per see. spikes and waves). In the other patient, 2 ~ y e a r of age, the EEG showed diffuse slowing with a low calcium blood level but normal frequencies for the age after treatment with A.T. 10.
104
CHR. H A N S T E D and S. BRANDT
SUMMARY In two siblings with idiopathic hypoparathyroidism - - aged 19 and 21/.2 years - - the EEG showed widespread slow activity, which disappeared a f t e r the serum calcium level had returned to normal values. I n the adult patient who had had attacks suggestive of petit real paroxysmal discharges persisted even after treatment. Both patients have been free from tetanic symptoms after treatment with A.T. 10. No antiepileptic medication has been neeessary. REFERENCES ALBRIGHT, F., BURNETT, C. H., S:~ITH, P. I]~. and PARSON, W. Pseudo-hypoparathyroidism - - an example of L, Seabright-Bantam's ' ' syndrome. Endocrinology/, 1942, 30: 922-932. EIRICK~ H.~ ALBRIGIIT, F., BARTTER, F. (]., FORBES, A. P. and REEVES, J. D. Further studies on pseudo-hypoparathyroidism: Report of four new cases. Acta Endovrinologica, 1950, 5: ]99225.
GOTTA, H. and ODORIZ,J. B. The electroencephalogram in hypoparathyroidism with tetany and epilepsy. J. Clin. Endocrinology, 1948, 8: 674686. HA•STED, CHE. Fejldiagnoser ved idiopatisk hypoparathyreoidisme. Ugeskrift for Lewger, 19§2, 114: 840-844. MORTELL, E. J. Idiopatie hypoparathyroidism with mental deterioration: E f f e c t of treatment on intellectual function. J. C l i n Endocrinology, 1946, 6: 266-274. ODORIZ, J. B., MANFREDI, J. Po and DE LA BALZE, J. F. Parathyroid insufficiency and the human electroencephalogram. J. C l i n Endocrinology~ 1944, 4: 493-499. PETERMAN, M. G. and GARVEY, M. ]). Pseudohyperparathyroiclism. Pediatrics, 1949, 4: 790-797. SUTPmN, A., ALBRmHT, F. and McCuNE, D. J. Five cases (three in siblings) of idiopatic bypoparathyroidism associated with moniliasis. J. Clin. Endocrinology, 1943, 3: 625-634. TAURENHAUS, M. and ENGLE, H. :M. Clinical observations on a case of idiopatie tetany and epilepsy. J. C$in. Endocrinology, 1945, 5: 147-150.
Refercnw: H.~STlm, CHR. and BRANIr$, S. Electroeneephalographic changes in siblings with hypoealcemia due to hypoparathyroidism. EEG Clan. Neltrophysiol., 1963, 5: 101-104.