Convulsions in children

CONVULSIONS IN CHILDREN ttAams HOSEN, lV[.D. NEW OaLEANS, LA. n

CONVULSION is a series of involuntary contractions of a group or several groups of muscles usually associated with a loss of consciousness. Initiated by various stimuli, convulsions originate in the motor area of the cortex, which transmits impulses through the brain to the anterior horn cells of the spinal cord and finally to the muscles. This symptom-complex, though occurring during all stages of life, is notoriously frequent in children, the frequency of which is inversely propositional to the age of the child. A s the child grows older, the incidence of convulsions gradually decreases so tlhat t hey are relatively infrequent after six years of life. Morse 1 explains the frequency of infantile convulsions by the following two factors: a. In infancy there is a rapid growth of the brain, which makes it more vulnerable and irritable than its slower growing neighbors. b. The higher cerebral centers , inhibitory in action, are imperfectly developed in infancy and childhood and are thus less able to restrain discharges from lower centers than when perfect development occurs. That heredity undoubtedly plays some part in the selective action in the development of convulsions offers an explanation for the absence of this symptom-complex in some children and its presence in others. Children born of neurotic parents have a greater tendency to suffer from convulsive attacks than children who have a more stable family background. The exciting causes of convulsions are five in number, namely: toxic, organic, epileptic, reflex, and metabolic. 1. Toxic.-a. The onset of acute infectious diseases is often ushered in by convulsions. This usually occurs after the first three years of life. b. Autointoxication is a very frequent causative factor, especially in children under four years of age. c. Acute disease of the nervous system causes the severest type of convulsions I f convulsions persist in spite of symptomatic treatment, a diagnostic spinal puncture should be made. d. Toxic convulsions in the newborn, though relatively infrequent, are usually due to the presence of bacterial infections involving the skin, nasopharynx, or umbilicus. A more infrequent cause is the absorption of toxins through the circulation or milk of ec]amptie mothers. Lead poisoning caused by a nipple shield or salves on the nipples of the mother is a possible cause. An enlarged thymus (classed as F r o m the Touro I n f i r m a r y . 636

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~oxic or r e f l e x ) i s an i n f r e q u e n t factor. Syphilis is seldom a cause. 2. O r g a n i c . - - T h i s is the m o s t f r e q u e n t cause of convulsions in the n e w b o r n and is usually m a n i f e s t e d within the first m o n t h of life. a. I n t r a c r a n i a l h e m o r r h a g e , t r a u m a t i c or due to a s p h y x i a f r o m a p r o l o n g e d a n d difficult labor or associated with a h e m o r r h a g i c diathesis, is the m o s t comnlon cause. The convulsions m a y be either clonie or tonic, usualJy a p p e a r i n g w i t h i n the first f o r t y - e i g h t hours of life. B e t w e e n convulsions the p a t i e n t is drowsy, refuses to nurse, a n d :has a feeble cry a n d a possible b u l g i n g of the fontanel. The spinal fluid shows gross blood or a x a n t h o c h r o m i c fluid due to the destinlction of the r e d blood cells. The absence of blood m a y indicate the presence of h e m o r r h a g e within the b r a i n substance. b. Congenital anomalies are i n f r e q u e n t causes. 3. I d i o p a t h i c E p i l e p s y . - - A c c o r d i n g to B o y e r " a seizure to be t r u l y e p i l e p t i f o r m m u s t be transient, m u s t i m p a i r or cause loss of consciousness a n d m u s t u l t i m a t e l y result in some change, h o w e v e r slight, in the p e r s o n a l i t y of the p a t i e n t . " This t y p e of convulsion is not accomp a n i e d b y a n y visible pathologic features. I t occurs most f r e q u e n t l y b e t w e e n the ages of five a n d ten years. 4. R e f l e x . - - T h i s f a c t o r is almost negligible, in spite of the l a r g e n u m b e r of eases a t t r i b u t e d to teething, worms, phimosis, and foreign bodies in the ear or nose. Teething a t the m o s t will cause slight fever, n a s o p h a r y n g i t i s , otitis media, anorexia, a n d some restlessness. An e n l a r g e d t h y m u s which m a y be classed as either toxic or reflex is an i n f r e q u e n t cause. 5. 3/ietabolie.--Spasmophilia or t e t a n y composes the metabolic group. I t occurs most f r e q u e n t l y in children between eight a n d t h i r t y - s i x m o n t h s of age. I t s seasonal incidence is usually f r o m M a y to June. The calcium content of the blood s t r e a m is usually below 7.5 rag., and often 5 rag., p e r 100 c.c. of blood. The a t t a c k s occur s p o n t a n e o u s l y w h e n the calcium level is as low as 7 rag. p e r 100 c.e. of blood. L a t e n t tetany, the calcium content of which is less t h a n 8.5 rag., is m a d e active w h e n an a d d e d i m p e t u s is present, as slight toxemias, constipation, etc. The etiology of convulsions has been v a r i o u s l y t r e a t e d b y m a n y writers, most of w h o m m a k e the general s t a t e m e n t t h a t the m a j o r i t y of convulsions in children are based on the presence of a latent t e t a n y . I n forty-five eases of convulsions at Touro I n f i r m a r y p e r s o n a l l y observed or i n v e s t i g a t e d d u r i n g a five-year period, the f r e q u e n c y of latent t e t a n y is not substantiated. Of the forty-five cases, eighteen were diagnosed as autointoxication, t h r e e epilepsy, five tetany, one cerebrospinal i n j u r y , one acute tonsillitis, one syphilis, and sixteen as " c o n v u l s i o n s " (no etiological diagnosis).

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Calcium and phosphorus determinations permitted a diagnosis of tetany in five, or II.I per cent of these cases. Whaley, ~4 chemist at Touro Infirmary for the past ten years, states that he has observed only a minor connection between convulsions and latent tetany. As shown by the clinical picture and laboratory findings in this series, the illnesses were for the most part mild in nature. These are the minor disturbances which are usnally classed as the initiators of convulsions in cases of latent tetany. In this series the calcium and phosphorus determinations are used as the criteria for the diagnosis of tetany although the writer realizes that occasionally true tetany occurs when the calcium is normal. In such cases there is a negative calcium balance in which more calcium is excreted than consumed. The importance of this is negligible because of its infrequency. The normal calcium is assmned to be from 9 to Ii rag. per I00 c.c. blood, this being based on the findings of Trumper and Cantarow ~ and Eng]ebach2 The normal phosphorus level in children is from 4 to 6 rag. per i00 c.c. of blood. A calcium level of 8.5 rag. or less is assumed as a basis for a diagnosis of tetany. TABLE,

I NU/~{BER AVERAGE POSITIVI CALCIP]KOS WASSER' UM PIIORUS MANN

NUMBE~ AVERAG~ AVER~GEI DIFFERTEMPER0F W.B.C. [ ENTIAL CASES A,TUR~ 18

1. A u t o i n t o x i c a tion

-

102 ~

AVERAGE AGE

10,8 - 5.5

1

3 yr.

11.i

0

5 yr.

L 3 9 _ _

_ _

E 1

2. E p i l e p s y

98 ~

-

5.3

L39

3. T e t a n y

7.7 - 3.8

]00 o

2 yr.

;L48 EP, 4. C e r e b r o s p i n a l injury 5. A c u t e tonsi].litis

-

--~--

~l-NTO

I

9.0 - 3.9 11.1

5ao

6. C o n v u l s i o n s L44 E3 7. S y p h i l i s

98~

0

I~ too.

0

8 too.

Lso

6,000 I

N69 L31

[

I

i lo2 ~

I

'

I I

98 ~ I

-

5.2

10.8 - 5.0

489 yr.

10.0 - 4.9

4 yr.

I

I t is g e n e r a l l y a g r e e d t h a t t e t a n y is i n t i m a t e l y associated with rickets. Consequently there is a t e n d e n c y to diagnose as l a t e n t t e t a n y most of the eases of convulsions in which there are signs of rickets. T r m n p e r a n d C a n t a r o w 2 stress the f a c t t h a t in the g r e a t m a j o r i t y of eases of rickets the serum calcium is within n o r m a l limits, the m o s t p r o m i n e n t f e a t u r e being a decrease in the level of the serum phosphate. In some instances, however, h y p o e a l e e m i a occurs with manifestations of t e t a n y .

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Thus it is seen t h a t while t e t a n y is almost a l w a y s associated w i t h rickets, rickets is i n f r e q u e n t l y associated w i t h a low serum calcium and, consequently, tetany. On this basis the careless diagnosis of l a t e n t t e t a n y based on the presence of rickets should be l a r g e l y disregarded. The d a m a g e sustained b y the central nervous system as a result of convulsions is an i m p o r t a n t consideration in t:he light of clinical investigation. The time-honored s t a t e m e n t of m a n y pediatricians and general p r a c t i t i o n e r s t h a t convulsions in children need not be considered seriously is u n w a r r a n t e d , as there seems to be a relation bet w e e n infantile convulsions and b r a i n damage. B u t it must be borne in m i n d t h a t the convulsion m a y be a s y m p t o m of a d a m a g e d n e r v o u s system or t h a t the convulsion m a y h a v e p r o d u c e d the damage. I n a series of 265 unseleeted cases with a h i s t o r y of infantile convulsions Thorn ~ found 29 p e r cent to be mentally deficient, or epileptie. StilP h a s p o i n t e d out t h a t a e o m p a r a t i v e l y small n u m b e r of the individuals who h a v e convulsions ever become epileptie. On the other h a n d Osler 6 f o u n d t h a t 40 p e r cent of the cases u n d e r his observation which w e r e diagnosed as epileptic g a v e a h i s t o r y of infantile convulsions. General statistics compiled b y neurologists show t h a t 22 per cent of the eases of infantile convulsions l a t e r develop epilepsy as c o m p a r e d to the p e d i a t r i c i a n s ' statisties showing 7 per eent. One case observed b y the w r i t e r stresses the p r i m e i m p o r t a n c e of convulsions as related to b r a i n damage, a n d c o n s e q u e n t l y the f u t u r e w e l f a r e of the individual. This patient, a g e d nine months, h a d a severe a t t a c k of convulsions lasting a b o u t one h o u r ; they were eaused a p p a r e n t l y b y intestinal influenza. T w e n t y - f o u r hours l a t e r a spastic h e m i p l e g i a developed. A f t e r a w e e k a p a r t i a l r e t u r n of a c t i v i t y occurred. A t the present time six months h a v e elapsed with a complete r e t u r n to n o r m a l i t y as f a r as ean be observed. W h a t the m e n t a l cap a c i t y in the f u t u r e will be is y e t to be determined. I n this ease an evident cerebral h e m o r r h a g e occurred. One can only surmise the frequency of minute, unreeognizab]e h e m o r r h a g e s sustained in convulsions. I n the light of such findings infantile convulsions should b e looked u p o n m o r e seriously a n d a g r e a t e r effort be m a d e to p r e v e n t t h e i r occurrence during e a r l y life. I n this w a y m u c h epilepsy and m e n t a l defleieney will be prevented. The t r e a t m e n t of convulsions should aim t o w a r d an early dissolution of the s y m p t o m s for the sake of the w e l f a r e of the child a n d the relief of the m e n t a l strain of the family. The first p a r t of the t r e a t m e n t consists of a cold b a t h w h e n f e v e r is p r e s e n t or a w a r m b a t h w h e n the t e m p e r a t u r e is normal. This is t h e n followed by a high enema.

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I f relief is not obtained at once, the free use of d r u g s should be instituted, n a m e l y : morphine, chloral h y d r a t e , sodium b r o m i d e or luminal. Chloral h y d r a t e in combination with the b r o m i d e is well t o l e r a t e d b y i n f a n t s ; no h e s i t a n c y should be felt in r e p e a t i n g the dose as often as necessary. The c o m b i n a t i o n of chloral h y d r a t e a n d bromide is best a d m i n i s t e r e d b y rectum. I f good results are not o b t a i n e d in a short time, the use of c h l o r o f o r m or ether is s t r o n g l y recommended. The f a c t t h a t the l o n g e r the convulsion lasts, the g r e a t e r is tlle chance of d a m a g e to the n e r v o u s system, should be b o r n e in mind. Continuous muscle t w i t c h i n g not relieved b y the a b o v e - m e n t i o n e d t r e a t m e n t is an indication f o r a spinal puncture. This is of more diagnostic t h a n t h e r a p e u t i c use. As soon as possible, a p u r g a t i v e should be t h e n given the patient. A f t e r complete relief of the s y m p t o m s , a diagnosis should be m a d e a n d t r e a t m e n t instituted. Cases w i t h d o u b t f u l etiology should be given the benefit of detailed l a b o r a t o r y investigation. In this w a y v a g u e conditions m a y be relieved thus p r e v e n t i n g f u t u r e a t t a c k s of convulsions with subsequent m e n t a l d e t e r i o r a t i o n a n d epilepsy. CONCLUSIONS

1. The exciting causes of convulsions are five in number, n a m e l y : toxic, organic, epileptic, reflex, and metabolic. 2. L a t e n t t e t a n y is an i n f r e q u e n t cause of convulsions. 3. I n forty-five cases of convulsions t e t a n y was p r e s e n t in five, or 11.1 p e r cent. 4. ~_ diagnosis of t e t a n y or l a t e n t t e t a n y should be m a d e only when there is less t h a n 8.5 mg. of calcium p e r 100 e.c. of blood. 5. Convulsions as a possible cause of epilepsy and m e n t a l deterioration are to be stressed. 6. I m m e d i a t e control of convulsions is necessary to decrease the incidence of d a m a g e to the n e r v o u s system. REFERENCES i. Morse, J. IJ.: Am. J. Dis. Child. 19: 73, 1919. 2. Trumper~ M., Cantarow, A.: Biochemistry in Internal IViedicine, Philadelphia, 1932, W. B. Saunders Co. 3. Engelbaeh, W. : Endocrine Medicine, Vol. 2, Springfield, Ill.: 1932, C. C. Thomas. 4. Them, D.A.: Am. 5. Psyehiat. 6:6137 1927. 5. Still, C. F.: Common Disorders and Diseases of Childhood, London~ 1920, :Frowde. 6. Osler, W., McCrae) T. : The Principle and Practice of Medicine, ~ e w York, ]912, D. Appleton and Co. 7. Burr, O . W . : Arch. Pedlar. 39: 303, 1922. 8. Walton, G. L., Carter, C . Y . : Boston IV[. & S. J. 125: 485~ 1891. 9. ~r J. L.: J . A. M. A. 78: 175~ 1922. 10. Turner, A . J . : M. J. AustrMia 2: 203, 1922. 11. Buffum, W. T., Jr.: l~hod~ Isla.n4 ~ . J. 5: 287, 1922. 12. Stephen, E. A . M . : M. ft. Australia 2: 231, 1931. 13. Choun, Gordon: Canad. :~r A. 5. 7: 191, 1927. 14. Whaley, 5. It.: Personal communication. 3439 PRYTAZ'TIA STREET