The side-effects of antiepileptic drugs – post anoxic myoclonus


Was somewhat atypical and the histology unknown, showed little, if any, response to

Cobalt irradiation.

As a result of the attention being paid to it i n the journals, the âdiencephalic syndrome of

Severe emaciation in early infancyâ is likely to be diagnosed earlier and more often. How

Far earlier diagnosis and advances in irradiation techniques will affect the prognosis remains

To be seen.

Department of child life and health,

17 hatton place, edinburgh 9.



1 . Babonneix, L., hutinel, J. (1925) âpolyurie liee sans doute ii un glium de la region tubirienne. gcrz.

2, bain, H.

W., darte, J. M. M., keith, W. S., kruyff, E. (1966) âthe diencephalic syndrome of early

3. Braun, F.Post anoxic myoclonus C., forney, W. R. (1959) âdiencephalic syndrome of early infancy associated with brain

4. Cooper, K. E. (1966) âtemperature regulation and hypothalamus. brit. Tired. Bid/., 22, 238.

5. Dodds, L. (1957) âa diencephalic syndrome of early infancy. meri. 1. Aiist., ii, 689.

6. Fitzsirnons, J. T. (1966) âthe hypothalamus and drinking. brit. Fried. E d / . , 22, 232.

7. Ford, F. R. (1966) diseases of the nervous system in infancy, childhood and adolescence. 5th ed.

8. Goebel, F. Von. (1932) â âhypophysare kachexieâ beirn kleinkind ohne zwergwuchs bei intakter

9. Hausmann, C. (1 926) âein gliom der lnfundibulargegend auf dysontogenetischer grundlage. virchows

H@. (paris), 98, 389.

Infancy due to silent brain tumors: with special reference to treatment. pediatrics, 38, 473.Post anoxic myoclonus

Tumors. pediatrics, 24, 609.

Springfield, 111.: thomas.

Hypophyse. Z. Kinderheilk., 53, 575.


Arch. Path. Anat., 262, 572.

10. Hilton, S. M. (1966) âhypothalamic regulation of the cardiovascular system. brit. Med. BirN., 22, 243.

11. Russell, A. (1951) âa diencephalic syndrome of emaciation in infancy and childhood. arch. Dis. C/ii/d/z.,


12. —{1959) âa diencephalic syndrome of hyperkinetic emaciation typically linked to predominant

Elation in infancy and early childhood. first international congress of neurological sciences, 1957.

London: pergamon, vol. I, p. 435.

13. Smith, K. R., weinburg, W. A., mcalister, W. H. (1965) âfailure to thrive. The diencephalic syndrome

Of infancy and childhood. J .Post anoxic myoclonus neirrosurg., 23, 348.

14. Wilkins, L. (1965) the diagnosis and treatment of endocrine disorders in childhood and adolescence.

Springfield, I l l . : thomas.


EVERYONE has their good and bad days, but this variability of performance seems to be a

Particular characteristic of the child with epilepsy. Side-effects of the treatment are often

Blamed, and in many cases this may be justifiable. But before such effects are considered

An indication for changing the treatment other alternatives may have to be excluded. If

Frequent seizures are occurring, even when they are of a very minor type, there is likely

To be a period, before, during and after the attack, when the function of the brain is

post anoxic myoclonus

Impaired. Also there is evidence that even when no clinical seizures are occurring, subliminal

Epileptic activity can disturb cerebral function. A correlation has been found between the

Results of psychological tests and the occurrence of specific epileptic discharges in the

E E G . Inappropriate or âdonât knowâ responses occurred when there was paroxysmal activity

In the EEG. Suggesting a limitation of integrative processes.:â HUTT and his colleaguesâ

Have also demonstrated a defect of recall after epilepsy precipitated by photic stimulation.

As the EEC; only records from the surface of the brain, i t is possible for epileptic discharges

To disorder the activity of the subcortical areas in the absence of clinical fits and EEG

post anoxic myoclonus

Abnormalities. MIRSKY and VAN BUR EN’S^ findings with continuous performance tests i n



Patients with petit ma1 epilepsy support this contention. In contrast to cases of focal

Epilepsy, patients with centrencephalic epilepsy showed a significant impairment o n

Continuous performance tests, even when they were having no clinical fits and showing

No EEG abnormalities. This may represent a relatively static difficulty due to some permanent

Neurological dysfunction but is more likely to reflect seizure episodes which involve only

Subcortical structures.

Emotional disturbances, which are common enough among epileptic children, may well

Affect their behaviour and account for their lack of progress a t school.Post anoxic myoclonus the child’s in-

Telligence must be taken into account, and also the hyperkinetic behaviour of some of

These children. O U N S T E D ~ estimated that the hyperkinetic syndrome occurred in 8 per cent

Of a large unselected series of epileptic children. It is best to avoid giving these children

Barbiturates because they often aggravate the behaviour disorder. It seems paradoxical

For a sedative to make a restless child more restless, but a possible explanation may be

That the hyperkinesis is due to a failure in the selection of sensory input. These children

May not inhibit the majority of the sensory stimuli reaching the cerebral cortex, SO that

They react first to one stimulus and then to another, a t short intervals.Post anoxic myoclonus the effect of

Barbiturate sedation would then be to make an inefficient function even more inefficient.

When these various factors have been considered, it may be decided that the child’s

Treatment is a t least partly responsible for variability of behaviour and over-sedation,

And that this is a n indication for changing it. It can be better to risk occasional

Seizures than to have the child half asleep all day. Most of the effectiveanticonvulsants

Number drowsiness among their toxic effects, but the individual response to them varies

Considerably. It is always worth while ringing the changes and giving them in various

Combinations, keeping the dose of each as low as possible. Toxic effects other than

post anoxic myoclonus

Drowsiness also have to be taken into account when a patient taking anticonvulsants shows

Evidence of intellectual deterioration. For instance, it seems possible that prolonged folic

Acid deficiency may have a harmful effect o n protein synthesis (GORDON~). It is also claimed

That barbiturates taken over a long period can lower the blood-sugar level.5. !’

Occasionally a patient, or his relatives, will report that since stopping treatment the fits

Have been less frequent. This may be a mortifying remark for the doctor who is trying

To do the patient good by giving him drugs, but it is a phenomenon worthy of further

Consideration. It seems possible that anticonvulsant treatment may pass over the top of

post anoxic myoclonus

The therapeutic curve, if given in increasing doses, and start to harm the patient. It is

Well established that in certain types of epilepsy, such as fits arising in the temporal lobe,

The epileptic discharges are most likely to be recorded in the EEG during drowsiness and

Sleep. It follows that, i f the patient is made excessively drowsy by treatment, his epilepsy

May be activated rather than suppressed. LEVY and fti

ANNO-I A riws

Treatment as an alternative to drugs, but, if due attention is paid to removing tinnccessary

Stresses aiid strains in the patient’s life, the dosage can sometimes be reduced.

N E I L G O K I I ~ N

FEG department,

Booth hall children’s hospital,

Charleston road. Blacklev. Manchebter. 9

post anoxic myoclonus

K EFEK t ncts

I . Gordon, N . ( 1967) ‘folic acid deticiency from anticonvulsant therapy.’ to be published.

2. Hutt, S. J., lee, D., ounsted. C. (1963) ‘digit memory and evoked discharges i n f o u r light-wnstitivc

Epileptic children.’ drveloip. Med. Child neiirol., 5, 559.

3. Kooi, K. A., hovey, li. B. (1957) ‘alterations in i i lei iki l function and piiradoxical cerebral aciivity.’

Arch. Neiirol. P.V,,c./ticir. (chic..) 78, 264.

4. Levy, L. L., fenichel. G . K. ( 1965) ‘uiphenyi1~ydantc)i i i -act iv~tte~ \ei/ureh.. Nri,ro/og.I. (miu/iwp.),

15, 716.

5. Merivale, W. H. H.. Hunter, K . A. (1954) ‘abnoi-ma1 glticose-toleriiiice test5 in patient\ rreated \ r i t h

Sedative drugs.’ lmicvt, i i , 939.

6.Post anoxic myoclonus mirsky, A. F.. Van buren, J. M . (1965) ‘on the nature of thc abwice i n centreticephalic epilepsy.’

7. Ounsted, C. (1955) ‘the hyperkinetic syndrome in epileptic children.’ loric-r!, i i , 303.

8. — lindsay, J. , norman, R . (1966) biological factors i n temporal lobe epilepsy. London: spastic\

9. Tod, H. (1935) ‘the effect of hypnotics on glucose tolerance.’ hioc./ir,ii. J . , 29, 914.

Electrorttcvpli. Clitt. Neiiropli.V.Siol., 18, 325,



THE introduction of histochemical techniques in the examination of muscle biopsy material

Has added new aspects to the study of niuscle diseases. FENICHEL:+ has applied these tech-

Niques to the study of developing muscle in 25 foetuses obtained from therapeutic abortions.Post anoxic myoclonus

With a gestational age of 5-20 weeks. Three groups of histochemical reactions were covered

Oxidative enzymes for mitochondria, myosin awase for myofibrils and phosphorylase.

And PAS for sarcoplasni. Muscle fibres with a high content of oxidative enzymes are us~tally

Classified as type 1. Aiid those with a high content o f phosphorylase and myosin A ~ U W

A s type 11. I n these foetuses paspositive material was noted i n all the fibres throughour

The age-range studied. N o phosphorylase activity was demonstrated. Probably for technical

Reasons, as other workers have found phosphorylase activity i n foetal mice. Mitochondria1

Enzyme reactions were of uniform intensity i n all mliscle tibres during the period of iiiyo-

post anoxic myoclonus

Fibrillary formation. These reactions could thus nor be used for fibre-typing u n t i l the trail+

T’ormation from niyotube to niattire myocyte was completed. The myosin A’rpase reactioii

Proved the most useful for early fibre typing. A s new niyotubes could he identified a s dark

(type I1 fibres) or light (type I. Fibres).

I n the youngest foetuses (5-8 weeks), FENIC’HI~I. Found that most of the cells formed a

Syncytium of preniyoblasts. Sonie myoblasts could be identified and a few were converted

To myotubes by the formation of myofilaments. Fibre typing could not be done. I n the

Next age-group (8-10 weeks) myotubes were the predominant cellular form. They co~i ld

Easily be classified as type 11 (dark myotubes) or type I (light myotubes) fibres.Post anoxic myoclonus type l r

Were more numerous and larger (diameter 15-20 microns) than type t (5-10 microns). I n

The oldest foetuses (10-20 weeks) mature myocytes appeared, and this was the predominant

Cellular form towards the end of the period. Thus, oxidative enzyme reactions could also

Be used for typing these fibres. At this age type 1 atid 1.1 fibres were eq~ially nlimerolis. But

Type I fibres were n o n larger than type 11. The B fibres, described by W O H I . ~ A I ~ T ; ~ could be

24 I