strength of 5 TU/0.1 mL negative. Chest roentgenogram showed a primary complex. The EEG showed bilateral dysfunction, with the left side being more involved. Left carotid angiography disclosed partial occlusion of test with PPD was

the internal carotid artery in the neck and late visualization of the middle cerebral artery. Two years later, his speech was improved and there was residual hemipare¬

sis.

Comment—The occurrence of caro¬ tid occlusion in identical twins has not, to our knowledge, been reported

previously.

The Dean of the Government Gen¬ eral Hospital, Madras, India, gave permission for us to use hospital records in preparing· this report. K. Srinivas, DM, FRCP M. Narayanan, MB, BS S. Gopal, MB, BS K. Jagannathan, MD, DTM Institute of Neurology

Government General Madras, India

Hospital

Fatal Guillain-Barre Syndrome With Reduced-dose Antirabies Vaccination

To the Editor.\p=m-\Shortly before publication in the Archives of our article titled "Neuroparalytic Accidents of Antirabies Vaccination With Suckling Mouse Brain (SMB) Rabies Vaccine" (34:694-700, 1977), we had the opportunity to study a new fatal case of Guillain-Barre syndrome.

Report of a Case.\p=m-\A71-year-old man received seven subcutaneous doses of SMB rabies vaccine for postexposure prophylaxis. The symptoms appeared six days after termination of the vaccination and the clinical picture was characterized by facial diplegia, bulbar muscle involvement, and descending quadriplegia with generalized areflexia. Cerebrospinal fluid values were normal with a slight increase of the IgG level (0.72 mg/dl). The patient was treated with high doses of corticoids and required respiratory assistance from the second day of evolution. Two weeks after the onset of the symptoms, the patient died suddenly.

Autopsy

was

not

performed. Virological

studies of the vaccine batch were done with negative results. Encephalitogenic activity of concentrated vaccine was also negative. The patient's serum had an antirabies titer of 1:50 and an antimyelin antibody titer of 1:40.

Com ment -This is the first case of Guillain-Barre syndrome following SMB rabies vaccination in Colombia since 1974 when the vaccination regi¬ men was reduced to seven subcuta¬ neous doses with two booster doses. Although the frequency of neuropara¬ lytic accidents has notoriously de¬ creased in Colombia since the reduc¬ tion of the vaccination schedule, it is

apparent from the

case reported here that this is not the definite solution. An epidemiological survey was launched by the National Institute of Health of Colombia to detect the presence of minor reactions to the vaccination.

I.

Vergara, MD

G. Toro, MD G. Rom\l=a'\n,MD G. Mendoza, MD Natl Institute of Health of Colombia Avenida Eldorado Con Carrera 50 Zona 6 o Apartados Aeros

later differed in mental and neurolog¬ ical outcome from those who remained seizure free. It seems, therefore, impossible to draw from the authors' data the conclusion that febrile convulsions have no deleterious consequences at least in part of the affected infants. Thus, any firm position concerning chronic anticonvulsant therapy is un¬ warranted. J. Aicardi, MD J. J. Chevrie, MD INSERM U 154 H\l=o^\pitalSaint Vincent de Paul 75674 Paris Cedex 14, France

80080 y 80334

Bogota, DE, Colombia

Febrile Seizures in Children To the Editor.\p=m-\In a recent article in the Archives (35:17-21, 1978), Ellenberg and Nelson found no difference in later intellectual performance between children who had had febrile seizures and their seizure free siblings. On this basis, they claim that "febrile seizures, initial or recurrent, are not likely to cost the child a measurable decrement in intelligence or early academic achievement." We are not convinced that this claim may really be derived from their data. In fact, a group of patients with febrile convulsions had, according to the authors' own data, an unfavorable mental outcome: those in whom afebrile seizures developed after febrile fits. Of 52 infants in this group, 14 (27%) at least were neurologically and/or mentally abnormal.1 Excluding these patients from analysis necessarily leads to an optimistic result that applies only to infants without afebrile seizures. It is not possible, however, to know beforehand in which particular infants with febrile convulsions will afebrile seizures develop later. Even admitting that those children in whom afebrile seizures evolved were, in their majority, "suspect" or "abnormal" prior to their first febrile convulsion,1 the high proportion (22%) of such infants in the authors' series does not permit to improve greatly the possi¬ bilities of prediction of later epilepsy and of associated mental retardation. It is known that mental retardation after febrile convulsions is strongly linked with the existence of later epileptic fits.2 Furthermore, it is conceivable that febrile convulsions aggravate preexisting defects. It would have been interesting in this regard to know whether those infants classified as suspect or abnormal in the Collaborative Perinatal Project in whom febrile convulsions developed

1. Nelson KB, Ellenberg JH: Predictors of epilepsy in children who have experienced febrile seizures. N Engl J Med 295:1029-1033, 1976.

2. Aicardi J, Chevrie JJ: Febrile convulsions:

Neurological sequelae and mental retardation, in Brazier MAB, Coceani F (eds): Brain Dysfunction in Infantile Febrile Convulsions. New York, Raven Press Inc, 1976, vol 2, pp 247-257.

Reply.\p=m-\ Our recent study investigated the effect of febrile seizures on intelligence in children in whom afebrile seizures did not develop subsequently\p=m-\thatis, 97% of children In

with febrile seizures\p=m-\andfound there to be no impairment. This result is not challenged by Drs Aicardi and Chev-

rie. With respect to the 3% of the children in whom afebrile seizures did develop after febrile, we agree with Drs Aicardi and Chevrie that they

demonstrated an increased frequency of mental impairment.1,2 However, contrary to the statement by Chevrie and Aicardi, it is possible to know beforehand which infants with febrile convulsions are at substantially heightened risk for later afebrile seizures. A small subset of children with febrile seizures (6%)2 can be identified who have a high risk of epilepsy and potentially of associated intellectual deficit. The small subgroup of children with febrile seizures who are at relatively high risk of afebrile seizures might be considered candidates for chronic anticonvulsant therapy. Pending further information as to the efficacy of such prophylaxis, some clinicians may elect to treat such children. However, we know of no evidence that prophylactic treatment initiated after a first (or later) febrile seizure can prevent later epilepsy or mental retardation. J. H. Ellenberg, MD Karin B. Nelson, MD

1. Nelson KB, Ellenberg JH: Predictors of epilepsy in children who have experienced febrile seizures. N Engl J Med 295:1029-1033, 1976. 2. Nelson KB, Ellenberg JH: Prognosis in chil-

dren with febrile seizures. Pediatrics 61:720-727, 1978.

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Febrile seizures in children.

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