ferent weights represent, as well as data to illuminate the clinically im¬ portant neuroendocrinological mecha¬ nisms that may be involved in the synchronization of a particular body composition and reproductive ability. ROSE E. FRISCH, PHD Harvard University 9 Bow St Cambridge, MA 02138 1. Frisch

RE, Revelle R: Variations in

body weights and the age of the adolescent growth spurt among Latin American and Asian populations in relation to calorie supplies. Hum Biol 41:185-212, 1969. 2. Frisch RE, Revelle R, Cook S: Height, weight and age at menarche and the "critical weight" hypothesis. Science 174:1148\x=req-\ 1149, 1971. 3. Frisch RE, Revelle R: Height and weight at menarche and a hypothesis of

menarche. Arch Dis Child 46:695-701,1971. 4. Frisch RE: Critical weight at menarche: Initiation of the adolescent growth spurt and control of puberty, in Grumbach MM, Grave GD, Mayer FE (eds): Control of the Onset of Puberty. New York, John Wiley & Sons Inc, 1974, pp 403-423. 5. Frisch RE: A method of prediction of age of menarche from height and weight at ages 9 through 13 years. Pediatrics 53:384-390, 1974. 6. Frisch RE, McArthur JW: Menstrual cycles: Fatness as a determinant of minimum weight for height necessary for their maintenance or onset. Science 185:949-951, 1974. 7. Frisch RE, Revelle R: Height and weight at menarche and a hypothesis of critical body weights and adolescent events. Science 169:397-399, 1970. 8. Frisch RE: Demographic implications of the biological determinants of female fecundity. Soc Biol, to be published. 9. Coale A: The history of the human population. Sci Am 231:40-51, 1974. 10. Revelle R: Food and population. Sci Am 231:160-171, 1974. 11. Kolata GB: !Kung hunter-gatherers: Feminism, diet, and birth control. Science 185(4155):932-934, 1974. 12. Osler D, Crawford J: Examination of the hypothesis of a critical weight at menarche in ambulatory and bedridden mentally retarded girls. Pediatrics 51:675-679, 1974.

Reply Sir.\p=m-\Ingeneral, Dr. Frisch's remarks merely reiterate ideas expressed in earlier publications with which we have dealt in our article. However, there is one important change in her position, as well as in recent work (eg, her reference 6). She now refers to an "average critical weight" (italics mine) for her various samples. Since, in our article, we have shown that this average weight differs not only among racial groups but also among normal samples of the same race, this seems to indicate an acceptance by all that the weight at

menarche is not only an individual characteristic, but also one of the most variable of such characteristics

associated with development. Thus, the mean weight at menarche, as expressed by Dr. Frisch, is not a "critical" weight, but a central tendency. Now, Dr. Frisch has merely repeated her earlier contention that the significant variable, in an individual, is the lean body mass. As we have noted, the evidence that she has pre¬ sented in support of this is indirect rather than physiological, and her findings may be explained by an inappropriate use of statistics. FRANCIS E. JOHNSTON, PHD Department of Anthropology University of Pennsylvania Philadelphia, PA 19174 The Use of Bromides for Epilepsy

Sir.\p=m-\Weare writing to compliment Joynt on his excellent review of an important and interesting event in medical history, the introduction of bromide as an antiepileptic agent, which appeared in the September issue of the Journal (128:362, 1974).

However, his statement that bromide has not "been supplanted by treatments devised by modern methods of drug manufacture" is not supported by many current authors in the field of epilepsy. Because of the enthusiasm for the newer anticonvulsant drugs, bromide is not used extensively at present, and some investigators consider it to be only of historical interest. In fact, several writings on the treatment of epilepsy merely cite the past importance of bromides and then summarily dismiss them as ineffective and relatively toxic. It is thus readily comprehensible why so few younger physicians have little knowledge of the use of bromide as an anticonvulsant and have generally excluded this drug from their antiepileptic armamentarium. Based on the results of treatment of at least 1,100 patients, we are con¬ vinced that bromide still has a very definite place in the therapy for ep¬ ilepsy. Since this appears to be con¬ trary to prevailing opinion and be¬ cause there is little information in the recent literature relative to the use of bromide in epilepsy, we believe we are obligated to place in modern per¬ spective a drug that has obviously fallen "out of style." Our initial report on the use of bro-

Downloaded From: http://archpedi.jamanetwork.com/ by a UQ Library User on 06/16/2015

mides in the control of epileptic sei¬ appeared in the Journal in 1953. The study group consisted of 196 children with severe brain dam¬ age who exhibited predominantly ma¬

zures

jor

motor

(grand mal)

or

myoclonic

both. The majority, 102 patients, had not responded to previ¬ ous anticonvulsant therapy. One hun¬ dred eleven (61%) of the 182 patients with major motor or myoclonic sei¬ zures, or both, benefited substantial¬ ly from bromide therapy. During the subsequent 21 years, we treated ap¬ proximately 900 additional patients with bromide, and although we have not yet completed our statistical eval¬ uation of the data, the results at hand essentially parallel those reported in 1953. Because of space limitation, the reader is referred to two recent publi¬ cations for our methods of adminis¬ tering bromide2 and for the dosages employed in our center.3 In our experience, the margin of safety in bromide therapy is consid¬ erable. We emphasize that infants and children tolerate bromides ex¬ ceedingly well, and with carefully su¬ pervised administration, toxicity is negligible. Drowsiness and cutaneous

seizures,

or

reactions, particularly bromoderma, the only two significant side ef¬

were

fects observed in

our patients. Con¬ experience in adults, psy¬ choses and neurologic manifestations are only rarely encountered in chil¬

trary to

our

dren. Detailed discussions relative to the prevention, detection, and man¬ agement of specific adverse reactions of bromide are presented in a previ¬ ous

publication.2

SAMUEL LIVINGSTON, MD LYDIA L. PAULI, MD The Samuel Livingston Epilepsy Diagnostic and Treatment Center 1039 St. Paul St

Baltimore, MD 21202 1. Livingston S, Pearson PH: Bromides in the treatment of epilepsy in children. Am J Dis Child 86:717-720, 1953. 2. Livingston S: Comprehensive Management of Epilepsy in Infancy, Childhood and Adolescence. Springfield, Ill, Charles C 1972. Publisher, Livingston S: Seizure disorders, in Gellis S, Kagan BM (eds): Current Pediatric Therapy. Philadelphia, WB Saunders Co, 1973, pp 78-92. Thomas 3.

Sir.\p=m-\RobertJ. Joynt made a significant contribution to the Journal in his excellent article that appeared in the September issue (128:362, 1974). His statement that "It is also unusual

Letter: The use of bromides for epilepsy.

ferent weights represent, as well as data to illuminate the clinically im¬ portant neuroendocrinological mecha¬ nisms that may be involved in the sync...
NAN Sizes 0 Downloads 0 Views