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cal improvement was dramatic. After the second exchange, thepatient could feed himself and stand unaided. After the fourthexchange, he could walk. Forced vital capacity, forced expira-tory volume in Is, and peak expiratory flow improved 164%,153%, and 140%, respectively. 4 weeks after the last exchange,the patient continued to improve and could once again drivehis truck and enjoy gardening.

Recent reports have implicated both humoral and cellularcomponents in the pathogenesis of the Guillain-Barre syn-drome. Cook et al. demonstrated complement-dependent mye-linotoxic activity in both 19S and 7S serum fractions, andfurther, showed that a serum concentration reduction from50% to 33% resulted in significantly less in-vitro myelinotoxicactivity.2 Nyland and Aarli found increased IgG binding toperipheral nerve tissue in 15 of 30 patient sera.3 Sheramataand colleagues have emphasised a cellular, delayed hyper-sensitivity mechanism.4,5Our patient was off all medications for 3 months before the

exchange and at no time were cytotoxic drugs administered. Itis very unlikely that the abrupt improvement was fortuitous.In moderate and severe cases, plasma exchange may wellbecome the treatment of choice for both the acute and chronic,atypical forms of the Guillain-Barre syndrome. Certainly,further assessment of this treatment is warranted.

Departments of Neurology and Pathology,Dartmouth-Hitchcock Medical Center,Hanover, New Hampshire 03755, U.S.A.

RICHARD L. LEVYRUSSELL NEWKIRK

JOSÉ OCHOA

BIRTH-RATE AND SUDDEN INFANT DEATH

SIR,-Farber and Chandra’ suggested that analysis of theseasonal variation of sudden-infant-death syndrome (SIDS)should take into account the variation in the number of infantsat risk for SIDS. In analysing SIDS incidence data from thestate of Colorado, we concluded that the effect of fluctuatingbirth-rates was negligible.

In the years 1977 and 1978, there were 186 confirmed SIDSdeaths of children born in the State of Colorado. Using Color-ado Department of Health birth statistics, we calculated the

2. Cook SD, Dowling PC, Murray MR, Whitaker JN. Circulating demyelinat-ing factors in acute idiopathic polyneuropathy. Arch Neurol 1971; 24:136-44.

3. Nyland H, Aarli JA. Guillain-Barré syndrome: demonstration of antibodiesto peripheral nerve tissue. Acta Neurol Scand 1978; 58: 35-43.

4. Sheramata W, Colby S, Lusky G, Cosgrove JBR. Cellular hypersensitizationto peripheral nervous antigens in the Guillain-Barré syndrome. Neurology1975; 25: 833-39.

5. Sheramata W, Rocklin RE, David JR. Cellular hypersensitivity in the Guil-lain-Barre syndrome. Can Med Assoc J 1974; 110: 1245-47.

1. Farber MD, Chandra V. Seasonal variation in sudden-infant-death syn-drome. Lancet 1978; ii: 473.

Rate of SIDS deaths by month (per 100 000 child-months).

number of children at risk each month. For example, childrenat risk in August, 1978, include those born from August, 1977,to July, 1978. We calculated the rate of SIDS deaths per100 000 child-months of risk (see figure). One child-month ofrisk is defined as one child living at risk for one month. Thisrate takes into account the fluctuating birth-rates.

In order to determine if the observed fluctuations in the

monthly rates of SIDS deaths could be due to chance alone,we applied Pearson’s chi square goodness-of-fit test. The chisquare value was 26-22 (11 degrees of freedom; p=0.006) andwe concluded that the rate is not constant throughout the year.When we performed the same test on the raw data, ignoringthe fluctuations in the monthly birth-rate, the chi square valuewas 26.13 (11 d.f.; p=0-0062).The difference in the values of the chi square test statistic

was slight because the monthly fluctuations in the number ofchildren at risk were small. In the month in which mostchildren were at risk (December) there were only 3-7% morechildren at risk than in the month with the least (January) inthis two-year period. The effect of the varying length of themonths was greater than the effect of fluctuating number ofchildren at risk in our study, because a 31-day month is 10.7%longer than a 28-day month.

Because there was little difference in the number of infantsat risk from month to month in our study, the effect of fluc-tuating birth-rates did not significantly affect the results of theanalysis.

This work was supported in part by NICHHD grant HD12365-Ol.

Department of Pathology,Children’s Hospital,Denver, Colorado 80218, U.S.A.

DENNIS P. ZOGLODENNIS W. LUCKEYARLENE L. FRAIKOR

WHOLEMEAL BREAD AND SATIETY

SIR,-Among the advantages claimed for dietary fibre isthat it enhances satiety: "A person on a high fibre diet is muchmore likely to reach the point of satisfaction before he eats toomuch".1 Conversely, it is suggested that refined carbohydratepromotes an increased energy intake.2,3 This view was sup-ported by Grimes and Gordon who offered twelve volunteerseither wholemeal or white bread in randomised sequence to eat"to a point of comfortable fullness", and noted that a non-para-metric ranking test indicated that in these circumstances theirintake of white bread was significantly greater than that ofwholemeal bread (p<0-05).We have repeated and extended Grimes’ and Gordon’s

work, and come to a different conclusion. Ten healthy volun-teers were offered unlimited quantities of bread, butter, andjam on four successive Tuesdays at lunchtime. They wereasked to record their food intake from the time of rising onTuesday to lunchtime on the following Wednesday. The studywas approved by the hospital ethical committee.The figure shows the average energy intake at lunchtime of

each volunteer on the two days when white bread was offered(group mean 1032&plusmn;322 kcal; 1 kcal=4.18 MJ), plottedagainst the average when wholemeal bread was offered (groupmean 1117&plusmn;361 kcal). The difference between individuals isfar larger than the difference between breads. When the totalintake of energy, protein, fat, or carbohydrate from Tuesdaymorning to noon on Wednesday is compared by paired t testthere is no significant difference between the days on whichwhite or wholemeal bread was offered.Our results conflict with those of Grimes and Gordon,4 but

1. Reuben D. The save your life diet. London: Ebury Press, 1976.2. Cleave TL. The saccharine disease. Bristol: John Wright, 1974.3. Heaton KW. Food fibre as an obstacle to energy intake. Lancet 1973; ii;

1418-21.4. Grimes DS, Gordon C. Satiety value of wholemeal and white bread. Lancet

1978; ii; 106.