Abstract â–¡ 83

Disturbances in the respiratory system, specifically in the phrenic nerve and diaphragm may be part of a cascade of events leading to Sudden Infant Death Syndrome.

Left side phrenic nerves (from the pericardial region) of 13 control cases (ranging in age from birth to 7 months), 17 SIDS cases of normal birth weight (NBW), (ranging in age between 1 and 8 months) and 10 SIDS low birth weight (LBW) cases (ranging in age between 2 and 8 months) were selected from archived or prospectively collected material. Each phrenic nerve was bisected transversely, one half was processed to wax and stained with H&E. The other half was processed to resin and stained with 1% toludine blue. The transectional area of each phrenic nerve and axon density was estimated and multiplied together to obtain the total number of myelinated axons.

A piece of diaphragmatic muscle was taken from the left side of the diaphragm of 10 control cases, 7 SIDS NBW and 9 SIDS LBW cases. Each piece was processed to wax and immuno-cytochemically stained for type II muscle fibres using a specific antibody to fast acting myosin. The TS area of both type I and type II muscle fibres was estimated using a point counting system. Results were analysed using linear regression analysis over age and the Mann-Whitney rank sum test, for comparison between groups.

There was no significant difference in TS area of phrenic nerve between control cases and either SIDS NBW or SIDS LBW cases. Both SIDS NBW (p=0.038) and SIDS LBW (p=0.011) cases demonstrated a reduced axon density when compared with control cases. There was a significant difference (P<0.001) in the total number of myelinated axons between SIDS LBW cases and control cases, SIDS LBW cases also demonstrated a qualitative reduction in myelin around each axon. There was no statistically significant increase with age in either phrenic nerve area, axon density or total number of myelinated axons in any of the groups analysed.

There was a significant increase in the TS area of type I muscle fibres in both SIDS NBW (p=0.009) and SIDS LBW (p=0.001) cases when compared with control cases. Type II muscle fibres also demonstrated an increase in TS area in both SIDS NBW (p=0.008) and SIDS LBW (p<0.001) cases when compared with control cases. There was no statistically significant increase any of the groups with age in TS area of either type I or type II muscle.

It is possible that some SIDS cases, irrespective of birth weight, may be defined by specific micro-anatomical deficiencies which have their origins in developmental delay or arrest during gestation.