Abstract â–¡ 82

Neuro-pathological deficiencies resulting from developmental delay or arrest have been inferred as possible elements in the chain of events leading to Sudden Infant Death Syndrome (SIDS). A developmental delay/arrest in either the axon number, or in the myelin surrounding each axon, may have repercussions on the functional capabilities of the associated tissue. Affected axonal tracts within the CNS may present as a pathogenesis for SIDS.

9 control cases, 11 SIDS NBW and 8 SIDS NBW cases were selected from archived material or prospectively collected. All cases ranged in age from 3 days to 8 months. The area of the corpus callosum was first estimated using a point counting technique. A punch biopsy of tissue was taken from the splenium, genu and body regions of the corpus callosum and processed to wax. Each section was immuno cytochemically stained, using anti-human neurofilament and luxol fast blue and the total number of axons estimated. The brainstem from 7 control cases, 10 SIDS NBW and 8 SIDS LBW cases were processed to resin and serially sectioned at 25µm. Every 4th section was stained with H&E and the area of the solitary tract estimated using a point counting technique. Results were analysed using Mann-Whitney rank sum test for comparison between groups and linear regression analysis for any change with age.

There was no significant difference in the area of the corpus callosum between either the SIDS NBW (p=0.949) or the SIDS LBW (p=0.201) cases and control cases. Nor was there a significant difference in the area of the corpus callosum with age, in any of the groups. There was a statistically significant difference in axon density between SIDS NBW and control cases (p=0.026). In the splenium region of the corpus callosum, SIDS LBW cases demonstrated a significant difference in axon density, when compared with the control cases (p=0.040). There was no significant difference in the total number of axons in either of the SIDS group when compared with the control group. Results from the solitary nuclei are at the moment incomplete but will be presented at the meeting.

Since myelination of the corpus callosum is initiated postnatally and continues during the first decade of life, it was not possible to determine whether the quality of the myelin surrounding each axon has been affected. A decrease in axon number may act as a pointer towards later deficiencies in myelin. A delay/arrest in axonal numbers or in the area in certain axonal tracts and not in other tracts, may points towards a hierarchical developmental delay/arrest originating in utero.