Interpretation: These results are in accordance with the findings that whereas over half of all lesions in an MS cord are seen in the upper cervical cord, most of the pathology in HAM/TSP is seen in the thoracolumbar cord, which in turn may be responsible for more extensive cord atrophy seen in HAM/TSP. An imaging marker such as SCCSA might serve as a surrogate endpoint in clinical trials, especially to assess the neuroprotective impact of various therapies.
It’s not straightforward to interpret these findings as the cohort was relatively small, and assumptions from MRI measures about what is happening in the tissue are notoriously not more than that: assumptions.
One likes to think of nerve fibres (axons) connecting the brain with nerve cells in the spinal cord as ‘cables’, and once fibre-damage occurs in MS, these fibres are removed and thus can no longer contribute to the overall diameter of the spinal cord leading – theoretically – to volume loss (= atrophy).
However, atrophy can be compensated for by other cellular changes, including inflammation and astrocyte activation, confounding the use of atrophy as a direct correlate of ‘nerve fibre loss’.
It becomes even more twisted when, as has been repeatedly reported, lesions in the spinal cord have very little association with the underlying nerve fibre loss, which seems to occur almost independently of spinal cord lesions, at least in later stages of MS.
Thus, whilst spinal cord atrophy is nevertheless a promising tool to predict future disability, the explanation for the differences between MS and HAM/TSP reported here will require confirmation, ideally using combined MRI/pathology studies of post mortem spinal cord.