Hit and Run or Should I say Hit and Crawl. The speed at which white matter damage leads to grey matter changes

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We often hear “I swapped to drug X or Y and I still feel I am getting worse”. This not surprising because it takes time for the attacks to run their course, So in this study they looked to see how quickly damage to the white matter (myelinated axons= nerve body) took to show itself by loss of neurons in the grey matter (nerve heads). Here they imaged people repeatedly and they looked at a few grey matter areas. These were the thalamus

The thalamus is a paired structure of gray matter located in the forebrain, near the center of the brain, with nerve fibers projecting out to the cerebral cortex in all directions. The thalamus has multiple functions, generally believed to act as a relay station, or hub, relaying information between different subcortical areas and the cerebral cortex. In particular, every sensory system (with the exception of the olfactory system) includes a thalamic nucleus that receives sensory signals and sends them to the associated primary cortical area and deep grey matter

Thalamus small.gif
Thalamus in red Source wikipedia reproduced under CC-BY-SA-2.1-jp

After damage to white matter tracts that connect with the thalamus and Deep grey matter, they could see shrinkage 1 year later, but not 2-4 years so it takes about a year for the same to evolve and complete. Therefore it must be born in mind that it will take time for benefit of treatment to show itself. This is what we have termed “therapeutic lag”

Carolus K, Fuchs TA, Bergsland N, Ramasamy D, Tran H, Uher T, Horakova D, Vaneckova M, Havrdova E, Benedict RHB, Zivadinov R, Dwyer MG. Time course of lesion-induced atrophy in multiple sclerosis. J Neurol. 2022 Apr 8. doi: 10.1007/s00415-022-11094-y.

Background and purpose: White matter (WM) tract disruption impacts volume loss in connected deep gray matter (DGM) over 5 years in people with multiple sclerosis (PwMS). However, the timeline of this phenomenon remains poorly characterized.

Materials and methods: Annual serial MRI for 181 PwMS was retrospectively analyzed from a 10-year clinical trial database. Annualized thalamic atrophy, DGM atrophy, and disruption of connected WM tracts were measured. For time series analysis, ~700 epochs were collated using a sliding 5-year window, and regression models predicting 1-year atrophy were applied to characterize the influence of new tract disruption from preceding years, while controlling for whole brain atrophy and other relevant factors.

Results: Disruptions of WM tracts connected to the thalamus were significantly associated with thalamic atrophy 1 year later (β: 0.048-0.103). This effect was not observed for thalamic tract disruption concurrent with the time of atrophy nor for thalamic tract disruption preceding the atrophy by 2-4 years. Similarly, disruptions of white matter tracts connected to the DGM were significantly associated with DGM atrophy 1 year later (β: 0.078-0.111), but not for tract disruption concurrent with, nor preceding the atrophy by 2-4 years.

Conclusion: Increased rates of thalamic and DGM atrophy were restricted to 1 year following newly developed disruption in connected WM tracts. In research and clinical settings, additional gray matter atrophy may be expected 1 year following new lesion growth in connected white matter.

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