Brain resilience correlates with cognitive performance in MS

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What causes cognitive issues in MS?

Not a straightforward question to answer. It has been postulated that there is a global cognitive dysfunction in MS largely due to connectivity issues (for example, thalamic grey matter volume loss and also lobar connectivity due to interruptions by MS lesions), but also secondary to cortical MS lesions. What is unknown is the resilience of the whole system and the ability to recover function. We do know that a certain degree of plasticity exists within the the adult nervous system, because without it we would not be able to learn new things and formulate new memories.

In this new study from Germany they found that the repair/recovery capacity (called synaptic plasticity) of the brain influenced a persons overall cognitive function. They used a technique called repetitive transcranial magnetic stimulation (TMS, see Figure below) of the brain cortex to stimulate the cortex into activation using an electrical current. With repetitive stimulation you can control the overall cortical excitability by inducing changes at a synaptic level (i.e. effectively plasticity) – or at least that is the theory.

In the past it has been shown that during an MS relapse, recovery in function is associated with this plasticity.

See the source image
Figure: Transcranial magnetic stimulation (source everipedia.org)

Interestingly, what they found was that in RRMS as opposed to healthy controls (HCs, see Figure below), there was a correlation between the potential amplitude generated by the stimulated motor cortex and measures of cognition. What this means is that lower your difference in amplitude pre and post TMS the poorer the potential for plasticity and henceforth similarly your cognitive outcomes.

They interpreted the lack of a good correlation in the HCs as having to have had lost a certain degree of cognitive function before this association becomes apparent (i.e. you need to drop to a certain threshold).

It is, nonetheless, concerning that this effect even exists at the RRMS level, but we do no that many individuals with RRMS do have cognitive deficits.

Fig. 2
Figure: Correlations of the difference between pre and post QPS Motor evoked potential (MEP) amplitude with SDMT and BVMT-R in patients with RRMS (a,b) and HCs (c,d) This figure shows the correlations of the difference between the pre and post QPS MEP amplitude with the SDMT as a measure of information processing speed and the BVMT-R as a measure of visuospatial short-term memory and learning separately for patients with RRMS and HCs

When they looked at their data in a different way, studying the induced plasticity (QPS) according to RRMS individuals with and without cognitive deficits, this difference again materialised (see Figure below [c]).

Fig. 3
Figure: Quadripulse (QPS)-induced plasticity in patients with RRMS compared to matched HCs (a,b) and in RRMS patients with cognitive impairment compared to patients without cognitive impairment (c,d). (b) and (d) show the predicted MEP amplitude based on the fixed effects of the linear mixed models. This figure shows the level of QPS-induced plasticity in different clinical subgroups. The upper part of the figure (a,b) displays QPS-induced plasticity in patients with RRMS compared to matched HCs. The lower part of the figure (c,d) shows QPS-induced plasticity in RRMS patients with and without cognitive impairment. The left part of the figure (a,c) shows the averaged difference between the pre and post QPS MEP amplitude per time point. The right part of the figure (b,d) shows the predicted MEP amplitude based on the fixed effects of the linear mixed models.

One of the main issues with this study is that you’re studying the motor cortex plasticity and the changes observed maybe secondary to lesion involvement along the pathway. They did control for latency (i.e. a delay in conduction) in this case and found that the original associations held. Also, this is just a snapshot of the excitatory pathways and not generalisable to the whole brain (which is composed of both excitatory and inhibitory pathways). As the authors suggest if they had integrated more MRI measures into this (for example MTR – marker of recovery/remyelination), this would have added more to their findings.

Regardless, their overall findings are very interesting. As an added comment, I would like to see what influence if any cardiovascular exercise has on this.

Abstract

Brain Stimul. 2022 Feb 16;S1935-861X(22)00035-3. doi: 10.1016/j.brs.2022.02.007. Online ahead of print.

The degree of cortical plasticity correlates with cognitive performance in patients with Multiple Sclerosis

Carolin BalloffIris-Katharina PennerMeng Ma Iason Georgiades Lina ScalaNina TroullinakisJonas Graf David KremerOrhan Aktas Hans-Peter Hartung Sven Günther MeuthAlfons Schnitzler Stefan Jun Groiss Philipp Albrecht 

Background: Cortical reorganization and plasticity may compensate for structural damage in Multiple Sclerosis (MS). It is important to establish sensitive methods to measure these compensatory mechanisms, as they may be of prognostic value.

Objective: To investigate the association between the degree of cortical plasticity and cognitive performance and to compare plasticity between MS patients and healthy controls (HCs).

Methods: The amplitudes of the motor evoked potential (MEP) pre and post quadripulse stimulation (QPS) applied over the contralateral motor cortex served as measure of the degree of cortical plasticity in 63 patients with relapsing-remitting MS (RRMS) and 55 matched HCs. The main outcomes were the correlation coefficients between the difference of MEP amplitudes post and pre QPS and the Symbol Digit Modalities Test (SDMT) and Brief Visuospatial Memory Test-Revised (BVMT-R), and the QPSxgroup interaction in a mixed model predicting the MEP amplitude.

Results: SDMT and BVMT-R correlated significantly with QPS-induced cortical plasticity in RRMS patients. Plasticity was significantly reduced in patients with cognitive impairment compared to patients with preserved cognitive function and the degree of plasticity differentiated between both patient groups. Interestingly, the overall RRMS patient cohort did not show reduced plasticity compared to HCs.

Conclusions: We provide first evidence that QPS-induced plasticity may inform about the global synaptic plasticity in RRMS which correlates with cognitive performance as well as clinical disability. Larger longitudinal studies on patients with MS are needed to investigate the relevance and prognostic value of this measure for disease progression and recovery.

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Neuro Doc Gnanapavan

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