Multiple sclerosis is an autoimmune chronic disease that causes neurological problems and progressive disability. Brain atrophy related to MS is a result of both underlying pathology (neuro inflammation) and neuro-axonal loss. In MS patients, brain volume loss occurs in a faster rate than in the healthy population: 0.5–1.0% vs. 0.1–0.3% per year [28]. Early in the disease course atrophy may be found even before detection of clinical symptoms and lead to long-term neurological disability [29].
Magnetic resonance imaging (MRI) is an important tool not only in diagnosis of MS disease, but also in the monitoring of disease activity and prediction of effects of treatment [30].
The primary objective of this study was to evaluate the brain atrophic changes in MS patients using MR-based quantitative volume measurements.
MRI-based brain volumetry at a single time point was applied to MS patients in our study, to evaluate its possible role in identifying MS patients at risk of disease progression. Patients were divided into six groups as following: Those with no thalamic or BP atrophy i.e., both within the normal range; z-scores greater than − 1.96(group 0), whole brain atrophy (z score below − 1.96(Group 1): thalamic and BP atrophy both z-scores below − 1.96(Group 2): thalamic (z-score below − 1.96) but no BP atrophy z-score greater than − 1.96(Group 3) whole brain atrophy with other structure atrophy (rather than thalamus) (group 4), multiple structure atrophy (Group 5).
We demonstrated twenty eight out of thirty MS patients showed BP atrophy according to the predefined z-score cut-off of − 1.96. Only two of MS patients showed no brain atrophy despite of long duration of illness 6 and 7 years. This indicated that whole brain atrophy is the most frequent pattern of atrophy and this was most probably due to the long duration of illness that led to global brain atrophy.
We showed that seventeen patients (56.7%) had whole brain atrophy associated with isolated thalamic atrophy as compared to 2 patients with whole brain atrophy and isolated corpus callosum atrophy 1 patient with whole brain atrophy with corpus callosum and caudate, one patient brain atrophy with caudate and putamen atrophy without thalamic atrophy. This indicates that the thalamus is the most frequent structure to be affected with whole brain atrophy (56.7%).
Study done by Alaleh et al. [23] agreed with us that corpus callosum, putamen and the caudate nucleus show a lower susceptibility for atrophic processes compared with the thalamus. The frequency of corpus callosum, caudate and putamen atrophy in our study was much lower than of the thalamus in 17 patients (56.7%) as compared to corpus callosum atrophy in 7 patients (23.3%), caudate atrophy in 7 patients (23.3%) and 2 patients with putamen atrophy (6.7%).
In our study, we showed that no patients with thalamic, caudate, putamen or corpus callosum atrophy without whole brain atrophy this may suggest that the whole brain volume affected more than isolated structure atrophy, or this may be due to long disease duration (mean duration of the cases was 6.1 years ± 2 SD) that affected the whole brain volume.
Our study showed ten patients (33.3%) with multiple structure atrophy.
Our findings differed from those documented in previous study done by Alaleh et al. [23], their study demonstrated thalamic atrophy without whole brain atrophy furthermore, almost no patients show whole brain atrophy, without thalamus atrophy. This disagreed with us as we noticed that 28 of 30 MS patients (93.3%) showed whole brain atrophy and the remaining 2 patients (6.7%) without whole brain atrophy did not show any other structure atrophy. No thalamic or other structures atrophy occurred without whole brain atrophy. In our research we did not detect a subgroup of MS patients with isolated thalamic atrophy in contrary to their study.
Our study results were matching with those detected by Sonia et al. [21] who reported a significant reduction of basal ganglia and thalamic volumes in MS patients relative to normal controls. DGM atrophy was most prominent for thalamus as compared to caudate and putamen.
The study done by Bergsland et al. [31] showed similar results to us, as they found that the early RRMS group showed significant decreases in multiple SDGM (thalamus, caudate and globus pallidus). They differed from us as they compared deep grey matter atrophy between patients with RRMS and patient with CIS. In our study, we compared atrophy of different grey matter structures and of corpus callosum in patients with RRMS to detect the most frequently affected structure that can be an early indicator of brain atrophy and disease progression.
A previous study done by Massimiliano et al. [32] detected presence of thalamic atrophy in remitting relapsing MS as in our study and found that the regional analysis of deep and cortical grey matter atrophy suggests an association between the neurodegenerative process taking place in the striatum—thalamus—frontal cortex pathway and the development of fatigue in relapsing—remitting multiple sclerosis.
In our study, we found no significant association between the presence of whole brain atrophy, isolated thalamic atrophy or multiple structure atrophy and increase of EDSS, this may be due to narrow range of variation of EDSS between MS patients and small sample size.
In our study, we showed no significant relation detected between the presence of cognitive impairment and, presence of whole brain, thalamic and multiple structure atrophy.
We were agreeing with Alaleh et al. [23], in that they did not found significant relation between increase in EDSS and presence of isolated thalamic atrophy but they successed to prove that there was significant relation between higher EDSS and subgroup of whole brain and associated thalamic atrophy.
We disagreed with Datta et al. [23], who found a weak association between EDSS and thalamic volume.
We found that no significant relation between the disease duration and degree of thalamic atrophy as well as between the disease duration and presence of multiple structures atrophy. The relation between the duration of illness and degree of loss of whole brain volume was insignificant and this might be due to the small sample size as its P value was 0.069 approaching significance, increase the sample size might increase significance. There was no significant relation between the presence of thalamic atrophy and disease duration. We could not assess the relation between the longer the disease duration and presence of whole brain atrophy as the number of patients without atrophy was too small to study this relation.
Our results regarding the effect of duration of illness were different from those found by Alaleh et al. [23], as they studied only the effect of duration on the presence of thalamic and whole brain atrophy and they found significant relation between the longer disease duration and presence of atrophy (P value = 0.036).
The limitations of our study were the small number of patients group the more number of cases the more the accuracy and impact of the study. The patients included in our study were diagnosed with remising and relapsing MS no patients with primary or secondary progressive MS. Relative long duration of illness (mean disease duration of the cases was 6.1 years ± 2 SD) short disease duration allows detection of early atrophic changes.
Other studies with larger number of cases and more variable types of MS subtype are highly recommended. In spite of small size of our sample and lack of variability of MS subtypes, we recommend to use MR volumetry technique in all patients diagnosed with MS for early detection of brain atrophic changes (which indicates progressive course of the disease and need of more aggressive therapy), as well as in the follow up of therapy to ensure the efficacy of the used medication.