The development of cortical lesions in MS seems to correlate with the clinical course and the degree of patients’ disability independent from white matter (WM) evolution [10]. More attention has been drawn to the function of the gray matter and its involvement in the early stages of MS [11].
The current study was conducted over eighty-two people with a mean age of 34.5 + 8.12 years; of which 60 patients were females. According to the type of MS at first diagnosis, there were 59 cases of relapsing–remitting MS, 5 cases of secondary progressive MS, 4 cases of primary progressive MS, 8 clinically isolated syndrome cases and 6 radiologically isolated syndrome cases. A study by Hamed et al. [8] included 90 patients with a mean age of 33.24 + − 8.93, of which the majority were relapsing–remitting multiple sclerosis cases (91.1%).
DIR suppresses the signal of both CSF and white matter allowing much better contrast between both gray and white matter with consequent superior delineation of the gray matter and its cortical subtypes. FLAIR sequence, on the other hand, cannot exactly or clearly show the border between the cortex and subcortical white matter. Type I lesions extend through both the white matter and the gray matter, type II lesions are entirely located within the cerebral cortex, do not make contact with the subcortical white matter or the pia mater and are small. Type III lesions are subpial in location, usually not extending beyond layers 3 and 4 of the cortex. finally, type IV lesions extend over the entire width of the cortex and do not extend into the subcortical white matter and might cover several gyri or entire lobes [12].
In this study, the number of cortical plaques types 1, 2, 3 and 4 detected by 3D DIR sequence was significantly more than the FLAIR sequence with 185%, 234%, 258% and 152% percent improvement (p < 0.001). The current study results were similar to that of Guerts et al. [13] who showed that the DIR sequence resulted in a 152% increase in the cortical lesion detection rate. Elnekeidy et al. [14] and Vural et al. [15] also reported the highest accuracy of the DIR in the detection of intracortical lesions. A study by Ertan et al. [16] acknowledged that the 3D DIR sequence detected intracortical lesions five times more than that of the 3D FLAIR sequence. In a study by Calabese et al. [17], several patients presented only with ‘Cortical onset’ of MS. Pirko et al. [18] also reported that many MRI studies have shown that gray matter pathology is already present at the clinical onset of the disease, independent of white matter pathology which is subtle or very limited.
3D DIR in this study was superior in the detection of all overall cortical types as well as juxtacortical, juxtacortical extended MS plaques with 204%, 119% and 169% plaque gain in comparison to FLAIR (p = < 0.001, 0.010 and < 0.001, respectively). In a study by Ertan et al. [16], DIR detected 1.76 times more JX lesions than FLAIR which was not significant statistically, Guerts et al. [13] also showed more JX lesions on DIR. On the other side, Moraal et al. [19] and Vural et al. [15] reported a higher number of juxtacortical lesions with FLAIR than DIR sequence, yet both studies showed no significant difference.
3D DIR was significantly better than FLAIR for MS plaque number detection in the periventricular white matter, subcortical white matter, infratentorial region and the overall MS plaques burden with a relative improvement of 115%, 112%, 131% and 122%, respectively (p < 0.001, 0.038, < 0.001, < 0.001, respectively). Different studies as with this study showed that the DIR was superior in detecting plaques in all these anatomical regions [11, 13,14,15].
The current study revealed no significant difference between 3D DIR and FLAIR for plaques number detection in deep white matter (p = 0.344) and deep gray matter (p = 0.104). However, Elnekeidy et al. [14] showed more DWM lesions on the DIR. On the other hand, few other studies found that the FLAIR rather than DIR detected a higher number of lesions in DWM [13, 15, 20]. The contrary outcomes throughout various studies revealed that the DIR and FLAIR have remarkably similar detection rates for the DWM plaques, which could be due to the plaques' location away from the cortical and periventricular regions.
According to a study by Haider et al. [21], the cause and clinical significance of deep gray matter injury in MS remains unknown but their study highlighted the importance of only the caudate nucleus and hypothalamus of which their pathogenic processes included demyelination, neurodegeneration and accumulation of oxidative injury. This study revealed no significant difference between 3D DIR and FLAIR for plaques number detection in the deep gray matter (p = 0.104). Ertan et al. [16] and Geurts et al. [13] showed that more lesions were detected by the DIR sequence compared to the FLAIR sequence in the deep GM regions. Ertan et al., however, showed no difference between DIR and FLAIR in the number of lesions in the thalamus.
Hamed et al. [8], Vural et al. [15] and Calabrese et al. [22] observed a positive association of cortical lesion load with the clinical outcome and EDSS of the patient. This study as well showed a significant correlation between MS disease duration, number of attacks and EDSS in relation to the overall cortical MS plaque types, juxtacortical expanded lesions, periventricular white matter lesions and the overall MS plaque burden. On the other hand, no significant correlation was seen for the deep white matter and infratentorial MS plaques. Elkholy et al. [23] showed a positive correlation yet not statistically significant between EDSS and the number of periventricular lesions, deep white matter lesions and infratentorial lesions in both FLAIR and DIR.
We recommended that using artificial DIR, which can create high contrast images from standard input, can detect cortical lesions with high reliability, significantly improving lesion detection in MS patients [5, 24].
Limitations
The first limitation was the relatively small number of patients. Secondly, cortical lesion volume was not included in this study which would have increased our knowledge of MS pathobiology and disease evolution.