## 1 Introduction  
Multiple sclerosis (MS) is a chronic autoimmune inflammatory disease characterized by demyelination and axonal loss in central nervous system neurons of the brain, spine, and optic nerves [1] that affects approximately 2.8 million people worldwide [2]. There are secular trends of increasing disease incidence and prevalence that are non-homogeneously distributed across populations due to complex gene-gene and gene-environmental interactions and increasing incidence among females. Uncertainties regarding the ascertainment of MS diagnosis and censoring of survival data after diagnosis may confound accurate estimations of incidence and prevalence rates, respectively [3]. Notwithstanding this, it remains indisputable that MS has exacted high economic costs on the healthcare systems of both developed [4] and low- to middle-income countries [5]. The main drivers of healthcare resource utilization are the costs of disease-modifying therapies (DMTs) and the non-medical costs associated with the management of chronic disability in the early and advanced stages of the disease, respectively [4; 5]. While patients and their families frequently bear the costs of non-medical interventions, these interventions are nevertheless associated with increased long-term medical and total societal costs [4]. This underscores the need for early diagnosis and intervention with DMTs, which can potentially control disease progression [1; 6; 7] and have been shown to be cost-effective in improving patients' quality of life [8]. This provides ample justification and motivation for the ongoing quest for more sensitive and accurate methods of MS diagnosis. There is no single pathognonomic clinical or laboratory finding that can secure a definitive diagnosis of MS. Rather, the diagnosis is made based on consensus clinical, imaging, and laboratory criteria [1; 6]. The 2017 McDonald criteria [9] define typical clinical signs and symptoms as well as lesions on magnetic resonance imaging (MRI) [10] that manifest in time and space, which can be combined with auxiliary examination findings (cerebrospinal fluid examination, visual and somatosensory evoked potentials) to establish the diagnosis of MS. Of note, MRI plays an instrumental role in the identification and localization of characteristic demyelinating plaques in the white matter of the brain and spine that constitute the pathological basis of MS and underpin its neurological presentations [10; 11; 12]. In particular, T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI [13] offers the optimal contrast-to-noise image signal properties for sensitive detection of plaque lesions and is routinely performed for anatomical MRI screening of the central nervous system in suspected cases of MS [12]. Interpretation of MRI images requires experts to manually scrutinize multiple contiguous image sections for the presence of white matter lesions, with care being taken to distinguish MS plaques from lesions associated with diseases that present with similar symptoms, e.g., ischemic gliosis and central nervous system vasculitis [14; 15; 16]. MS plaques are hyperintense in T2 sequence, oval-round shaped, at least 3 mm in size, with asymmetric distribution. The typical location of MS plaques is as follows: (1) periventricular: adjacent to the lateral ventricles; (2) juxtracortical and cortical: localized to U fibers; (3) infratentorial: located unilaterally or bilaterally paramedian adjacent to the brain stem, cerebellum, and 4 th ventricle; (4) spinal cord: cervical and thoracic localized, shorter than two vertebral segments, axially wedge-shaped, sagittal cigarette shaped, localized in peripherally located posterior and lateral columns [12]. The process of clinical scan reading is time-intensive, fatiguing, and susceptible to intra- and inter-observer variability.