Multiple Sclerosis: Clinical Features, Pathophysiology, Neuroimaging and Future Therapies

Abstract

Multiple sclerosis (MS) is a common immune-mediated progressive neurodegenerative disease of the CNS that typically manifests with periods of disease activity followed by intervals of remission. The etiology of MS remains unknown; however, existing evidence indicates that MS is a ‘whole-brain disease’ that is driven by a potent immune response against CNS antigen(s), particularly myelin peptide antigens. The immunopathogenesis of MS includes both the cell- and humorally-mediated arms of the immune system. Genetic and environmental factors play important roles in the development of MS. Application of various neuroimaging techniques to the world of MS have expanded our knowledge concerning its pathogenesis and assist us in the more accurate diagnosis of MS versus its imitators. Current treatments target acute attacks and aim to reduce future clinical relapses. A summary of the potential future therapies for MS is presented.

Fractalkine (CX3CL1) levels in patients with Behçet's disease and Neuro-Behçet's disease

“…A significant increase in serum CX3CL1 levels was demonstrated in the only study conducted in MS patients [8]. Despite clinical similarities, the pathogenesis of NBD and MS differ in several aspects, however there are no specific markers for either disease [6,[21][22][23][24].…”

Some neuropsychiatric and MRI manifestations in patients with multiple sclerosis

“…Motor symptoms in MS mainly originate from corticospinal tract involvement and patients complain of weakness, heaviness, stiffness, or even pain in the affected limbs. Development of demyelinating lesions in the corticospinal tract may occur at the medullary pyramids, basis pontis, cerebral peduncles, deep hemispheric WM, or, Cerebellar manifestations in MS result from vermian and hemispheric cerebellar (a favorite location for MS) demyelinating lesions, and clinically present with gait ataxia, dysmetria, intention tremor on the finger-to-nose test, dysdiadochokinesia, difficulty with the heel-to-shin test, rubral tremor, and failure to perform on tandem gait examination [32].…”

“…Other abnormalities of ocular motility, which may be observed as part of MS, consist of one-and-a-half syndrome, skew deviation, paresis of single cranial nerves innervating extraocular muscles (III, IX, and IX), horizontal or vertical gaze paresis, and impairment of smooth visual pursuit. Involvement of the lower parts of the brainstem is associated with unilateral or bilateral facial paresis, dysarthria, nasal speech, pseudobulbar palsy, vertigo, tinnitus, dysphagia, blepharospasm, and rarely hearing loss, although the latter is rare [32].…”

“…Upon neuro-ophthalmologic examination, varying degrees of visual acuity loss, central scotoma, papillitis (swollen optic nerve head with hemorrhages or exudates), or normal optic disk (in cases of retrobulbar optic neuritis) are detected. In addition, these patients have impairment of color vision, prolonged visual-evoked potentials, and a positive 'swinging flashlight test', which points toward an afferent pupillary defect (also known as Marcus Gunn pupil), as well as various forms of visual field defects [32].…”

“…In addition, MS is a potentially painful disease and several painful syndromes, such as trigeminal neuralgia glossopharyngeal neuralgia [45], radicular pain, and 'central pain', may occur during the course of the disease. Central pain is observed in 15-85% of MS patients [32].…”