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Received : 18-03-2021

Accepted : 22-03-2021



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Get Permission Jain, Shukla, Agrawal, and Sharma: A review: Pathophysiology, diagnosis and management of multiple sclerosis


Introduction

Multiple sclerosis is an auto immune disorder that affectscentral nervous system and it leads to severe physical and cognitive incapacitation as well as neurological problems in young adults. However MS is somewhat influenced by B cells through a variety of mechanisms, including ectopic lymphoid follicles in the CNS, present antigen , production of cytokine and production of antibiotics. Multiple sclerosis is considered the most common cause of neurological disability while inflammatory lesions associated with MS may affect a large range of systems and cause a variety of neurological symptoms.1, 2

Multiple sclerosis presents between 20 and 40 years of age and the women are more susceptible than men. The exact pathophysiology of multiple sclerosis in not known but it seems to be autoimmune in nature.3

Types of Multiple Sclerosis4, 5, 6

Multiple sclerosis is extremely variable with symptoms that may be appear, disappear or sometimes worsen over time and it is possible and to classify people according to the course of their disease.

  1. Relapsing remitting multiple sclerosis

  2. Secondary progressive multiple sclerosis

  3. Primary progressive multiple sclerosis

  4. Progressive relapsing multiple sclerosis

The treatment strategy for multiple sclerosis is broadly based on disease – modifying drugs such as interferon – β and glatiramer acetate. Multifocal zones of inflammation due to T- lymphocyte and macrophage infiltrations and are the primary causes of myelin sheath destruction that result in the formation of CNS plaques.

Pathogenesis of Multiple Sclerosis

Multiple sclerosis shows a variety of neurological symptoms that spread in different parts of the CNS. It may occur alone or combined. These symptoms are quite vary from patient to patient but it may involve sensory disturbance, dysfunction of bladder, vision loss limb weakness, fatigue and troubles in bowel. Typically the disease starts with the sudden onset of neurological deficits.7, 8

Only small percentage of patients feel a gradually progressive clinical course from the onset of the disease such as clinical course refers to the principal progressive from of MS. Therefore the steady progression of symptoms associated with primary progressive MS leads to disability from the beginning.9, 10

Figure 1

Pathogenesis of multiple sclerosis with immune cell and their cytokines

https://s3-us-west-2.amazonaws.com/typeset-prod-media-server/7cc054c8-623f-4e60-976e-4915ad09579aimage1.jpeg

Diagnosis Approaches

Basically the diagnosis of multiple sclerosis is based on the demonstration of MS- typical CNS lesions disseminated in space and time which based upon clinical findings alone or it a combination of clinical and MRI approach. It’s also being diagnosed with the demonstration of neurological sign and symptoms.10, 11, 12

Table 1

More common symptoms of Multiple Sclerosis (MS)

Primary symptoms

More common symptoms

Dizziness, emotional impairment, vision problems and walking difficulty

Less common symptoms

Hearing, Headache, breathing and Speech problems and swallowing etc.

Secondary symptoms

Urinary tract infections

Tertiary symptoms

Depression, Psychological and social complications.

Nowadays the diagnosis of MS based on the result of MRI examination. For MRI examination a contrast agent like gadolinium used to highlight active plaques, MRI allows detecting plaques that are ongoing to destruction of the BBB. Apart of this diagnosis tools various potentials test including visual, brain stem auditory and somatosensory, these furnished the information about demyelization in the optic nerve and CNS. In addition, CSF analysis for myelin basic protein and immunoglobulin gamma (Ig G) determination and blood sample analysis for detection of vitamin deficiencies may be helpful.13, 14

Management of Multiple Sclerosis

In previous studies we know that there is no current treatment of multiple sclerosis but Therapeutic management may be useful. Therapeutic management can be dividing into relapse treatment, Symptomatic treatment and disease- modifying treatment. In relapse treatment the Methylprednisolone at dose of 1 g/day or 500 mg/day for 305 days with or without oral tapering. Alternatively the treatment continues with equal dose via oral administration.

In disease- modifying treatment, potentially ameliorate the disease course are studied and in case the clinical course is dominated by relapses as for the clinically isolated syndrome RRMS and occasionally SPMS.

The basic therapeutics deals with immunomodulators like IFN β and glatiramer acetate are used as first line therapeutics which help in reducing the relapse rate and do not cause any severe side effect. Teriflunomide and fingolimod are also used as basic therapeutics.

Basic therapeutics Apart from above treatment some therapies like Escalation therapy and Symptomatic treatment etc. are also available which more beneficial in the treatment of multiple sclerosis.15, 16

Conclusion

The actual cause of multiple sclerosis is unknown. Various factors influences play an important role in the pathogenesis of this disease. Several drugs having therapeutic effect anti inflammatory drugs, immunomodulators in multiple sclerosis have been studied. In present research, current treatment is not available but beside drug therapies like ADSCs which gives the idea of cell transplantation. This idea may provide a novel strategy for the treatment of neurological disease.

Source of Funding

None.

Conflict of Interest

The authors declare that there is no conflict of interest.

References

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C Bjartmar JR Wujek BD Trapp Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the diseaseJ Neurol Sci200320621657110.1016/s0022-510x(02)00069-2

2 

T Jersild Penicillin in Scarlet FeverBMJ1948131810.1136/bmj.1.4545.318-c

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BD Trapp KA Nave Multiple Sclerosis: An Immune or Neurodegenerative Disorder?Annu Rev Neurosci20083112476910.1146/annurev.neuro.30.051606.094313

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A Alonso MA Hermain Temporal trends in the incidence of multiple sclerosis: a systemic reviewNeurology200087112935

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R Gandhi A Laroni HL Weiner Role of the innate immune system in the pathogenesis of multiple sclerosisJ Neuroimmunol20102211-271410.1016/j.jneuroim.2009.10.015

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NG Torkildsen SA Lie HL Nyland Survival and cause of death in multi sclerosisNeurol Mult Scaler20081411999

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EG Celius C Smestad Change in sex ratio, disease course and age at diagnosis in Oslo MS patients through seven decadesActa Neurol Scand200912027910.1111/j.1600-0404.2009.01208.x

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IF Charo RM Ransohoff The Many Roles of Chemokines and Chemokine Receptors in InflammationN Engl J Med200635466102110.1056/nejmra052723

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FD Lublin SC Reingold Defining the clinical course of multiple sclerosis: results of an international survey. National Multiple Sclerosis Society (USA) Advisory Committee on Clinical Trials of New Agents in Multiple SclerosisNeurology19964690711

10 

AJ Coles A Cox E Page J Jones SA Trip J Deans The window of therapeutic opportunity in multiple sclerosisJ Neurol200625319810810.1007/s00415-005-0934-5

11 

A Feinstein The clinical neuropsychiatry of multiple sclerosis2nd EditionCambridge University PressNew York, NY2007

12 

RA Marrie R Rudick R Horwitz G Cutter T Tyry D Campagnolo Vascular comorbidity is associated with more rapid disability progression in multiple sclerosisNeurology201074131041710.1212/wnl.0b013e3181d6b125

13 

DH Mahad BD Trapp H Lassmann Pathological mechanisms in progressive multiple sclerosisLancet Neurol20151421839310.1016/s1474-4422(14)70256-x

14 

R Milo A Miller Revised diagnostic criteria of multiple sclerosisAutoimmun Rev2014134-55182410.1016/j.autrev.2014.01.012

15 

B Ferguson MK Matyszak MM Esiri VH Perry Axonal damage in acute multiple sclerosis lesionsBrain19971203939

16 

F Khan L Turner T Kilpatrick Multidisciplinary rehabilitation for adults with multiple sclerosisJ Neural Neurosurg Psychiatry2008792114



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