MS attacks myelinated axons in central nervous system immune-mediated inflammatory. 

Disease follows relapsing-remitting pattern with short-term neurologic deficits that resolve. 

It is a mix of genetic factors and external triggers resulting in an autoimmune disorder attacking the CNS. 

Multiple sclerosis diagnosis requires multiple clinical attacks with lesions separated in time and space. 

MS is divided into the following categories: 

Relapsing-remitting MS  

Secondary progressive MS 

Primary progressive MS  

Progressive-relapsing MS 

Physician should not immediately diagnose MS after first demyelination attack due to other possible diseases. 

The prevalence in the US ranges from 58 to 95 per 100,000 population. It affects 2.1 million people worldwide, crosses all regions and races with varying prevalence rates. 

Racial and ethnic differences impact risk with more incidence  rate is reported in various regions. 

Autoimmune diseases are more prevalent in women. The ratio of female-to-male incidence has risen from 1.4 in 1955 to 2.3 in 2000. 

Improved adhesion molecule expression on lymphocytes and macrophages allows inflammatory cells to breach blood-brain barrier. 

It is an inflammatory CNS disease with demyelinating plaques. Plaques appear as indurated areas in specimens. 

Multiple sclerosis is CNS disease with demyelinating plaques causing inflammation and sclerosis in pathologic specimens. 

Patients shows demyelinating lesions in spinal cord and brain, with myelin loss, oligodendrocyte destruction, and axon sparing. 

In MS, neural inflammation resolves with some remyelination. Recovery in patients may be due to nervous system plasticity. 

Unknown cause of MS suggests multiple factors contribute to trigger or sustain disease. It occurs when environmental factors combine with genetics to disrupt immunity. 

First-degree relatives of MS patients have a seven times higher risk of MS, but their excess lifetime risk is low.  

Gene variants within the general population, known as polymorphisms, can cause various levels of gene and protein expression. 

Without treatment, over 30% of MS patients face severe disability in 20-25 years.  

Some disease-modifying agents for MS slowed disability progression in research trials, long-term effects are uncertain. 

5% to10% of MS patients experience a milder phenotype with no significant disability after decades. 

Men with primary progressive MS have poor prognosis and limited treatment response. Patients have slightly shorter life expectancy, that is linked to disability and severity. 

Multiple Sclerosis is diagnosed in people between the age group of 20 and 40 years old.  

Cranial Nerve Examination 

Sensory System Examination 

Motor System Examination 

Symptoms quickly emerge with subsequent partial or full recovery. 

Symptoms slowly worsen from RRMS to steady progressive form without relapses. Gradual symptom progression with intermittent relapses. 

Multiple sclerosis treatment includes immunomodulatory therapy (IMT) for immune disorders and symptom management therapies. 

IMT aims to reduce relapses and slow MS progression, with most agents approved for relapsing forms. 

Emergency department treats symptoms and risk factors of acute exacerbation to improve medical condition. 

Therapies for relapsing MS reduce attack frequency and severity, slow disability progression, and decrease lesion accumulation in the brain/spinal cord. 

Patient lifestyle, tolerance, and injection side effects impact choice of DMAMS. Physician preference and experience with medications also influence selection. 

Cyclophosphamide induction and glatiramer maintenance reduced relapse risk and were well tolerated. 

Neurology

Psychological support essential for managing stress, anxiety, and depression in patients. 

Lifestyle modification like intake of healthy nutritional supplements and proper hydration should be followed by patients. 

Proper education and awareness about multiple sclerosis should be provided and its related causes, and how to stop it with management strategies. 

Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort. 

Neurology

• Interferon beta-1b: Interferon beta stops pro-inflammatory cytokine expression, including IL-1 beta, TNF-alpha, TNF-beta, IFN-gamma, and IL-6. 
• Interferon beta-1a: It is approved for treating relapsing MS slows disability accumulation and frequency decrease in patients. 
• Alemtuzumab: It is a monoclonal antibody targeting CD52 to treat relapsing forms of multiple sclerosis. 
• Natalizumab: It is a bioengineered antibody that blocks alpha-4 integrin adhesion function. 
• Teriflunomide: It reduces inflammation that inhibits dihydroorotate dehydrogenase enzyme. 
• Ocrelizumab:  It targets CD20 antigen on pre-B and mature B lymphocytes with selectivity. 

Neurology

Methylprednisolone: 

It decreases inflammation that reverses capillary permeability. 

Prednisone: 

It suppresses inflammation and immune responses at high doses. 

Neurology

Azathioprine: 

Immunosuppressive drug derived from 6-mercaptopurine converted to 6-thiouric acid by xanthine oxidase. 

Methotrexate:  

It inhibits DNA processes that block dihydrofolic acid reductase, impeding thymidylate and purine synthesis. 

Mitoxantrone:  

It is approved for secondary progressive or aggressive relapsing-remitting MS to reduce disability and clinical relapses in patients. 

Cladribine:  

It is a prodrug of Cd-ATP used for multiple sclerosis. The mechanism involves cytotoxic effects on lymphocytes through DNA synthesis impairment. 

Neurology

Siponimod: 

It is used for adults with relapsing forms of MS including active secondary progressive disease. 

Fingolimod: 

This activity reduces lymphocyte migration into the central nervous system. 

Neurology

Amantadine: 

It is approved for influenza A and Parkinson’s, also used off-label for fatigue in MS patients. 

Neurology

Baclofen: 

It decreases excitatory neurotransmitter release at spinal level to inhibit reflexes. 

Neurology

OnabotulinumA toxin: 

It is an injectable toxin that blocks nerve-muscle connections for muscle relaxation. 

Neurology

Tizanidine:  

Alpha-adrenergic agonist decreases spasticity that increases motor neuron inhibition. 

Neurology

Clonazepam:  

It is a benzodiazepine that enhances GABA inhibition to reduce reflexes. 

Diazepam:  

It increases presynaptic inhibition by modulating GABA-A transmission. 

Neurology

Modafinil:  

It is a Schedule IV controlled substance that promotes wakefulness and treats fatigue without disrupting sleep. 

Armodafinil: 

It promotes wakefulness like sympathomimetic agents, but with a different pharmacologic profile. 

Neurology

Carbamazepine  

It blocks sodium channels, usually relieves pain in 80% MS patients in 24 to 48 hours. 

Gabapentin  

It is used for pain management and sedation in neuropathic patients. 

Neurology

Duloxetine 

It inhibits serotonin and norepinephrine uptake, treats depression and neuropathic pain. 

Neurology

Ibuprofen 

It is preferred for mild to moderate pain to reduce inflammation and prostaglandin synthesis. 

Neurology

Oxybutynin 

It is an antispasmodic that relaxes bladder smooth muscle to inhibits muscarinic effects of acetylcholine on muscle. 

Neurology

Docusate sodium:  

It softens stools to incorporate water and fat, that ensure easy and natural passage. 

Methylcellulose:  

It bulks stool, increases bowel motility and reduces transit time. 

Use of Acetylcholinesterase Inhibitors: 

Donepezil:  

It inhibits acetylcholinesterase to enhance acetylcholine levels for improved cognitive function. 

Neurology

Dalfampridine 

It is approved to improve walking in patients. 

Neurology

Medications for Disease-Modifying Therapy in MS reduce relapses, disability progression, and immune system attacks on myelin sheath. 

Plasmapheresis removes plasma from the blood and replaces it with a substitute to treat severe MS relapses unresponsive to steroids. 

Neurology

In the diagnosis phase, evaluation includes medical history, physical examination, and neurological tests to confirm diagnosis. 

Pharmacologic therapy is very effective in the treatment phase as it includes use of immunomodulator, corticosteroids, dopamine agonist, neuromuscular blocker, benzodiazepines and surgical intervention. 

In supportive care and management phase, patients should receive required attention in the form of postoperative care and rehabilitation. 

The regular follow-up visits with the neurologist are schedule to check the improvement of patients along with treatment response.