Multiple sclerosis is an inflammatory demyelinating disorder of the central nervous system that is more common in northern latitudes and among Caucasian populations. It typically presents with sensory disturbances, weakness, and visual problems and is diagnosed based on disseminated lesions found on MRI. Management involves immunosuppression and physical/occupational therapy to address symptoms and maintain function. Prognosis depends on factors like age of onset, relapse rate, and the degree of disability.

1. Multiple sclerosis Ramesh Debur

2. Definition It is a inflammatory, demyelinating disorder involving the white matter of the central nervous system

3. Etiology

4. Eitology and Demographics More in the northern hemisphere than in the southern hemisphere More in Europe, Canada, North America than the rest Risk Stratification White > Asian > African

6. Etiology / Demographics Anywhere between 10 to 60 years Peak onset between 20 to 40 years Female > Male Genetic factors 20 times increase if the first degree relative is affected Monozygotic twins 30% greater chance Migrants to europe at increased risk Environment

7. Onset Insidious onset Optic Neuritis - Complaint of mono occular weakness and pain most common Parasthesias, Weakness Pain Impaired coordination

8. Clinical Features

9. Initial Signs and clinical features Action tremor ascending numbness starting in the feet; bilateral hand numbness; hemiparesthesia; dysesthesia in one of the above distributions; generalized heat intolerance Motor weakness with UMN symptoms

10. Later clinical features Motor System Weakness (mono, quadri, etc), Spasticity, + ve Babinski’s, Cerebellar Dysdiodochokinesia, ataxia, scanning speech, incordination, loss of balance. Sensory Lhermitte's sign, dysesthetic pain, paresthesia, numbness Posterior column loss heat intolerance

11. Urinary Incontinence, increased frequency, incomplete emptying, UTI Optic disc pallor, atrophy, blurred vision, diplopia, nystagmus, oscillopsia, intranuclear ophthalmoplegia, central scotomas or other visual field defects

12. Symptoms Depression Lhermitte’s sign Weakness Fatigue Dizziness or vertigo Heat sensitivity Sexual dysfunction

13. Diagnosis Standard Criteria History of at least two attacks; Clinical evidence of at least one lesion and clinical or para clinical evidence of another lesion

14. Hallmarks Disseminated white matter lesions of the CNS were first described by a French neurologist Charcot in late 19 th Century perivascular inflammation and demyelination Periventricular distribution of plaques is often seen.

15. Mechanisms of Plaque Evolution blood-brain barrier is disrupted at the onset of symptoms , acute inflammatory response of lymphocytes, plasma cells and macrophages can produce demyelination by direct or indirect mechanisms . The macrophages in those lesions contain myelin fragments or myelin breakdown products. Lymphocytes contribute to pathologic processes by means of antibody- and cell-mediated immunity (direct mechanism) or by secretion of lymphocytes and cytokines (indirect mechanism

20. Results of Demyelination conduction block at the site of lesion slower conduction time along the affected nerve increased subjective feeling of fatigue secondary to compensation for neurologic deficits

21. Clinical Diagnosis Interneculear opthalmoplegia Optic neuritis Positive rhomberg sign Lhermitte’s sign Atleast 2 episodes of weakness with spontaneous resolution of symptoms

22. Differential diagnosis CNS infection (e.g., Lyme disease, syphilis, human immunodeficiency virus infection, human T-lymphotrophic virus type I) CNS inflammatory condition (e.g., sarcoidosis, systemic lupus erythematosus, Sjögren's syndrome) CNS microvascular disease (e.g., disease caused by hypertension, diabetes mellitus, vasculitis, ) Genetic disorder (e.g., leukodystrophy, hereditary myelopathy, mitochondrial disease) Structural or compressive condition of the brain and spinal cord (e.g., cervical spondylosis, tumor, herniated disc, Chiari's malformation) Vitamin B12 deficiency

23. Types Benign MS 10% Relapsing-remitting MS 40% Secondary chronic progressive 40% Primary progressive MS 10%

24. Treatment Immunosupression (ATCH)- initial phase Steroidal therapy- maintenance Beta-Interferon – treatment of relapses Immuno Globulin g - prevention of relapse

25. Physiotherapy Management

26. Alternative Therapies

27. Nutrition Good Omega-6 oils (borage, evening primrose, black currant oils) B-complex vitamins, especially B12 (1,000 mcg per day) and B6 (100 mg per day), and minerals, such as calcium (1,000 mg per day) and magnesium (500 mg per day) Vitamin C (250 to 500 mg twice per day), vitamin E (400 IU per day), and coenzyme Q10 (100 mg twice Bad Avoid food allergens such as wheat, dairy, eggs, soy, citrus, tomatoes, corn, chocolate, fish, and peanuts—eliminate these foods, then reintroduce one at a time, watching for reactions. Many individuals with MS are sensitive to foods that contain gluten. Eliminate refined foods, alcohol, caffeine, saturated fats (animal products), and additives (MSG and aspartame)

28. Complimentary therapies Homeopathy Combination remedies may be used for fatigue, spasm, and to help rid the body of impurities. Acupuncture Acupuncture may be used to alleviate symptoms. Massage Massage is important for maintaining flexibility and reducing Spasticity, as well as improving the overall sense of well-being

29. Factors that influence prognosis Favorable Females Low rate of relapses per year Complete recovery from the first attack Long interval between first and second attack Symptoms predominantly from afferent systems (i.e.,. sensory symptoms) Younger age of onset Low disability at 2 to 5 years from the disease onset Later cerebellar involvement Involvement of only one CNS system at the time of onset Unfavorable Males High rate of relapses per year Incomplete recovery from the first attack Short interval between first and second attack Symptoms predominantly from efferent systems (i.e.,. symptoms of motor tract involvement) Older age of onset Significant disability at 2 to 5 years from the onset acute onset Early cerebellar involvement Involvement of more than one CNS system at the time of onset

30. Physiotherapy Management Philosophy of Neuro Rehabilitation: Education and Self Management

31. Assessment Strength Tone Range of Motion Balance Co-ordination Ambulation Fatigue Cardio vascular and respiratory status Bed Mobility Bowel/Bladder/Sexual Status Swallowing Visual Status Sensory Impairment ADL Cognition Vocational status Psychological status Physical environment

32. Goals Intial Phases Maintain JROM, Reduce pain, Reduce fatigue, maintain muscle properties Later stages Maintain muscle properties, Reduce Fatigue, strengthing program Remission phases Functional independence, focus on recovery of residual muscles, Optimisation of the remaining muscle strength Relapses Maintain previous levels of activity *Revaluate patient for complications and deterioration

33. Management Three levels of treatment based on : Symptomatic treatment Standardized profiles Patient Driven goals

34. Symptomatic Fatigue Factors contributing : sleep deprivation, neuromuscular fatigue, depression, etc Management: Energy conservation, exercise planning, rest activities, enviromental adaptaion Aerobic exercise, general endurance exercises, general conditioning exercises,

35. Weakness: could be due to Spasticity, disuse, fatigue, Deconditioning, etc, Treatment: slow progressive exercises, PNF, compensatory strengthing techniques, bracing, mobility aids, orthotics. Spasticity: due to the UMN syndrome Treatment: Stretching, RIP, Surgical & medical management

36. Balance & coordination: due to cerebellar problems Treatment: Strengthing proximal musculature, using visual cues, biofeedback, weighted cuffs, Sensory problems: Dorsal column problems Treatment: compensatory strategies, retraining methods, counter irritant therapy,

37. Cognitive dysfunction: Due to central demyelination Treatment: Compensatory strategies such as memory book, etc, Clear reasoning strategies, short term recall (e.g.. For ADL), General Deconditioning Treatment: Aerobic exercises, swimming etc,

38. Standardised profiles General Measures Functional Independence Measures (FIM) Barthel Index Disease Specific Krutzke Scale for multiple sclerosis Modified fatigue impact inventory Mental health inventory QOL SF – 36 Modified Social Support survey