Multiple sclerosis

Ramesh Debur

Definition

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

Etiology

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

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

Onset

Insidious onset

Optic Neuritis - Complaint of mono occular

weakness and pain most common

Parasthesias,

Weakness

Pain

Impaired coordination

Clinical Features

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

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

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

Symptoms

Depression

Lhermitte’s sign

Weakness

Fatigue

Dizziness or vertigo

Heat sensitivity

Sexual dysfunction

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

Hallmarks

Disseminated white matter lesions of the CNS

were first described by a French neurologist

Charcot in late 19th Century

perivascular inflammation and

demyelination

Periventricular distribution of plaques is

often seen.

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

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

Clinical Diagnosis

Interneculear opthalmoplegia

Optic neuritis

Positive rhomberg sign

Lhermitte’s sign

Atleast 2 episodes of weakness with

spontaneous resolution of symptoms

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

Types

Benign MS 10%

Relapsing-remitting MS 40%

Secondary chronic progressive 40%

Primary progressive MS 10%

Treatment

Immunosupression (ATCH)- initial phase

Steroidal therapy- maintenance

Beta-Interferon – treatment of relapses

Immuno Globulin g - prevention of relapse

Physiotherapy Management

Alternative Therapies

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)

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

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

Physiotherapy Management

Philosophy of Neuro Rehabilitation: Education and Self Management

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

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

Management

Three levels of treatment based on :

Symptomatic treatment

Standardized profiles

Patient Driven goals

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,

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

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,

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,

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