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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
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