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Clinical Medicine III > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

Define multiple sclerosis

A
  • Inflammatory, autoimmune, demyelinating disease of the CNS
  • Characterized by multiple lesions in the CNS called sclerotic plaques caused by the body’s immune system attacking & stripping the myelin sheath of nerves
  • It blocks or impairs neural transmission resulting in various kinds of impairments: motor & sensory loss, weakness/fatigue, coordination problems, pain, cognitive problems
  • Since multiple body systems may be involved, need multi-disciplinary approach for optimal care: disease of variabilities
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2
Q

What are the general 4 types of progression

A
  • Relapsing-remitting MS (RRMS)
  • Secondary progressive MS (SPMS)
  • Primary progressive MS (PPMS)
  • Progressive relapsing MS (PRMS)
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3
Q

Describe relapsing-remitting MS

A
  • Most common type (85% of new cases)
  • Defining a relapsing attack: new symptom just last at least 24 hrs & be separated from other symptoms by at least 30 days to qualify as a new attack
  • 60% progress to secondary progressive type in 2 decades
  • The 1st demyelinating attack may be clinically isolated attack for some it could be a single isolated event, most others could go on to have 2nd & subsequent attacks
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4
Q

Incidence of MS

A
  • MS is a disease of the temperate climates with highest prevalence in Scotland and Scandinavia
  • Very rare in Japan and Africa
  • Age of onset is 20-50 yrs
  • Females > males
  • Men transmit disease to children more than women
  • Pregnancy reduces relapse rates
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5
Q

Etiology of MS

A
  • Exact cause is unknown but has genetic & environment factors
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6
Q

Genetic factors related to MS

A
  • Child of MS parent has 5 fold increased risk
  • Increased presence of gene for HLA-DR2 (immune system protein)
  • Absence of inhibitory KIR2DL3 is associated with MS
  • Majority with MS also have other autoimmune diseases: Hashimoto thyroiditis, psoriasis, IBD, RA
  • Families with Hx of MS also have other autoimmune diseases: MS develops on a background of increased susceptibility to autoimmune disorders
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7
Q

Environmental factors related to MS

A
  • Vitamin D deficiency: may explain higher occurrence rates in northern & southern hemispheres
  • Viral infections are also thought to trigger MS; more than 1/3 relapses are preceded by infections: EB virus, Measles virus, Herpes virus, Retrovirus
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8
Q

Describe the primary pathology of MS

A
  • Primary pathology is demyelination of CNS nerve fibers
  • Immune system erroneously attacks myelin protein, confusing it with herpes viral protein
    -Demyelination causes initial abnormalities in nerve conduction and correlate with immediate functional impairments after attacks
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9
Q

Describe the pathogenesis of MS

A
  • Myelin loss starts around small vessels
  • Plaques appear as focal lesions in white matter of cerebral hemispheres, brainstem, spinal cord, and white matter around ventricles (PWM), optic nerves, corpus callous, and also in grey matter areas
  • Inflammation of myelinated areas -> demyelination of nerves -> axonal loss
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10
Q

What is the primary cause of long term disability in MS

A
  • Although demyelination may cause relapses, long term disability is primarily caused by irreversible axon loss & cell death
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11
Q

Describe the cellular pathogenesis level of MS

A
  • Starts with inflammatory process against myelin by the immune system
  • Cell mediated immune reaction: T-cells are activated against myelin antigen & cross BBB
  • Activated T-cell changes the BBB to allow more T-cells to cross
  • Activated T-cell release pro-inflammatory cytokines like interleukins & TNF alpha which dilates BBB
  • Dilated BBB allows more types of immune cells (B-cells & macrophages)
  • Activated T-cells also release other inflammatory cells (microglia, reactive astrocytes)
  • B-cells mark myelin basic protein (MBP) with antibodies to be then attacked by phagocytosis cells
  • Demyelinated areas appear as sclerotic plaques
  • W/o myelin, axons start to malfunction, can correlate to relapsing periods early in MS
  • Regulatory T-cells temporarily stop inflammatory process (remission)
  • Demyelination capacity reduces leading to axonal loss through inflammatory attack
  • Disease progression & long term disability occurs
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12
Q

What stage of MS does remission happen better

A
  • Remission happens better during the early stages of MS
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13
Q

Describe plaques

A
  • Plaques are filled by macrophages, T-cells, immunoglobulins, & microglia
  • New plaques appear pink w/faint borders exhibiting intense inflammatory activity
  • Old inactive plaques appear gray with sharp edges
  • New lesions frequently appear at the sites of previous lesions which contribute to failed remyelination
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14
Q

What regions in the CNS are plaques frequently found

A
  • Periventricular
  • Juxtacortical
  • Infratentorial region
  • Spinal cord
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15
Q

Describe general clinical manifestations of MS

A
  • In most individuals MS is characterized by progressive disability over time but amount of accumulated disability varies widely “disease of variability”
  • 20% may show benign course with 1 or a few relapse attacks followed by complete remission
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16
Q

What does the type and extent of disability in MS depend on

A
  • Type of MS
  • CNS area affected
  • Capacity of the brain to adapt to lesions
  • Individual’s threshold of appearance of symptoms
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17
Q

What is the most common presentation of primary progressive type

A
  • Myelopathy (spasticity, paraparesis, pain, gait impairments, balance problems)
  • Progressive sensory loss & motor weakening
  • Pain
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18
Q

Describe optic neuritis

A
  • One of the 1st manifestations of MS
  • Optic nerve is part of CNS tracts and is subject to demyelination
  • Typically unilateral painful decrease in vision: usually temporary during relapse, pain in periocular area, good healing with remission
  • Decreased color vision, changes in pupillary light reflex, reduced clarity, blurry vision, visual field defects
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19
Q

Ocular problems associated with MS

A
  • Gaze palsies
  • Nystagmus
  • Inability to fix gaze: caused by lesions in the pons, vestibular nuclei of brainstem, or cerebellum
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20
Q

Describe fatigue as a clinical manifestation of MS

A
  • Single most common & disabling symptom in MS
  • Often precedes diagnosis by years
  • Presents as severe tiredness along with mental fatigue/fuzziness
21
Q

Describe central fatigue

A
  • Due to demyelination
  • Nerve fibers start to short circuit after repetitive firing when called upon to do repetitive task
  • Repetitive exercises w/o rest could lead to feeling of increased weakness and should be avoided
22
Q

Unique characteristics of MS fatigue

A
  • Simple ADLs can cause fatigue
  • May occur early in the morning even after a restful night’s sleep
  • Generally occurs on a daily basis
  • Tends to worsen as the day progresses
  • Tends to be aggravated by heat & humidity
  • Unpredictable: comes on easily & suddenly
  • Generally more severe than normal fatigue
23
Q

Describe cognitive problems associated with MS

A
  • AKA “Cog fog”
  • Occurs in 50% of MS patients
  • Memory loss: forgetfulness
  • Attention deficits
  • Depression can occur either bc of actual changes in brain or due to knowledge of disease
  • Medications can cause cognitive problems like sedation, confusion, or depression
24
Q

Common sensory changes related to MS

A
  • Somatosensory symptoms: hypoesthesia, parasthesia, or dysesthesia
  • Loss of sense of vibration, position, 2-point discrimination: which all could lead to balance problems
  • May begin in part of one extremity, face, trunk, or perineum
  • Symptoms may not be substantiated by objective findings as remission might have happened by the time patient shows up for examination
25
Q

Weakness/paresis related to MS

A
  • Result of decreased neuromuscular firing secondary to demyelination & axonal loss
  • Loss of orderly recruitment of motor units
  • Disrupted agonist-antagonist relationships
  • Heat increases weakness due to conduction block
  • Cooling improves strength & function
26
Q

Spasticity related to MS

A
  • UMN lesion very common with MS
  • More common in LE
  • Severity can vary from non-existent to severe in same person from time to time making it challenging to manage with meds
  • Noxious stimuli can exacerbate spasticity
  • Often Ms patients can use their spasticity to walk, transfer, & manage ADLs
  • Spasms may accompany spasticity: more severe at night
  • Clonus, Babinski’s sign
27
Q

Cerebellar symptoms related to MS

A
  • Axonal loss and/or atrophy
  • Incoordination, tremor, and ataxia in extremities or trunk
  • May be symmetric or asymmetric
  • Dysarthria: scanning speech
  • Occur mostly during progressive phases
28
Q

Balance, coordination, & dizziness problems related to MS

A
  • Due to impairments in any/all balance regulating systems: sensory, motor, & cognitive
  • Due to excessive fatigue, raise in body temperature, or lesions in brainstem, cerebellar structures, or from BPPV
29
Q

Cranial nerve dysfunction related to MS

A
  • when lesions are in brainstem affecting CN nuclei
  • CNs 3-12 at the nuclei level
  • Trigeminal neuralgia/Tic Douloureux (CN 5)
  • Spasms or weakness of facial muscles (CN 7)
  • Vertigo, N/V, balance problems if vestibular nuclei are affected
  • Dysarthria/dysphagia (CN 9-10)
30
Q

Pain related to MS

A
  • Common in MS (50%)
  • Usually neuropathic type pain (burning, stabbing, sharp) may occur with dysesthesias (like squeezing sensations)
  • Distribution may/may not follow any sensory pattern of involvement
  • Fairly constant with nocturnal worsening
  • Pain meds offer minor relief
  • Trigeminal neuralgia: shock like pain in face, characteristic in young person
  • Lhermitte sign: momentary electric shock like sensation evoked by flexing neck or cough; more likely to occur when fatigued or overheated
31
Q

Bladder and bowel symptoms related to MS

A
  • Urge incontinence: spastic small (fail to store) bladder, frequent night time urination (nocturia)
  • Stress incontinence: weakened pelvic floor muscle
  • Overflow incontinence (less common): large (fail to empty) bladder, higher risk of UTI, spasticity/dyssynergia b/w bladder & urinary sphincter
  • Bowel incontinence (diarrhea) or constipation: occurs less frequently
32
Q

What is used to diagnosed MS

A
  • McDonald criteria
33
Q

Define dissemination in space and dissemination in time

A
  • Space: presence of >1 lesions in different CNS regions in an MRI scan
  • Time: simultaneous presence of active (inflammatory) & inactive (old) lesions in different CNS regions in an MRI scan; done using contrast enhancing technique
34
Q

Describe ADEM (acute disseminating encephalomyelitis)

A
  • Acute attack during childhood
  • Characterized by inflammatory attack of the brain & spinal cord that damages myelin with features of encephalitis (fever, headache, seizures, & coma)
  • Usually occurs just once
  • Could convert to MS later with relapses
35
Q

Describe diagnosis of MS using imaging

A
  • Plaques & brain atrophy seen in MS brain
  • During early stages or in relapsing-remitting type plaques correlate with clinical picture but not much during chronic stages or with progressive types of MS
  • Correlation b/w periods of clinical worsening & total number of plaques/lesions, # of new lesions, & total area of gadolinium contrast enhancement
36
Q

What is the hallmark of progressive forms of MS

A
  • Cortical demyelination
  • For both primary & secondary progressive types & provide better indication of disease progression & disability
37
Q

Diagnosis of progressive forms of MS

A
  • Measures of brain atrophy using MRI imaging volume quantification of grey & white matter areas can provide better correlations with functional disability & disease progression than white matter lesion (plaque) activity
38
Q

Grey matter atrophy is partly related to what

A
  • Neuropsychological impairment
  • Impairments in verbal memory, euphoria, & disinhibition
39
Q

Describe treatment for MS

A
  • Goal is to stop the destructive inflammatory process by the activated immune system
  • Disease modifying drugs can significantly decrease relapse rates, new cortical lesions, cortical atrophy progression, disability progression, & transition to secondary progressive MS
  • Disease modifying drugs (DMDs): (the ABCs) Avonex, Betaseron, Copaxone
  • Interferons modify or interfere with the immune response
40
Q

List non-interferon DMDs

A
  • Mitoxantrone
  • Natalizumab
  • Fingolimod
  • reduce relapses, secondary progression, & long term increase in disability
  • Dalfampridine: improve conduction by blocking potassium leaks
41
Q

Other drugs that provide symptomatic management for MS

A
  • Muscle relaxants (Baclofen, Botox injections) for spasticity
  • Gabapentin for pain
  • Stimulants (Modafinil, Amantadine) for fatigue
  • Sedatives (Diazepam) for inducing sleep
  • Corticosteroids: 1st line Tx against acute exacerbations; can alter all aspects of inflammation
42
Q

Describe typical prognosis of MS

A
  • Life expectancy is modestly reduced
  • Average number of attacks is 1 per year
  • If untreated 50% of MS cases will require AD to walk after 15 yrs & 50% will be w/c bound at 20 yrs
  • Physical rehab improves functional independence but cognitive problems & ataxia tend to be refractory
43
Q

Factors that predict worse MS prognosis

A
  • Motor & cerebellar symptoms
  • Short time between attacks
  • Numerous attacks within 1st year or initial years
  • Rapid disability after 1st attacks
44
Q

Factors that predict better MS prognosis

A
  • Sensory symptoms
  • Infrequent attacks
  • Full recovery after a relapse
  • Low level of disability after 5-7 yrs of onset
45
Q

Implications of MS for PT

A
  • Goal: improve/maintain functional mobility status in house & community
  • Visit mostly for complaints of fatigue & weakness
  • Aerobic exercise with balance training & socialization improves fitness/function in mild MS & function in moderate-severe MS
  • Avoid fatigue & overheating: distributed practice might be helpful, submit aerobic training might be better
  • Use MFIS to monitor level of fatigue level
46
Q

Describe Kurtzke expanded disability status scale (EDSS)

A
  • Documents disease severity and progression: helpful for quantifying movement disability
  • Defines functional systems as follows: Pyramidal, Cerebellar, Brainstem, Sensory, Bowel and Bladder, Visual, Cerebral. Other
47
Q

MS severity categorization using EDSS

A
  • EDSS = 0-3.5: mild disability; full ambulatory w/o AD
  • EDSS = 4-6.5: moderate disability; ambulatory to specific distances w/o or w/ AD
  • EDSS = 7-9.5: severe disability; very limited ambulation even w/ aid; w/c or bed bound
48
Q

Roles for PT related to MS

A
  • Be involved with dosing of intrathecal baclofen to relieve spasticity
  • Be involved with determining appropriate muscles for botox injections
  • Need good task analysis skills, consult with team for planning of botox injections
  • Submax strength training
  • Balance training, gait training
  • Exacerbation of sx like increased reflex activity, increased extensor tone & difficulty with flexion are also signs of increased fatigue/heat intolerance
  • Cooling vests

Clinical Medicine III (20 decks)

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