Management of Select Neurological Diseases Flashcards

1
Q

Guillan-Barre Syndrome

A

Acute inflammatory demyelinating polyneuropathy (AIDP)

immune mediated disorder of the PNS myelin

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2
Q

Guillain Barre Syndrome

age of onset

A

15-35 and 50-75 years of age. Older population don’t do as well

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3
Q

Hallmark Signs of GBS

A

Fine parathesias begins with hands/feet

Progressive symmetric ascending paralysis

Tachycradia, hypotension, sweating

Bowel/Bladder dysfunction

Hyporeflexia

Slow progression of Sx over 10-12 days

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4
Q

Hx: Patient c/o of paralysis that started in the feet and hands, after a few days, they feel paralyze in the shin and forearm. What Neurological conditions do you suspect?

A

GBS

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5
Q

Clinical Course of GBS

A

Progressive weakness until a plateau (disease nadir)

Respiratory deficits may be present if respiratory mm is affected (pt will go on vent)

After “nadir” they will slowly recover taking up to 2 years

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6
Q

Recovery rate of GBS

A

50-95%

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7
Q

Prognosis of GBS

A

depends on severity of disease

Poorer prognosis associated with:

  • rapid onset of sx
  • older age
  • prolonged vent (>1 mo)
  • slower recovery after nadir
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8
Q

DD of GBS

A

lyme, HIV, sarcoidosis, transverse myelitis (loss of sensation on a distinct line)

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9
Q

Testing for GBS

A

slow NCV

ECG

monitor respiratory status/DVTs

IV immune globulin or plasmophoresis

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10
Q

Steroidal use and GBS

A

not recommended b/c inhibit myelin recovery

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11
Q

PT & GBS

A

Goal: maximize function

Tolerance of upright activity (good seating system)

being gentle stretching, mm reed, postural contro/balance retraining

Functional training

Aqutics

AVOID overworking weak mm (rest before they get tired)

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12
Q

Post Polio Syndrome

A

Complex combination of primary and secondary impairments as a result of polio virus

refers to residual deficits that are further complicated by new onset of sx:

  • ms weakness
  • joint and ms pain
  • fatigue
  • cold intolerance
  • progressive atrophy
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13
Q

complications associated with post polio syndrome

A
  • ms weakness
  • joint and ms pain (flaccid paralysis, joint not proper therefore increase compensation
  • fatigue
  • cold intolerance
  • progressive atrophy
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14
Q

Onset of PPS

A

~35 years post polio-myelitis infection

Acute polio myelitis: Acute infectious disease caused by an enteric virus.

Paralytic form causs death of anterior horn cells in SC and motor neuron cells in brain

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15
Q

Acute paralytic polio recovery

A

@ beg: almost all motor units are affected

overtime some recover, some gets destroyed

pt recover with less motor units therefore sprouting has to occur to the affected motor fibers. mm hypertrophy may occur with rehab

utilize compensation techniques

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16
Q

Incidence of PPS

A

due to aging

excessive metabolic stress

autoimmune process

28-64% of patients with polio (1/3 to 2/3)

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17
Q

PPS Risk factors

A

Severeity of acute poliomyletic paralysis

age of onset

amount of recovery

greater physical activity during intervening years

18
Q

Inclusion criteria for Dx of PPS

A
  1. Prior episode of PM with residual with residual motor loss
  2. Period of at least 15 years of neuro/functional stability
  3. Gradual onset of new weakness or abnormal ms fatigue, atrophy or general fatigue
19
Q

Signs and Symptoms of PPS

A

progressive mm atrophy & weakness that is usually asymmetrical (unlike GBS) which is proximal, distal or patchy, slowly progressive

Abnormal mm fatigue

mm pain d/t overuse of weak mm

ms tenderness on palpation

joint pain

respiratory insufficiency (2nd to resp mm weakness)

20
Q

Medical mmgt of PPS

A

Meds to manage pain/fatigue

pt education (compromise joint alignment)

address psychological sequelae (Type A ppl)

21
Q

PT management of PPS (areas to work on)

A

Fatigue: life style changes (energy conservation, wt loss program, use of AD/orthoses)

weakness (nonfatiguing exercise program, use of submax/max str ex with short reps)

Avoid overuse of weakened mm

22
Q

PT prescription for PPS

A

exercise in short intervals with rest in b/w

exercise on alternate days

gentle cardiac conditioning

aquatics

pt education/ support

23
Q

Which patient population should you educate to rest before they get tired?

A

GBS

MS

24
Q

Multiple Sclerosis

A

Idiopathic autoimmune disease process of UMN (suspect environmental exposure prior to onset and then virus) (onset much earlier compare to GBS which is more recent virus)

25
Q

Onset of MS

A

2nd or 3rd decade of life

female predominance 2-3:1

Progressive, often relapsin and remitting

26
Q

Types of MS

A

Relapsin remitting (RR)

Secondary progressive (SP)

Primary Progressive (PP)

Progressive Relapsin (PR)

27
Q

Characteristics of relapsin remitting MS

A

partial or total recovery after relapse/flare or exacerbation

28
Q

Characteristics of secondary progressive MS

A

Follows RR and characterized by steady progression, minor remissions and plateau

without treatment 1/2 RR => SP in 10 years

pt are never dx as SP, they always convert from RR=>SP

29
Q

Characteristics of Primary Progressive MS

A

progressive course from onset with or without plateaus and minor remission

30
Q

Characteristics of progressive relapsing MS

A

progressive course from onset with acute relapses

steeper decline and each relapse is worst

31
Q

Positive prognosis of MS

A

Female (more common, but better b/c of hormone)

onset before 35 years

monoregional attack (e.g. only in the back)

complete recovery after exacerbation

low frequency attacks

32
Q

Negative prognosis factors of MS

A

Male

onset after 35

polyregional attack

poor recovery after exacerbation

high frequency attacks

33
Q

Signs of MS

A

Paresthesias

change in vision

weakness

gait and balance dysfunction (Rhomberg M/L & circular sway)

34
Q

Symptoms of MS

A

Fatigue

difficulty walking/balance deficits

B&B problems

pain

visual disturbances

cognitive changes

tremors

35
Q

How to Dx MS

A

Dx with Brain/C spine MRI with contrast, CSF analysis

Pattern of sx

r/o other causes of s/s

36
Q

EDSS

A

Ordinal scale (0-10.0), Half point increments, lower score = higher function

Quantifies disability in 8 functional systems

0 = no clinical signs of MS

10= death

<5.5 Ind ambulating

>5.5 need AD

37
Q

Pharmacological MMt

A

Disease modifying agents (interfereon Beta 1a/1b which is injection every other day or tiw, copaxone (daily))

Amprya - supplemental drug for functional fatigue

corticosteroids for acute Sx

Vit D (4000 IU/day b/c MS usually low in Vit D)

38
Q

Goals for PT managament of MS

A

Manage Fall Risk/balance impairments (50% fall rate, 60% of the fall get injured)

Establish regular exercise routine

Emphasize health and wellness

Equipment Procurement

return of functional status prior to last exacerbation

Connect client to National MS society

39
Q

PT Management (What to DO)

A

address balance dysfunction

consider fatigue (primary and secondary)

consider secondary impairments

consider thermosensitivity (inc. temp by 1/2 F slow conductivity, cool by 1F improvement)

consider progressive nature

40
Q

PT management (Don’t)

A

Overheat

over fatigue

assume primary disease has caused all the impairments

assume each pt will progress similarly

41
Q

PT management

A

Maintain flexibilty/str, endurance (ms and cv)

balance based torso weighting vest

brain derived neurotrophic growth factor (amount affected by exercise) help with neuroplasticity

Fall Risk

Pt education

42
Q

Why do MS fall?

A

Decreased proprioception in LEs

heat sensitivity

divided attention

fatigue

reduced MS endurance

AD use

fear of falling decline in function

(fatigue and divided attention)