Management of Select Neurological Diseases Flashcards
Guillan-Barre Syndrome
Acute inflammatory demyelinating polyneuropathy (AIDP)
immune mediated disorder of the PNS myelin
Guillain Barre Syndrome
age of onset
15-35 and 50-75 years of age. Older population don’t do as well
Hallmark Signs of GBS
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
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?
GBS
Clinical Course of GBS
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
Recovery rate of GBS
50-95%
Prognosis of GBS
depends on severity of disease
Poorer prognosis associated with:
- rapid onset of sx
- older age
- prolonged vent (>1 mo)
- slower recovery after nadir
DD of GBS
lyme, HIV, sarcoidosis, transverse myelitis (loss of sensation on a distinct line)
Testing for GBS
slow NCV
ECG
monitor respiratory status/DVTs
IV immune globulin or plasmophoresis
Steroidal use and GBS
not recommended b/c inhibit myelin recovery
PT & GBS
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)
Post Polio Syndrome
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
complications associated with post polio syndrome
- ms weakness
- joint and ms pain (flaccid paralysis, joint not proper therefore increase compensation
- fatigue
- cold intolerance
- progressive atrophy
Onset of PPS
~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
Acute paralytic polio recovery
@ 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
Incidence of PPS
due to aging
excessive metabolic stress
autoimmune process
28-64% of patients with polio (1/3 to 2/3)
PPS Risk factors
Severeity of acute poliomyletic paralysis
age of onset
amount of recovery
greater physical activity during intervening years
Inclusion criteria for Dx of PPS
- Prior episode of PM with residual with residual motor loss
- Period of at least 15 years of neuro/functional stability
- Gradual onset of new weakness or abnormal ms fatigue, atrophy or general fatigue
Signs and Symptoms of PPS
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)
Medical mmgt of PPS
Meds to manage pain/fatigue
pt education (compromise joint alignment)
address psychological sequelae (Type A ppl)
PT management of PPS (areas to work on)
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
PT prescription for PPS
exercise in short intervals with rest in b/w
exercise on alternate days
gentle cardiac conditioning
aquatics
pt education/ support
Which patient population should you educate to rest before they get tired?
GBS
MS
Multiple Sclerosis
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)
Onset of MS
2nd or 3rd decade of life
female predominance 2-3:1
Progressive, often relapsin and remitting
Types of MS
Relapsin remitting (RR)
Secondary progressive (SP)
Primary Progressive (PP)
Progressive Relapsin (PR)
Characteristics of relapsin remitting MS
partial or total recovery after relapse/flare or exacerbation
Characteristics of secondary progressive MS
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
Characteristics of Primary Progressive MS
progressive course from onset with or without plateaus and minor remission
Characteristics of progressive relapsing MS
progressive course from onset with acute relapses
steeper decline and each relapse is worst
Positive prognosis of MS
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
Negative prognosis factors of MS
Male
onset after 35
polyregional attack
poor recovery after exacerbation
high frequency attacks
Signs of MS
Paresthesias
change in vision
weakness
gait and balance dysfunction (Rhomberg M/L & circular sway)
Symptoms of MS
Fatigue
difficulty walking/balance deficits
B&B problems
pain
visual disturbances
cognitive changes
tremors
How to Dx MS
Dx with Brain/C spine MRI with contrast, CSF analysis
Pattern of sx
r/o other causes of s/s
EDSS
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
Pharmacological MMt
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)
Goals for PT managament of MS
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
PT Management (What to DO)
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
PT management (Don’t)
Overheat
over fatigue
assume primary disease has caused all the impairments
assume each pt will progress similarly
PT management
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
Why do MS fall?
Decreased proprioception in LEs
heat sensitivity
divided attention
fatigue
reduced MS endurance
AD use
fear of falling decline in function
(fatigue and divided attention)
