Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
49 Cards in this Set
- Front
- Back
|
7 symptoms of UMN syndrome
|
1. paresis 2. loss of fractionation 3. abnormal reflexes 4. myoplastic hyperstiffness 5. co-contraction 6. abnormal synergies 7. mm overactivity
|
|
|
What tract is responsible for loss of fractionation?
|
LCST - fine, graded movts
|
|
|
2 stimuli causing hyperrefexia
|
Abnormal cutaneous reflexes and muscle stretch hyperreflexia
|
|
|
Causes of myoplastic hyperstiffness
|
contracture, weak actin-myosin binding, selective atrophy of type II fibers
|
|
|
How does the mm spindle stay sensitive to stretch? 1 during stretch and 2 during contraction
|
1. during stretch, the ends of the intrafusal fibers connect to extrafusal fibers so stretching of the muscle stretches the mm spindles. 2. During contraction, g-MNs fire at the same time a-MNs fire - which cause contraction of the ends of the mm spindle
|
|
|
How does the g-MN make sure the mm spindles stays sensitive to stretch?
|
g-MN fires whenever the a-MN fires. g-MN innervates the ends of the intrafusal fibers (polar ends of mm spindles). Contraction of the ends of spindles stretches the central region of the mm spindle. The central region of the mm spindle can thus detect stretch at shortened ranges
|
|
|
Name and describe the different types of mm spindles fibers. What type of afferents wrap around them?
|
Dynamic nuclear bag fibers - 1a afferent wrap around them. Static nuclear bag fibers and nuclear chain fibers - type II afferent wrap around them.
|
|
|
What do primary endings of type Ia afferents report to the CNS?
|
Because type Ia afferent endings wrap around dynamic nuclear bag fibers, they detect phasic/quick/velocity dependent types of stretch
|
|
|
What do secondary endings of type II afferents report to the CNS?
|
Report position - independent of velocity. Reports tonic stretch.
|
|
|
Explain how the MAS can evaluate both primary type Ia and secondary type II afferents.
|
A quick catch is due to hypersensitivity of Ia afferents. A resistance t/o the rest of the range would be due to hypersensitivity of type II afferents (Tonic). Although the latter could be due to hyperstiffness
|
|
|
What is the basic premise behind hyperreflexia?
|
Threshold is reduced resulting in larger and and sooner stretch reflex. Many theories on how this threshhold is reduced
|
|
|
Explain the g-MN hypersensitivity theory of hyperreflexia.
|
g-MN responsible for contracting the ends of the mm spindles and making the middle of the spindles taut. The more taut the spindle, the more "sensitive" it is. Results in a exaggerated response - Ia or type II afferents b/c will stretch both
|
|
|
Theory of how myoplastic changes in the mm can cause hyperreflexia?
|
Spindles are parallel to muscle and the ends connect to the extrafusal fibers. Forces from the mm can be directly transmitted onto spindles.
|
|
|
Explain the a-MN hypersensitivity of hyperreflexia.
|
a-MN is set closer to threshhold for firing - afferents coming in from the SC need less of a stimuli to depolarize the a-MN
|
|
|
What intrafusal fibers are responsible for "wind-up" and "quick" stretches
|
Wind-up = static nuclear bag and nuclear chain Quick = dynamic nuclear bag
|
|
|
What controls Flexor Response Afferent is normal ppl? Why is it disrupted in UMN syndromes?
|
LCST is largely responsible for "gating" cutaneous responses (ie. babinski doesn't cause a complete LE withdrawl). With TBI and other UMN shiot, the descending systems are disrupted on not gating properly so we have an exaggerated response
|
|
|
How do mm synergies link mm together?
|
At the SC - propriospinal neurons that stay in the SC have connections across multiple segments
|
|
|
Theory of abnormal mm synergies.
|
Result of constant loading being applied to an extremity (ie. gravity). Causes type II afferent to fire, causing reflex contraction
|
|
|
What causes co-contraction?
|
Disruption of descending systems.
|
|
|
Explain reciprocal inhibition. What other systems contribute to reciprocal inhibition?
|
Type Ia afferents respond to quick stretch, synapse on Ia inhibitory interneurons in SC, and inhibit the antagonist mm group. Cutaneous, joint afferents, and descending systems all contribute to silencing the antagonist
|
|
|
What is autogenic inhibition?
|
GTOs in the tendon respond to tension, sends info via Ib afferents to synapse on Ib interneurons in the SC and inhibit the agonist. This allows tension to be adjusted, changing force for better mo control
|
|
|
When is a Renshaw Cell activated and what does it do?
|
Has a recurrent loop with a-MN, so it fires when ever the a-MN fires
Inhibits synergist and disinhibits 1a inhibitory interneuron (contracts the antagonist pretty much) |
|
|
What is the overall job of the Renshaw Cell?
|
Causes contraction of the antagonist (like GTO), and help to regulate and grade movement
|
|
|
What happens with UMN lesion to the Renshaw Cell?
|
Becomes overactive and contracts antagonist more = not smooth
|
|
|
5 Meds used to tx spasticity
|
Lioresal (Baclofen)
Dantrium (Dantrolene Sulfate) Valium (Diazepam) Neurontin (Gabapentin) Zanaflex (Tizanidine) |
|
|
What is the role of GABA? What meds suppress GABA?
|
GABA decreases the release of excitatory NTs
Baclofen and Valium |
|
|
How does Dantrium exert its efffects? Side effects?
|
Directly on the mm - dec Ca release from SR
mm weakness, hepatotoxicity, nausea, lethargy |
|
|
Why is valium not used much anymore to tx spasticity?
|
Very drowsy and chance of dependency
|
|
|
How does Nuerontin exert its effects? Side effect dis-similar to other meds?
|
Mechanism unknown - we think it causes inhibition of a-MN, but it does not bind to GABA receptors.
Ataxia |
|
|
How does Zanaflex exert its effects? Benefit?
|
Binds to alpha 2 receptors in CNS and inhibits interneurons that speak to a-MN. Fewer side effects and less generalized weakness
|
|
|
Negative effect of Zanaflex? Other side effects?
|
It may inhibit recovery after a TBI. Other side effects: dry mouth, dizzy, sedation
|
|
|
Where is the Baclofen pump implanted?
|
Abdomen subcutatenously threaed back and enters SC @ L2. Used to only thread as high at T6 b/c worried about diaphragm, but we need to dec spasticity in UEs too!
|
|
|
Criteria to be eligible for a Baclofen pump?
|
1. 3-4 on MAS
2. Multijt spas thats limiting fxt 3. Can't tolerate oral meds |
|
|
What is the test we do before implanting a Baclofen Pump?
|
Test it - PTs must measure MAS every 2 hours after injection for 8 hrs.
Will give higher doses up to 3 days - MAS needs to dec. by 2 to implant a pump |
|
|
What does the PT do after a Baclofen pump is implanted?
|
Bed rest for a few days, then must work on ROM and stretching. Also re-examine transfers b/c less spasticity. Must teach family. May need dif DME so assess ADs
|
|
|
What should be avoided with a Baclofen pump?
|
Forceful trunk activity
Head modalities near pump or systemically Do not abruptly withdrawl = seizures and autnomic disreflexia |
|
|
Consequences of abrupt withdrawl from Balofen pump?
|
Fever, altered mental state, inc tone, drowsy
Seizures, autonomic dysreflexia |
|
|
What is chemodenervation?
|
denervation by chemicals - produce focal effects for specific mm
|
|
|
What does botox do and how long does it last?
|
Interferes with ACH release in mm (block peripheral transmission)
Onset: 24-72 hrs Lasts: 3-4 months |
|
|
What is a diagnostic block?
|
Licodace that works for 4-8 hrs, so you can see if you want to use botox or phenyl.
|
|
|
Where is phenyl or botox injected? Why phenyl vs. botox?
|
Trunk of a nerve of Motor Point Block (more specific, but more difficult). Phenyl less toxic and used on larger mm
|
|
|
Contraindications for chemodenervation?
|
Pt uses spasticity for fxt activities
Anticoagulants (relative b/c injection site) Pt unable to cooperate (or family) Pts w/ joint deformities or contractures |
|
|
What should we avoid for 1-3 days after chemodenervation injection? Can we apply inhibitory casting after this?
|
stretching the area - very painful injection site. After this, intense PT
Not for 7-10 days |
|
|
Theories for why inhibitory casting works
|
1. Neurophysiological: dec input from Ia fibers
2. Biomechanical: long duration, low load 3. Nueral warmth promotes relaxiation with padding |
|
|
How do we apply inhibitory casting?
|
5-10 deg from end range and cast them for 5-7 days (TO says only a couple days)
Take cast off, inc. ROM and recast |
|
|
How many castings can we do?
|
3 max b/c lots of bad things happens with immobilization.
|
|
|
F/u after we are done with inhbitory casting?
|
Splint to maintain ROM for hrs a day and sleeping at night
We want WB Bivalve cast allows us to reapply it |
|
|
Contraindications to casting?
|
Rigid spasticity, unstable medical condition
Absent sensation, poor skin conditions Open wounds, cognitive deficitys, very young children |
|
|
Precautions for casting
|
Apply early in week
Pad areas of inc. pressure Check capillary refilling Write date, intials, and day its coming off |
