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;
71 Cards in this Set
- Front
- Back
|
What does ALS stand for
|
Amytrophic Lateral Sclerosis
|
|
|
where can the pathology of ALS be located
|
-motor cortex
-corticobulbar pathway -cranial nerve nuclei in the brainstem -spinal cord -anterior horn cells |
|
|
what is pseudobulbar palsy
|
UMN pathology, spasticity, change in effect, emotional labilty. May have an impact on chewing, swallowing, speech but because of spasticity
|
|
|
what is progressive bulbar palsy
|
LMN pathology, flaccid, weakness in mm of swallowing, chewing speech, facial expression, oculomotor system often intact
|
|
|
what movements are typically spared with ALS
|
-eye movements
-sensory -bowel and bladder (know that they have to go to relieve themselves, but don't have the ability to control) -coordination -cognition |
|
|
How to dx of ALS
|
-clinical presentation: cramping, twitching, weakness
-EMG shows fibrillations and fasciculations with giant MN spikes -elevated creatine phosphokinase levels -threshold of percieved weakness |
|
|
T/F: by the time most patient complain of weakness, they have lost about 80% of mn in the area of weakness
|
False, by the time pts c/o weakness they have lost 80% of mn in the area of weakness
|
|
|
what is the prognosis for pts who have ALS
|
-initial onset of bulbar signs leads to a poorer prognosis
-has a relentless px -death usually within 2-5 years; median of 4 years, |
|
|
what do pts with ALS usually die from
|
complications of respiratory problems; pneumonia, respiratory failure
|
|
|
what treatment is involved with ALS
|
-no cure or definitive treatment
-Riluzole (antiglutimate drug) has been shown to prolong life by months -treat symptoms |
|
|
what symptoms often need to be treated in pts with ALS
|
-spasms (meds, stretching)
-nutrition issues (due to swallowing,mouth and tongue problems) -fatigue mangement (energy conservation, respiratory care) |
|
|
What can PT does ALS
|
-education
-functional training -assistive and adaptive device -exercise |
|
|
what do you need to take into consider for exercise for a pt with ALS
|
-some support in literature for exercise protocols
-less decline in function in ex vs non-ex groups -need to find happy medium: prevent overuse fatigue and prevent disuse atrophy -no adverse effects, small effect size of improvement |
|
|
T/F: can tell the stage by a pts immediate presentation
|
False- may have good ambulation by significant distal UE weakness.
|
|
|
what UE mm tend to be weak
|
-hand and cervical extensors
|
|
|
T/F: Polio is common
|
False, is rare in the U.S about 10 cases a year due vaccination problems. Is more common in third world countries.
|
|
|
for those with post polio syndrome what are symptoms that may be feel
|
-new fatigue, weakness, pain and decreased function
|
|
|
what type of injury is polio
|
-attach of the anterior horn, LMN injury
|
|
|
what pt population is polio similar to in terms of how PTs treat
|
-similar to SCI, but may have unique presentations for example, may have one leg and UE on opposite side, or have no proximal UE control but have distal UE control
|
|
|
what is the pathology of polio
|
-febrile illness & destruction of mn/anterior horn cells
-motor neurons may be affected, recovered, or destroyed |
|
|
how can return of function in polio be explained
|
-recovered neurons develop terminal axon sprouts to re-innervate orphaned mm fibers (creating Giant Motor Units)
-Hypertrophy of innervated fibers (denervation hypertrophy) -physiological compensation/neuronal adapation -functional compensation |
|
|
what percentage of AHC did pts with Polio lose but still have a 5/5 MMT
|
60% of AHC
|
|
|
what percentage of AHC did pts with Polio lose but still have a 4/5 MMT
|
60%-90%
|
|
|
what percentage of AHC did pts with Polio lose but still have a 1-3/5 MMT
|
90%-98%
|
|
|
What is significant about 30% of motor units functioning
|
-if LESS than 30% of motor units are functioning the strenous exercise is DETRIMENTAL to pts
-if greater than 30% motor units are functioning, then strenous exercise will result in hypertrophy |
|
|
what was observed in pts with MMT of 2 or 3 in pts with polio
|
would get WEAKER with exercise
|
|
|
what was observed in pts wtih MMT of 4 or 5 in pts with polio
|
would get stronger with exercise
|
|
|
when does post polio syndrome usually occur
|
-approximately 35 yrs later
|
|
|
what is the post polio syndrome sequellae
|
-combination of neurological,musculoskeletal and psychosocial manifestations
|
|
|
what symptoms tend to occur in pts with post polio syndrome
|
-profound fatigue
-pain -new weakness that may or may not have been in the same area |
|
|
what is the etiology of post polio syndrome
|
-no evidence to support reactivation of virus or autoimmune response
-normal agining with loss of neurons of age 60 may be a factor -giant motor unit may have increased metabolic demand -problem at neuromuscular junction of giant motor units -however is mostly unclear |
|
|
what is the main mode of treatment in pts with post polio syndrome
|
strengthen what they have and use what they have
|
|
|
what are components in education for pts with post polio syndrome
|
-pacing themselves and not stressing areas of weakness
|
|
|
what are musculoskeletal issues that need to be addressed
|
-pain management
-modify workload of muscles relative to their limited capacity -correct/minimize gait and postural deviations -orthotic assessment -promote function, safety, QOL |
|
|
what are the post polio syndrome PT guidelines
|
-weight management should be done with nutritional means, not exercise
-maintain function by doing things the easy way, take advantage of modern technology -relaxation and imagery can be used to maximize rest periods -avoid unessential physical activity -preserve and protected limited mm & joint capacity, utilize energy conservation; break up tasks, take rests, condense activities -avoid exhaustion |
|
|
what was the rehab like when pts were initially dx with polio
|
-pts worked very hard in rehab with strenous exercise to regain motor function, but upon PPS dx, this is NOT the tx of choice, so pts are being told the OPPOSITE of what they remember
|
|
|
Guillain Barre Syndrome is traditionally placed in what category
|
demyelination polyradiculoneuropathies
|
|
|
What two categories can GBS be like
|
-axonal neuropathies and demyelination neuropathies
|
|
|
what does GBS affect
|
-affects mixed peripheral nerves- damage to myeline sheath disturbs propagation of action potential resulting in slowed conduction, dysynchrony of conduction or conduction block
|
|
|
what is GBS usually are result of
|
-probably autoimmune response, ~60% follow respiratory of GI illness
|
|
|
what are sxs of GBS
|
-progressive ascending motor weakness that develops rapidly
-rekativey symmetrical -distal to proximal -areflexia of distal DTR's -may have sensory symptoms -may have autonomic symptoms |
|
|
what is the prognosis for pts with GBS
|
-lowest (nadir) point usually within a week, 90% hit lowest point (nadir) within 3 weeks and then recovery begins
|
|
|
what is the px of ambulation for pts with GBS
|
-80% ambulatory within 6 months
|
|
|
what is the px for functional mobility for pts with GBS
|
-50% will have minor neurological deficit without functional deficit
-15% will have functional deficit -5% will die from complications (usually respirtatory) |
|
|
what is the medical management for pts with GBS
|
-respiratory observation and support
-plasmapheresis -IVIG (intravenous immunogobulin) |
|
|
what is the role in PT for pts with GBS
|
-attention to respiratory function and swallowing function
-attention to skin and contracture risk -adaptive, assistive & orthotic equipment |
|
|
How will exercise affect GBS
|
will not hasten or improve nerve regeneration; must avoid fatigue; rest periods must be frequent
|
|
|
what may persist in pts demostrating "full recovery"
|
-sub clinical deficits
|
|
|
what is charcot-marie-tooth disease
|
-hereditary motor and sensory neuropathy; peroneal mm atrophy
-most common inherited disorder affecting nerves -initally involves peroneal nerve and foot; later can involve forearms and hands -1 in 2500 persons |
|
|
what is the etiology of CMT
|
-autosomal dominant (most cases)
-causes mutations in proteins responsible for Schwann cell myelination in PNS -Two distinct chromosomal etiologies, but clinically they present the same |
|
|
what is the clinical presentation for CMT
|
-slow, progressive disorder
-distally symmetric mm weakness, atrophy, diminished DTRs -Pes cavus deformity (high arch) & hammer toes -foot drop; steppage gait -progresses to wasting and weakness in distal UE |
|
|
what is the tx for CMT
|
-no real medical ts to alter its course
-symtomatic tx: to minimize deformity and maximize function |
|
|
what role does PT have in CMT tx
|
-orthotic assessment
-education -functional training -prevention of contractures -skin breakdown |
|
|
what is the course of tx for CMT with rigid deformities
|
-surgery, triple arthrodesis may preserve function
|
|
|
what is triple arthrodesis
|
results in fusion of subtalar, calcaneocuboid, and talonavicular joints
|
|
|
what orthotic would be appropriate for CMT
|
patellar tendon bearing in order to offload the weight on the foot and ankle
|
|
|
If the pt is in early progression, what is your role as a PT
|
-strengthen what they have, try to mange alignment since it is not a fast progressive disease
|
|
|
what is mysathenia gravis characterized by
|
-FLUCTUATING weakness and fatigability of skeletal mm
-weakness with increase repetitions due to decrease transmission at NMJ |
|
|
what is the etiology of MG (generally, classification location)
|
-autoimmune disorder
-associated with thymic disorders -defect at NMJ |
|
|
what is malfunctioning at the NMJ
|
-anti-ACh receptor antibodies decrease the # of available receptors of ACh resulting in decreased transmission of ACh across NMJ
|
|
|
how is MG dx
|
-use acetylcholinesterase inhibitor and if pt improves, then they have MG because the the inhibitor in system the ACh is able to get to the receptors that would be blocked by antibodies otherwise
|
|
|
clinical presentation of Mysthenia gravis
|
-weakness, fatigability
-repetition causes fatigue and rest restores function -muscle of eyes and other cranial nerve innervated mm are often first to show weakness -in MOST cases: fluctuating weakness of proximal mm |
|
|
what other eye related symptoms can a pt with MG have
|
-ptosis (droopy eyelid)
-diplopia |
|
|
T/F: the course of MG is consistent from day to day
|
-FALSE, slowly progressive, fluctuations in intensity day to day, week to week
|
|
|
T/F: In pts with MS, they may have exacerbations
|
TRUE- may lead to MG crisis that can endanger respirtatory status and may progress to medical emergency
|
|
|
T/F: energy conservation is huge for this pt
|
True,most end up using a W/C for get around
|
|
|
what are some things that may cause exacerbation or MG crisis:
|
-non compliance of medications
-infection -change in temperature -change in emotional state -some medications antibiotics, antidysrhymics (beta blockers, ca channel blockers), lithium, corticosteriods, mm relaxants |
|
|
what are some physcial findings that a pt with MG may be in exacerbation
|
-facial mm may be slack
-slack jaw -unable to support head -voice changes -flaccidity -absent gag reflex -respiratory distress |
|
|
What types of tx are involved with MG
|
-thymectomy
-AChE inhibitors, treats symptoms but not underlying cause -immunosuppresion-corticosteriods -plasmaphersesis _IVIG |
|
|
what role does PT have in MG
|
-education of energy conservation
-functional training -alternate task movements |
|
|
what are the long term side effects of corticosteriods
|
-increased appetite and weight gain
-deposits of fat in chest, face, upper back, and stomach -water and salt retention leading to swelling and edema -high blood pressure -diabetes -slowed healing of wounds -osteoporosis -muscle weakness -immunosupprestion -depression |
