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;
111 Cards in this Set
- Front
- Back
|
what three diseases affect the CNS initially
|
-multiple sclerosis
-parkinson's disease -Huntington Disease |
|
|
what 2 diseases affect the CNS & PNS
|
-Amyotrophic lateral sclerosis
|
|
|
what 4 disease affect the PNS
|
-Polio/post-polio syndrome
-guillian Barre Syndrome -charcot-Marie-Tooth disease -Myasthenia gravis |
|
|
What are the three different sets of possible etiology for MS
|
1) MS is an autoimmune disease induced by viral/infectious agent (30-45%)
2) immune response triggers production of T-lymphoctyes,macrophages, and immunoglobins (that end up being toxic to the nervous system)(5-15%) 3)autoimmune cytotoxic effect on myelin in CNS |
|
|
With MS describe what happens when try to have an action potential
|
-not able to make leaps across the Gaps where there is damaged myelin. In early stages of MS can see return to function b/c myelin can repair itself, over time, the myelin is less capacble of repairing itself resulting to a constant loss of function over time.
|
|
|
what is the role of myelin,
|
-speeds conduction of action potential
-insulate the nerves |
|
|
what is the role of oligodendorcytes, and effect of MS
|
-myelin production cells that can handle the damage amount in early stages of MS, but over time, are less capable of reproducing myelin
|
|
|
What are the areas of predilection (preference) for plagues in patients with MS
|
-optic nerves
-periventricular white matter -spinal cord (CST tract, posterior columns) -cerebellar peduncles |
|
|
what is normally the first complaint pts with MS have
|
-vision disturbances that are caused by plaques on the optic nerve
|
|
|
what is Lamat's sign
|
tingling, pain assoacited with long stretch in sitting. (indictive of involvement of posterior columns?)
|
|
|
what is the criteria for dx of MS
|
-find evidence of damage in at least two separate area
-damage that occurred at least a month apart -rule out all other possible dx. ** see new lesions 6 months post |
|
|
T/F: there is a definitive MS DX test
|
FALSE
|
|
|
MRI visualizes plaques in what % of pts with clinical defined MS
|
95%
|
|
|
How is cerebrospinal fluid used in dx of MS
|
-identifies elevated immunoglobin, and presence of oligoclonal IgG bands in 90-95% of pts
|
|
|
how does evoked potentials play a role in dx of MS
|
-abnormal in 90% of pts with MS, VEP most useful of MS dx.
|
|
|
Name 3 disease modifying agents for MS
|
-synthetic interferon drugs (betaseron, avonex)
-glatiramer acetate (copaxone) -mitoxontrone (novantrone) |
|
|
what drugs are used to treat relapses in MS
|
-corticosteriods
-adrenocorticotropic (ACTH) |
|
|
Describe the following clinical course for MS:
Relapsing-remitting MS |
- a pt has exacerbations that may allow them to return to baseline with rehab post exacerbation. Overtime they may see an overall decline in function, pts often progress into secondary progressing MS
|
|
|
Describe the following clinical course for MS:
secondary progressive MS |
-most pts are initially dx with relapsing remitting MS. Some pts have a decrease or no more relapses. Those that have relapses each relapse is more progressive.
|
|
|
Describe the following clinical course for MS:
Progressive Relapsing MS |
-the disease is progressive from the beginning and may occasionally have relapses that are progressive in nature
|
|
|
Describe the following clinical course for MS:
Primary Progressive MS |
-diease has a constant decline of function that there is no periods of exacerabation or remission, their may be periods of plateua or faster progression but is overall continuous in nature
|
|
|
Benign MS
|
- pts have enough of the neurological sxs to be dx with MS, but don't see changes in functional mobility for 10-20 years
|
|
|
Malignant MS (marburg's variant)
|
-AKA acute MS= very rapid and progressice decline in function in a very short amount of time, fortunately very rare
|
|
|
What are some exacerbating factors associated wtih MS
|
-deteriorating health
-organ system disease -viral and bacterial infections -stress -heat:psedoexacerbation |
|
|
what is Uhthoff's phenomenon
|
-the observation that after pts exercise they temporarily have an exacerbation. This lead to the hot bath test that was the main dx tool from the 1890 to about 1920 for MS
|
|
|
what types of pain issues may occur due to MS
|
-tic doulourex (trigeminal neuralgia)
-Lhermitte's sign -dysesthesias -hyperpathia -HA -chronic neuropathic pain |
|
|
what is Lhermittes' sign
|
flexion of the neck produces and electric shock like sensation down the spine & LE, indicative of posterior column involvement
|
|
|
what is Dysesthesias
|
-burning, aching pain, especially in LE
|
|
|
what is hyperpathia
|
-light touch elicits severe pain
|
|
|
what % of pts with MS complain of severe pain
|
80%, (55% is "significant pain_
|
|
|
what % of pts with MS complain of vision problems
|
80%
|
|
|
what types of vision deficits are seen in pts with MS
|
-optic neuritis
-scotoma -marcus gunn pupil -nystagmus -internuclear opthalmoplegia -diplopia |
|
|
symptoms of optic neuritis
|
pain behind the eye with blurred vision; blindness in one eye
|
|
|
describe Scotoma
|
-dark spot in center of visual field
|
|
|
describe Marcus Gunn Pupil
|
-change in light reflexes, dilates the opposite eye when shine light
|
|
|
describe internuclear opthalmoplegia
|
lateral gaze palsy with nystagmus of other eye (problem with MLF)
|
|
|
what type of patient that walks into outpatient PT, you may use MS as differential dx
|
-pt with vestibular issues. If you shine the light and get the Marcus Gunn Pupil, complete the rest of your eval and refer back to MD for MS work up
|
|
|
what issues can pts with MS develop overtime
|
-speech and swallowing dysfunction
-cognitive & affective changes (depression 50% of pts) and emotionallability -autonomic changes such as CV dysautonomia, B&B dysfunction (80%) and sexual dysfunction (70% women, 90%men) |
|
|
Describe CV dysautonomia
|
including indifference to pain, diminished secretion of tears, poor vasomotor control, motor incoordination, labile cardiovascular reactions, frequent attacks of bronchial pneumonia, and hypersalivation with aspiration and trouble in swallowing???
|
|
|
what types of motor dysfunction may occur lter in pts with MS
|
-weakness (ranges from mild to paralysis)
-fatigue (75-95% of pts c/o fatigue, 50-60% say fatigue is their most troubling sx -spasticity -80% -balance and coordination deficits -ambulation and mobility deficits |
|
|
How does fatigue effects pts with MS
|
-100% of pts c/o fatigue
-significantly impacts daily life -important to educate family and pt about planning and pacing -thought to be a central phenomenon; impairment of volitional drive to descending motor pathways. believed to be a dysfunction of circuits involving thalamus, BG and frontal cortex -higher brain working load required to perform a given mental or physical activity |
|
|
what are some PT interventions for management of sensory deficit and skin care
|
-educate
-positoining -desentization |
|
|
what are some PT interventions for management of pain
|
-modalities
|
|
|
what are some PT interventions for management of fatigue
|
-energy conservation
-aerobic conditoning -importance of normal schedule, good eating habits |
|
|
T/F: studies have shown that endurance training reduces fatigue
|
False, the pts increase speed, endurance and efficiency but report the same amount of fatigue. Is hypothesized that faitgue may be unrelated. It is important to show pts how much more they have been able to do.
|
|
|
What are the "Take home"points for fatigue for pts with MS
|
-Fatigue is prevalent, is often identified as both physical andmental,pathophysiology of fatigue unique to MS, endurance will improve with training in persons with MS, endruance training may not necessarily impact sense of fatigue (lassitude)
|
|
|
What are some PT inerventions for pts with MS
|
-strength training at Submax
-aerobic conditioning -flexibility training -respiratory training -balance training -locomotor training -patient caregiver education |
|
|
what are the MS exercise guideline for strength training
|
8-15RM, 2-3 sets, 2-3 weeks
4-8 exercises total, LE focus AVOID FREE WEIGHTS |
|
|
what are the MS exercise guidelines for endurance training
|
-50-70% VO2 max
-60-80% max HR -10-40min;2-3 weeks |
|
|
what do many studies associated with physcial activity in pts with MS
|
-decreased neurological impairment and increased QoL in MS pts
|
|
|
what are the "take home"points for balance
|
-balance training should be functional and challenging and address sensory and motor components of the balance system
-balance based torso weighting may be promising intervention to ameloirate ataxia |
|
|
what are the strucutres that can be involved with PD
|
-caudate
-putament -globus pallidus -subthalamic nuclie -substantia nigra |
|
|
what is the role of the basal ganglia
|
-important role in production of voluntary movement and control of postural adjustments associated with voluntary movement.
-within BG information is intergrated and modulated from cortex and thalamus through multiple parallel channels -direct and indirect pathways facilitate flow of signals to thalamus activating movements/inhibiting/suppressing movements |
|
|
what is the etiology/pathophysiology of PD
|
-damaage to BG can result in hyper or hypokinetic disorder, depending on whether the pathology affects direct or indirect pathways
|
|
|
what is PD associated with
|
-degeneration of dopaminergic neurons that produce dopamineq
|
|
|
when are signs and symptoms of PD seen
|
after degeneration of approximately 80% of neurons has occured
|
|
|
what are the 4 cardinal features of PD
|
-ridigity
-bradykinesia/akinesia -tremor -postural instability |
|
|
Describe the components of rigidity
|
-not velocity dependent; reflexes may be normal
-cogwheel (feels like breaking adhesions) vs lead pipe rigidity ( constant resistance throughout range) -trunk rigidity -reflexes are NORMAL |
|
|
how does rigidity make movement difficult
|
-with rigidity pts will move less, therefore will lose range
|
|
|
Bradykinesia or Akinesia is seen in what % of pts with PD
|
80%
|
|
|
Describe tremor
|
-a resting tremor aka pill rolling is the first sign in approximately 50% of pts with PD
|
|
|
What are the mechanics of disruption that are seen in pts with PD that cause postural instability
|
-difficulty in anticipatory adjustments
-rigid body unable to use normal postural synergies -postural changes shift CoG anteriorly |
|
|
With the anterior COG shift in pts with PD, what does it result in
|
B/C of the anterior COG shift and inability to plan movement well, pts are constantly trying to "Catch up" so they don't fall
|
|
|
what are the clinical manifestations seen in pts with PD
|
-lack of movement
-fatigue -masked face/hypomimia (decreased expression) -musculoskeletal changes -gait disturbances -motor planning and learning deficits -sensory disturbances -swallowing and communication dysfunction -cognitive and behavioral dysfuntion -autonomic dysfuntion -cardiopulmonary dysfunction -shy-drager syndrome/multiple system atrophy (hallmar:autonomic instability) |
|
|
describe how the movement of a pt with PD may change
|
-may have decreased movement that looses degrees of freedom and become uniplanar. This may be because it requires so much cortical function in order to elicit appropriate movement
|
|
|
what musculoskeletal changes may occur with pts with PD
|
-atrophy
-ROM decrease in shoulder flexion, hip extension, retraction, pecs, pulmonary excursion, knee extension, |
|
|
T/F: Prone is a GREAT position for all stages of PD
|
False- only in the early stages of PD because in late PD, the pt becomes flexed so if lay down, difficulty breathing. Supine is a good position, but will have a "phantom pillow:
|
|
|
What do pts with PD usually die of
|
pnuemonia
|
|
|
what are "red flags" to look for in pts with PD
|
-autonomic dysfunction
-cardiopulmonary dysfucntion |
|
|
approximately what % of pts have dementia
|
40%
|
|
|
what other cognitive issue can a pt with PD have
|
problem solving
|
|
|
How is PD medically Dx
|
-hard to definitively dx early
-hx and clinical exam with at least 2 of the 4 cardinal signs present |
|
|
what are 3 diagnosis that need to be differentiated from PD
|
-progressive supranuclear palsy
-corticobasal degeneration -multiply system atrophy or Shy Drager Syndrome |
|
|
what are characteristics from progressive supranuclear palsy (2)
|
-personality changes
-inability to gaze downward |
|
|
How do you differentiate corticobasal degeneration from PD
|
-lovdopa meds help with PD, but not with corticobasal degeneration
|
|
|
what are signs associated with multiple system atrophy or Shy Drager Syndrome
|
-dizziness
-fainting -orthostatic hypotension |
|
|
Describe the course of PD
|
-slowly progressive with long sub-cortical period (5 years)
-tremor as first sign-more benign progression -postural instability or gait disturbance as first sign has a more pronounced, faster deterioration, more often have functional disability and cognitive changes |
|
|
with L-dopa therapy after 5 years....
|
9% are severally functionally diabiled or dead
|
|
|
With L-dopa therapy after 10 years...
|
21% are severly functionally disabled or dead
|
|
|
With L-dopa therapy after 15 years....
|
37.5% are several functional disabled or dead
|
|
|
what is the mainstay treatment for pts with PD
|
-dopamine replacement- sinemet (levadopa and Carbidopa)
|
|
|
Other than dopamine therapy, what are some medical management drugs for pts with PD
|
-early protective :MAO inhibitor (seligilineor Deprenyl)
-dopamine agonist (Bromocriptine, Ropinirole) -Anticholinergics (Bentropin, Trihexyphenidyl) |
|
|
how long is the therapeutic effect for Lovdopa and why
|
5-7 years, because body stops making own dopamine, therefore the L-dopa isn't enough to sustain function
|
|
|
what is important about the "on-off" phenomenon
|
-on off phenomenon is when the body as little or a lot of medicine in the system the Vallies is when there is little and the pts sxs are prominent and the peaks when there is a lot of medicine in the system and the pts symptoms are subtle. You need to see the range you are dealing with the better help the pt deal with the vallies and make the most of the peaks
|
|
|
what is a drug holiday
|
-when the pt does not take the L-dopa for a period of time. The aim of this is to extend the use time of the L-dopa
|
|
|
what are the types of surgical management for pts with PD
|
-ablative surgery (stereotatic obliteration {pallidotomy, thalamtomy})
-deep brain stimulation -neural transplantaion |
|
|
Components of the PT examination for pts wtih PD includes
|
-Rigidity (narrative description)
-bradykinesia (timed movement) -tremor(narration, what impacts) -postural instability (balance tests) -gait -function |
|
|
For PT intervention what are some relaxation techniques
|
-gentle rocking, rotaiton activities
-breathing exercises, roching chair, audio tapes, yoga, meditation, Feldenkrais, stress management) |
|
|
what are some PT Interventions
|
-Relaxation techniques
-PNF Rhythmic initiation -ROM/flexibility -intergrate breathing exercises with UE/posture activities to minimize secondary respiratory complications -functional mobility training (task specific training) -balance activities (task specific training) -gait training(task specific training) -strength training -endurance training -motor learning strategies -functional adaptations -respiratory exercises -aerobic exercise -group exercise and HEP -patient and family education |
|
|
what are some techniques you can use for ROM/Flexibility and what areas do you need to focus on
|
-positioning
-PNF -Focus on neck, trunk -joint mobs and stretching as needed |
|
|
What is BIG
|
a program that emphasis exaggerated movemnts in order to encourage pts with PD to to make (for them) large mvmtns which compared to "normals" is more "normal"
|
|
|
what are some points that need to be incorporated into interventions with PD according to recent literature
|
-effects of PT are task specific and context specific
-suggest training of meaningful tasks in home environment -decline following treatment suggests ongoing management necessary |
|
|
According to recent literature what are 4 specific tx recommendations
|
-cueing strategies to improve gait
-cognitive movement strategies to improve transfers -exercises to improve balance -training of joint mobility and mm power to improve physical capacity |
|
|
what does recent literature say about LE strength in pts with PD
|
-not as strong as age-matched peers
-leg strength was correlated to TUG time |
|
|
what are 3 elements in management of gait in pts with PD
|
-strategy training
-management of secondary sequelae -promotion of physical activity |
|
|
according to recent literature what types of strategy training is recommended for PD to facilitate movement
|
-compensatory strategies to bypass BG (cues)
-learning strategies to improve performance through practice |
|
|
according to recent literuatre what types of management of secondary sequelae is recommended
|
-musculoskeletal
-cardiorespiratory |
|
|
what does literature say about exercise and balance
|
-moderate evidence that exercise results in improvements in postural stability.
-optimal delivery and content to exercise intervetions (dosing, component exercise) at different stages of the disease are not clear -both adaptive (flexibility, strength, motor coordination and balance) and intensive (adaptive plus aerobic) exercise programs were effective in improving mobility and balance |
|
|
what is the etiology/pathophysicology of huntington Disease
|
-neuronal loss in caudate and putamen. and is genetic
-symptons begin between 30-50 symtpoms include cognitive, psychiatric and movement disorders that increase as disease progresses |
|
|
what cognitive deficits are seen in pts with huntington disease
|
-an early sign on disease, slowed thinking, imparied ability to manipulate inofrmation, difficulty dual tasking,memory deficits, global dementia
|
|
|
what are psychiatric symptoms of pts with HD
|
depression,irritabiity, anxiety and apathy,
|
|
|
what are behavioral manifestations of pts with HD
|
aggression, impulsivity, social withdrawal, suicidal thoughts
|
|
|
what mvmnt disorders are associated with HD
|
involuntary movements and voluntary movements
|
|
|
Describe Chorea
|
rhything, asymmetrical movements that the pt has no control over.
|
|
|
Describe dystonia
|
abnormal posturing of trunk that is not functional. hands and feet may be set or may be able to relieve
|
|
|
what are the problems with voluntary movements that may come with HD
|
-uncoordinated, slow movements
-abnormalities of postural control (with dystonia and uncoordinated movements) -hypokinesia and may be because of fighting chorea |
|
|
how is HD dx
|
genetic test
|
|
|
what is the treatment for HD
|
none available
|
|
|
What is the prognosis for pt with HD
|
death typically occurs 15-25 years after appearance of symptoms
|
|
|
what pharmacological treatments that are associated with HD
|
-to treat psyche symptoms
|
|
|
what role for PT play for pts with HD
|
-PT for strengthening, balance training
|
