MS Flashcards
1
Q
who gets MS
A
female, onset age 30-60 high risk US/europe/canada/new zealand australia (low risk africa/aisia) genetics stress trigger
Genetic + environment
most complain about ambulation and not getting PT
2
Q
Relapse and Remitting
A
most common form
- medication
- worse (relapse) and improves (remission-degress of recovery to a degree but getting worse over tiem)
(not exacerbation which is an increase in disease activity, it is just a worsening of sx)
3
Q
Relapse - progressive
A
varied relapse and then stabilize, relapse and stabilize (describe behavior not severity)
4
Q
Chronic Progressive
A
(primary progressive)
no improvement: slowing of progression can happen but it progresses over time
5
Q
Secondary progressive
A
start as more benign then becomes a straight slope of progressing
6
Q
Benign
A
occasional sx without significant functional impairment
7
Q
fulminant
A
rapid progressive
early severe disability and death
8
Q
Dx MS
A
mcdonald
- attacks of:
Spatial: 2 regions
temporal: 6 months apart - lab evidence of 2 or more distinct regions
- no other better explanation
9
Q
what evoked potential slows
A
slow conduction velocity
10
Q
his view on exacerbation
A
exacerbation is an acute demyelinating event
exercise doesnt cause this. fatigue, temperature, stress cause worsten of sx but not an exacerbation
11
Q
EDSS
A
most used scale to measure severity of MS
disability scale measure 8 Functional systems: pyramidal (motor), cerebellar, brainstem, sensory B&B visual cerebral and other
only measure ambulation by distance and AD**
mild: 0-3.5
mod: 4-6.5
severe: 7-9.5
12
Q
fatigue in MS
primary vs secondary
A
primary –lassitude/motor fatigue
secondary is treatable
-infection -tx the infection (drugs inhibit immune system so susceptible to infection which incr temp)
- spasticity: E cost -tx baclophen
- ataxia: high E cost
weakness: sedentary cause disuse atrophy tx exercise
depression: tx medicine
sleep deprivation (speascticity, B&B, polyuriam,)
Polypharmacy: too many medications
13
Q
6MWT MS
A
each minute less distance covered than in the minute before
14
Q
can exercise cause exacerbation
A
no
it can cause fatigue
will not cause more neuro damage or increase likelihood of relapse or exacerbation
15
Q
some MS sx
12 primary
6 secondary
A
1-FATIGUE
2-SENSORY changes: anastehsia, Lhermitte sign (posterior cord)
3-TRIGEMINAL NEURALGIA (trig nerve inflammed)
4-WEAKNESS: plaque in pyramidal, disuse
5-OPTIC NEURITIS: abrupt lose vision 2-3 days, blur vision..usually transient
6-SPASTICITY: UMN involve, worse with time
7-HEAT SENSITIVITY: transient worse sx, (wont cause permanent damage, some pts benefit from cooling before exercise)
8. ATAXIA: cerebellar involve or posterior column
9. can disdiakokinsestia, tremor, vestibulopathy, dysmetria get vertigo(–BPPV is preipheral: more common in ms)
10) PSYCH
11) BLADDER
12) SPEECH/LANGUAGE
SECONDARY
1) musculoskeletal (bc innapropriate movement patterns)
2) weakness (not the primary of demylenation but resulting disuse)
3) change in respiration (primary death: lose muscle control of respiration or deconditioned)
4) posture (positionning)
5) osteoporosis (disuse/steroids)
infections (UTI)
6) balance loss (bc primary effeects of weak/spasticity, ataxia, sensory loss, loss motor control and vision ALSO secondary of weakness and contractures)
- if fall rhomber eyes closed it bc visual dom in balance, train eyes closed
- do better on balance when they not fatigued
16
Q
nystagmus in CNS vs PNS
A
Central: Nystagmus Direction changes Rotary or linear nystagmus and not both nystagmus can be seperate from vertigo unable to suppress with fixation
Peripheral unidirectional nystagmus rotary AND linear components nystagmus nystagmus matches with vertigo suppresses with fixation
17
Q
MS drugs
A
A) Disease modifying:
CRAB: copaxone, rebif, avonex, betaseron
- copaxone: limit inflammatory PROPERTY of cells that cross BBB
- beta interferon: PREVENT immune cells into BBB (avonex, bataseron, rebif)
- Tysabri: BLOCK inflammatory cells cross BBB
- -can cause PML
Gilenya: prevent WBC leaving lymph nodes
B) Second order:
Mitoxantrone: sepress immmune
STEROIDS: limit inflammation process
C) Sx
Spasticity:
Baclophen: spasticity (specificity issue)
Zanaflex: Tizanidine: decr spasticity but lose tone elsewhere (specificity issue)
Dantrium: NMJ
Fatigue:
Ampyra: potasium channel blocker to improve nerve conduction
Provigil: act like missing myelin
18
Q
Baclofen
Tizanidine
Dantrolene
A
Baclofen: spasticity of spinal origin (not as effective if cerebral origin)
i. Maximal dose effect: 80-100mg: after that patient gets drowsy and lethargic
ii. Past that amount get Drowsiness, lethargy
1. If not getting relief from spasticity at 80-100mg use a baclofen pump
iii. Act on level of CNS
Tizanidine, clonidine: (second order medication for spasticity, less effective but less drowsiness issue)
i. For Spasticity
ii. pain reducing effects
iii. Act on level of CNS
Dantrolene: (third order drug, works at PNS: NMJ, not at CNS)
–acts as the level of contractile unit, not the CNS
it works on the peripheral nervous system, the NMJ. If person has too much drowsiness with baclofen it is good to give them dantrolene.
The problem is it has a more global effect: reduce the tone in other muscles too (so get the spastic muscle to normal and get low tone in the other muscles): this happens to a greater extent than it does with the other medications
19
Q
copaxone
A
: limit inflammatory PROPERTY of cells that cross BBB
20
Q
beta interferon:
A
PREVENT immune cells into BBB (avonex, bataseron, rebif)
21
Q
Tysabri
A
: BLOCK inflammatory cells cross BBB
–can cause PML
22
Q
Gilenya
A
: prevent WBC leaving lymph nodes
23
Q
Mitoxantrone
A
: sepress immmune
24
Q
STEROIDS
A
: limit inflammation process
25
Ampyra
: potasium channel blocker to improve nerve conduction
| against fatigue
26
Provigil
: act like missing myelin
| against fatigue
27
if see exacerbation what may it be
UTI
28
MS BANDING
pain
feel like band pressing you around the middle
feel like being squeezed --but neuro cause
given neurontin / gabapentin
do TNES,
PT/OT: posture, gait, neiro affect ortho too , dont want compensations
29
does exercise help MS patients
yes
and not exacerbate
he found in his study that cooling helped them walk farther (before and during can cool them)
aquatic therapy good (study didnt show increased gait, did have strength increase)
30
how to exercise with MS
intermittent: we dont want the fatigue to come on but need amt for progress
**vital signs not always accurate indicator of fatigue
get more dose if more rest breaks: volume
MMT can be misleading, first few reps are strong then begin to deteriorate
strengthened with rest breaks and improved without fatigue
**THEY CAN EXERCISE (only pseudoexacerbations can occur): can get fatigue and thermosensitive so do cooling for more volume of exercise INTERMITTENT
31
is berg good for MS
no get fatigued later in day and fall;
32
a main cause of lack of fitness in MS
lack of training
33
Cerebellum
afferent
efferent
Afferent: from somatic, proprioceptors, visual, vestibular, auditory, motor and nonmotor cerebral cortex
Efferent: brainstem, midbrain, cerebral cortex
34
Paleocerebellum
input from spinocerebellar/cuneocerebellar/trigemninalcerebellar tracts with SOMATOSENSORY information from LIMBS and FACE
input from sensory and motor cortices
*unconscious proprioception
lesion of the spinocerebellum results in overshooting when reaching for something reach past object: abnormality in maintaining the muscle tone (ie in a rebound test)
abnormality in maintaining the muscle tone
35
Neocerebellum
input from: sensory, premotor, motor cortex
voluntary movement: planning and timing (skilled movements, more presice with practice)
**if lose hard to acquire lost skills in PT
```
(control of rapid movements, sudden movements (throw a ball and he quickly reacts to catch it)
precise movement control
motor planning)
dysmetria
disdiadokinesia
```
36
Cerebellum in motor control
gets sensory input:
- -somatic, vestibular, visual, auditory
- -motor commands
defines body status : compare intent with actual movement *posture/equilibrium corrections for maintaining balance
MOTOR output to brainstem motor nuclei/motor /premotor cortex
37
major role of cerebellum
1. coordinates activity, fluid movement and postures
2. comparison of motor activities to intend plan and modify it if not achieved (continual loop)
3. modification of motor output based on sensory input and motor output: continuous loop
4. compensation for motor tasks: predictive / anticipatory
big role in predictive movement: feed forward, anticipatory *if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance
5. major role in learning new motor programs because of its modifying function
38
if cerebellum damaged
learning new motor programs is limited: challenge in PT because we depend on motor learning -- here plasticity cannot occur
*if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance
depending on where lesion is in the cerebellum can change deficits
39
Signs of Cerebellar Dysfunction
| 5 traits
1. Dysmetria
2. Asynergia/dysnergia
3. Rebound phenomena
4. Tremor
5. Hypotonia
40
vestibulocerebellum
posture and equilibrium
lesion: inability to maintain balance with rapid change of position
almost predominantly vestibulocerebellum
receives feedback from vestibular system (semicircular canals, etc) to determine changes in direction of self motion
almost instantaneously institutes corrections in postural motor signals necessary for maintain balance after these changes in positioning
lesions in result in inability to maintain balance with rapid changes in position
41
initiation of movement: do cerebellum do too early or too late?
late
42
Friedreichs ataxia
one of the most common hereditary disorders of CNS
CNS & PNS
sx begin at 8-15yo
progressive ataxia, loss of DTR’s, impaired proprioception
scoliosis & pes cavus
abnormal eye movements
cardiomyopathy
ataxia due to loss of proprioception and tract involvement
o gait common first symptom
43
Olivopnotoverebellar atrophy
combined degeneration
progressive ataxia with later onset
initially pure cerebellar, w/ later pyramidal tract, BG and autonomic signs
44
nutrition issues cerebellum
thiamine deficiency
alcoholism
B12- deficiency
E-deficiency
45
neoplasms cerebellum
primary tumors
metastatic disease
paraneoplastic syndrome
46
Arnold Chiari Malformatios
most common developmental malformation of the posterior fossa
o herniation of cerebellusm, medulla & pons throught the foramen magnum
into upper c-spinal canal
47
cerebellum vascular disorders
vascular disorders
ischemia and hemorrhage
mechanical trauma
focal or multifocal
48
Cerebellum tx
weighting
used to keep ataxic arms down but possibly just strengthening arm =>
if pt has too much movements for walker, this is good
pool
dampens tremor while they are in pool
no functional overflow
abdominal binders--quiets trunk
vestibular rehab
only works if pure vestibular & central lesion (and unilateral)
3 sites: cortex, pons and cerebellar
controlling degrees of freedom
using movement decomposition for compensation
depends on etiology
single, focal, stable lesion => better chances
degenerative or multi- focal (MS) => poor chance
plasticity?
not really because ‘skill producer’ is what is affected
motor learning (small errors)
dependent on the learner detecting the errors and correcting them
pt is currently using ‘too large’ errors (large complex)
more forceful ataxia
use single digit movements => limb
49
Tonic clonic seizure = grand mal seizure
ENTIRE cerebral cortex
15-30 seconds of intermittnet contractions major muscle groups followed by jerking of extermities
followed by unconsious up to five minutes
dont hold them down, clear away furniture
**no aura
50
absence (petite-mal) seizure
called this because many people wouldn’t even notice
can see eye blinking (3/sec) or hand twitching
short- term loss of awareness or consciousness
can occur in clusters (someone can have 5-10 in 1 day)
4-12 y.o most common age range
no aura
51
partial (focal) seizure
MOST COMMON
- --usually caused by local (focal) brain involvement
* stroke, AVN, head trauma, slow bleed post fall, tumor
```
---various presentations, twitching (from primary motor area), vision ‘abnormal sensation’ or hearing ‘abnormal sensation’ (not quite hallucination)--depends on where it is :
auditory lobe
occipital obe
motor cortex
etc
```
52
Myoclonic seizure
brief, shock-like jerks of a muscle or a group of muscles
get a few contractions in one or 2 muscles
due to increased excitability of the motor system
53
Multifocal Seizure
affect multiple areas of brain
presentation depend on where in brain
*AUORA* (only seizure he said had aura)
54
cause of seizure
newborn or infant- due to something that occurred at birth (birth issue or anoxia) or a metabolic issue
-can occur with high fever and be benign
o up thru adolescence usually idiopathic
adults: trauma, tumors, aneurysm, drug toxicity, alcohol abuse/withdrawal,
arterial venous malformation (AVM)
55
how do you know LOC and not seizure
another LOC after seizure isnt seizure, it is syncope ,
if it is syncope they will not clench teeth
56
is brain pain innervated
no
57
Primary Headaches
1. Migraine
2. Tension Headache
3. Cluster Headache
58
Migraine
multisystem,
at least 5 attacks to diagnose
4 hours-4 days
light and sound sensitive (also nausea and vomit)
unilateral, pulsating, mod-severe intensity, aggravated by exercise
genetic
NOT VASCULAR (maybe hypothalamus/upper brainstem issue)
Type 1: get aura : visual/ auditory/ sensory hallucination: if medicate here less sx
can affect c-spine
Without Aura: MORE COMMON : can be bilateral, can affect c-spine
59
Tension Headaches
ACUTE type tension headache: due to posture/stress: muscular
muscle origin: traps, levator, c-spine muscle tension
can get from clenched teeth: TMJ induced
-----------------------------------------------------
CHRONIC tension headache: neurotransmitter deficient causes ongoing chroninc (progress from acute, this one isnt muscular origin)
```
Chronic tension headache dx:
15 headaches/month for at least 6 months
+ at least 2:
1) pressing non pulsating pain
2) mild/mod intensity
3) bilateral location
4) not aggrevated by ADL
```
will have nausea or photosensitive or phonosenstiive
60
Cluster Headaches
come in clusters
-alot in a period, go away, come back in a cluster
Men, trigger: alcohol, smoking, lack sleep
15 minutes - 3 hrs
unilateral near eye or frontal
*eyes tears, nose run*
can have ptosis of eyelid
Maybe ANS issue, medications affect bloodflow (some need vasoconstrict, others need dialate)
61
Secondary Headaches
1. Sinus headaches
2. headache from lumbar puncture
3. pathologies cause headaches:
- --meningitis
- --encephalitis
- --AVM (incr pressure, especcially if develope glaucoma)
- --aneurism
- --glaucoma
- --small hemorrhage
*headache from small hemorrhage or aneurism will be worst headache of their life
****RULEL OUT: TMJ
62
Headache tx
1. diary of food and environment and stuff
2. biofeedback if tension headache
3. relax, meditate, manage stress
4. posture eval: alingment
5. trigger point massage
6. rapid cooling flourimethane spray and stretch
7. constant coutnerstrain and muscle energy techniques
8. mobilization of nervous system-tension testing of nerve, nerve flossing
9. exercise for endorphins EXCEPT FOR MIGRAIGNe
63
most demanding task in gait cycle
```
weight acceptance (initial contact and loading)
--shock absorb, initial limb stability, preservation of progression
```
hip extensors, quads, DF
64
if tell elderly to walk faster wheat to they increase
increase hip power (but young will increase at all joints)
65
is there a direct correlation between E cost and instability?
NO
66
Facotors of elderly gait
high A/P and M/L limb acceleration, more medial to lateral COG displacement, lateral sway
Low A/P pushoff
increased hip flexion, knee flexion, ankle has decrease in plantarflexio, and has toe out angle
more land footflat downstairs
high falls and tripping , high heel contact skid velocity, late hamstring activation,
DIMINISHED LE ROM: hip extension and ankle DF
67
implications elderly gait
diminished: limit of sway, control of narrow BOS,
limits of stable stance approached earlier
postural responses called in earlier
postural response may require less activation
elderly have increased sway when balance is challenged by removing a modality or rendering a modality unreliable
therefore diminished postural responses when need it
ELDERLY HAVE MULTIPLE CHANGES IN MOBILITY
STEREOTYPIC
LEADS TO DIMINISHED MOVEMENT, ACTIVITY, FALLS
PT INTERVENTIONS AVAILABLE
68
Muscular Dystrophy
Muscle disease, not motor neuron
Dystrophin deficit, spontaneous degeneration of muscle
defect determines age and spread of progression
Type II fibers: fast phasic involved (Force)
*check blood for CPK bc proteins leak into blood from unstable muscle
PROXIMAL weakness and EXTENSOR weakness first
(if younger age onset, it progresses faster)
69
Beckers Muscular Dystrophy
x linked
benign form of Muscular Dystrophy
PROXIMAL WEAKNESS
able to ambulate until mid teens
SLOWER PROGRESSION
*PT tx like DMD
70
Fascioscapulohumeral Muscular Dystrophy
autosomal dominant
onset at any age, most have by age 20yrs
FACE, SCAPULA, HUMERAL
WINGING SCAPULA: scapula elevated,
weak face: obicularis oris, obicularis occuli (cannot close eyes, drink from straw, transverse smile, wrinkle forehead)
weak Upper arms: arm usually IR , pec atrophy, Lordosis
weak Shoulders *deltoid spared
weak ABDOMINALS
PT: clavicle strap, orthotic for LORDOSIS, eyedrops to keep moist, adaptive devices ADL independence, AFO if footdrop
71
Limb Girdle Muscular Dystrophy
onset in 30s (autosomal recessive)
HIP and SHOULDER weakness (biceps, pecs)
* popeye arm: proximal weakness and so distal arms look larger
* antigravity muscles affected, ADL
SLOW PROGRESSION to all muscles 20 years after dx
PT: tx functional difficulties, raised toilet seat, elevated chair, elevate furniture, spring cushion
72
Myotonic Muscular Dystrophy
autosomal dominant
combination of myotonia and dystrophy
1st sign: myotonia: cannot relax a muscle after a contraction or stimulation--more in cold weather
Progressive weakness to all muscle groups --dystrophy:
ptosis, bland expression, temporal atrophy, hands, feet, face, neck flexors, frontal balding
* CRANIAL NERVE INVOLVED
* BULBAR INVOLVED: swallow, chew, speech, weak
PT tx: functional sx,: AFO, ADL, AD, eval, home assess
73
Duchennes Muscular Dystrophy
x linked
* gowers sign, meryon sign (lift under axilla and not shoulder depress bv weak extensors)
* LE weak (thigh and hip muscles 1st) --> then proximal shoulder and arm
* enlarged calves
Wc by 10-12 yrs
POSTURE: to move wt line post hip, ant knee
Lumbar lordosis, hip abduction, hip flexion (weak extensors), knee flexion, equinovarus (hand on hip)--walk in abduction, PF + inversion
* **TIGHT: gastroc, TFL, illiopsoas***
(contractures: sacromere shorten)
GIVE STEROIDS
Death: cardiac/pneumonia
PT tx: strengthen low intensity (3-5 reps/dont want disuse atrophy of the ones they dont use, not to fatigue), stretch, ADL, respiratory (weak resp muscles), keep mobility, scoliosis if iin wc, positioning (leg in extension), nightsplints,
- orthotics when cannot climb stairs, LLB, tilt table
* if surgery make them ambulatory the nxt day
74
What is tight in Duchennes Muscular Dystrophy
TIGHT: gastroc, TFL, illiopsoas***
Age 2-3: illiopsoas
Age 3-4: heelcord
Age 4: TFL
75
Duchennes Muscular Dystrophy tx
PT tx: strengthen low intensity (3-5 reps/dont want disuse atrophy of the ones they dont use, not to fatigue), stretch, ADL, respiratory (weak resp muscles), keep mobility, scoliosis if iin wc, positioning (leg in extension), nightsplints,
stretch: gastroc, TFL, illiopsoas***
Age 2-3: illiopsoas
Age 3-4: heelcord
Age 4: TFL
76
which has enlarged calves
DMD
77
which has popeye arm
Limb Girdle Muscular Dystrophy
78
Scoliosis bracing
Boston low profile: clamshell
dynamic pad for counterpressure
cushion fabricated
Rigo cheneu orthotic: schroth: mult pts of pressure to leave open areas at CONCAVE side of curve so person can try to self correct in brace
75-90% ots with DMD
surgery vs conservative was same results by age 17
79
Hoehna and Yard Stage 1
Mild UNILATERAL Disease:
1) impaired Diadochokinesis (rapid alternating: they have slow movements)
2) decreased FASCIAL EXPRESSION
3) decreased INITIATION of movements,
4) decreased speech VOLUME
5) loss of some EQUILIBRIUM REACTIONS
6) Slight RIGIDITY
Balance ok
Gait Ok
ADL ok
80
Hoehn and Yahr Scale:
Stage 2:
STAGE 2: bilateral involvement
1) independent ADL
2) IMPAIRED POSTURE, postural changes,
3) BILATERAL RESTING TREMOR
4) BRADYKINESIA, DECREASED SPONTANEOUS movements
5) NO FACIALl expressions
6) SHUFFLING gait, difficulty TURNING
7) DEPRESSION
Postural changes (more flexed)
Gait Changes (shuffling gait, difficulty turning, less armswing, less trunk rotation)
FUNCTIONAL FOR ADL
81
Hoehn and Yahr Scale:
Stage 3
BILATERAL INVOLVEMENT; MODERATE DIFFICULTY IN ADL
1) BALANCE IMPAIRED
2) loss of equilibrium reactions (no protective reactions)
3) Bradykinesia, akinesia
4) retropulsion: forward chasing of COG:
smaller more rapid steps with trunk flexed forward
5) FREEZING during gait (they know what they want to do but cant do it)
6) horrendous turning during gait
7) difficulty with dressing (initiation-not apraxia), ADL DIFFICULT
Impaired Balance
Impaired gait: retropulsion, freezing, bad turning
ADL: difficult
82
Hoehn and Yahr Scale:
Stage 4:
SEVERE DISABILITY, MARKED GAIT DISTURBANCE
1) RIGIDITY increased
2) worse bradykinesia-->AKINESIA
3) bed mobility difficult (not weakness, a motor control issue)
4) "poor" balance
5) decreased dexterity
* ALL ADL DECREASED*
83
Hoehn and Yahr Scale:
Stage 5:
CONFINED TO WC OR BED
1) non-ambulatory
2) severe rigidity
3) bradykinesia, akinetic: very few voluntary movements
4) Flexion posture
5) Drooling, dysphagia (eating difficult)
6) Decubeti (bed position, contractures and skin breakdown)
7) respiratory function decreased due to akinesia
AKINESIA: few voluntary movements
84
PSP
progressive supranucleus palsy
cannot do up and down gaze
similar to PD
*face expression and back head tilt (to see up) key features
work on balance and eyes
the SCALE for psp only documents function, not for dx
85
Dystonia
torticollis most common
also can be foot and hand
ABNORMAL INVOLUNTARY MOVEMENTS
sustained muscle contractions that produce twisting and repete motions and abnormal posturing
UKNOWN CAUSE
tx:
86
Essential Tremor
happens when moving (unlike PD)
progresss slowly
87
Huntingtons
CNS degeneration, choreaform movements --rapid, no purpose uncoordinated
high dopamine
weird gait
decrease mental function, ocular movements deteriorate, head and neck control too
cerebral and caudate nucleus issue
tx with adding Ach or getting rid of dopamine (opposite of PD)
***RESPIRATORY THERAPY
88
Wilsons Disease
extrapyramidal (like PD) but under age 40
cannot metabolize COPPER and neurotoxic level: TREATABLE
medication to bind to copper to remove it
