Random Mix Flashcards
Parkinson’s tremor dominant vs Postural instability and gait disturbances
- Tremor dominant = earlier onset, better prognosis, and cognition intact
- Postural instability and gait = quicker progression, worse prognosis, and cognition IS affected.
Progressive supranuclear palsy characteristics PSP
- ocular motor disturbances, unable to move eyes up or down (vertical palsy) c/o blurred vision
- rapid progression
- retropulsion/startle reflex
- Early postural instability / falls
- rigid trunk
- WBOS
- dysarthria/dysphasia
- Levodopa has little to no effect
- caused by damage to the brainstem
Differences between parkinson plus syndromes vs idiopathic PD
Parkinson’s Plus:
- lack/decreased response to levodopa
- early onset of dementia
- early onset of postural instability
- marked symmetry of signs early on vs PD starts unilaterally
- trunk involved more than limbs
- ocular signs (vertical gaze and nystagmus)
- early autonomic signs (IE hypotension and incontinence)
Multiple Systems Atrophy MSA
- autonomic failure
- severe orthostatic hypotension
- urinary dysfunction
- erectile dysfunction
- sustained gazed evoked nystagmus
- changes in cognition is LESS common
- WBOS ataxic gait
- caused by damage to the basal ganglia, cerebellum, and brainstem
cortical basal degeneration CBD
- caused by damage to the frontal lobe, parietal lob, and dopamine in substantia nigra.
- Progressive dementia
- limb apraxia, usually unilateral
- apraxic speech (non-fluent)
- prominent sensory symptoms (alien hand, spatial neglect)
- impaired upward and horizontal gaze
- parkinsonism (rigid trunk, bradykinesia, NO resting tremor, marked dystonia, myoclonus)
Lesion to substantia Nigra
Narrow and shuffling gait, decrease arm swing, freezing of gait, falls in late stage of the disease (PD)
striatum vs lentiform nucleus
Striatum = caudate and putamen
Lentiform nucleus = putamen and globus pallidus.
Damage to the globus pallidus
Causes Huntington’s disease (B athetoid and chorea movements)
PD is caused by damage to what structure? How many neurons have to be loss before physical signs?
- damage to basal ganglia, (SNpc) substantia nigra pars compacta (nigra because dopamaine is black on imaging) located in the midbrain
- 60-80% are loss before physical signs
Sporadic vs genetic presentation of PD
Genetic PD (10%) = Atypical presentation: younger onset, dystonia, early dementia
H&Y scale
0-5: higher is worse (+1.5 and +2.5)
0 = no signs or sx
1 = unilateral sx
1.5 = unilateral plus axial
2 = Bilateral but NO balance sx
2.5 = Bilateral and MILD balance (negative pull test)
3 = mild to moderate progression with Balance deficits
4 = severe disability but still able to stand and walk independently
5 = bedridden or w/c bound if not assisted.
non- motor signs/symptoms of PD
- sleep disturbances
- dysautonomia (especially orthostatic hypotension)
- constipation
- cognitive: executive function, memory, motivation, memory, attention, in later stages dementia
- affects the limbic system, depressed dopamine causes: depression, apathy, anxiety, anhedonia (inability to feel pleasure)
- increased dopamine causes (later stages with shrinking therapeutic levels): euphoria, mania, impulsivity, pleasure seeking/risky behavior
Evidence based treatment for PD:
Evidence supports: - Pace controlled treadmill training - forced cycling - LSVT Loud and Big - Dance - boxing some research Mixed evidence: Tai Chi No evidence yet: yoga, PWR! Other: include cardiorespiratory training. Dual task helps with single and dual tasks but not balance. Exercise is disease modifying
Where do cervical, thoracic, lumbar, and sacral spinal nerves exit
Cervical spinal nerves exit ABOVE the corresponding vertebral body
Thoracic and Lumbar spinal nerves exit BELOW
Sacral spinal nerves exit at the end of the spinal cord (L1-L2)
Main nerve for Ankle DF
Anterior Tib innervated by the deep fibular nerve (L4 - S1) . Nerve wraps around fibular head.
Modified Rankin Score
- recommended for acute care stroke and rehab stroke
- score: 0- 5; higher = worse
- 0: no symptoms at all
- 1: no significant disability despite symptoms. Can carry out all usual activities
- 2: slight disability; unable to carryout all previous activities but look after own affairs
- 3: Moderate disability: requires some help but able to walk without assistance
- 4: Moderate - severe disability: unable to walk without assistance and able to attend to own bodily needs without assistance
- 5: severe disability: bedridden and requiring constant nursing care and attention
- 6: Dead
What is the highest level of complete SCI where it’s POSSIBLE to perform EVEN transfers Independently
possible at C6 (independent to some assistance)
What is the highest level of complete SCI where it’s POSSIBLE to perform UNEVEN transfers Independently
possible at C7 (independent to some assistance)
What is the highest level of complete SCI where it’s POSSIBLE to be independent with manual w/c indoors
C6
What is the highest level of complete SCI where it’s POSSIBLE to be independent with manual w/c outdoors
outdoors level ONLY = C7
What SCI level starts functional ambulation?
Functional ambulation starts at T10
Highest SCI level someone could be independent with Ambulation?
T10 -L1 patient could be independent (or require some assistance) to amb with KAFO and AD short distances
Highest SCI level for limited household ambulation
T11- T12
Highest SCI level for independent house hold ambulation
L1
Highest SCI level for limited community ambulation
L1
Highest SCI level for full community ambulation
L3
nominal vs ordinal vs interval vs ratio
- nominal: yes/no; male/female
- ordinal: ranking order with no set intervals IE first, second, third or good, fair, poor
- intervals: has set intervals IE temperature, but NO true zero
- Ratio: set intervals and true zero. IE ambulation distance and time.
symptoms for AICA stroke
- AKA lateral pontine stroke
- symptoms: same side ataxia, contrallateral weakness, contrallateral decreased pain and temperature, vertigo/nausea
symptoms for PICA stroke
- aka lateral medullar stroke or wallenberg syndrome
- symptoms: same side ataxia, contralateral decreased pain and temperature of the body, same side for face, dysphagia/dysarthria, nausea/vertigo, horners syndrome (ptosis (eyelid droop), mtosis (pupil constriction), and decreased sweating on same side due to sympathetic trunk involvement)
definition of therapeutic index
The RATIO between toxic dose in 50% of subjects to the effective dose in 50% of subjects
watershed stroke
- ischemia to distal branches of main cerebral arteries, caused by hypofusion
- results in proximal weakness with distal strength ok
- “barrel man”
Lacunar stroke
stroke to distal branches of MCA which supply the basal ganglia and internal capsule
- high incident in elderly and with HTN
what functions are spared in ALS?
sensory, bowel and bladder, cognition, and ocular motor
Primary Lateral sclerosis (PLS)
UMN only; better prognosis then classic ALS but may progress to classic ALS
Progressive Spinal Muscular atrophy (PMA)
LMN only
typical ALS
UMN early on, followed by LMN signs
Chronic inflammatory demyelinating polyneuropathy (CIDP) vs GBS
CIDP has chronic progressive course of 2 or more months or relapsing weakness vs BGS rapidly progresses 2-6 weeks. CIDP is more likely to have sensory signs (paresthesia, pain, loss of somatosensory feedback), CIDP is less likely to have preceding illness; independent amb is often maintained in CIDP, autonomic dysfunction and respiratory insufficiency is less common in CIDP.
- FOR BOTH: it’s important to monitor overwork weakness and DOMS 1-5 days post activity
GBS test results
- Nerve conduction velocities are abnormal/decreased.
- distal compound motor action potential (CMAP) predicts prognosis. poor outcome is CMAP is < 20% of normal at 3-5 weeks
- elevated CSF proteins
CIDP test results
- elevated CSF protein levels
- slowed/decreased nerve conduction velocities
- prolonged distal motor latency
- partial motor conduction block
better prognosis if diagnosis earlier
ALS and MS
also worse prognosis if male for MS
ALS test results
- nerve conduction velocity testing: usually normal BUT could be slightly slowed.
- EMG: reduction in the number of motor units, fibrillations (small) and positive sharp waves, fasciculations (larger). Signs of reinnervation = long duration polyphasic units
MS test results
- MRI of brain and SC will see plaques and atrophy ( need 2 lesions and 2 attacks to dx unless > 1 yr then just 2 lesions)
- evoked potentials (visual) - just tells you if optic tract is intact
- CSF: oligoclonal bands (just tells you if there is inflammation)
EDSS scoring
1 - 10 with .5 increments; Higher = worse
0 - 4.5 = Independent ambulation
5.0 - 7.5 = Impaired / limited ambulation
8.0 - 9.5 = restricted to w/c or bed
10 = dead
Ambulation:
- 0 = 200 meters
- 5 = 100 meter
- 0 = unilateral / intermittent assistance
- 5 = constant or bilateral assistance
- 0 = 5 meters
- 5 = steps
0 - 3.5 = normal to mild
- 0 -5.5 = mild to moderate
- 0 -7.5 = mod to serve
- 0 -9.5 = severe
Error based learning vs reinforcement learning locations
- Error based learning (error data and trial by error) = cerebellum
- Reinforcement learning (No error data; binary outcome only; successful movements will be reinforced) = basal ganglia
Feed forward vs feed back mechanism motor responses
- Feed forward (anticipatory / know it’s coming) = cerebellar
- Feed back (reactionary / don’t know it’s coming) = brain stem and SC
Evidence Based Treatment: Cerebellar
- external cueing (rhythmic auditory stimulation, EMG, and visual biofeedback
- case studies for loading trunk (considered compensatory), no evidence for loading limbs
- balance training to include static, dynamic, and optokinetic stimulation
- dynamic balance and whole body movements over limb coordination
- utilize reactive feed back reactions (Brain stem and SC) and reinforcement learning (BG) to compensate for damaged cerebellar
Evidence Based Treatment: Cerebellar
- adaptation exercises (VOR retraining): used mostly for unilateral hypofunction
- substitution (dissociation of head and eye movement): used for CNS dysfunction and bilateral hypofunction, when there is no vestibular system.
- Habituation (desensitization): unilateral hypofunction and central vestibular
Evidence Based Treatment: TBI
• Address self efficacy
• Increase executive function
• Restrict activities/environment first then add distractions and environmental challenges / dual tasks as motor ability improves
• Encourage cardiorespiratory fitness program
• Address coordination and posture
.Address balance deficits because they are more related to h/o falls than attention/dual tasks
CIMT protocol
need 10 degrees finger extension, 20 degrees wrist extension, no cog or sensory deficit. Training paretic UE for 6hrs a day x 2 weeks. Restraint of UE 90% of waking hours during this time
how to prevent shoulder pain in manual w/c
- Strengthening of posterior shoulder muscles for power and endurance
- Strengthening of shoulder external rotators
- Stretching anterior shoulder structures
- Biofeedback training
- Arm ergometry
- move wheels forward
- push with a semicircular pattern which has more time in push phase vs recovery phase and hands fall below the push rim during the recovery phase.
- move the wheels forward, although this makes the w/c less stable.
