Stroke
Flexion vs extension synergy
Flexion: shoulder abduction, elbow flexion, wrist and finger felxion
Extension: shouldef adduction, elbow extension, wrist and finger flexion
What diagnoses PD
Bradykinesia, rigidity, tremor
What is roLe of cerebellum
Adapts response timing and magnitude of APA based on past experience
Describe types of balance control
Steady state: sensory inputs = somatosensory, vestibular visual. Motor outputs: antigravity postural tone
issues lead to alignment issues and verticality and increased postural sqay
Anticipatyr balance control: sensory inputs= somatosensory, vestibular, visual. Can’t be observed, but can see during task perfromance
reactive balance control: sensory inputs= Propioception and vestibular. motor outputs= motor tracts to catch self
Define spasticity
Enhanced stretch reflex behavior resulting in hypersensitivity of muscle to elongation which results in increased resistance of limb to imposed movements
Biomechanical factors impaired with stroke
Force genreation
decrease number of muscle fiber size
atrophyHow does direct pathway work
Define dysdiadochokinesia
Impaired ability to sustain rhythm or force in rapid alternating movement
error in rate and regularity of movement
Muscle afferents
1a= primary spindle for muscle length and rate of change (velocity)
II= secondayr spindle for muscle length without velocity
Ib= golgi tendon organ for muscle tension (force)
III= free nerve endings for pain, chemical stimuli, temeprature
IV= free nerve endings for pain chemical stimuli ands temperature
What stage of movement do stroke, PD, and cerebellar originate in
Stroke: execution
PD: preparation
cerebellar: preparation
Describe what you will see for a baby with a stroke pre and post natal
Pre natal: less strength deficits but significant mirror movements
Post natal: strong strength deficit and distal weaker than proximal and no mirror movements, strong synergies due to pruning
What type of intervention would you do?
External cues—> not able to use SMA BG pathway, need to use premotor cerebellar pathway with external cueing
What type of learning intervention would you do
Hebbain learning, cant use trial and error because you wont learn from your mistakes, no feed forward and feedback response as there is no update from system on how the movement is going. No difference between motor command and what actually happened (in inferior olive). Can’t make adjustment
compare PICS for SCI and stroke
SCI: spams!! disinhibited deep dorsal horn interneurones, 5HT receptor is always active and no longer ligand binding, becomes sensitive to monoamines present
Stroke: spasticity!!! Increase in monamines present from CBST and motor neurons become hyperexciable causing hyperactive stretch reflex
DCML vs anterolateral path
if someone had a lesion at L2 left hemi spinal cord on, what will they loose?
If someone had a lesion in L cortex, what will they show?
DCML= fine touch, vibration, propioception
Dorsal horn—> fasciculus gracilis/cuneatus—> synapse at nucleus gracilis/cuneatus—> Cross at internal capsule—> ascend medial lemniscus—> synapse at VPL—> cortex
Anterolateral= crude touch, pain, temperature
dorsal horn—> ascend/descend 1-2 levels Lissaurs tract—> synapse at dorsal root—> ascend and cross anterior commissure—> ascends anterolateral matter—> synapse VPL and intralaminar nuceli—> cortex
Hemicord lesion: loss of contralateral pain, temperature, and crude touch and ipsilateral loss of discriminatve touch, propioception, and vibration a few levels below lesion
Lesion in L cortex: effect DCML and anterolateral on contralateral side
What are the motor control factors underlying the impairment/movement problem?
Neural
- strength —> decreased descending input, decreased firing frequency
- impaired selectivity —> reduction of CST and increase of CBSPT leading to diffuse synaptic distributions, reduction of brain areas for fine selective movements
What are the motor control factors underlying the impairment/movement problem
Neural
- Bradykinesia—> impaired muscle scaling activation, abnormal firing pattern with increased beta band oscillations, increased inhibition of thalamus from lack of dopamine in the substantsa Nigra pars compacta
- Rigidity—> abnormal long latency reflex, impaired shortening reaction, stretch induced inhibition
What are the motor control factors underlying The impairment/movement problem?
- Asynergia—> impaired ability to coordinate timing and amplitude of muscles in multisegmental movements because they can’t take into account multiple muscle torques.
Compare the CST and CBST.
CST:
originates in M1 (primary motor Cortex)
terminates in ventral horn
synapses 1 times
dexterity and limb movements
high temporal resoliution
high spatial resolution
faster
CBST:
originates in premotor cortex and SMA
terminates in intermediate horn
synapses with at least 3 internerurons
postural control and neck and trunk control
Low temporal resolution
low spatial resolution
slow
Define APA
Describe what happens with the APAs in the following 3 diagnoses: stroke, PD, cerebellar
Any time your body has to to a movement that disrupts balance/posture, there is a preemptive drive to help minimize the disruptance.
Stroke: decreased APAs due to decreased firing rate
PD: short small bursts
Cerebellar: altered timing
Interventions?
Ortho she’s to help increase gait speed, mobility, and dynamic balance
aerobic high intensity training
backwards walking imporves forward gait speed
Locomotor requirements missing
Coordination of rhythmical stepping, progression during stance, swing limb advancement, anticipatory dynamic balance, adaptability, inititation
Motor control impairments
Decreased strength, impaired ability to alternate rapid movements, diminished balance, limited coordination, hard to adapt, cognition
Premotor lesion vs SMA lesionvs area 4
Premotor lesion:proximal limb weakness, difficulty reaching, apraxia
SMA lesion: biannual coordination, impaired initiatin
4 lesion: lack of dexterity, hypotonia
1a afferent from muscle spindle when muscle is stretched
efferent to homonymous muscle and synergistic muscles
1a inhibitory inter nervous and efferent to antagonist to be inhibited