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Neuromuscular Development/Control I > Stroke Interventions > Flashcards

Stroke Interventions Flashcards

1
Q

Goals of assessment in emergency department/acute care

A
  • Neurological signs: BE FAST (balance, eyesight, face, arm, speech, time)
  • Determine type of stroke (ischemic vs hemorrhagic)
  • Severity, prognosis, & D/C potentials: NIHSS helpful with determining severity (≥16 high probability of death/severe disability, ≤6 good recovery)
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2
Q

Describe assessment of orofacial deficits

A
  • Facial asymmetry due to unilateral muscle weakness: drooped face/mouth, nasolabial fold, mouth closure, palpebral fissure, ask pt to close eyes/wrinkle forehead
  • Inadequate lip closure: difficulty controlling saliva
  • Dysphagia: difficulty swallowing/chewing/tongue movements
  • Poor coordination b/w eating & breathing: risk aspiration, pneumonia, poor nutrition
  • DDX of stroke vs facial palsy
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3
Q

Ways to help determine type of stroke syndrome

A
  • Neuroimaging to help determine the where of stroke: MRI
  • Other exams include HINTS
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4
Q

Assessment of stroke syndromes

A
  • Neurological manifestations of stroke follow predictable clinical findings based on functional areas affected & cerebral vessel occluded/damaged
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5
Q

Clinical manifestations of MCA syndrome

A
  • Supplies: primary motor & sensory cortices, Broca’s area, & Wernicke’s area
  • Contralateral weakness UE and face
  • Contralateral sensory loss UE and face
  • Aphasia (L/dominant hemisphere): expressive, receptive, global
  • Neglect (R/nondominant hemisphere)
  • Superior occlusion = Broca’s
  • Inferior occlusion = Wernicke’s
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6
Q

Clinical manifestations of ACA syndrome

A
  • Supplies: primary motor & sensory (LE), supplementary motor, & prefrontal cortex
  • Contralateral sensory loss LE
  • Contralateral weakness LE
  • Altered mental status: frontal lobe behavioral abnormalities
  • Aphasia: speech preservation (Broca’s)
  • Abulia: lack of drive/will power
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7
Q

Clinical manifestations of PCA syndrome

A
  • Supplies: occipital lobe, inferior/lateral temporal lobe (hippocampus), diencephalon (thalamus & subthalamus), cerebral peduncles & midbrain
  • Contralateral homonymous hemianopia
  • Contralateral weakness
  • Thalamic pain syndrome: abnormal sensations
  • Disruption of anterior supply: apathy, amnesia
  • Disruption of posterior supply: neglect, aphasia
  • Visual agnosia, anomia
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8
Q

Clinical manifestations of Lacunar syndrome

A
  • Affects: basal ganglia, internal capsule, thalamus, pons
  • Pure contralateral weakness
  • Pure contralateral sensory loss
  • Parkinsonism
  • Large majority are asymptomatic
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9
Q

Clinical manifestations of vertebrobasilar artery syndrome

A
  • Supplies: corticospinal tracts, corticobulbar tracts, medial & superior cerebellar peduncles, spinothalamic tracts, & several cranial nerve nuclei
  • Headache, D/N/V, nystagmus, diplopia, dysarthria, dysphagia
  • Ipsilateral ataxia, hemiparesis, dysmetria
  • Bilateral effects
  • Locked in syndrome: total body paralysis while sparing eye movement/blinking, cognition & hearing intact, all sensation decreased
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10
Q

Clinical manifestations of superior cerebellar artery syndrome

A
  • Supplies: superior cerebellar cortex, superior cerebellar peduncle, cerebellar nuclei, small portions of midbrain/pons
  • Headache, D/N/V, nystagmus, diplopia, dysarthria
  • Dysmetria
  • Ipsilateral limb/gait ataxia
  • Ipsilateral Horner’s syndrome
  • Contralateral loss of touch/pain/temp
  • Contralateral mild hemiparesis
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11
Q

Clinical manifestations of anterior inferior cerebellar artery

A
  • Supplies: anterior inferior cerebellum, cerebellar nuclei, portions of the pons & medulla (CNs V/VII/VIII), vestibular & hearing organs in inner ear
  • Lateral pontine syndrome
  • D/N/V, nystagmus, diplopia, dysarthria, dysmetria
  • Ipsilateral deafness
  • Ipsilateral ataxia & loss of balance
  • Ipsilateral Horner’s syndrome
  • Ipsilateral loss of touch/pain/temp & weakness in face
  • Contralateral loss of pain/temp & weakness in limbs
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12
Q

Clinical manifestations of posterior inferior cerebellar artery syndrome

A
  • Supplies: posterior inferior cerebellar hemispheres, central nuclei of cerebellum & dorsolateral medulla (CNs V/VIII/IX/X)
  • Lateral medullary syndrome/Wallenburg syndrome
  • D/N/V, nystagmus, dysarthria, dysmetria
  • Ipsilateral ataxia & loss of balance
  • Ipsilateral Horner’s syndrome
  • Dysphagia (CN IX/X)
  • Hoarseness of voice (CN IX/X)
  • Ipsilateral loss of touch/pain/temp of face (CN V)
  • Contralateral loss of pain/temp on body
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13
Q

Clinical manifestations of spinal artery & vertebral arteries

A
  • Supplies: medial medulla
  • Medial medullary syndrome
  • Contralateral paresis of UE & LE
  • Contralateral loss of touch & proprioception
  • Ipsilateral tongue deviation (hypoglossal nucleus)
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14
Q

Common set of signs/symptoms in posterior circulation strokes (Vertebro-basilar, SCA, AICA, PICA)

A
  • Together known as acute vestibular syndrome
  • D/N/V
  • Vertigo
  • Nystagmus lasting for days
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15
Q

Bedside HINTS exam to diagnose stroke versus peripheral vestibulopathy

A
  • HINTS = Head Impulse test, Nystagmus, & Test of skew
  • Stroke: Normal HIT, direction changing/vertical/purely torsional nystagmus, positive skew with cover/uncover test
  • Peripheral vestibular problem: Abnormal HIT, direction fixed/horizontal nystagmus, negative skew with cover/uncover test
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16
Q

Describe the validity of HINTS

A
  • Very good bedside exam in ED/Acute care
  • Better than MRI for detecting stroke in the 1st 24-48hrs
  • Pts mostly gets referred to PTs for this
  • Use this for determining the need for further stroke work-up and/or further imaging or D/C to an OP clinic
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17
Q

Goals for vital management for ischemic stroke in ED/Acute care

A
  • Administer r-tPA within 4.5hrs, after infusion keep BP less than 180/105mmHg
  • Once neurologically stable keep BP 140/90mmHg
  • MAP around 110mmHg
  • ICP goal between 60-80mmHg
  • Maintain O2 >94%
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18
Q

Goals for vital management for hemorrhagic stroke in ED/Acute care

A
  • Maintain SBP <140mmHg
  • Recommended to use anti-hypertensives is systolic >160-180mmHg and diastolic 105mmHg
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19
Q

Goals for therapy and contraindications against early mobilization

A
  • Goals: monitor vitals, early mobilization (as indicated)
  • Contraindications: not until 24hrs later, increased ICP, lower levels of consciousness (sedation), any unstable heart conditions
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20
Q

Recovery potential from stroke

A
  • Varies based on location of injury, severity, extent of tissue damage, age, PLOF, comorbidities, acuity
    -Most significant recovery occurs within first 3-6mo post stroke, slower recovery up to 2-3yrs
  • Pt’s who receive IPR show better recovery than those who don’t
  • Ambulation capacity is a primary factor in determining D/C destination, gait speed in a reliable/valid measure of post stroke functional mobility
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21
Q

Sensory impairments seen during IPR stay (subacute stroke period = few days-few wks)

A
  • Primary sensory loss
  • Superficial, deep (proprioception), & higher cortical sensations affected
  • Spatial perceptual deficits: causes problems with postural control
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22
Q

Motor impairments during subacute stroke

A
  • Paresis with force production deficit: less motor unit recruitment, abnormal timing, torque too initiate & sustain functional movements
  • Atrophy of some muscles
  • Motor planning deficits: apraxia, speech planning deficit (non-fluent aphasia), mostly with L hemisphere involvement
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23
Q

Abnormal synergistic patterns of stroke

A
  • UE synergistic postures: scapular ADD/depression, shoulder ADD/IR, elbow flexion, forearm supination/pronation, wrist/finger flexion
  • LE synergistic postures: pelvic retraction, hip ADD/IR, knee extension, ankle PF/inversion, toe flexion
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24
Q

Describe the Brunnstrom stages of recovery from acute through subacute phases of stroke spasticity

A
  • Stage 1: Flaccidity
  • Stage 2: Spasticity begins to develop
  • Stage 3: Spasticity increases & reaches its peak
  • Stage 4: Spasticity begins to decrease
  • Stage 5: Spasticity continues to decrease
  • Stage 6: Spasticity is essentially absent
  • Stage 7: Return to normal function
25
Q

Communication deficits related to stroke

A
  • 30% of all CVAs have some degree of language dysfunction
  • Aphasia: Broca’s (expressive), Wernicke’s (reception), Global
  • Dysarthria
  • Emotional lability: R hemisphere CVAs = unable to control emotions
  • Referral to SLPs
26
Q

CV impairments related to stroke

A
  • CV complications are 2nd leading cause of post stroke mortality
  • Dyspnea & chest pain
  • Reduced LV EF
  • Cardiac arrhythmias (abnormal ECG)
  • Increased cardiac enzymes (troponin
  • Weakened heart muscles (heart failure)
  • Lack of activity/deconditioning after stroke
27
Q

Respiratory complications related to stroke

A
  • Hemiparesis of respiratory muscles: Reduced lung expansion due to decreased control/weakness of diaphragm & intercostal muscles
  • Poor vital capacity: patient is forced to increased RR (respiratory rate)
  • Lung volumes reduced by 30-40%
  • Reduced VO2, decreased tolerance to exercise, fatigue
  • Reduced cough effectiveness due to weakness of abdominal muscles
28
Q

Describe Pusher syndrome (Contraversive pushing)

A
  • Stroke in L/R posterolateral thalamus, insular cortex, superior temporal gyrus, operculum, internal capsule
  • Loses perception/sense of upright posture: pt posture tilted toward semi side/pt actively pushes toward semi side
  • Visual vertical is intact but vestibular vertical with eyes closed is impaired
  • Passive correction of posture is met with resistance from the patient
29
Q

Diagnosis of Pusher syndrome/Contraversive pushing

A
  • Visual assessment of tilted posture
  • ABD/extension of nonpareil UE/LE
  • Resistance to passive correction
30
Q

Treatment for Pusher syndrome/Contraversive pushing

A
  • Increase visual vertical feedback: place vertical structures in environment & have them feel visual feedback correct
  • Place pillow under unaffected side to correct posture passively (w/o pushing) & have them feel that they are not falling and that it aligns with visual vertical
31
Q

Differential diagnosis between Pusher syndrome and neglect

A

-For neglect the patient may slump towards affected side due to not paying attention to the neglected side/weakness/bumping into objects on that side but NOT pushing

32
Q

Position interventions for stroke patients in acute/IPR

A
  • Goal is to position out of synergistic patterns
  • Helps to maintain normal posture, ROM, reduces risk for MSK deformities, contractures
  • Helps to improve sensory awareness/perception of correct posture
  • Help drive motor areas for more active postural maintenance
  • Better sensory info = better movement
  • Improve respiration & minimizes pressure points
  • Alternate between supine, unaffected, and affected side
    -Shoulder & pelvic positioning needs more attention early on as they tend to be retracted
33
Q

Considerations during positioning stroke patients

A
  • Avoid putting wash clothes/soft squeezable ball inside involved hand (increases spasticity & facilitates primitive palmar grasp reflex)
  • Resting hand splint can be beneficial
  • Footboard to prevent PF is not helpful
  • A pair of shoes may be helpful
34
Q

Therapy intensities for stroke patients recommendations

A
  • Measure of difficulty: different types of exercises/activities
  • Must achieve higher volumes which can be achieved using FITT principles
  • 3hrs or longer per day is associated with greatest functional improvements
  • Strong evidence that early intensive therapy may improve gait & general motor function
35
Q

Task specific training for stroke patients

A
  • LE: may improve functional ambulation, balance, & ADLs post stroke; NDT approach may improve ADLs compared to conventional care; has longer lasting cortical reorganization; intense locomotor training has been shown to improve gait speed & endurance
  • UE: may improve motor function, spasticity, ROM, & muscle strength but not stroke severity or ADLs (CIMT is best example of UE task specific training)
36
Q

Partial BW support treadmill training (PBWSTT) recommendations

A
  • Doesn’t improve ADLs or stroke severity with gait & functional ambulation
  • May not improve gait or balance outcomes compared to conventional interventions
  • Can be considered for patients with low ambulatory function especially when other mobility strategies are inappropriate or unsafe
37
Q

Treadmill training in the absence of partial BW support recommendations

A
  • May improve functional ambulation but may not impact balance, ADLs, & motor function
  • Treadmill w/o BW support can be used when over ground gait training is not available or appropriate
  • Treadmill is NOT superior to over ground gait training
38
Q

Strength training recommendations for stroke patients

A
  • Strong evidence that LE training improves balance but not functional mobility
  • Mixed evidence in LE training improves ADLs, muscle strength, functional ambulation or gait
  • UE may improve motor function & ROM but not dexterity or spasticity
39
Q

Balance training recommendations for stroke patients

A
  • Sit to stand may improve gait & muscle strength but not balance
40
Q

CV/aerobic training recommendations for stroke patients

A
  • Cycle ergometer training help improve motor function, balance, & ADLs. but not functional mobility, gait spasticity, or muscle strength
  • Treadmill may improve functional ambulation but not balance, ADLs, & motor function
41
Q

FES/FES based neuro-orthosis for functional training recommendations for stroke patients

A
  • LE: improves ADLs, muscle strength, functional ambulation, & gait; may help motor function & spasticity
  • UE: May improve motor function & dexterity
42
Q

Motor imagery.mental practice recommendations

A
  • LE: May improve gait, balance, functional ambulation, & motor function
  • UE: May improve motor function & muscle strength
43
Q

Mirror therapy recommendations

A
  • May improve motor function, dexterity, proprioception, & stroke severity
44
Q

Use fo AFOs recommendations

A
  • May improve gait & functional ambulation
45
Q

Strong recommendations for stroke patients related to early mobilization, amount of rehab, cardiorespiratory fitness, & task specific strategies

A
  • Commence mobilization out of bed activity within 48hrs of stroke onset unless otherwise contraindicated
  • Provide as much scheduled therapy as possible
  • Group circuit class therapy should be used to increase scheduled therapy time
  • Include individually tailored exercise interventions to improve cardiorespiratory fitness
  • Task specific recommendations: sitting, sit to stand, standing balance, arm activity
46
Q

Describe rolling PNF based techniques

A
  • Rhythmic initiation w/ or w/o prepositioning of LE into flexion/adduction
  • Rhythmic rotation: reduce truncal tone, facilitates pelvic protraction, which is necessary for all functional activities like rolling, sup-to-sit, transfers
  • Hold relax active movement: to enhance ability to roll through greater range
  • Slow reversal, slow reversal hold, controlled mobility
  • Agonistic reversals: controlled mobility
  • Combine with D1F of UE or LE to encourage rolling from supine<>sidelying
  • D1E of UE or LE sidelying<>supine
  • Chops and Lifts during rolling
47
Q

Describe scooting NDT based techniques

A
  • PT holds the entire foot to avoid stimulating plantar flexion response
  • If patient exhibits better control of proximal parts of LE, PT can use a more distal handhold at toes to inhibit toe flexion and promote ankle DF
  • Hip extension over edge of surface: early activation of glut max and hamstring to break primitive synergies
48
Q

Describe scooting PNF based techniques

A
  • Joint facilitation/approximation: activate joint receptors for weight bearing
  • May need to provide additional tactile cues at gluteal muscles or use sheet
49
Q

Describe supine to sitting PNF based techniques

A
  • Alternating isometrics and rhythmic stabilization at partial sidelying on affected elbow to improve stability
  • Agonistic reversals during sidelying to sitting; to improve controlled mobility
50
Q

Describe sitting NDT based techniques

A
  • Key point of control to improve lumbar extension: forward and up
  • Key point of control to improve thoracic extension: forward and down
  • Thoracolumbar extension together
  • Another key point of contact for thoracic extension: below the clavicles
  • Anterior pelvic tilt from the side and from the front
  • Posterior pelvic tilt using abdominals from the side
  • Neutral pelvis from the side and from the front (using 4 and pinky finger)
  • Ideas about progression: bi-manual outstretched arms (affected arm being held by unaffected arm in antispastic posture), make it more dynamic
51
Q

Describe sit to stand NDT based techniques key points of control for flexion momentum

A
  • From the side: have person practice reaching while maintaining posture
  • From the front
52
Q

Describe sit to stand NDT based techniques key points of control momentum transfer/lift off

A
  • Therapist on paretic side, one manual cue below clavicles, other behind on paraspinals
  • Therapist sitting in front, both manual cues on side of trunk, position paretic arm appropriately
  • Therapist on paretic side, one manual cue on thigh, other on paraspinals or positioning the paretic arm appropriately
  • If more points of control needed, therapist on paretic side, one manual cue below clavicle, other on paraspinals, therapist leg controlling the knee forward movement by providing manual contact on Tib Ant
  • Alternate way (not ideal): therapist in front, both manual cues on side of trunk, therapist leg guarding the knee (can restrict forward knee movement)
53
Q

Describe sit to stand PNF based techniques

A

-To improve forward lean of trunk: hold relax active movement
- To improve controlled trunk movement forward: slow reversals & agonistic reversals
- To improve control during lift-off: agonistic reversals, may need to adjust manual contacts on upper trunk/pelvis during sit<>stand task depending on pt’s abilities and weakness
- Approximation on pelvis may help

54
Q

Describe a squat pivot transfer task oriented technique

A
  • Initial conditions: seat height (from and to), w/c preparation
  • Patient preparation: BOS at EOB, feet placement staggered, hands placement for creating ‘pre-twist’
  • Therapist preparation: hand placement (key points of control), feet placement, sit away from patient in a diagonal fashion
  • Initiation/forward flexion: have patient move forward with hip flex/trunk extended position
  • Execution/momentum transfer: trunk rotation cue with hands and therapist knee during pivoting (allow tibial forward movement)
  • Termination: avoid flopping down
55
Q

Describe pre-gait activities task oriented approach using mixed techniques (part practice)

A
  • Use ‘dorsiwrap’ as needed – practice dorsi-wrapping
  • Therapist sitting/standing on affected side
  • Practice swinging and stepping with the affected LE: key points behind retracted pelvis (for elbow cueing) and on paraspinals/opposite trunk, verbal cue for stepping ‘big’, provide ‘elbow protraction’ cue using elbow during pre-swing phase
  • May need additional key point control at the end of swing to stop knee buckling at IC: may be achieved by shifting cue from clavicles to knee, or may need to also use the therapist knee to stop patient knee buckle
  • Try these with therapist standing and sitting on a stool
  • Progression/regression: remove manual cues, small step to big steps, step over high obstacles, add LE ankle weight, or UE weight
56
Q

Describe pre-gait PNF based techniques to improve stability in symmetrical or midstance standing

A
  • Approximation on pelvis: downward and posteriorly or downward and anteriorly
  • Approximation on trunk: downward
  • Alternating isometrics
  • Rhythmic stabilization
57
Q

Slide 65

A
58
Q

Describe gait PNF based techniques

A
  • Quick stretch technique to facilitate muscle recruitment for pelvic anterior elevation/protraction to initiate swing

Neuromuscular Development/Control I (22 decks)

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