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Motor Control > Neuromuscular Physical Therapy Practice Patterns > Flashcards

Neuromuscular Physical Therapy Practice Patterns Flashcards

1
Q

A sign is . . .

A

– Objective findings of pathology

– Can be determined by physical examination

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2
Q

A symptom is . . .

A

– Subject’s experience of the pathology

– Perceived by the patient

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3
Q

Positive Sign

A

– Release of abnormal behaviors – Presence of abnormal reflexes – Spasticity

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4
Q

Negative Sign

A

– Loss of normal behaviors
– Paresis
– Loss of sensation

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5
Q

Primary Effects

A

– Impairment in the same system as the pathology
– Direct result of pathology
• Paresis, loss of sensation, loss of speech

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6
Q

Secondary Effects

A

– Impairment in different system from pathology
– Develop as a result of the pathology often over time
• Change in muscle length or decubitus ulcers

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7
Q

Neuromuscular Diseases

A

– Motor unit

– LMN signs

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8
Q

Disease of Central Motor Control

A

– Control of the motor unit

– UMN signs

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9
Q

Myalgia signs and symptoms

A
  • Common, but rarely a main complaint

* Onset can be abrupt, slow, or insidious

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10
Q

Myalgias may be due to . . .

A 
– Over-exertion/strain
– Metabolic myopathy
– Infections
– Fibromyalgia
– Autoimmune disorders (MS, lupus)
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11
Q

Signs/Symptoms: Weakness

A

• Rate of progression varies
• Distribution varies
– See Fredericks and Saladin table 12-1
• Complete or partial loss of strength
– Paralysis or plegia indicates complete loss
– Paresis indicates partial loss

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12
Q

Signs/Symptoms: Myasthenia

A

• Muscle Fatigability
– Performance declines with repeated contractions
– This is not a typical fatigue

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13
Q

Signs/Symptoms: Atrophy

A

– Myopathy = little atrophy with profound weakness
– Denervation = profound atrophy and weakness
– Cancer = severe atrophy with little weakness

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14
Q

Signs/Symptoms: Hypertrophy

A

– Unaffected muscles may look relatively larger
– Compensatory hypertrophy due to increased work load of synergistically-related muscles
– Pseudohypertrophy can occur where muscle tissue is replaced with fat and connective tissue

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15
Q

Myogenic Hyperactivity: Fasciculation

A

Twitch of group of muscle fibers

visible

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16
Q

Myogenic Hyperactivity:

Myokymia

A

Rippling contraction (visible), especially in the face

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17
Q

Myogenic Hyperactivity: Spasm

A

Forceful, involuntary contraction

that may interfere with function

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18
Q

Myogenic Hyperactivity: Cramp

A

Powerful, painful, involuntary spasmodic contraction in single muscle

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19
Q

Myogenic Hyperactivity: Tetany

A

Sustained spasmodic contraction in multiple muscles

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20
Q

Myogenic Hyperactivity: Fibrillation

A

Contraction of single muscle fiver (not visible)

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21
Q

Myogenic Hyperactivity: Myotonia

A

Delayed ability for muscle to relax; alteration in

muscle membrane

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22
Q

Myogenic Hyperactivity: Contracture

A

Involuntary shortening of fibers in electrically quiet muscle

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23
Q

Signs/Symptoms: Hypotonia

A

• Reduction in muscle tone that impacts function
– May occur with or without hyporeflexia
– Common in neuromuscular diseases (LMN)
– Feels soft and flabby
– Produces less than normal resistance to stretch

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24
Q

Anesthesia

A

Loss of sensation, especially pain

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25
Q

Hypoesthesia

A

Decreased sensitivity to sensation

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26
Q

Paresthesia

A

Abnormal sensations (burning, prickling, tingling)

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27
Q

Dysesthesia

A

Unpleasant abnormal sensation produced by innocuous stimuli

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28
Q

Hyperesthesia

A

Exaggerated unpleasant sensitivity to innocuous stimuli

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29
Q

Hypoalgia

A

Diminished sensitivity to painful stimuli

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30
Q

Hyperalgia

A

Excessive sensitivity to painful stimuli

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31
Q

Hyperpathia

A

Exaggerated unpleasant response to painful stimuli that persists after removal of stimuli

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32
Q

Glove-and- stocking pattern

A

Forearms distally and mid-calf distally lack sensation (common in neuropathies)

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33
Q

Deep Tendon Reflex Scoring

A

0 Absent No visible contraction
1+ Hyporeflexia Sluggish contraction with little to no joint movement
2 Normal Slight contraction with slight joint movement
3+ Hyperreflexia Clearly visible, brisk contraction with moderate joint movement
4+ Abnormal 1-3 beats clonus; may spread to contralateral side
5+ Abnormal Sustained clonus; may spread to contralateral side

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34
Q

Central Motor Control Disorders include . . .

A 
– Stroke
– SCI
– Parkinson’s Disease 
– TBI
– Multiple Sclerosis
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35
Q

Hypertonia: Spasticity

A

– Velocity dependent increase in muscle tone accompanied
by hyperactive DTR
– Severity varies greatly depending on site and extent of damage
– Predominately in antigravity muscles
– Clasp-knife phenomenon = sustained stretch results in
sudden disappearance of resistance

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36
Q

Hypertonia: Rigidity

A 
– Heightened resistance to passive movement independent
of velocity of stretch
– Relatively uniform throughout ROM
– Most predominant in flexors
– Can be lead-pipe or cogwheel
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37
Q

Posturing: Midbrain or bilateral forebrain lesions

A

– Posturing may be responsive to position, loud
noise, and pain
– Persistence is a poor prognostic indicator

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38
Q

Posturing: Decorticate

A

blah

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39
Q

Posturing: Decerebrate

A

blah

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40
Q

Signs/Symptoms: Hypotonia

A

• Decreased resistance to passive stretch

– Usually associated with diminished DTR

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41
Q

Spinal shock and Diaschisis

A

– Sudden alteration of function, usually following
injury or insult
– Seen following TBI, CVA, and SCI

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42
Q

Signs/Symptoms: Weakness and Fatigability

A

Impaired activation of the motor unit ranging from mild to total paralysis

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43
Q

Hemiparesis

A

• Contralateral = lesion above decussation of pyramidal
tracts
• Ipsilateral = unilateral cerebellar lesion

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44
Q

Quadriparesis

A

• Supraspinal bilateral lesion

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45
Q

Quadriplegia (tetraplegia)

A

• SCI T1 or above

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46
Q

Paraplegia (diplegia)

A

SCI below T1

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47
Q

Loss of Fractionation

A

Inability to move to a single joint independently of other joints

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48
Q

Abnormal Synergies

A

– Dominant muscle synergies that emerge when voluntary activation of one joint movement is invariable accompanied by predictable movement at other joints
– Flexion synergy common in UE and extension synergy common in LE
– Know Table 12-6

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49
Q

Coactivation Changes

A

Agonist and antagonist contract

together during movement

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50
Q

Timing Anomalies

A

Increased reaction time and movement time

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51
Q

Tremor

A

Rhythmic oscillating movement occurring at rest or with movement

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52
Q

Dystonia

A

Powerful, sustained contraction of groups of muscles causing twisting or writhing of whole body; can be fast, slow, or painful

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53
Q

Athetosis

A

Writhing, twisting movement of limbs, head, trunk, face, or tongue without fixed posture

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54
Q

Associated Reactions

A

Unintentional movement of one part of the body occurring with intentional movement of another part

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55
Q

Ataxia

A

Unsteadiness, incoordination, clumsiness; can be halting, jerky, and imprecise movement and difficulty in regulating force, range, direction, velocity, and rhythm of movement

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56
Q

Dysmetria

A

Error in distance estimation

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57
Q

Dyssynergia

A

Errors in timing or sequencing resulting in lack of fluidity

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58
Q

Dysdiadochokinesia

A

Abnormal rhythm and incoordination especially during rapidly alternating movements

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59
Q

Signs/Symptoms: Apraxia

A

Inability to perform goal-directed movements in absence of motor or sensory dysfunction

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60
Q

Ideomotor Apraxia

A
  • Awkward, clumsy response to understood command
  • Unable to use sensory feedback to correct movement
  • Lesions typically of premotor area
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61
Q

Ideational Apraxia

A
  • Inability to recognize objects and their uses
  • Inability to form appropriate motor program in response to command for habitual movement
  • Lesions in dominant hemisphere
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62
Q

Signs/Symptoms: Hypokinesia

A

Slowness of movement independent of problems with muscle power or coordination

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63
Q

Akinesia

A

Lack of movement

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64
Q

Bradykinesia

A

Slowness of movement

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65
Q

Signs/Symptoms: Reflexes

A

• Superficial (cutaneous)
– Muscle response elicited by stimulation of skin
• Tendon Reflexes

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66
Q

Give the difference between normal plantar reflex and Babinski

A
  • Normal is plantar flexion of toes
  • Positive is dorsiflexion of toes with separation and fanning of toes 2-5
  • Indicative of pyramidal system damage
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67
Q

Signs/Symptoms: Balance and Sensation

A

• Balance is reduced through altered motor, reduced reaction and movement time, abnormal tone, and/or poor postural control
• Sensation deficits are related to location and extent of lesion
– Include DCML and Anterolateral systems and their respective sensory modalities

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68
Q

Give the cardinal risk factors for CVA

A

– Hypertension
– Diabetes
– Heart Disease

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69
Q

Non-modifiable risk factors for CVA

A

– Age, race, sex, family history, history of CVA

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70
Q

Modifiable risk factors for CVA

A

– Primary: HTN, DM, hyperlipidemia, hypercholesterolemia,
Chronic inflammatory processes
– Non-primary: inactivity, obesity, smoking, alcohol abuse, drug abuse, oral contraceptives

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71
Q

Warning Signs of CVA

A

• Sudden numbness or weakness in face, arm, or leg, especially when unilateral
• Sudden confusion, trouble speaking, understanding
• Sudden trouble with vision
• Sudden trouble walking, dizziness, loss of
balance, or incoordination
• Sudden severe headache with no know cause

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72
Q

Transient Ischemic Attacks

A

• Signs and symptoms last less than 24 hours
– Strong predictor of impending stroke
– Symptoms similar to stroke
• Occasionally, you will see reversible neurologic deficits that last longer than 24 hours but resolve within 3 weeks

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73
Q

Ischemic Stroke Types

A

– Large artery disease resulting in atherothrombosis
or thromboembolism
– Cardio embolism or embolism of other source
– Lacunar infarcts: small deep infarcts in the distal distribution of penetrating vessels (lenticulostriate, thalamoperforating, pontine perforating arteries, recurrent artery of Heubner). They result from occlusion of one of the small penetrating end arteries at the base of the brain and are due to fibrinoid degeneration.

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74
Q

Ischemic Strokes often occur . . .

A

During sleep

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75
Q

Ischemic: Thrombotic Strokes Cause

A

– Atheroma forms and occludes artery, causing turbulence
– Turbulence leads to development of platelet plaque called atherothrombus, further occluding artery
– May fragment to become thromboembolism or hemorrhage to further occlude artery
– Variable onset from minutes to hours

76
Q

Ischemic: Embolic Strokes Cause

A

– Clot most commonly of cardiac origin
– Can also be thromboembolism, cancer metastasis, or fat from bone trauma
– Often via internal carotid artery and into the middle cerebral artery and its branches
– Rapid onset from seconds to minutes with focal deficits

77
Q

Ischemic: Lacunar Strokes Cause

A

– Small vessel disease
– Pure sensory strokes are predictive of deep, small lacunar infarcts from a single penetrating artery
– Pure motor hemiparesis can occur from arterial occlusion of branches of the distal medial cerebral artery

78
Q

Hemorrhagic Strokes: Intra-cerebral hemorrhage

A
  • Often due to chronic
    hypertension
    • 10% of all strokes
    • Higher 30-day morbidity and mortality than ischemic
79
Q

Hemorrhagic Strokes: Subarachnoid hemorrhage

A

Can result from ruptured aneurysm or AVM or trauma
• 3-5% of all strokes
• Severe and sudden headache described as “worse ever”
• Nausea, vomiting, impaired consciousness, nuchal rigidity, and seizures are signs
• Diagnosed vis CT or MRI; may also see xanthochromia of CSF

80
Q

Hemorrhagic Stroke Effects

A

– Decreased perfusion leads to global ischemia

– Acute mortality rate is as high as 30-50%

81
Q

Effects of Infarct: Penumbra

A

• Core of ischemic tissue from cell death
• Surrounding is zone of injured and potentially
viable tissue called the penumbra
• Early reperfusion is critical in preserving the tissue potential in the penumbra

82
Q

Give the steps of the metabolic cascade prompted by infarct:

A

• Loss of blood flow results in depletion of ATP
• This results in membrane depolarization as ionic
transport ceases
• Calcium influx causes mass release of neurotransmitters including glutamate
• Glutamate activates NMDA and excitatory receptors, resulting in further depolarization of surrounding neurons and further calcium influx, perpetuating the process
• Calcium influx also leads to degradation of the cellular structure through the excessive activation of enzymes
• Byproducts of the cascade result in further cellular inflammation, vascular compromise and damage
• Within hours of the initial infarct event, the penumbra is often consumed and coalesced with the infarcted core
• Medical treatment focuses on preserving the penumbra via restoring blood flow

83
Q

Localization of Impairment: Frontal Lobe

A

Primary movement, personality changes, cognitive impairments, delayed initiation, language deficits (Broca’s)

84
Q

Localization of Impairments: Temporal Lobe

A

Auditory and perceptual changes, memory and learning impairments, aphasia (Wernicke’s)

85
Q

Localization of Impairments: Parietal Lobe

A

Somatosensory changes, impaired spatial relations, homonymous visual deficits, agnosia, language comprehension impairments

86
Q

Localization of Impairments: Occipital Lobe

A

Homonymous hemianopsia, impaired extra ocular muscle movement

87
Q

Localization of Impairments: Cerebellum

A

Ataxia, ipsilateral dysmetria, dysdiadochokinesia, intention tremor

88
Q

Localization of Impairments: Brainstem

A

Gait disturbance, diplopia, focal weakness, altered consciousness and attention

89
Q

Middle Cerebral Artery Syndrome

A
  • Contralateral paralysis and sensory deficits
    • Due to infarct of internal capsule
    • UE more involved than LE
    • Somatic and motor areas involved
  • Speech impairments
    • Broca’s area (dominant hemisphere) = motor
    • Wernicke’s area (dominant hemisphere) = receptive • Global = both Broca’s and Wernicke’s
  • Unilateral neglect
    • Parietal lobe (non-dominant hemisphere)
  • Contralateral homonymous hemianopsia
    • Disruption of optic radiation
90
Q

Anterior Cerebral Artery Syndrome

A
  • Contralateral paralysis and sensory deficits
    • Due to infarct of internal capsule
    • LE more involved than UE
  • Contralateral cortical sensory loss
    • Stereognosis, graphesthesia, tactile extinction
  • Slowness, delay of spontaneity, motor inaction
  • Problems with bilateral manual tasks
    • Due to infarct of corpus callosum
91
Q

Posterior Cerebral Artery Syndrom: Peripheral Territory

A

– Contralateral homonymous hemianopsia (primary visual cortex or
optic radiation disruption)
• May see macular sparing due to collateral circulation from MCA to occipital pole
– Visual agnosia or prosopagnosia (left occipital lobe)
– Memory deficits (infero-medial temporal lobe)
– Topographical disorientation (non-dominant primary visual area)

92
Q

Posterior Cerebral Artery Syndrom: Central Territory

A

– Thalamic pain (VPN of thalamus)
– Involuntary movement (subthalamic nucleus)
– Contralateral hemiplegia (cerebral peduncle of midbrain)
– Weber’s syndrome (CN3)
– Paresis of vertical eye movements, ptosis (supranuclear fibers to CN3)

93
Q

Medial Medullary Syndrome

A

• Ipsilateral to Lesion
– Paralysis of 1⁄2 of tongue (CN12 or nucleus)
• Deviates to paralyzed side with protrusion
• Contralateral to Lesion
– Hemiparesis (UE and LE due to corticospinal tract disruption)
– Impaired tactile and proprioceptive sense (medial lemniscus)

94
Q

Lateral Medullary Syndrome (Wallenberg’s)

A

• Ipsilateral to Lesion
– Cerebellar ataxia (cerebellum or inferior cerebellar
peduncles)
– Decreased sensation (pain and temperature on face and tactile in limbs due to CN5 disruption)
– Vertigo (vestibular nuclei)
– Nystagmus (vestibular nuclei)
– Dysphagia (CN9 and 10)
– Horner’s syndrome (descending sympathetic tracts)
• Contralateral to Lesion
– Impaired pain and temperature sensation of 50% of body and sometimes the face (spinothalamic tract)

95
Q

Horner’s Syndrome

A 
• Ptosis
     – Drooping upper eye lid
• Miosis
     – Decreased pupillary size
• Anhidrosis
     – Decreases sweating on ipsilateral face and neck
96
Q

Locked-In Syndrome

A

– Results in tetraplegia and often bilateral cranial
nerve palsy (sparing of upward gaze)
– Coma (if reticular activating systems disrupted) – Sparing of cognition

97
Q

What are primary impairments?

A 
Direct Result of Pathology:
Weakness
Abnormal muscle tone 
Muscle activation problem Alteration in sensation 
Alteration in cognition 
Alteration in perception 
Speech & language dysfunction
Alteration in emotional system & behavior
98
Q

What are secondary impairments?

A

Indirect consequence; secondary system:
Orthopedic changes in alignment & mobility
Change in muscle & soft tissue length
Pain
Edema

99
Q

What are composite impairments?

A

Interaction of multiple systems:
Impaired balance
Impaired walking
Shoulder subluxation Inappropriate learned compensations

100
Q

Lethargy

A

Mildly depressed LOC; easily aroused

101
Q

Obtunded

A

Depressed LOC; difficult to arouse

102
Q

Stupor

A

Not able to be aroused from sleep-like state

103
Q

Coma

A

Inability to make any purposeful response to environment

104
Q

Fluent Aphasia

A

– Wernicke’s or Receptive
– “Sounds” correct, but is nonsensical
– Auditory comprehension is impaired
– Results from lesion of left posterior-lateral temporal lobe

105
Q

Non-fluent Aphasia

A

– Broca’s or Expressive
– Flow is slow and hesitant, vocabulary limited and syntax impaired
– Speech production is labored or lost
– Auditory comprehension is good
– Results from lesion of premotor area of left posterior frontal lobe

106
Q

Dysphagia

A

• Difficulty or inability to swallow
– Very common with brainstem strokes (80%) and
seen commonly in other strokes
– Aspiration occurs in 30% of patients

107
Q

Cognitive Dysfunction: Attention

A

– Ability to focus on specific stimulus without distraction

– May confabulate

108
Q

Cognitive Dysfunction: Orientation

A

person, place, time

109
Q

Cognitive Dysfunction: Memory

A

– Registration, encoding, storage, recall, retrieval

– Test with Mini-Mental Status Exam

110
Q

Cognitive Dysfunction: Multi-infarct dementia

A

– Onset may be abrupt with fluctuating deficits in attention and memory; occurs after multiple small infarcts

111
Q

Cognitive Dysfunction: Delirium (Acute Confused State)

A

– Seen most often during acute stage following CVA; characterized by clouding of consciousness and impaired alertness

112
Q

Cognitive Dysfunction: Problem Solving

A

Manipulate knowledge and apply to new situations

113
Q

What is pseudobulbar affect?

A

Emotional lability or emotional dysregulation syndrome

114
Q

How common is depression in patients who have experienced a CVA?

A

Around 35%

115
Q

Unilateral Neglect

A
  • Perceptual problem of impaired awareness of one side of space (usually the left)
  • Test with line bisection or letter cancellation tests
  • Often includes asomatognosia, a tendency to ignore or neglect one side of the body
116
Q

Visual Deficits: Homonymous hemianopsia

A

– Loss of vision on one side of visual field (named
for lost visual field)
– Left hemianopsia = loss of left nasal and right temporal hemiretina
– Can teach compensation

117
Q

Cardiopulmonary and Musculoskeletal Issues

A

• Often underlying coronary artery disease
– May be deconditioned prior to stroke
•Impaired pulmonary function due to decreased lung volume, perfusion, and vital capacity
• Risk of DVT and pulmonary embolism acutely
• Osteoporosis and fracture risk is commonly
increased in elderly
– Fall risk increases in many with chronic stroke

118
Q

What are the main goals for medical management post CVA?

A

– Improve cerebral perfusion
– Maintain BP and cardiac output
– Restore/maintain fluid and electrolyte balance
– Maintain blood glucose levels
– Control seizures and infection
– Control edema, intracranial pressure, and herniation
– Maintain bowel and bladder function
– Maintain skin integrity
– Decrease risk for complications like DVT, aspiration, ulcers, etc.

119
Q

Brunnston Stages of Recovery

A

1: Flaccidity, no DTR. No movement of the limbs can be elicited
2: Associated reactions or minimal voluntary movement
3: Voluntary control of abnormal synergies
4: Movement combinations that are not exclusively part of either synergy
5: More difficult movement combinations possible
6: Disappearance of spasticity, individual joint movements possible

120
Q

Stages of Rehabilitation: Acute Phase

A

– Low-intensity starts as soon as medically stable
– Strong evidence that early specialized care results in better outcomes
• Neurological ICU
• Specialized stroke units
• Acute care (average stay is about 5 days)
– PT Intervention Focus: stability and early mobility
• Monitor vitals and prevent ulcers
• Position out of synergistic patterns
• Early bed mobility: rolling, bridging, scooting
• Postural control in sitting
• Transfers from bed to/from wheelchair or standard chair
• Standing weight shifts or gait training for more mild strokes

121
Q

Stages of Rehabilitation: Subacute Phase

A

– Patients with moderate to severe impairments benefit from inpatient rehabilitation
• Must tolerate 3 hours of active rehabilitation 6 days/week
– Strong evidence that intensive rehab within 20 days of stroke onset results in improved function
• Freestanding comprehensive rehab facilities
• Rehab units in acute care hospitals
– PT Intervention Focus: functional mobility
• Bed mobility
• Transfers: bed, chair, couch, toilet, shower/tub, car
• Gait training: various surfaces including curbs/ramps/stairs
• Task-specific training and motor control

122
Q

Stages of Rehabilitation: Chronic Phase

A

– Outpatient services after first few months
– PT Intervention Focus: higher function
• Constraint-induced movement therapy
• Locomotor training (Body-weight supported treadmill training)
• Strengthening
• Balance
• Task-specific training and motor control

123
Q

what is Central Post-Stroke Pain?

A

– Arises as direction consequence of brain lesion
– Occurs in 10%, usually with involvement of thalamus
– Pain, often persistent, described as burning, aching, or shooting

124
Q

What are the components of sensation examination?

A

– Superficial: light touch, pressure, sharp/dull
– Deep: proprioception, kinesthesia, vibration
– Combined: stereognosis, tactile localization, two-point discrimination, texture recognition

125
Q

What are some common hyper- and hypo-mobility presentations post stroke?

A

– Shoulder and wrist are susceptible to instability and alignment problems
– Limitations common in shoulder flexion, abduction, external rotation
– Contractures common in elbow flexors, wrist and finger flexors, and forearm pronators
– Limitations common in hip flexors, adductors, and hamstrings with contractures likely in plantar flexors

126
Q

Hypotonia due to acute diaschisis is replaced by ___________; if hypotonia persists, it is a ________ prognostic indicator

A

Spasticity

Poor

127
Q

Spasticity describes?

A

hyper-reflexia, abnormal movement patterns, co-contraction, and hypertonia:
– Characterized by velocity-dependent increase in tonic stretch reflex
– It is modified by muscle length and increases over time
– Though it can be strong, it is often unrelated to functional disability

128
Q

Give the modified Ashworth scale.

A

0 No increase in muscle tone

1 Slight increase in muscle tone, manifested by catch and release OR minimal resistance at end rang of motion

1+ Slight increase in muscle tone, manifested by catch followed by minimal resistance through less than 1⁄2 rang of motion

2 More marked increase in muscle tone through greater than 1⁄2 ROM but affected part is easily moved

3 Considerable increase in muscle tone with passive movement difficult

4 Affected parts are rigid in flexion or extension (not true rigidity)

129
Q

Describe the Tardieu Scale

A

See lecture 2 slide 14

130
Q

Voluntary Movement Changes: Increased reaction and movement times

A

common due to central deficits in muscle activation

131
Q

Voluntary Movement Changes: Abnormal patterns of movement

A

seen and may be due to compensation for weakness, changes to soft tissue, or altered central activation patterns

132
Q

Voluntary Movement Changes: Decreased fractionation

A

decrease in inability to activate individual muscles independent of other muscles

133
Q

Voluntary Movement Changes:: Associated movements

A

possible, especially with effort or stress

134
Q

Voluntary Movement Changes: Synergy Patterns, is strength training contraindicated for a synergy pattern?

A

– Not solely or necessarily indicative of spasticity, but may
also reflect adaptations to muscle weakness
– Strength training is NOT contraindicated

135
Q

Synergy Patterns: UE Flexion Synergy

A 
Scapular retraction/elevation
Shoulder abduction and ER
Elbow flexion
Forearm supination
Wrist and finger flexion
136
Q

Synergy Patterns: UE Extension Synergy

A 
Scapular protraction
Shoulder adduction and IR
Elbow extension
Forearm pronation
Wrist and finger flexion
137
Q

Synergy Patterns: LE Flexion Synergy

A

Hip flexion, abduction, and ER
Knee Flexion
Ankle DF and inversion
Toe extension

138
Q

Synergy Patterns: LE Extension Synergy

A

Hip extension, adduction, and IR
Knee Extension
Ankle PF and inversion
Toe Flexion

139
Q

Fugl-Meyer Assessment

A

Good validity and reliability for the motor component of the test with excellent inter- rater reliability (r=0.92 – 0.99)
• Interpretation
– Severe Stroke: Motor score

140
Q

Motor Assessment Scale (See lecture 4, slide 19)

A

• Tests Mobility skills after stroke • 6-point ordinal scale

141
Q

Chedoke-McMaster Stroke Assessment See lecture 4, slide 22)

A
  • Valid and reliable test measuring physical impairment (shoulder pain, postural control, arm, hand, leg, and foot) and activity limitations (rolling, sitting, transfers, standing, walking, stairs)
  • Based on FIM scale
  • Impairments correspond to stage of motor recovery with max score of 100
142
Q

Issues with coordination

A

Results from deficits in transmission of sensorimotor signals in the CNS
– Impacts ability to meet task or environmental demands
– Incoordination often associated with weakness, but is a separate impairment

143
Q

Apraxia

A

Is the inability to plan and execute coordinated movements:

• Results from lesions in premotor frontal cortex, left inferior parietal lobe, and corpus callosum

144
Q

Ideational Apraxia

A

no understanding of how to do task

145
Q

Ideomotor Apraxia

A

May produce movement automatically but struggles when given command

146
Q

where is muscle weakness typically seen?

A

Weakness is typically seen contralaterally with distal muscles usually weaker than proximal and upper extremity weaker than lower extremity.

147
Q

Ipsilateral weakness can be seen with?

A

Cerebellar Strokes

148
Q

Quadriparesis can be seen with?

A

Brainstem lesions

149
Q

Neural weakness

A

result of decrease in descending inputs to motor unit (primary source of weakness following stroke)
• Changes in number and type of motor units recruited and their discharge frequency

150
Q

Disuse weakness

A

Disuse weakness: secondary impairment:
– Has large impact of function and there may be varying degrees of
weakness depending on joint position and task
– Trunk typically has less weakness likely due to bilateral innervation
– MMT is problematic due to difficulty in isolating individual muscles and presence of spasticity which may impact results
– Motoricity Test

151
Q

Motoricity Test (see lecture 4, slide 26)

A 
• Measure of limb function after
stroke
• Maximum score of 100 (normal) per extremity
• Severe paralysis score of 0-32
• Moderate paralysis score of 33-64
• Mild paralysis score of 65-99
152
Q

Abnormal Balance Reactions

A

– Reduced voluntary sway in standing
– Inappropriate muscles used in response strategy
– Reduced amplitude of reactive forces in paretic limb
– Increased latency of balance reactions in paretic limb

153
Q

PASS (See lecture 4, slide 28)

A
  • Measures balance in acute recovery

* Appropriatefor individuals with severe stroke and little mobility

154
Q

Berg Balance Scale

A
  • Quantitative assessment of balance
  • Maintains positions or complete movements of varying difficulty (14 items with max score of 56)
  • Excellent test-retest reliability for stroke
  • High specificity for predicting non-fallers and moderate sensitivity for predicting falls
155
Q

Timed Up and Go

A

• Basic mobility and balance test

- > 30 is high risk for falls and 20 - 30 is at risk for falls

156
Q

Postural Alignment: Pelvis

A

- Shift to weight bearing on stronger side

  • Reluctance (fear) of shifting weight to the affected side
  • Posterior Pelvic tilt in sitting (sacral sitting)
  • Unilateral retraction and elevation of pelvis in standing on affected side
157
Q

Postural Alignment: Trunk

A
  • Flattened lumbar curve and exaggerated thoracic curve and forward head in sitting (due to posterior pelvic tilt)
  • Lateral Flexion with trunk shortened on affected side
158
Q

Postural Alignment: Shoulders

A
  • Unequal height with depression on affected side
  • Humeral subluxation with scapular downward rotation and lateral flex of trunk
  • Scapular instability with winging
159
Q

Postural Alignment: Head/Neck

A

Protraction and lateral flexion/rotation away from the affected side

160
Q

Postural Alignment: UE

A
  • More UE held in flexed, adducted position with IR and elbow flexion, forearm pronation, and wrist/finger flexion; typically NWB
  • Stronger UE used for postural support
161
Q

Postural Alignment: LE

A
  • In sitting, affected LE held in hip abduction and ER with hip/knee flexion
  • In standing, affected LE held in hip/knee extension with hip adduction and IR (scissoring) and plantar flexion
  • Unequal weight bearing on feed, similar to pelvis in sitting
    
162
Q

Pusher Syndrome (contraversive pushing)

A

– Associated with verticality perceptual disorder (tilt 20 degrees toward hemiparetic side)
– Associated with damage to posterolateral thalamus
– Patient pushes strongly with stronger arm/leg toward hemiplegic side which results in falling to hemiplegic side
– Scale for Contraversive Pushing (SCP) (see lecture 4, slide 33)
• Scores 0-6 with higher score indicated increased severity

163
Q

Emory Functional Ambulation Profile

A

Timed measure of walking under 5 environmental conditions
– Floor
– Carpet
– Up and go
– Obstacles
– Stairs
• Reliable gait assessment for stroke survivors

164
Q

Rancho Los Amigos Gait Analysis

A

See lecture 4, slide 36

165
Q

mGARS

A 
Quantifiesand documents three categories of gait abnormalities
– General
– Lower Extremity
– Head, arms, trunk
segments
166
Q

Stroke Impact Scale

A

Self-ReportMeasure
– 15 minutes to complete with good reliability and
validity
– 59 items in 8 domains
• Strength, hand function, ADL, Mobility, Communication, Emotion, Memory and Thinking, Social Participation
– Scored with 5-point ordinal scales • Higher score = higher function
– Example
• “In the past week, how would you rate the strength of your
arm that was most affected by your stroke?”
– 5 = A lot of strength, 1 = No strength at all

167
Q

Tests for Impairments at Body Function and Structures

A 
– Sensory Integrity and Integration
• Somatosensation, modality distribution
• Pain intensity and location
– Cranial Nerve Integrity
– Joint Integrity, Alignment and Mobility
• Active/Passive ROM, muscle length, etc
– Posture Alignment and Symmetry
– MotorFunction
• Motoricity Test
• Lateral Step-up Test
• Spasticity: Modified Ashworth and Tardieu
– DiagnosisSpecific(Stroke)
• Fugl-Meyer
• Stroke Rehabilitation Assessment of Movement (STREAM)
• Chedoke-McMasters Stroke Assessment
• Motor Assessment Scale
• Wolf Motor Function Test
• Scale for Contraversive Pusing
168
Q

Tests and Measures by ICF Classification; Tests for Activities

A

– Functional Status
• FIM (transfers, locomotion, stairs, dressing, bowel/bladder, eating, communication)
– Balance
• Postural Assessment Scale for Stroke (PASS)
• BergBalanceScale
• TimedUpandGo
• Short Physical Performance Battery
– Wheelchair Mobility and Parts Manipulation
• Wheelchair Skills Test
– Gait Assessment
• EmoryFunctionalAmbulationProfile
• Rancho Los Amigos Gait Analysis Form
• Modified Gait Assessment Rating Scale (mGARS)
– Aerobic Capacity
• 3 or 6 Minute Walk Test

169
Q

Tests and Measures by ICF Classification: Tests for Participation

A

– Stroke Impact Scale
– NIH Stroke Scale
– Barthel Activities of Daily Living

170
Q

FIM Procedures (see algorithm lecture 4, slide 46)

A

• Collect admissions data within 72 hours of admission; collect discharge data within 72 hours of discharge
– Follow-up data collected 80-180 days after discharge
• Record scores that best describe patient’s usual level of
function for every FIM item
• Setup is rated as a “5/7” for all items
• Risk for injury if tested or if patient does not perform activity is rated as a “1/7”
• Requiring two helpers is rated as a “1/7”
• If patient requires supervision, they are NOT independent

171
Q

Bladder/Bowel Management FIM

A

– Continence and assistance level
– Includes complete intentional control of equipment and/or agents for bladder control
– 7/7 = complete and intentional control; never incontinent
– 6/7 = requires urinal, bedpan, catheter, pad, diaper, etc or
uses medication for control; no accidents
– 5/7 = may require supervision or have occasional bladder accidents (less than 10/2 weeks)
– 4/7 = minimal contact less often than weekly (2-3 per month)
– 3/7 = moderate assistance less often than daily (2-3 per week)
– 2/7 and 1/7 = almost daily assistance

172
Q

Bowel Management FIM

A

– Includes complete intentional control of

equipment and/or agents for bowel control – Similar scoring to bladder

173
Q

Principles to Improve Motor Learning

A

• CognitiveStage
– Use instructions and demonstrations (whole and part)
– Active participation is vital – Use physical guidance
• AssociativeStage
– Decrease verbal cues and guidance
– Add variability to practice
– Include self-assessment and problem solving
• MentalPractice
– Mental practice alone is not beneficial, it must be combined with actual practice but can improve performance

174
Q

Principles of Feedback

A

• ExtrinsicFeedback
– Provided by the therapist
– Provide specific extrinsic feedback early in learning (cognitive stage)
• IntrinsicFeedback
– Occurs naturally as part of the movement; e.g.
kinesthetic feedback
– As the patient is able to do the task with minimal assistance transition to more intrinsic feedback

175
Q

Principles of Practice

A

• Blocked practice improves initial performance and so should be used in the cognitive (early) stage of learning.
• Distributed practice session is helpful when the patient fatigues quickly
• As the patient progresses introduce variable practice using serial or random order practice
• Environment
– Ensure early success moving to more challenges later
– Move from closed to open environment

176
Q

Intervention Strategies

A

• Compensation (Adaptation)
– Assistive device or orthotic
– Modify task or environment
– Substitution of a different sensory system or muscle group
• Correction (Remediation) = True Recovery – Improving impairments and activity limitations
• Prevention
– Minimize potential impairments or complications

177
Q

Categories of Motor Skills: Transitional Mobility

A
  • Ability to move from one posture to another (changing BOS or COM)
  • Rolling; supine-to-sit; sit-to- stand; transfers
178
Q

Categories of Motor Skills: Static Postural Control (Stability)

A
  • Ability to maintain postural stability and orientation within the COM when BOS is fixed
  • Holding postures: quadruped, sitting, kneeling, standing
179
Q

Categories of Motor Skills: Dynamic Postural Control (Controlled Mobility)

A
  • Ability to maintain postural stability and orientation with the COM over fixed BOS while parts of the body are in motion
  • Weight shifting; UE reaching
180
Q

Categories of Motor Skills: Skill

A
  • Coordinated UE and LE movement sequences to investigate & interact with environment
  • UE grasp and manipulation LE Stepping and Walking
181
Q

General Sequence of Progression

A

• TrunkControl
– Prerequisite to limb (and head) control
– Proximal stability is generally required for distal mobility
• Isometric -> Eccentric -> Concentric
• Closed Chain -> Open Chain
• Small ROM -> Large ROM
• Gravity Minimized ->  AgainstGravity ->  Resisted
• Single Joint -> Complex Movement
• More Support -> Less Support

182
Q

Enhancing Plasticity: Best Recovery

A

occurs when contralateral pathways normally used to control movement are reactivated

183
Q

Enhancing Plasticity: Poor Recovery

A

occurs when ipsilateral pathway remains sole active pathway

184
Q

Enhancing Plasticity: Critical mass of recovery

A

needed for improvement to occur
– Several weeks of intense training
– Need enough restored function to realize that limb is useful and improvements make movement easier

185
Q

Enhancing Plasticity: Intrinsic Factors Influencing Recovery

A

• Size of Lesion
– Inverse relationship between size and recovery
• Age
– Small impact on ultimate outcome
• Training
– Enriched environments, training, & rehab increase cortical representations and functional recovery
– Care in stroke units is associated with decreased death, disability and need for institutional care
• Timing & Intensity
– Clear relationship between early intensive rehab and
functional outcomes
– Begin as soon as medically stable

186
Q

Learned Disuse

A

– Learned phenomena that it is easier to use intact limb

– Seems to be related to sensory loss more than motor loss

187
Q

Strategies to Improve Learned Disuse

A
  • Encourage weight bearing
  • Educate for protection
    Sensory Retraining:
    • Mirror therapy
    • Repetitive discrimination activities
    • Bilateral simultaneous movement
    • Repetitive task practice
    Sensory Stimulation:
    • Compression
    • Mobilization
    • Electric stimulation
    • Thermal stimulation

Motor Control (1 decks)

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