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NMR II > Exam 3: Stroke Impairments > Flashcards

Exam 3: Stroke Impairments Flashcards

1
Q

What percentage of stroke patients experience some form of weakness?

A

80-90%

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2
Q

Are UE or LE more likely effected?

A

UE

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3
Q

20% of individuals with what type of stroke will fail to regain any functional use of their UE?

A

MCA stroke

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4
Q

Will distal or proximal muscles experience greater strength deficits?

A

Distal

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5
Q

What are the dominant synergies of the UE and LE?

A

UE flexion and LE extension

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6
Q

What are the non-dominant synergies of the UE and LE?

A

UE extension and LE flexion

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7
Q

What components are included in UE flexion synergy?

A

Scapular retraction and elevation
Shoulder abduction and ER
Elbow flexion
Forearm supination
Wrist flexion
Finger flexion

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8
Q

What is the strongest component of UE flexion synergy?

A

Elbow flexion

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9
Q

What components are included in UE extension synergy?

A

Scapular protraction
Shoulder adduction and IR
Elbow extension
Forearm pronation
Wrist flexion
Finger flexion

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10
Q

What is the strongest component of UE extension synergy?

A

Shoulder adduction

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11
Q

What components are included in LE flexion synergy?

A

Hip flexion, abduction, ER
Knee flexion
Ankle dorsiflexion, inversion
Toe dorsiflexion

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12
Q

What is the strongest component of LE flexion synergy?

A

Hip flexion

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13
Q

What components are included in LE extension synergy?

A

Hip extension, adduction, IR
Knee extension
Ankle plantarflexion, inversion
Toe plantarflexion

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14
Q

What is the strongest component of LE extension synergy?

A

Hip adduction, knee extension, and ankle plantarflexion

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15
Q

Describe Stage 1 of Motor Recovery

A

Period of flaccidity, no movement of the limbs can be elicited

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16
Q

Describe Stage 2 of Motor Recovery

A

Some facilitated movement, minimal voluntary movement responses. Spasticity begins to develop, particularly in muscles of dominant synergy

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17
Q

Describe Stage 3 of Motor Recovery

A

Both flexion and extension synergies present and elicited voluntarily. Active movement occurs within the synergy. Spasticity peaks

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18
Q

Describe Stage 4 of Motor Recovery

A

Some movement combinations that do not follow path of basic synergies are mastered. Spasticity begins to decline

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19
Q

Describe Stage 5 of Motor Recovery

A

Synergies lose their dominance. More difficulty out of synergy movement combinations are mastered. Spasticity continues to decline

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20
Q

Describe Stage 6 of Motor Recovery

A

Individual joint movements. Improving coordination

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21
Q

Describe Stage 7 of Motor Recovery

A

Normal function

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22
Q

When will a patient with a stroke experience hypotonicity?

A

Immediately following a stroke due to cerebral shock

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23
Q

When will hyperreflexia emerge?

A

With the development of spasticity and synergy

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23
Q

When will a patient with a stroke present with hyporeflexia?

A

Initially following the stroke during the period of flaccidity

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24
Q

Describe the prevalence and general characteristics of hypertonicity?

A

Present in 90% of cases. Affects antigravity muscles, and can lead to contractures

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25
Q

Describe coordination deficits in a patient with stroke

A

Difficulty with timing and sequencing and limited ability to adapt to task demands

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26
Q

How will a patient present with a cerebellar stroke in terms of coordination?

A

Ataxia

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27
Q

How will a patient present with a stroke affecting the basal ganglia in terms of coordination?

A

Slow movement (bradykinesia), involuntary movements including chorea or hemiballismus

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28
Q

What is apraxia?

A

Difficulty planning and executing movements that can not be accounted for by another reason (strength, coordination, or cognition)

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29
Q

Where are lesions located that cause apraxia?

A

Premotor frontal cortex, left parietal lobe, corpus callosum

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30
Q

What is ideational apraxia?

A

Inability to produce movement on command or automatically due to breakdown in conceptualization of the complete task

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31
Q

What is ideomotor apraxia?

A

Inability to produce movement on command or imitation, but may produce automatically

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32
Q

What ROMs may be limited due to contractures?

A

Shoulder flexion, abduction, ER
Elbow extension
Forearm supination
Wrist and finger extension

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33
Q

What causes joint malalignment at the wrist and shoulder?

A

Edema at the wrist and shoulder subluxation

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34
Q

What two factors result in shoulder subluxation in stroke patients?

A

Muscle inactivity and biomechanical alignment

35
Q

What impaired muscle activation contributes to GH instability?

A

Deltoid and rotator cuff

36
Q

How is the scapula positioned in stroke patients at risk of shoulder subluxation?

A

Scapula is abducted, elevated, and downwardly rotated

37
Q

What other factors contribute to shoulder subluxation besides muscle inactivation and scapular position?

A

Poor posture with asymmetry and a flexed trunk, humeral head not supported by labrum resulting in gravity pulling down the humerus and stretching the capsule and ligaments

38
Q

Where will a patient with a cortical lesion experience somatosensation deficits?

A

Localized contralateral deficits

39
Q

Where will a patient with a deep lesion experience somatosensation deficits?

A

Diffuse involvement contralateral

40
Q

Where will a patient with a brainstem lesion experience somatosensation deficits?

A

Ipsilateral face and contralateral trunk and limb

41
Q

What are patients with deficits in somatosensation at risk for?

A

Neglect, learned nonuse, and increased risk of injury

42
Q

What does CPSP stand for?

A

Central Post-Stroke Pain

43
Q

What is CPSP?

A

Lesions to the somatosensory pathway, especially the thalamus

44
Q

Describe the characteristics of CPSP?

A

Severe burning, aching, intermittent stabbing, shooting pains, exaggerated response to touch, pressure or thermal stimuli

45
Q

When does CPSP develop?

A

First few months following a stroke

46
Q

Do patients recover from CPSP?

A

Recovery is rare and it limited rehab participation

47
Q

What visual deficits are common following stroke?

A

Homonymous hemianopsia and visual inattention or perceptual neglect

48
Q

Where would a lesion causing perception deficits likely be located?

A

Right parietal cortex

49
Q

What perceptual deficits are common with stroke?

A

Body image disorders (neglect), spatial relation syndromes, agnosia

50
Q

What are spatial relation syndromes?

A

Difficulty perceiving the relationship between self and environment

51
Q

What is the common postural alignment of the trunk in sitting?

A

PPT/sacral sitting with a flat lumbar curve, asymmetry in the frontal plane

Presentation will vary depending on location of COM

52
Q

What is the common postural alignment of the limbs in sitting?

A

Involved limbs fall into alignment with gravity, can vary due to tone and COM

53
Q

What is the common postural alignment of the head in sitting?

A

Secondary cervical hyperextension, may rotate away from the affected side

54
Q

What contributes to impaired postural control in sitting?

A

Visual, perceptual, and sensory impairments and the reduced ability to recruit, modulate, and control the trunk and limb muscles

55
Q

What is the effect of the lack of activation of leg muscles during postural control in sitting?

A

Decreased support and balance during reaching activities

56
Q

Describe postural alignment in standing from the frontal plane

A

Decreased activation on the involved side and unequal weight distribution

57
Q

Describe the postural alignment of the trunk in standing

A

Inactive thoracic extensors and abdominals

58
Q

Describe the postural alignment at the hip and pelvis in standing

A

Inactive hip extensors and abductors resulting in hip flexion and adduction. Pelvis will be retracted and elevated

59
Q

Describe the postural alignment at the knee in standing

A

GRF is anterior and medial to the knee, resulting in hyperextension

60
Q

Describe the postural alignment at the ankle and foot in standing

A

Relative plantarflexion and inversion

61
Q

Describe hemiparesis in terms of postural control

A

Uneven weight distribution, increased postural sway in standing, disorganization of normal postural synergies, and frequent loss of balance

62
Q

What type of ataxia will result with a midline cerebellar lesion?

A

Truncal ataxia

63
Q

What type of ataxia will result with a lateral cerebellar lesion?

A

Ipsilateral limb symptoms

64
Q

Describe common symptoms of cerebellar ataxia

A

Gait and balance abnormalities, may occur with vestibular symptoms if there is brainstem involvement

65
Q

What is sensory ataxia?

A

Disrupted proprioceptive input to the CNS resulting in gait and balance abnormalities

66
Q

What compensation can aid with sensory ataxia?

A

Reliance on vision, will see increased symptoms with eyes closed

67
Q

What three ways can ataxia affect postural control?

A

Inability to sustain coactivation

Inability to grade and time trunk muscle coactivation with limb movement resulting in poor anticipatory postural adjustment

Inability to grade and time agonist vs antagonist muscles in limbs resulting in decreased coordination

68
Q

What are common hemiparetic gait deviations during stance phase?

A

Asymmetrical weight distribution, inadequate weight shift onto involve LE, hip flexion and trendelenburg, knee hyperextension, short step with involved limb, lack of trailing limb during terminal stance, decreased sensory input and kinesthetic awareness

69
Q

What are common hemiparetic gait deviations during swing phase?

A

Difficulty initiating swing, extensor tone, decreased hip and knee flexion, circumduction or hike of pelvis, decreased dorsiflexion and foot clearance, lack of heel strike

70
Q

What sided lesion will result in speech or language deficits?

A

Dominant

71
Q

What is dysarthria?

A

Difficulty with speech production due to impaired motor function. Can also affect respiration, articulation, phonation, resonance, or sensory feedback

72
Q

What are common problems with dysphagia?

A

Delayed swallowing reflex, reduced pharyngeal peristalsis, reduced lingual control

73
Q

What are risks associated with dysphagia?

A

Risk of aspiration, dehydration, and compromised nutrition

74
Q

What type of stroke will result in dysphagia?

A

Brainstem stroke

75
Q

What cognitive effects are associated with stroke?

A

Deficits in attention, orientation, short-term memory impairment, executive function, dementia

76
Q

What emotional effects are associated with stroke?

A

Emotional changes, pseudobulbar affect, apathy, euphoria, depression

77
Q

Where are lesions likely located that result in emotional changes?

A

Frontal lobe, hypothalamus, limbic system

78
Q

What changes in urinary function can result due to stroke?

A

Incontinence related to hyperreflexia, hyporeflexia, disturbed sphincter control, sensory loss

79
Q

What are causes of functional incontinence in stroke patients?

A

Inattention, mental status, or immobility

80
Q

What changes in bowel function can occur in stroke patients?

A

Incontinence, diarrhea, constipation, impaction

81
Q

Why is cardiovascular and pulmonary dysfunction relevant in stroke patients?

A

Underlying vascular disease and coronary artery disease. Leads to decreased vital capacity. May limit exercise tolerance

82
Q

When are stroke patients at risk for DVT or a pulmonary embolism?

A

High risk during the acute phase

83
Q

When does the majority of recovery from a stroke occur?

A

First few weeks or months

84
Q

At what point does a stroke patient tend to plateau in terms of recovery?

A

6 months

NMR II (27 decks)

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