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NMR II > Stroke > Flashcards

Stroke Flashcards

1
Q

What side will patients with a left (dominant) hemisphere stroke have hemiparesis/hemiplegia & sensory impairments?

A

Right

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2
Q

Which hemisphere stroke do patients tend to be slow, cautious & disorganized when approaching unfamiliar tasks?

A

patients with a left (dominant) hemisphere stroke

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3
Q

Which hemisphere stroke are patients easily frustrated and angered with communication difficulties?

A

patients with a left (dominant) hemisphere stroke

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4
Q

Are patients with a left (dominant) hemisphere stroke aware of their problems?

A

Yes and often respond with anxiety

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5
Q

Which hemisphere stroke do patients tend to profit from gestures and non-verbal instructions?

A

patients with a left (dominant) hemisphere stroke

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6
Q

Which hemisphere stroke do patients have difficulty planning & sequencing movements?

A

patients with a left (dominant) hemisphere stroke

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7
Q

T/F: You should immediately repeat information if a patients with a left (dominant) hemisphere stroke does not respond verbally or with gestures

A

False- They need time tp process information and respond

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8
Q

Which hemisphere stroke have difficulty with recognition of objects, use of objects or word recall?

A

patients with a left (dominant) hemisphere stroke

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9
Q

patients with a left (dominant) hemisphere stroke tend to suffer from what language disorder?

A
  • Aphasia
  • Possible dysphagia
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10
Q

A patient with a right (non-dominant) Hemisphere stroke will have hemiparesis/hemiplegia & sensory impairments & neglect on which side?

A

Left

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11
Q

Which hemisphere stroke do patients have difficulty with spatial perceptual tasks & visuospatial disorders?

A

Right Hemisphere Stroke

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12
Q

Which hemisphere stroke has poor insight & awareness of impairments?

A

Right Hemisphere stroke

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13
Q

Which hemisphere stroke is
- safety awareness diminished
- they tend to move impulsively
- Overestimate own abilities to perform task

A

Right Hemisphere Stroke

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14
Q

Which hemisphere stroke has difficulty with abstract reasoning and is rigid in thought?

A

Right Hemisphere Stroke

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15
Q

Which hemisphere stroke profits from verbal instructions more than gestures?

A

Right Hemisphere Stroke

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16
Q

Which hemisphere stroke needs cues to take thing one step at a time & detect/correct errors?

A

Right Hemisphere Stroke

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17
Q

If a patient suffered a right sided lesion where do a majority of motor symptoms manifest? Is UE or LE more affected?

A
  • Left (usually contralateral to lesion)
  • UE > LE
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18
Q

Do proximal or distal muscles exhibit greater strength deficits?

A

Distal

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19
Q

A patient suffered a lesion on the right side, why may they present with some weakness on the right side?

A
  • Anterior corticospinal tract causes some ipsilateral weakness
  • Most weakness will be contralateral
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20
Q

T/F: All motor symptoms after stroke are due to neural changes

A

False

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21
Q

What are the dominant synergies?

A
  • UE Flexion
  • LE Extension
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22
Q

What are the non-dominant synergies?

A
  • UE Extension
  • LE Flexion
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23
Q

T/F: Muscles not involved in either synergy are easy to activate

A

False

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24
Q

What is the flexion synergy of the UE?

A
  • Scapular retraction/elevation
  • Shoulder ABD, ER
  • Elbow Flexion
  • Forearm supination
  • Wrist Flexion
  • Finger flexion
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25
Q

What is the extension synergy of the UE?

A
  • Scapular protraction
  • Shoulder ADD, IR
  • Elbow extension
  • Forearm pronation
  • Wrist flexion
  • Finger flexion
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26
Q

What is the LE flexion synergy?

A
  • Hip flexion, ABD, ER
  • Knee flexion
  • Ankle DF, INV
  • Toe DF
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27
Q

What is the LE Extension synergy?

A
  • Hip extension, ADD, IR
  • Knee extension
  • Ankle PF, INV
  • Toe PF
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28
Q

What are the strongest components of the UE flexion synergy?

A
  • Elbow flexion
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29
Q

What are the strongest components of the UE extension synergy?

A

Shoulder ADD

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30
Q

What are the strongest components of the LE flexion synergy?

A

Hip flexion

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31
Q

What are the strongest components of the LE extension synergy?

A
  • Hip ADD
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32
Q

Describe Stage 1 of Sequential Motor Recovery Stages Following Stroke

A
  • Period of flaccidity
  • No movement of the limbs can be elicited
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33
Q

Describe Stage 2 of Sequential Motor Recovery Stages Following Stroke

A
  • Some facilitated movement
  • Minimal voluntary movement responses
  • Spasticity begins to develop (particularly in muscles of dominant synergy)
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34
Q

Describe Stage 3 of Sequential Motor Recovery Stages Following Stroke

A
  • Both flexion & extension synergies present & elicited voluntarily
  • Active movement occurs within synergy
  • Spasticity peaks
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35
Q

Describe Stage 4 of Sequential Motor Recovery Stages Following Stroke

A
  • Some movement combinations that do not follow path of basic synergies are mastered
  • Spasticity begins to decline
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36
Q

Describe Stage 5 of Sequential Motor Recovery Stages Following Stroke

A
  • Synergies lose their dominance
  • More difficult out of synergy movement combination are mastered
  • Spasticity begins to decline
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37
Q

Describe Stage 6 of Sequential Motor Recovery Stages Following Stroke

A
  • Individual joint movements
  • Improving coordination
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38
Q

Describe Stage 7 of Sequential Motor Recovery Stages Following Stroke

A

Normal

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39
Q

When does hypotonicity (flaccidity) typically occur?

A

Immediately post stroke (cerebral shock)

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40
Q

T/F: A patient will only experience hypotonicity (flaccidity) immediately post stroke

A

False
- Persists in some with lesion to primary motor cortex or cerebellum

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41
Q

In 90% of cases patients post stroke with experience what type of tone? What muscles does this tone present int?

A
  • Hypertonicity (spasticity)
  • Antigravity muscles
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42
Q

Initially post stroke patients will experience (hyporeflexia or hyperreflexia)?

A

Hyporeflexia during period of flaccidity

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43
Q

Post stroke, hyperreflexia emerges with what? What are some reflexes that are increased?

A

Spasticity & synergies

  • Increase in DTR, clonus, pos babinski
  • Tonic reflexes
  • Associated reactions
44
Q

If a patient has a stoke in the cerebellum what is the biggest deficit they will have?

A
  • Coordination
  • Ataxia
45
Q

In regards to coordination how will a patient with a stroke in the basal ganglia present?

A
  • Like a movement disorder
  • Slow movement (bradykinesia)
  • Involuntary movements (Chorea, hemiballismus)
46
Q

What is apraxia?

A

Difficulty planning/ executing movements that can not be accounted for by another reason

47
Q

Lesions where can result in apraxia?

A
  • Premotor frontal cortex
  • Left parietal lobe
  • Corpus callosum
48
Q

What is ideational apraxia?

A
  • Inability to produce movement on command or automatically due to breakdown in conceptualization of the complete task
  • Typically multistep sequential movement impaired
49
Q

What is ideomotor apraxia?

A

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

50
Q

What are common ROM limitations a patient post stroke will experience?

A
  • Shoulder flexion, abduction & ER
  • Elbow extension
  • Forearm supination
  • Wrist & finger extension
51
Q

What are some common joint malalignments post stroke?

A
  • Wrist (edema)
  • Shoulder (subluxation)
52
Q

Is AROM always possible for patients post - stroke? If not why?

A
  • No because synergies, spasticity or contractures
53
Q

Shoulder subluxations post stroke are the consequence of muscle inactivity & biomechanics alignment. Describe why this occurs

A
  • Impaired activation of deltoid muscle and rotator cuff contribute to glenohumeral instability
  • Scapula – abducted, elevated, downwardly rotated
  • poor posture (flexed trunk, asymmetrical)
  • Muscle imbalances of scapula
  • Humeral head not supported by glenoid labrum
  • Gravity pulls humerus down and over time capsule and ligaments stretch
54
Q

T/F: Somatosenstion is often absent

A

False- Often impaired not absent

55
Q

If a patient suffers from a cortical lesion where do they experience somatosensation deficits?

A

Localized contralateral deficits

56
Q

If a patient suffers from deeper lesion where do they experience somatosensation deficits?

A

Diffuse involvement contralateral

57
Q

If a patient suffers from brainstem lesions where do they experience somatosensation deficits?

A
  • Ipsilateral face
  • contralateral trunk & limb
58
Q

T/F: Somatosensation impairments often contribute to neglect, learned nonuse & risk of injury

59
Q

What can central post-stroke pain (CPSP) present as?

A
  • Severe burning, aching
  • Intermittent stabbing or shooting pains
  • Exaggerated response to touch, pressure or thermal stimuli
60
Q

Lesions where tend to cause CPSP?

A

somatosensory pathways, especially thalamus

61
Q

When does CPSP often develop? Do patients recover?

A
  • Most often develops in first few months of stroke
  • Recovery is rare
  • Limits rehabilitation participation
62
Q

What vision deficits may a patient experience post stroke?

A
  • Homonymous hemianopsia (can accommodate)
  • Visual inattention (neglect, perceptual) (often unaware, worse problem)
63
Q

What is spatial relation syndromes?

A

Difficulty perceiving relationship between self & environment

64
Q

A lesion where tends to cause perception deficits?

A
  • Usually lesion to R parietal cortex
65
Q

What are some perception deficits may a patient experience post-stroke?

A
  • Body scheme/body image disorder
  • Spatial relation syndromes
  • Agnosia
66
Q

Post Stroke how is the trunk usually aligned in sitting?

A
  • PPT (sacral sitting); flat lumbar curve
  • Asymmetry (frontal plan)
67
Q

In regard to postural alignment in sitting post stroke, why does the presentation in the frontal plane vary?

A
  • Presentation varies depending upon location of COM
  • Passive elongation affected side
  • Shortening affected side
68
Q

When observing postural alignment in sitting how are the limbs and head positioned?

A
  • Limbs: Involved limbs fall into alignment with gravity, Varies with location of COM and tone
  • Head: Secondary cervical hyperextension, may rotate from affected side
69
Q

What are the contributing impairments that cause some malalignment in postural control of sitting?

A
  • Visual, perceptual and sensory impairments
  • Reduced ability to recruit, modulate and control trunk/ limb muscles
70
Q

Patients post-stroke demonstrate greater movement of upper or lower trunk in sitting?

A
  • Demonstrate greater movement of upper trunk
  • Limited movement of lower trunk (lumbar spine, pelvis)
  • Little to no APT
71
Q

T/F: Patients have a lack of activation of leg muscles for support & balance during reaching activities in sitting

72
Q

How do patients postural alignment in standing present in the frontal plane?

A
  • Decreased activation on involved side
  • Unequal weight distribution
73
Q

In standing what musculature is inactive in the trunk?

A
  • Thoracic extensors
  • Abdominals
74
Q

In standing what is inactive in the hip/pelvis? What does the alignment present as?

A
  • Inactive:Hip Extensors and Abductors
  • Alignment: Hip flexion +/- Adduction
  • Pelvis: retracted and elevated
75
Q

In standing what is the alignment of the knee & ankle/foot?

A
  • Knee: GRF now anterior / medial to knee so Hyperextension
  • Ankle / Foot: relative PF & INV
76
Q

Are biomechanics malalignments early on are often due to distal or proximal weakness?

A

Proximal weakness

77
Q

What will the postural control present as in a patient with hemiparesis?

A
  • Uneven weight distribution
  • Increased postural sway in standing
  • Disorganization of normal postural synergies
  • Frequent loss of balance
78
Q

How will postural control present as in patients with cerebellar ataxia?

A
  • Truncal or ipsilateral limb symptoms depending on lesion site
  • Gait & balance abnormalities
  • May occur with vestibular symptoms
79
Q

How does ataxia prevention differ between midline lesions & lateral lesions?

A
  • Midline lesion = truncal ataxia
  • Lateral lesions = ipsilateral limb symptoms
80
Q

What does postural control present as in sensory ataxia?

A
  • Gait & balance abnormalities
  • Rely on vision (symptoms with eyes closed or in dark)
81
Q

Lesion where cause cerebellar ataxia? And what causes sensory ataxia?

A
  • Lesion to cerebellum or its connections
  • Disrupted proprioception input to CNS
82
Q

Midline cerebellar lesions cause what type of ataxia? Lateral lesions cause what symptoms?

A
  • Truncal ataxia
  • Ipsilateral limb symptoms
83
Q

What are the symptoms of sensory ataxia?

A
  • Gait & balance abnormalities
  • Rely on vision
84
Q

Describe the postural control of patients with ataxia

A
  • Inability to sustain coactivation (trunk muscles)
  • Inability to grade & time trunk muscle coactivation w/ limb movement
  • Inability to grade & time agonist vs antagonist muscles in limbs
85
Q

Patients with ataxia struggle to grade & time trunk muscle coactivation with limb movement. What does this do their anticipatory and reactive postural control?

A
  • Poor anticipatory postural adjustment
  • Hypermetric reactive postural responses
86
Q

What are the hemiparetic gait deviation in stance phase?

A
  • Asymmetrical weight distribution
  • Inadequate wt shift onto involved LE
  • Hip flexion & trendelenburg
  • Knee hyperextension
  • Short step with uninvolved limb
  • Lack of trailing limb during terminal stance
  • decreased sensory input & kinesthetic awareness
87
Q

What are the hemiparetic gait deviation during swing phase?

A
  • Difficulty initiating swing
  • Extensor tone
  • Decreased hip/knee flexion
  • Circumduction/ hiking of pelvis
  • Decreased DF/ Foot clearance
  • Lack of heel strike
88
Q

If a patient presents with aphasia what hemisphere normally has a lesion?

A

Dominant hemisphere lesions (usually left)

89
Q

What is the difference between wernicke’s and Broca’s aphasia?

A
  • Wenicke’s is fluent but does not understand what you are saying
  • Broca’s is expressive they know what they want to say but difficult to say it
90
Q

What is dysarthria and what can it affect?

A
  • Difficulty w/ speech production due to impaired motor function
  • Can affect respiration, articulation, phonation, resonance or sensory feedback
91
Q

How should you communicate with individuals with aphasia?

A
  • Avoid noisy or distracting environments
  • Use short & simple sentences
  • Allow for processing & response time
  • Avoid open ended questions/ allow for “yes”/ “no” responses if accurate
  • Use physical cues (gestures, demonstration, facial expression)
  • Rephrase questions
  • Remain calm, encourage patient to try again later if frustrated
  • Communication boards
92
Q

What are the common problems that occur with dysphagia? And what is the patient at risk for?

A
  • Delayed swallowing reflex
  • Reduced pharyngeal peristalsis
  • Reduced lingual control
  • At risk for aspiration, dehydration & compromised nutrition
93
Q

A patient post-stroke, what is their executive function like?

A
  • Impulsiveness
  • Inflexible thinking
  • lack of abstract thinking
  • Impaired organization/ sequencing
  • Decreased insight
  • Impaired planning & judgement
94
Q

How is a patient’s memory post-stroke?

A
  • Short term impairment
  • Confusion
  • Confabulation
  • Perseveration
95
Q

Lesions where cause emotional changes?

A
  • Frontal lobe
  • Hypothalamus
  • Limbic system
96
Q

What are some emotional symptoms of patients post-stroke?

A
  • Pseudobulbar affect (emotional lability)
  • Apathy
  • Euphoria
97
Q

What is the bladder symptoms in a patient post-stroke?

A
  • Urinary incontinence
  • Hyperreflexia, hyporeflexia, disturbed sphincter control and/or sensory loss
  • Functional incontinence secondary inattention, mental status or immobility
98
Q

What is bowel function in a patient post-stroke?

A
  • Incontinence, diarrhea, constipation, impaction
  • Stool softener & physical activity may help
99
Q

What phase of stroke are patients at a high risk for DVT & Pulmonary Embolism?

A
  • High risk in acute phase
  • Immobility
100
Q

How are DVT & Pulmonary Embolism treated?

A
  • Anticoagulation meds
  • Initial rest followed by mobility once medicated
101
Q

How are DVT & Pulmonary Embolism prevented?

A
  • Prophylactic anticoagulation
  • Leg exercises
  • Support stocking
102
Q

Cardiovascular & Pulmonary dysfunction are often caused by what in patient post-stroke?

A

Underlying vascular disease & coronary artery disease

103
Q

When does the most amount of recovery occur?

A

1st weeks & months

104
Q

When does recovery begin to plateau?

105
Q

Does mild stroke or severe stroke have a prolonged recovery?

A
  • Severe stroke (usually more limited)
  • Mild stroke usually recovers rapidly
106
Q

How can late recovery be demonstrated?

A

With extensive task specific training

107
Q

What is considered late recovery?

A

Anything past 1 year

NMR II (14 decks)

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