Stroke Flashcards
1
Q
What side will patients with a left (dominant) hemisphere stroke have hemiparesis/hemiplegia & sensory impairments?
A
Right
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
3
Q
Which hemisphere stroke are patients easily frustrated and angered with communication difficulties?
A
patients with a left (dominant) hemisphere stroke
4
Q
Are patients with a left (dominant) hemisphere stroke aware of their problems?
A
Yes and often respond with anxiety
5
Q
Which hemisphere stroke do patients tend to profit from gestures and non-verbal instructions?
A
patients with a left (dominant) hemisphere stroke
6
Q
Which hemisphere stroke do patients have difficulty planning & sequencing movements?
A
patients with a left (dominant) hemisphere stroke
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
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
9
Q
patients with a left (dominant) hemisphere stroke tend to suffer from what language disorder?
A
- Aphasia
- Possible dysphagia
10
Q
A patient with a right (non-dominant) Hemisphere stroke will have hemiparesis/hemiplegia & sensory impairments & neglect on which side?
A
Left
11
Q
Which hemisphere stroke do patients have difficulty with spatial perceptual tasks & visuospatial disorders?
A
Right Hemisphere Stroke
12
Q
Which hemisphere stroke has poor insight & awareness of impairments?
A
Right Hemisphere stroke
13
Q
Which hemisphere stroke is
- safety awareness diminished
- they tend to move impulsively
- Overestimate own abilities to perform task
A
Right Hemisphere Stroke
14
Q
Which hemisphere stroke has difficulty with abstract reasoning and is rigid in thought?
A
Right Hemisphere Stroke
15
Q
Which hemisphere stroke profits from verbal instructions more than gestures?
A
Right Hemisphere Stroke
16
Q
Which hemisphere stroke needs cues to take thing one step at a time & detect/correct errors?
A
Right Hemisphere Stroke
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
18
Q
Do proximal or distal muscles exhibit greater strength deficits?
A
Distal
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
20
Q
T/F: All motor symptoms after stroke are due to neural changes
A
False
21
Q
What are the dominant synergies?
A
- UE Flexion
- LE Extension
22
Q
What are the non-dominant synergies?
A
- UE Extension
- LE Flexion
23
Q
T/F: Muscles not involved in either synergy are easy to activate
A
False
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
25
What is the extension synergy of the UE?
- Scapular protraction
- Shoulder ADD, IR
- Elbow extension
- Forearm pronation
- Wrist flexion
- Finger flexion
26
What is the LE flexion synergy?
- Hip flexion, ABD, ER
- Knee flexion
- Ankle DF, INV
- Toe DF
27
What is the LE Extension synergy?
- Hip extension, ADD, IR
- Knee extension
- Ankle PF, INV
- Toe PF
28
What are the strongest components of the UE flexion synergy?
- Elbow flexion
29
What are the strongest components of the UE extension synergy?
Shoulder ADD
30
What are the strongest components of the LE flexion synergy?
Hip flexion
31
What are the strongest components of the LE extension synergy?
- Hip ADD
32
Describe Stage 1 of Sequential Motor Recovery Stages Following Stroke
- Period of flaccidity
- No movement of the limbs can be elicited
33
Describe Stage 2 of Sequential Motor Recovery Stages Following Stroke
- Some facilitated movement
- Minimal voluntary movement responses
- Spasticity begins to develop (particularly in muscles of dominant synergy)
34
Describe Stage 3 of Sequential Motor Recovery Stages Following Stroke
- Both flexion & extension synergies present & elicited voluntarily
- Active movement occurs within synergy
- Spasticity peaks
35
Describe Stage 4 of Sequential Motor Recovery Stages Following Stroke
- Some movement combinations that do not follow path of basic synergies are mastered
- Spasticity begins to decline
36
Describe Stage 5 of Sequential Motor Recovery Stages Following Stroke
- Synergies lose their dominance
- More difficult out of synergy movement combination are mastered
- Spasticity begins to decline
37
Describe Stage 6 of Sequential Motor Recovery Stages Following Stroke
- Individual joint movements
- Improving coordination
38
Describe Stage 7 of Sequential Motor Recovery Stages Following Stroke
Normal
39
When does hypotonicity (flaccidity) typically occur?
Immediately post stroke (cerebral shock)
40
T/F: A patient will only experience hypotonicity (flaccidity) immediately post stroke
False
- Persists in some with lesion to primary motor cortex or cerebellum
41
In 90% of cases patients post stroke with experience what type of tone? What muscles does this tone present int?
- Hypertonicity (spasticity)
- Antigravity muscles
42
Initially post stroke patients will experience (hyporeflexia or hyperreflexia)?
Hyporeflexia during period of flaccidity
43
Post stroke, hyperreflexia emerges with what? What are some reflexes that are increased?
Spasticity & synergies
- Increase in DTR, clonus, pos babinski
- Tonic reflexes
- Associated reactions
44
If a patient has a stoke in the cerebellum what is the biggest deficit they will have?
- Coordination
- Ataxia
45
In regards to coordination how will a patient with a stroke in the basal ganglia present?
- Like a movement disorder
- Slow movement (bradykinesia)
- Involuntary movements (Chorea, hemiballismus)
46
What is apraxia?
Difficulty planning/ executing movements that can not be accounted for by another reason
47
Lesions where can result in apraxia?
- Premotor frontal cortex
- Left parietal lobe
- Corpus callosum
48
What is ideational apraxia?
- Inability to produce movement on command or automatically due to breakdown in conceptualization of the complete task
- Typically multistep sequential movement impaired
49
What is ideomotor apraxia?
Inability to produce movement on command or imitation, but may produce automatically
50
What are common ROM limitations a patient post stroke will experience?
- Shoulder flexion, abduction & ER
- Elbow extension
- Forearm supination
- Wrist & finger extension
51
What are some common joint malalignments post stroke?
- Wrist (edema)
- Shoulder (subluxation)
52
Is AROM always possible for patients post - stroke? If not why?
- No because synergies, spasticity or contractures
53
Shoulder subluxations post stroke are the consequence of muscle inactivity & biomechanics alignment. Describe why this occurs
- 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
T/F: Somatosenstion is often absent
False- Often impaired not absent
55
If a patient suffers from a cortical lesion where do they experience somatosensation deficits?
Localized contralateral deficits
56
If a patient suffers from deeper lesion where do they experience somatosensation deficits?
Diffuse involvement contralateral
57
If a patient suffers from brainstem lesions where do they experience somatosensation deficits?
- Ipsilateral face
- contralateral trunk & limb
58
T/F: Somatosensation impairments often contribute to neglect, learned nonuse & risk of injury
True
59
What can central post-stroke pain (CPSP) present as?
- Severe burning, aching
- Intermittent stabbing or shooting pains
- Exaggerated response to touch, pressure or thermal stimuli
60
Lesions where tend to cause CPSP?
somatosensory pathways, especially thalamus
61
When does CPSP often develop? Do patients recover?
- Most often develops in first few months of stroke
- Recovery is rare
- Limits rehabilitation participation
62
What vision deficits may a patient experience post stroke?
- Homonymous hemianopsia (can accommodate)
- Visual inattention (neglect, perceptual) (often unaware, worse problem)
63
What is spatial relation syndromes?
Difficulty perceiving relationship between self & environment
64
A lesion where tends to cause perception deficits?
- Usually lesion to R parietal cortex
65
What are some perception deficits may a patient experience post-stroke?
- Body scheme/body image disorder
- Spatial relation syndromes
- Agnosia
66
Post Stroke how is the trunk usually aligned in sitting?
- PPT (sacral sitting); flat lumbar curve
- Asymmetry (frontal plan)
67
In regard to postural alignment in sitting post stroke, why does the presentation in the frontal plane vary?
- Presentation varies depending upon location of COM
- Passive elongation affected side
- Shortening affected side
68
When observing postural alignment in sitting how are the limbs and head positioned?
- 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
What are the contributing impairments that cause some malalignment in postural control of sitting?
- Visual, perceptual and sensory impairments
- Reduced ability to recruit, modulate and control trunk/ limb muscles
70
Patients post-stroke demonstrate greater movement of upper or lower trunk in sitting?
- Demonstrate greater movement of upper trunk
- Limited movement of lower trunk (lumbar spine, pelvis)
- Little to no APT
71
T/F: Patients have a lack of activation of leg muscles for support & balance during reaching activities in sitting
True
72
How do patients postural alignment in standing present in the frontal plane?
- Decreased activation on involved side
- Unequal weight distribution
73
In standing what musculature is inactive in the trunk?
- Thoracic extensors
- Abdominals
74
In standing what is inactive in the hip/pelvis? What does the alignment present as?
- Inactive:Hip Extensors and Abductors
- Alignment: Hip flexion +/- Adduction
- Pelvis: retracted and elevated
75
In standing what is the alignment of the knee & ankle/foot?
- Knee: GRF now anterior / medial to knee so Hyperextension
- Ankle / Foot: relative PF & INV
76
Are biomechanics malalignments early on are often due to distal or proximal weakness?
Proximal weakness
77
What will the postural control present as in a patient with hemiparesis?
- Uneven weight distribution
- Increased postural sway in standing
- Disorganization of normal postural synergies
- Frequent loss of balance
78
How will postural control present as in patients with cerebellar ataxia?
- Truncal or ipsilateral limb symptoms depending on lesion site
- Gait & balance abnormalities
- May occur with vestibular symptoms
79
How does ataxia prevention differ between midline lesions & lateral lesions?
- Midline lesion = truncal ataxia
- Lateral lesions = ipsilateral limb symptoms
80
What does postural control present as in sensory ataxia?
- Gait & balance abnormalities
- Rely on vision (symptoms with eyes closed or in dark)
81
Lesion where cause cerebellar ataxia? And what causes sensory ataxia?
- Lesion to cerebellum or its connections
- Disrupted proprioception input to CNS
82
Midline cerebellar lesions cause what type of ataxia? Lateral lesions cause what symptoms?
- Truncal ataxia
- Ipsilateral limb symptoms
83
What are the symptoms of sensory ataxia?
- Gait & balance abnormalities
- Rely on vision
84
Describe the postural control of patients with ataxia
- 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
Patients with ataxia struggle to grade & time trunk muscle coactivation with limb movement. What does this do their anticipatory and reactive postural control?
- Poor anticipatory postural adjustment
- Hypermetric reactive postural responses
86
What are the hemiparetic gait deviation in stance phase?
- 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
What are the hemiparetic gait deviation during swing phase?
- Difficulty initiating swing
- Extensor tone
- Decreased hip/knee flexion
- Circumduction/ hiking of pelvis
- Decreased DF/ Foot clearance
- Lack of heel strike
88
If a patient presents with aphasia what hemisphere normally has a lesion?
Dominant hemisphere lesions (usually left)
89
What is the difference between wernicke's and Broca's aphasia?
- 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
What is dysarthria and what can it affect?
- Difficulty w/ speech production due to impaired motor function
- Can affect respiration, articulation, phonation, resonance or sensory feedback
91
How should you communicate with individuals with aphasia?
- 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
What are the common problems that occur with dysphagia? And what is the patient at risk for?
- Delayed swallowing reflex
- Reduced pharyngeal peristalsis
- Reduced lingual control
- At risk for aspiration, dehydration & compromised nutrition
93
A patient post-stroke, what is their executive function like?
- Impulsiveness
- Inflexible thinking
- lack of abstract thinking
- Impaired organization/ sequencing
- Decreased insight
- Impaired planning & judgement
94
How is a patient's memory post-stroke?
- Short term impairment
- Confusion
- Confabulation
- Perseveration
95
Lesions where cause emotional changes?
- Frontal lobe
- Hypothalamus
- Limbic system
96
What are some emotional symptoms of patients post-stroke?
- Pseudobulbar affect (emotional lability)
- Apathy
- Euphoria
97
What is the bladder symptoms in a patient post-stroke?
- Urinary incontinence
- Hyperreflexia, hyporeflexia, disturbed sphincter control and/or sensory loss
- Functional incontinence secondary inattention, mental status or immobility
98
What is bowel function in a patient post-stroke?
- Incontinence, diarrhea, constipation, impaction
- Stool softener & physical activity may help
99
What phase of stroke are patients at a high risk for DVT & Pulmonary Embolism?
- High risk in acute phase
- Immobility
100
How are DVT & Pulmonary Embolism treated?
- Anticoagulation meds
- Initial rest followed by mobility once medicated
101
How are DVT & Pulmonary Embolism prevented?
- Prophylactic anticoagulation
- Leg exercises
- Support stocking
102
Cardiovascular & Pulmonary dysfunction are often caused by what in patient post-stroke?
Underlying vascular disease & coronary artery disease
103
When does the most amount of recovery occur?
1st weeks & months
104
When does recovery begin to plateau?
6 months
105
Does mild stroke or severe stroke have a prolonged recovery?
- Severe stroke (usually more limited)
- Mild stroke usually recovers rapidly
106
How can late recovery be demonstrated?
With extensive task specific training
107
What is considered late recovery?
Anything past 1 year
