CVA Common Impairments pt 1/2 Flashcards
1
Q
CVA patterns of weakness are mainly seen involving what body part/s?
A
Extremity involvement»_space; trunk (trunk has bilateral innervation)
2
Q
Hemiparesis -
A
Mild to moderate weakness on contralateral side
3
Q
Hemiplegia -
A
Severe to profound weakness on contralateral side
4
Q
Dense hemiplegia -
A
no active movement observed
5
Q
T/F Mild ipsilateral weakness also can be seen
A
True, 10-25% of CST descend ipsilaterally (anterior CST)
6
Q
Primary neuromuscular impairments of CVA include:
A
- Damage to descending cortical drive
- Type I ↑, Type II ↓
- Loss of force production - Loss of motor units
- Asynchronous and abnormal motor unit firing
7
Q
Secondary neuromuscular impairments of CVA include:
A
- Increased fatigability
- Delayed reaction times
- Prolonged movement times
- Disuse muscular atrophy
- Length-tension changes
8
Q
Distal/proximal extremity has higher chance for more long standing and poorer prognosis for return?
A
Distal > proximal
9
Q
Facial weakness results from damage to what?
A
contralateral corticobulbar (CN VII, XII) pathways
10
Q
If UMN lesion, what part of face is affected?
A
Contralateral lower face, forehead has bilateral innervation
11
Q
If LMN lesion, what part of face is affected?
A
Ipsilateral lower and upper face
12
Q
Reactive motor control is (feedback/feedforward).
A
Feedback
13
Q
Proactive/anticipatory motor control is ((feedback/feedforward).
A
feedforward
14
Q
An idea or plan for purposeful movement that is made up of component motor programs
A
Motor plan
15
Q
An abstract representation that, when initiated, results in the production of a coordinated
movement sequence
A
Motor program
16
Q
A set of internal processes associated with feedback or practice leading to relatively permanent changes in the capability for motor skill
A
Motor learning
17
Q
The reappearance of motor patterns present prior to CNS injury performed in the same manner as prior to injury
A
Motor recovery
18
Q
The appearance of new motor patterns resulting from changes to CNS
- Adaptation
- Substitution
A
Motor compensation
19
Q
The process of initiating, directing, and grading purposeful voluntary movement
A
Motor control
20
Q
Stages of motor recovery post CVA:
A
Stage I: Initial flaccidity, hyporeflexia (LMN) no voluntary movement (cerebral shock)
Stage 2: Emergence of spasticity, hyperreflexia (UMN), and emergence of stereotypical synergies (mass patterns of movements)
Stage 3: Voluntary movement possible, but only in synergies, spasticity strong if present
Stage 4: Voluntary control in isolated joint movements emerging, corresponding decline of spasticity and synergies
Stage 5: Increasing voluntary control out of synergy; coordination deficits present
Stage 6: Control and coordination near normal
21
Q
Flexor synergy -
A
Scapula retraction and elevation, shoulder abduction and ER, elbow flexion*, supination, wrist and finger flexion
22
Q
Extensor synergy -
A
Hip extension, adduction, and IR, knee extension, ankle PF and inversion, toe PF
23
Q
Apraxia -
A
Inability to plan and execute purposeful movements that cannot be accounted for by any other reason
24
Q
Lesions where can lead to apraxia?
A
- Premotor frontal cortex (either side)
- Left inferior parietal lobe
- Corpus callosum
25
Ideomotor apraxia -
1. Inability to produce movement on command, but able to move automatically
2. Conceptualization of task remains intact
26
Ideational apraxia -
1. Inability to produce movement both on command or automatically
2. Complete breakdown of conceptualization of task
27
Because CVA patients often can't isolate muscle testing, how do we document strength?
Functional Strength Testing
28
Fugl-Meyer Assessment of Physical Performance is what type of outcome measure?
- Impairment based outcome measure
| - motor domain includes movement, coordination, and reflexes
29
MDC ad MCID of UE and LE CVA population on Fugl-Meyer Assessment of Physical Performance:
MDC UE = 5.4
MDC LE = 5
MCID UE = 10
MCID LE = 10
30
Rivermean Motor assessment us what type of outcome measure?
- Measures impact on mobility
| - Gross motor, leg and trunk, arm
31
MCID of CVA pop on Rivermean Motor assessment?
3
32
How does VO2 levels change for stroke patients?
- VO2 levels double with household chores
| - Up to 3x normal VO2 levels with ambulation on level ground
33
Chronotropic incompetence -
Inability for HR to increase proportionally to metabolic demands of activity
34
Deconditioning in post stroke patients is a result of what 3 things?
1. Acute illness
2. Bedrest
3. Limited activity levels
35
CVA patients deconditioning effect on neurological:
Degradation of neural circuits due to loss of active engagement
36
CVA patients deconditioning effect on cardiovascular:
↓ cardiac output, HRmax
| ↑ resting and exercise BP
37
CVA patients deconditioning effect on pulmonary:
↓ lung volume, pulmonary perfusion and vital capacity, altered chest wall excursion
↓ Respiratory lung output accompanied by ↑ oxygen demands of new movement patterns -> worsened fatigue and endurance
38
CVA patients deconditioning effect on MSK:
↓ muscle mass, bone mass, flexibility
39
CVA patients deconditioning effect on behavioral:
Depression, anxiety, fear
40
What two things recommended before beginning exercise program post-cva?
1. Graded exercise testing
| 2. ECG
41
Sub-max protocols for post CVA?
Peak HR 120 bpm or 70% age-predicted HRmax
| BP <250/115 mmHg
42
If unable to do graded exercise testing, what should happen?
1. Light-to-moderate exercise recommended while monitoring patient response
↑ training frequency, duration, or both to compensate for reduced intensity
2. Close monitoring of HR, BP
- Borg Rate of Perceived Exertion (RPE)
3. Outcome Measures
- 6-minute walk
- 2-minute walk – acute CVA
43
Critical components of coordination:
1. Sequencing
2. Timing
3. Grading
44
What is incoordination?
- Disruption of sequencing, timing, grading
| - Loss of coupling between synergistic joints and muscles
45
Lesions where can lead to incoordination?
1. motor cortex
2. basal ganglia
3. cerebellar lesions
46
impaired ability to perform rapid alternating movements (antagonist and agonist breakdown)
Dysdiadochokinesia
47
inability to judge distance or range of movement
dysmetria
| hypo or hyper
48
loss of ability to associate muscles together for complex movements (split up movements by joint movement)
Asynergia
49
inability to rapidly and sufficiently halt movement of a body part after a strong isometric force
rebound phenomenon
50
unintentional, oscillatory movement
tremor
| resting/intentional
51
fragmented movement patterns
dyssynergia
52
Ataxia -
- difficulties with fluidity/timing, accuracy, and speed of movements
- Also see impairments in steadiness, response orientation, and reaction and movement times
53
Cerebellar ataxia -
damage to cerebellum
54
sensory ataxia -
proprioceptive deficits (sensory input)
55
Potential examination findings with damage to cerebellum:
```
Ipsilateral
- trunk/limb/gait ataxia
- Dysmetria, dyssynergia, dysdiadochokinesia
- balance deficits
and
- oculomotor deficits
- lack of check reflex
- mild hypotonia
- intentional tremor
- slurred speech (dysarthria)
- difficulties with motor learning
```
56
Potential examination findings with damage to basal ganglia:
```
contralateral
- trunk/limb/gait ataxia
- Dysmetria, dyssynergia, dysdiadochokinesia
- balance deficits
and
- spasticity
- resting/intentional tremor
- Difficulty initiating movements
- considerable strength deficits
- slow movements
```
57
Potential examination findings with damage to dorsal column (sensory ataxia):
```
contralateral
- trunk/limb/gait ataxia
- Dysmetria, dyssynergia, dysdiadochokinesia
- balance deficits
and
- abnormal sensory exam (proprioception)
- unlikely to see tremor
```
58
What type of tone is velocity dependent?
spasticity
59
What type of tone is velocity independent?
hypertonicity
60
Decorticate posturing -
UE flexion, LE extension/IR/PF
| • Brainstem lesions above red nucleus
61
Decerebrate posturing -
UE and LE extension
| • Brainstem lesions below red nucleus
62
In acute UMN injuries why will you see temporary hypotonia and for how long?
Cause - cerebral or spinal shock
duration - days to weeks
63
```
Modified ashworth scale:
0 =
1 =
1+ =
2 =
3 =
4 =
```
Measurement of spasticity
0 = no increase tone
1 = Slight increase - catch and release of minimal resistance at EROM
1+ = slight increase - catch followed by minimal resistance
2 = More marked increase in tone through most ROM
3 = Passive movement difficult
4 = Rigid in flexion or extension
64
CN 2 Optic dysfunction -
Reduced visual acuity (blurry vision)
65
CN 3, 4, 6 dysfunction -
Gaze palsies -> double vision (diplopia)
| Ptosis
66
CN 5 Trigeminal dysfunction -
Loss of facial sensory input
Asymmetrical jaw movement and strength
Loss of mastication -> choking risk -> aspiration risk
67
CN 7 Facial dysfunction -
Facial weakness, loss of sensory tongue, impairment of salivary glands -> choking risk -> aspiration risk
Impairment of lacrimal glands -> impair vision
68
CN 8 Vestibulocochlear dysfunction -
Hearing loss
| Vestibular dysfunction -> vertigo, balance deficits
69
CN 9 glossopharyngeal dysfunction -
Dysphagia
Reduced taste & sensation on tongue, loss of gag reflex -> choking risk -> aspiration
risk
ANS: Cardiovascular dysfunction (HR, BP)
70
CN 10 Vagus dysfunction -
Pharyngeal and laryngeal weakness
Loss of gag reflex -> choking risk -> aspiration risk
ANS: Abnormalities of esophageal motility, gastric acid secretion, gallbladder emptying, cardiovascular dysfunction (HR)
71
CN 11 Spinal accesory dysfunction -
UTrap and sternocleidomastoid weakness -> inability to rotate the head or shrugging the shoulders
72
CN 12 hypoglossal dysfunction -
Tongue weakness -> choking risk -> aspiration risk
73
General slowing of cognitive & motor processes
Lethargy
74
Dulled or blunted sensitivity, difficult to arouse
Obtundation
75
State of semi-consciousness, only arouses with intense stimulation
stupor
76
Unconsciousness
coma
77
How do we measure level of consciousness?
```
Glasgow coma scale - prognostic test
- Measures 3 areas of consciousness (arousal): eye opening, motor response, verbal response
Scores 3-15
- < 8 severe
- 9-12 moderate
- 13-15 mild
```
78
T/F Total GCS score found to predict acute mortality with 88% accuracy
True
79
What can be excluded from GCS when communication deficits w/o loss of predictive value?
Verbal component
80
Cognitive evaluation of orientation:
| What cortical regions involved?
person, place, time, situation
| - Multiple cortical regions involved
81
Cognitive evaluation of attention (4 parts):
| What cortical regions involved?
```
sustained
selective
divided
alternating
- Prefrontal cortex, reticular formation
```
82
Cognitive evaluation of memory:
| What cortical regions involved?
```
immediate recall
short-term
long-term
- ST: prefrontal cortex, limbic system
- LT: hippocampus, temporal lobe
```
83
Cognitive evaluation of executive function:
| What cortical regions involved?
abstract thinking, problem-solving, judgment, reasoning, insight
- prefrontal cortex
84
Cognitive evaluation of communication:
| What cortical regions involved?
spontaneous speech, command following, repetitive and naming, articulation, fluency
85
Emotional changes caused by lesions affecting what part of brain?
frontal lobe, hypothalamus, and limbic
86
apathy -
shallow affect, blunted emotional responses
87
euphoria -
Exaggerated feelings of well-being
88
pseudobulbar affect -
| damage where?
state of emotional lability due to neurological insult
- Emotional outbursts of uncontrolled or exaggerated laughing or crying
- inferior frontal and inferior parietal lobe damage (R or L)
89
depression -
| damage where?
persistent feelings of sadness accompanied by feelings of hopelessness, worthlessness, and/or helplessness
- Correlation found with left frontal and right parietal lesions
- Also can happen as secondary sequelae of impact of injury
90
Behavioral Considerations based on Right hemispheric involvement:
a. Difficulty perceiving emotions
b. Difficulty with expression of negative emotions
c. Irritability, confusion
d. Impulsive, quick with movement
e. Poor judgement (impulsive)
f. Rigidity of thought
g. Absent or poor insight, awareness of impairments, may completely deny disability
i. Tendency to overestimate abilities
h. High safety risk! (fall risk)
91
Behavioral Considerations based on Left hemispheric involvement:
a. Difficulty with expression of positive emotions
b. Slow, anxious, cautious
c. Disorganized and distracted when attempting to complete a task
d. Compulsive behavior
e. Typically very aware of impairments and extent of disability; more realistic
f. May need extra coaxing to participate
g. High safety risk!
92
Integration of sensory impressions into information that physiological meaningful -
perception
93
Right hemi lesion perceptual considerations:
1. Body scheme impairments: Unilateral neglect, Pusher’s Syndrome, Anosognosia, Somatagnosia, R-L discrimination
2. Difficulties in general with spatial relationships: Hand-eye coordination, Figure-ground discrimination, Position-in-space, depth and distance, Topographical disorientation
3. Agnosias: Visual, auditory, sensory
94
Left hemi lesion perceptual considerations:
Apraxia common (aphasia often comes hand in hand)
- Ideational
- Ideomotor
95
Neglect involved what hemi/lobe?
right parietal
96
Infarcts to what artery most commonly causes neglect?
MCA
97
Most common manifestations of neglect:
visual (visuospatial)
98
Neglect is a good/poor prognostic factor for functional recovery:
* Poor prognostic indicator for functional recovery
| * Longer hospitalizations, functional dependency, long-term disability, increased fall risk
99
Improvement in neglect is seen at what point/stages of rehab?
early
100
Examination of neglect:
1. Observation - head rotation with gaze preference
2. Double Simultaneous Stimulation test (helps pull out what type of neglect)
3. Clock drawing, picture copying, cross-out tasks, line bisection
4. Consider presence of visual field loss (hemianopia) alongside neglect
101
lateral pulsion vs retropulsion:
Lateral pulsion – patient tendency to fall toward side of lesion (Wallenberg syndrome)
Retropulsion – Posterior loss of balance
102
Pusher's syndrome:
Lesion -
Features -
Lesion: R hemisphere centered in area of posterolateral thalamus
Features:
• Contralateral tilted posture with severe imbalance
• Head is able to orient to vertical with cues
• Tendency to push strongly towards paretic side with nonaffected limbs (away from side of lesion)
• Resistance to external corrections
103
Pusher's syndrome R hemi CVA commonly seen with what other symptoms?
* Commonly seen with left hemiplegia
| * High association with left spatial and sensory neglect
104
Pusher's syndrome L hemi CVA commonly seen with what other symptoms?
* Commonly seen with right hemiplegia
| * High association with aphasia
105
Examination for Pusher's syndrome:
- Outcome measures: minimal evidence
| - Observation: sitting, standing, exacerbating factors, response to corrections and cues?
106
Common visual dysfunctions post CVA with damage to cerebellum:
* Impaired pursuits and saccades
| * Diplopia (double vision)
107
Common visual dysfunctions post CVA with damage to CN III, IV, VI II nuclei and associated CNS areas (brainstem):
```
• Ptosis (droopy eyelid)
• Ocular motility disturbance
Diplopia (double vision)
Visual distortions
Dysconjugate gaze
Impaired vergence (convergence/divergence)
```
108
Lesion at the L optic nerve, where will you see the visual defect?
Left ipsilateral blindness
109
Lesion at the optic chiasm (bilateral lateral compression), where will you see the visual defect?
Binasal hemianopia (can't see out of nasal portion of both eyes)
110
Lesion at the midsagittal transection/pressure), where will you see the visual defect?
Bitemporal hemianopia (can't see out of temporal portion of both eyes)
111
Lesion at the optic tract (L), where will you see the visual defect?
Right hemianopia (can't see out of right side of both eyes)
112
Lesion at the optic radiation (L) lower division, where will you see the visual defect?
Right upper quadrantanopia
113
Lesion at the optic radiation (L) upper division, where will you see the visual defect?
Right lower quadrantanopia
114
Lesion at the optic radiation (L) both divisions, where will you see the visual defect?
Right hemianopia with macular sparing
115
What 2 arteries support the optic nerve and chiasm?
anterior cerebral
| anterior communicating
116
What 2 arteries support the optic tract?
posterior communicating
| anterior choroidal arteries
117
What 2 arteries support the optic radiation?
middle cerebral artery
| posterior cerebral artery
118
What artery supports the primary visual cortex?
PCA
119
Damage to cortical vestibular regions (PIVC, MST, VIR) impacts what?
Impacts integration and regulation of vestibular systems
120
Damage to brainstem vestibular regions (midbrain, pons) impacts what?
VOR, VSR, VCR dysfunction
121
Damage to flocculonodular lobe impacts what?
VOR dysfunction, postural instabilities
122
Transient ischemic attacks most common site is?
- vertebrobasilar artery
123
Intense symptoms of TIA at the vertebrobasilar artery include:
vertigo
| visual deficits
124
Posterior Inferior Cerebellar Artery (PICA) Stroke (Wallenberg’s Syndrome) S&S:
Vertigo, headache, facial pain (ipsilateral), disequilibrium, nausea and vomiting, ataxia (ipsilateral), hiccups, and contralateral limb burning pain / altered sensation of temperature
125
Anterior Inferior Cerebellar Artery (AICA) Stroke S&S:
* PICA symptoms + HEARING
| * May present with a combination of peripheral (unilateral sensory loss) and central vestibular damage
126
MCA/PCA infarcts on vestibular system:
* Vertigo typically not present, vestibular symptoms tend to be more mild (disequilibrium, vertical disorientation)
* Most common complaint with vestibular dysfunction: “DIZZINESS”
127
VOR -
| Ex: L head rotation
- Eye movements that equally counter head movements
EX: L head rotation
+ L semicircular canal -> + R abducens, + L oculomotor
- R semicircular canal -> - L abducens, - R oculomotor
EYES MOVE TO RIGHT
128
Cortical lesion effect on sensory systems:
specific localized areas of dysfunction
• Parietal lobe – homunculus tells us where we expect to see
• Dorsal column
129
Thalamic lesion effect on sensory systems:
diffuse involvement
130
Light touch, proprioception (>/=) temp and pain with CVA implications on sensory systems
Light touch, proprioception >> temperature, pain
131
Decreased sensitivity to sensory stimuli
hypoesthesia
132
Increased sensitivity to sensory stimuli
hyperesthesia
133
Abnormal sensation such as numbness, prickling, or tingling
paresthesia
134
Touch sensation experienced as pain
dysesthesia
135
Pain produced by non-noxious stimulus
allodynia
136
Complete loss of pain sensitivity
analgeisa
137
Increased sensitivity to pain
hyperalgesia
138
Inability to localize sensation
atopognosia
139
Most common predictors (acute/subacute) for fall risk post CVA:
* Functional impairment
* Cognitive deficits
* Impaired balance
140
CVA impairments and balance:
* Visual impairments: Diplopia, Hemianopia/quadrantanopia
* Vestibular dysfunction: Vertigo, dizziness, disequilibrium
* Sensory loss: Loss of real-time feedback of movements
* Perceptual deficits: Neglect, Midline orientation deficits
* Motor impairments: Weakness, Increased reaction times, disordered sequencing, Spasticity (acute: hypotonicity)
* Reduced endurance: Increased fatigability
* Cognitive considerations: Inattention, reduced carryover, insight, impulsivity, Arousal levels
* Miscellaneous: Orthostatic hypotension, Premorbid comorbidities
141
CVA impairments and balance can lead to impairments in what?
1. steady state (increased postural sway)
2. anticipatory control
3. and/or reactive responses (increased stepping response – can cause imbalance)
142
Evaluation for Presence of Fatigue post CVA:
1. Fatigue Severity Scale
| 2. Fatigue Impact Scale
143
Central Post-Stroke Pain/Thalamic Syndrome
Pain arising as a direct consequence of lesion to central somatosensory system
• Cortex, thalamus, medulla
• Thalamus = “Thalamic Syndrome” – most common site of involvement (VPL)
• “Neuropathic pain”
144
When will Central Post-Stroke Pain/Thalamic Syndrome usually begin?
Weeks to months post initial insult
145
Medical management of Central Post-Stroke Pain/Thalamic Syndrome:
Fluoxetine (anti-dep SSRIs) – increase neuroplasticity after brain injury or stroke
146
Most common site of musculoskeletal pain post stroke? Second?
1. Shoulder
| 2. Low back
147
What can lead to significantly higher risk of developing shoulder pain within first 8-10 weeks of CVA?
Severe UE hemiplegia and/or shoulder subluxation within 72 hours post CVA
148
Examination of hemiplegic shoulder subluxation:
* Fingerbreadth method: Subluxation = 1⁄2 fingerbreadth or more
* Radiographs
* Ultrasound
149
Shoulder-hand syndrome -
* Painful shoulder + painful and edematous hand/wrist
* +Allodynia, hyperalgesia
* Elbow typically spared
* R CVA > L CVA
