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Neuro 1 > CVA Common Impairments pt 1/2 > Flashcards

CVA Common Impairments pt 1/2 Flashcards

1
Q

CVA patterns of weakness are mainly seen involving what body part/s?

A

Extremity involvement&raquo_space; trunk (trunk has bilateral innervation)

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2
Q

Hemiparesis -

A

Mild to moderate weakness on contralateral side

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3
Q

Hemiplegia -

A

Severe to profound weakness on contralateral side

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4
Q

Dense hemiplegia -

A

no active movement observed

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5
Q

T/F Mild ipsilateral weakness also can be seen

A

True, 10-25% of CST descend ipsilaterally (anterior CST)

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6
Q

Primary neuromuscular impairments of CVA include:

A
  1. Damage to descending cortical drive
  2. Type I ↑, Type II ↓
    - Loss of force production
  3. Loss of motor units
  4. Asynchronous and abnormal motor unit firing
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7
Q

Secondary neuromuscular impairments of CVA include:

A
  1. Increased fatigability
  2. Delayed reaction times
  3. Prolonged movement times
  4. Disuse muscular atrophy
  5. Length-tension changes
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8
Q

Distal/proximal extremity has higher chance for more long standing and poorer prognosis for return?

A

Distal > proximal

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9
Q

Facial weakness results from damage to what?

A

contralateral corticobulbar (CN VII, XII) pathways

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10
Q

If UMN lesion, what part of face is affected?

A

Contralateral lower face, forehead has bilateral innervation

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11
Q

If LMN lesion, what part of face is affected?

A

Ipsilateral lower and upper face

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12
Q

Reactive motor control is (feedback/feedforward).

A

Feedback

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13
Q

Proactive/anticipatory motor control is ((feedback/feedforward).

A

feedforward

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14
Q

An idea or plan for purposeful movement that is made up of component motor programs

A

Motor plan

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15
Q

An abstract representation that, when initiated, results in the production of a coordinated
movement sequence

A

Motor program

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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

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17
Q

The reappearance of motor patterns present prior to CNS injury performed in the same manner as prior to injury

A

Motor recovery

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18
Q

The appearance of new motor patterns resulting from changes to CNS

  • Adaptation
  • Substitution
A

Motor compensation

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19
Q

The process of initiating, directing, and grading purposeful voluntary movement

A

Motor control

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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

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21
Q

Flexor synergy -

A

Scapula retraction and elevation, shoulder abduction and ER, elbow flexion*, supination, wrist and finger flexion

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22
Q

Extensor synergy -

A

Hip extension, adduction, and IR, knee extension, ankle PF and inversion, toe PF

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23
Q

Apraxia -

A

Inability to plan and execute purposeful movements that cannot be accounted for by any other reason

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24
Q

Lesions where can lead to apraxia?

A
  1. Premotor frontal cortex (either side)
  2. Left inferior parietal lobe
  3. Corpus callosum
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25
Q

Ideomotor apraxia -

A
  1. Inability to produce movement on command, but able to move automatically
  2. Conceptualization of task remains intact
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26
Q

Ideational apraxia -

A
  1. Inability to produce movement both on command or automatically
  2. Complete breakdown of conceptualization of task
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27
Q

Because CVA patients often can’t isolate muscle testing, how do we document strength?

A

Functional Strength Testing

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28
Q

Fugl-Meyer Assessment of Physical Performance is what type of outcome measure?

A
  • Impairment based outcome measure

- motor domain includes movement, coordination, and reflexes

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29
Q

MDC ad MCID of UE and LE CVA population on Fugl-Meyer Assessment of Physical Performance:

A

MDC UE = 5.4
MDC LE = 5

MCID UE = 10
MCID LE = 10

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30
Q

Rivermean Motor assessment us what type of outcome measure?

A
  • Measures impact on mobility

- Gross motor, leg and trunk, arm

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31
Q

MCID of CVA pop on Rivermean Motor assessment?

A

3

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32
Q

How does VO2 levels change for stroke patients?

A
  • VO2 levels double with household chores

- Up to 3x normal VO2 levels with ambulation on level ground

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33
Q

Chronotropic incompetence -

A

Inability for HR to increase proportionally to metabolic demands of activity

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34
Q

Deconditioning in post stroke patients is a result of what 3 things?

A
  1. Acute illness
  2. Bedrest
  3. Limited activity levels
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35
Q

CVA patients deconditioning effect on neurological:

A

Degradation of neural circuits due to loss of active engagement

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36
Q

CVA patients deconditioning effect on cardiovascular:

A

↓ cardiac output, HRmax

↑ resting and exercise BP

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37
Q

CVA patients deconditioning effect on pulmonary:

A

↓ 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

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38
Q

CVA patients deconditioning effect on MSK:

A

↓ muscle mass, bone mass, flexibility

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39
Q

CVA patients deconditioning effect on behavioral:

A

Depression, anxiety, fear

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40
Q

What two things recommended before beginning exercise program post-cva?

A
  1. Graded exercise testing

2. ECG

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41
Q

Sub-max protocols for post CVA?

A

Peak HR 120 bpm or 70% age-predicted HRmax

BP <250/115 mmHg

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42
Q

If unable to do graded exercise testing, what should happen?

A
  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
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43
Q

Critical components of coordination:

A
  1. Sequencing
  2. Timing
  3. Grading
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44
Q

What is incoordination?

A
  • Disruption of sequencing, timing, grading

- Loss of coupling between synergistic joints and muscles

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45
Q

Lesions where can lead to incoordination?

A
  1. motor cortex
  2. basal ganglia
  3. cerebellar lesions
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46
Q

impaired ability to perform rapid alternating movements (antagonist and agonist breakdown)

A

Dysdiadochokinesia

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47
Q

inability to judge distance or range of movement

A

dysmetria

hypo or hyper

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48
Q

loss of ability to associate muscles together for complex movements (split up movements by joint movement)

A

Asynergia

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49
Q

inability to rapidly and sufficiently halt movement of a body part after a strong isometric force

A

rebound phenomenon

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50
Q

unintentional, oscillatory movement

A

tremor

resting/intentional

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51
Q

fragmented movement patterns

A

dyssynergia

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52
Q

Ataxia -

A
  • difficulties with fluidity/timing, accuracy, and speed of movements
  • Also see impairments in steadiness, response orientation, and reaction and movement times
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53
Q

Cerebellar ataxia -

A

damage to cerebellum

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54
Q

sensory ataxia -

A

proprioceptive deficits (sensory input)

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55
Q

Potential examination findings with damage to cerebellum:

A 
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
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56
Q

Potential examination findings with damage to basal ganglia:

A 
contralateral
- trunk/limb/gait ataxia
- Dysmetria, dyssynergia, dysdiadochokinesia
- balance deficits
and
- spasticity
- resting/intentional tremor
- Difficulty initiating movements
- considerable strength deficits
- slow movements
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57
Q

Potential examination findings with damage to dorsal column (sensory ataxia):

A 
contralateral
- trunk/limb/gait ataxia
- Dysmetria, dyssynergia, dysdiadochokinesia
- balance deficits
and 
- abnormal sensory exam (proprioception)
- unlikely to see tremor
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58
Q

What type of tone is velocity dependent?

A

spasticity

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59
Q

What type of tone is velocity independent?

A

hypertonicity

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60
Q

Decorticate posturing -

A

UE flexion, LE extension/IR/PF

• Brainstem lesions above red nucleus

61
Q

Decerebrate posturing -

A

UE and LE extension

• Brainstem lesions below red nucleus

62
Q

In acute UMN injuries why will you see temporary hypotonia and for how long?

A

Cause - cerebral or spinal shock

duration - days to weeks

63
Q 
Modified ashworth scale:
0 = 
1 = 
1+ = 
2 = 
3 = 
4 =
A

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
Q

CN 2 Optic dysfunction -

A

Reduced visual acuity (blurry vision)

65
Q

CN 3, 4, 6 dysfunction -

A

Gaze palsies -> double vision (diplopia)

Ptosis

66
Q

CN 5 Trigeminal dysfunction -

A

Loss of facial sensory input
Asymmetrical jaw movement and strength
Loss of mastication -> choking risk -> aspiration risk

67
Q

CN 7 Facial dysfunction -

A

Facial weakness, loss of sensory tongue, impairment of salivary glands -> choking risk -> aspiration risk
Impairment of lacrimal glands -> impair vision

68
Q

CN 8 Vestibulocochlear dysfunction -

A

Hearing loss

Vestibular dysfunction -> vertigo, balance deficits

69
Q

CN 9 glossopharyngeal dysfunction -

A

Dysphagia
Reduced taste & sensation on tongue, loss of gag reflex -> choking risk -> aspiration
risk
ANS: Cardiovascular dysfunction (HR, BP)

70
Q

CN 10 Vagus dysfunction -

A

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
Q

CN 11 Spinal accesory dysfunction -

A

UTrap and sternocleidomastoid weakness -> inability to rotate the head or shrugging the shoulders

72
Q

CN 12 hypoglossal dysfunction -

A

Tongue weakness -> choking risk -> aspiration risk

73
Q

General slowing of cognitive & motor processes

A

Lethargy

74
Q

Dulled or blunted sensitivity, difficult to arouse

A

Obtundation

75
Q

State of semi-consciousness, only arouses with intense stimulation

A

stupor

76
Q

Unconsciousness

A

coma

77
Q

How do we measure level of consciousness?

A 
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
Q

T/F Total GCS score found to predict acute mortality with 88% accuracy

A

True

79
Q

What can be excluded from GCS when communication deficits w/o loss of predictive value?

A

Verbal component

80
Q

Cognitive evaluation of orientation:

What cortical regions involved?

A

person, place, time, situation

- Multiple cortical regions involved

81
Q

Cognitive evaluation of attention (4 parts):

What cortical regions involved?

A 
sustained
selective
divided
alternating
- Prefrontal cortex, reticular formation
82
Q

Cognitive evaluation of memory:

What cortical regions involved?

A 
immediate recall
short-term
long-term
- ST: prefrontal cortex, limbic system
- LT: hippocampus, temporal lobe
83
Q

Cognitive evaluation of executive function:

What cortical regions involved?

A

abstract thinking, problem-solving, judgment, reasoning, insight
- prefrontal cortex

84
Q

Cognitive evaluation of communication:

What cortical regions involved?

A

spontaneous speech, command following, repetitive and naming, articulation, fluency

85
Q

Emotional changes caused by lesions affecting what part of brain?

A

frontal lobe, hypothalamus, and limbic

86
Q

apathy -

A

shallow affect, blunted emotional responses

87
Q

euphoria -

A

Exaggerated feelings of well-being

88
Q

pseudobulbar affect -

damage where?

A

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
Q

depression -

damage where?

A

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
Q

Behavioral Considerations based on Right hemispheric involvement:

A

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
Q

Behavioral Considerations based on Left hemispheric involvement:

A

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
Q

Integration of sensory impressions into information that physiological meaningful -

A

perception

93
Q

Right hemi lesion perceptual considerations:

A
  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
Q

Left hemi lesion perceptual considerations:

A

Apraxia common (aphasia often comes hand in hand)

  • Ideational
  • Ideomotor
95
Q

Neglect involved what hemi/lobe?

A

right parietal

96
Q

Infarcts to what artery most commonly causes neglect?

A

MCA

97
Q

Most common manifestations of neglect:

A

visual (visuospatial)

98
Q

Neglect is a good/poor prognostic factor for functional recovery:

A
  • Poor prognostic indicator for functional recovery

* Longer hospitalizations, functional dependency, long-term disability, increased fall risk

99
Q

Improvement in neglect is seen at what point/stages of rehab?

A

early

100
Q

Examination of neglect:

A
  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
Q

lateral pulsion vs retropulsion:

A

Lateral pulsion – patient tendency to fall toward side of lesion (Wallenberg syndrome)

Retropulsion – Posterior loss of balance

102
Q

Pusher’s syndrome:
Lesion -
Features -

A

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
Q

Pusher’s syndrome R hemi CVA commonly seen with what other symptoms?

A
  • Commonly seen with left hemiplegia

* High association with left spatial and sensory neglect

104
Q

Pusher’s syndrome L hemi CVA commonly seen with what other symptoms?

A
  • Commonly seen with right hemiplegia

* High association with aphasia

105
Q

Examination for Pusher’s syndrome:

A
  • Outcome measures: minimal evidence

- Observation: sitting, standing, exacerbating factors, response to corrections and cues?

106
Q

Common visual dysfunctions post CVA with damage to cerebellum:

A
  • Impaired pursuits and saccades

* Diplopia (double vision)

107
Q

Common visual dysfunctions post CVA with damage to CN III, IV, VI II nuclei and associated CNS areas (brainstem):

A 
• Ptosis (droopy eyelid)
• Ocular motility disturbance
 Diplopia (double vision)
Visual distortions
Dysconjugate gaze  
Impaired vergence (convergence/divergence)
108
Q

Lesion at the L optic nerve, where will you see the visual defect?

A

Left ipsilateral blindness

109
Q

Lesion at the optic chiasm (bilateral lateral compression), where will you see the visual defect?

A

Binasal hemianopia (can’t see out of nasal portion of both eyes)

110
Q

Lesion at the midsagittal transection/pressure), where will you see the visual defect?

A

Bitemporal hemianopia (can’t see out of temporal portion of both eyes)

111
Q

Lesion at the optic tract (L), where will you see the visual defect?

A

Right hemianopia (can’t see out of right side of both eyes)

112
Q

Lesion at the optic radiation (L) lower division, where will you see the visual defect?

A

Right upper quadrantanopia

113
Q

Lesion at the optic radiation (L) upper division, where will you see the visual defect?

A

Right lower quadrantanopia

114
Q

Lesion at the optic radiation (L) both divisions, where will you see the visual defect?

A

Right hemianopia with macular sparing

115
Q

What 2 arteries support the optic nerve and chiasm?

A

anterior cerebral

anterior communicating

116
Q

What 2 arteries support the optic tract?

A

posterior communicating

anterior choroidal arteries

117
Q

What 2 arteries support the optic radiation?

A

middle cerebral artery

posterior cerebral artery

118
Q

What artery supports the primary visual cortex?

A

PCA

119
Q

Damage to cortical vestibular regions (PIVC, MST, VIR) impacts what?

A

Impacts integration and regulation of vestibular systems

120
Q

Damage to brainstem vestibular regions (midbrain, pons) impacts what?

A

VOR, VSR, VCR dysfunction

121
Q

Damage to flocculonodular lobe impacts what?

A

VOR dysfunction, postural instabilities

122
Q

Transient ischemic attacks most common site is?

A
  • vertebrobasilar artery
123
Q

Intense symptoms of TIA at the vertebrobasilar artery include:

A

vertigo

visual deficits

124
Q

Posterior Inferior Cerebellar Artery (PICA) Stroke (Wallenberg’s Syndrome) S&S:

A

Vertigo, headache, facial pain (ipsilateral), disequilibrium, nausea and vomiting, ataxia (ipsilateral), hiccups, and contralateral limb burning pain / altered sensation of temperature

125
Q

Anterior Inferior Cerebellar Artery (AICA) Stroke S&S:

A
  • PICA symptoms + HEARING

* May present with a combination of peripheral (unilateral sensory loss) and central vestibular damage

126
Q

MCA/PCA infarcts on vestibular system:

A
  • Vertigo typically not present, vestibular symptoms tend to be more mild (disequilibrium, vertical disorientation)
  • Most common complaint with vestibular dysfunction: “DIZZINESS”
127
Q

VOR -

Ex: L head rotation

A
  • 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
Q

Cortical lesion effect on sensory systems:

A

specific localized areas of dysfunction
• Parietal lobe – homunculus tells us where we expect to see
• Dorsal column

129
Q

Thalamic lesion effect on sensory systems:

A

diffuse involvement

130
Q

Light touch, proprioception (>/=) temp and pain with CVA implications on sensory systems

A

Light touch, proprioception&raquo_space; temperature, pain

131
Q

Decreased sensitivity to sensory stimuli

A

hypoesthesia

132
Q

Increased sensitivity to sensory stimuli

A

hyperesthesia

133
Q

Abnormal sensation such as numbness, prickling, or tingling

A

paresthesia

134
Q

Touch sensation experienced as pain

A

dysesthesia

135
Q

Pain produced by non-noxious stimulus

A

allodynia

136
Q

Complete loss of pain sensitivity

A

analgeisa

137
Q

Increased sensitivity to pain

A

hyperalgesia

138
Q

Inability to localize sensation

A

atopognosia

139
Q

Most common predictors (acute/subacute) for fall risk post CVA:

A
  • Functional impairment
  • Cognitive deficits
  • Impaired balance
140
Q

CVA impairments and balance:

A
  • 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
Q

CVA impairments and balance can lead to impairments in what?

A
  1. steady state (increased postural sway)
  2. anticipatory control
  3. and/or reactive responses (increased stepping response – can cause imbalance)
142
Q

Evaluation for Presence of Fatigue post CVA:

A
  1. Fatigue Severity Scale

2. Fatigue Impact Scale

143
Q

Central Post-Stroke Pain/Thalamic Syndrome

A

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
Q

When will Central Post-Stroke Pain/Thalamic Syndrome usually begin?

A

Weeks to months post initial insult

145
Q

Medical management of Central Post-Stroke Pain/Thalamic Syndrome:

A

Fluoxetine (anti-dep SSRIs) – increase neuroplasticity after brain injury or stroke

146
Q

Most common site of musculoskeletal pain post stroke? Second?

A
  1. Shoulder

2. Low back

147
Q

What can lead to significantly higher risk of developing shoulder pain within first 8-10 weeks of CVA?

A

Severe UE hemiplegia and/or shoulder subluxation within 72 hours post CVA

148
Q

Examination of hemiplegic shoulder subluxation:

A
  • Fingerbreadth method: Subluxation = 1⁄2 fingerbreadth or more
  • Radiographs
  • Ultrasound
149
Q

Shoulder-hand syndrome -

A
  • Painful shoulder + painful and edematous hand/wrist
  • +Allodynia, hyperalgesia
  • Elbow typically spared
  • R CVA > L CVA

Neuro 1 (5 decks)

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