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Neurology > CVA > Flashcards

CVA Flashcards

1
Q

Risk factors and early warning signs

A
  • sudden numbness or weakness of the face, arm, or leg, especially on one side of the body
  • sudden trouble walking, dizziness, loss of balance or coordination
  • sudden severe HA with no known cause
  • sudden trouble seeing with one or both eyes
  • sudden confusion, trouble speaking or understanding
  • possible urge to throw up
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2
Q

Ischemic CVA vs hemorrhagic CVA

A
  • ischemic CVA: a thrombus or embolus blocks blood flow to part of the brain
  • hemorrhagic CVA: blood spills out from break in blood vessel in the brain
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3
Q

what does the P wave, QRS complex, and T wave of the EKG combined represent?

A
  • The P wave, QRS complex, and T wave represent contractions of the heart
  • The P wave represents activity in the hearts upper chambers, while the QRS complex and T wave represent activity in the lower chambers
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4
Q

MRI vs CT scan for detection of CVA

A

CT:
•demonstrates poor sensitivity for detecting small infarcts and infarction in the posterior fossa
•sometimes during acute phase CT scans are negative
•acute bleeding/hemorrhaging are visible on CT scans
•CT scan can delineate cerebral edema within 3 days
•cerebral infarction is visible within 3 to 5 days with the addition of contrast material

MRI:
• more sensitive in the diagnosis of acute strokes
•allows detection of cerebral ischemia as early as 30 minutes after vascular occlusion and infarction within 2-6 hours
•details the extent of the infarction or hemorrhage
•can detect smaller lesions than CT scans

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5
Q

Middle cerebral artery deficits

A

•contralateral hemiparesis UE and face affected > LE
•contralateral hemisensory loss UE and face > LE
•Broca’s/motor/expressive/nonfluent aphasia
•Wernike’s/sensory/receptive/fluent aphasia
•global aphasia
•perceptial defecits: unilateral neglect, depth perception, spatial relations, agnosia (inability to interpret sensations) (R) CVA
•contralateral homonymous hemianopsia
• apraxia (neurological disorder characterized by loss of the ability to execute or carry out skilled movements and gestures)
*MOST COMMON site of occlusion in stroke- affects LATERAL frontal, parietal, and temporal lobes; subcortical structures- internal capsule, and portions of the basal ganglia

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6
Q

Anterior Cerebral artery deficits

A
  • contralateral hemiparesis, LE affected > UE and face
  • urinary incontinence
  • apraxia- problems with imitation and bimanual tasks
  • abulia (akinetic mutism)- slowness, delay/lack of spontaneity, motor inaction
  • supplies the MEDIAL aspect of the frontal and parietal lobes, subcortical structures- internal capsule, portions of the basal ganglia and most of the corpus collosum
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7
Q

Apraxia

A

neurological disorder characterized by loss of the ability to execute or carry out skilled movements and gestures

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8
Q

abulia (akinetic mutism)

A

slowness, delay/lack of spontaneity, motor inaction

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9
Q

Posterior cerebral artery deficits

A

•central post stroke thalamic pain syndrome
•involuntary movements- choreoathetosis
•Weber’s syndrome- occulomotor nerve palsy and contralateral hemiplegia
•contralateral homonymous hemianopsia
visual agnosia (inability to process visual sensory info)
•prosopagnosia- difficulty naming people on sight
•dyslexia
•memory defect
•topographic (the arrangement of an area) disorientation
•blindness
•supplies occipital lobes, medial and inferior temporal lobes, upper brainstem, midbrain, posterior diencephalon, and thalamus

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10
Q

Vertebro/basilar artery deficits

A
  • vertebral artery supplies the medulla and cerebellum
  • Basilar artery supplies the pons, internal ear and cerebellum
    •occlusions to the vertebrobasilar system can produce a wide variety of symptoms both ipsilateral and contralateral signs, because some of the tracts in the brainstem will have crossed and others have not
    •numerous cerebellar and cranial nerve abnormalities also are present
    •locked in syndrome occurs with basilar artery thrombosis with sudden onset, patient’s progress from acute hemiparesis to tetraplegia, paralysis of CN V-XII. Dysarthric mutism (pt has trouble controlling the muscles that produce words). Preserved consciousness and sensation. Cannot move or speak but remains alert and oriented, horizontal eye movement is impaired but horizontal eye movement and blinking remains intact
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11
Q

Dysarthric

A

occurs when the muscles you use for speech are weak or you have difficulty controlling them. Dysarthria often causes slurred or slow speech that can be difficult to understand

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12
Q

prosopagnosia

A

difficulty naming people on sight

•PCA

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13
Q

choreoathetosis

A

involuntary twitching or writhing

•PCA

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14
Q

Weber’s syndrome-

A

occulomotor nerve palsy and contralateral hemiplegia

•PCA

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15
Q

Medical management of CVA

A
  • reestablish circulation and oxygenation via O2. Pt in coma may need ventilation and suctioning
  • maintain adequate BP. Hypotension and hypertension is treated
  • maintain sufficient cardiac output. Control arrhythmias and cardiac de-compensation
  • restore/maintain fluid and electrolyte balance
  • maintain blood glucose levels within normal range
  • control seizures and infections
  • control edema, ICP, and herniation using antiedema agents
  • maintain bowel and bladder functions- may require cath
  • maintain skin and joint integrity
  • decrease risk of DVT, aspiration, decubitis ulcers
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16
Q

Pharmacological management of CVA

A
  • Thrombolytics
  • Anticoagulants
  • Antiplatelet therapy
  • Antihypertensive agents
  • Angiotensin II receptor agonists
  • Anticholesterol agents/Statins
  • Antispasmodics/spasmolytics
  • Antispastics
  • Anticonvulsants
  • Antidepresants
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17
Q

Thrombolytics

A

Meds: Activase or tPA

Function: dissolves clots and reestablishes blood flow- also used for CVT, PE, and coronary arteries

AE: bleeding and brain hemorrhage

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18
Q

Anticoagulants

A

Meds: Warfarin/Coumadin, Heparin, Pradaxa

Function: used to reduce the risk of blood clots, prevent existing clots from getting bigger by thinning the blood.

AE: bleeding, hemorrhage, hematomas

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19
Q

Antiplatelet therapy

A

Meds: Plavix

Function: decrease risk of thrombosis and recurrent stroke. May be recommended for patients with atrial fibrillation.

AE: gastric ulcers and bleeding

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20
Q

Antihypertensive agents

A

Meds: ACE inhibitors, alpha/beta/calcium channel blockers, vasodilators, diuretics

Function: control hypertension

AE: hypotension, dizziness

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21
Q

Angiotensin II receptor antagonists

A

Meds: Micardia, Cozaar

Function: enlarges blood vessels and reduces BP.

AE: hypotension and dizziness

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22
Q

Anticholesterol agents/ Statins

A

Meds: Lipitor, Crestor, Zocor, Simvastatin

Function: lowers cholesterol for management of hyperchoesterolemia

AE: dizziness, weakness, headache, insomnia

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23
Q

Antispasmodics/spasmolytics

A

Meds: Soma, Parafon, Forte, Flexeril, Diazepam/Valium, Robaxin, Norflex/Norgesics

Function: relax skeletal muscle and decreases muscle spasm

AE: drowsiness, dizziness, dry mouth

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24
Q

Antispastics

A

Meds: Baclofen/Lioresal, Dantrolene sodium/dantrium, Diazepam/Valium, Zanaflex

Function: relax skeletal muscle and decreases muscle spasm

AE: drowsiness, dizziness, confusion, weakness

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25
Q

Anticonvulsants

A

Meds: Tegretol, Klonopin, Valium, Phenobarbitol/Luminal, Dilantin

Function: controls seizures, acts as a generalized CNS depressant

AE: drowsiness, ataxia, sedation

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26
Q

Antidepressants

A

Meds: Prozac, Monoamine oxidase inhibitors, Zoloft, tricyclic/Amitriptyline

Function: controls depression

AE: tremor, anxiety, insomnia, nausea

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27
Q

TIA vs CVA

A

TIA
•trans ischemic attacks or mini-strokes result when a cerebral is temporarily, but not completely, blocked, decreasing blood flow to the brain. Problems with function are temporary.

CVA
Many strokes result from a complete blockage of a cerebral artery, leading to death of brain cells and permanent loss of certain functions

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28
Q

Glasgow coma scale

A
  • Consciousness: state of arousal and awareness of one’s environment
  • Lethargy: diminished level of arousal. Appears drowsy but when questioned can open eyes and respond briefly. Easily falls asleep if not continuously stimulated.
  • Obtunded: diminished arousal and awareness. Difficult to arouse from sleeping, once aroused- appears confused. Responds slowly and shows little interest in or awareness of environment, attempts at interaction are generally unproductive.
  • Stupor (semi-coma): can be aroused only with vigorous and unpleasant stimuli. Mass movement responses may be observed in response to painful stimuli or loud noises
  • Coma: unconscious and cannot be aroused. Eyes remain closed- no sleep wake cycles
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29
Q

Normal and abnormal states of consciousness: alert

A

Completely awake, attentive to normal levels of stimulation, able to interact meaningfully with clinician

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30
Q

Lethargic or somnolent

A

arousal with stimuli, falls asleep when not stimulated, decreased awareness, loss of train of thought

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31
Q

Obtunded

A

difficult to arouse, requires constant stimulation to maintain consciousness, confused when awake, interactions with therapist may be largely unproductive

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32
Q

Stupor (semi-coma)

A

arousal only with strong, generally noxious stimuli and returns to unconscious state when stimulation is stopped, patient is unable to interact with clinician. Mass movement responses may be observed in response to painful stimuli or loud noise.

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33
Q

Coma (deep coma)

A

unarousable to any type of stimulus, reflex motor responses may or may not be seen. Eyes remain closed.

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34
Q

Delirium

A

state of disorientation marked by irritability or agitation, paranoia, and hallucinations, patient demonstrates offensive, loud and talkative behaviors

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35
Q

Dementia

A

Alteration in mental processes secondary to organic disease that is not accompanied by a change in arousal

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36
Q

Right CVA vs Left CVA

A 
Right:
•paralyzed left side
• spatial perceptual deficits
•quick and impulsive behavioral style
•tends to minimize problems
•short attention span
•visual field deficits
•impaired judgement
•memory deficits
Left:
•paralyzed right side
•speech-language deficits
• slow, cautious behavior style
•visual field deficits
•aware of deficits, may be depressed or anxious
•memory deficits
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37
Q

Pusher syndrome

A

Ipsilateral pushing: 10% of patients with acute CVA
•patients sit or stand asymmetrically with most of weight shifted to WEAK hemiparetic side
•efforts to passively correct results in patient pushing more forcefully
•training needs to emphasize upright positions with active movement shifts towards the stronger side
•clinician may sit on patient’s uninvolved side and instruct them to “lean towards me”
•if visuospatial deficits are not present patient can look in mirror and be asked if their posture is upright - ask “what direction are you tilted” “where do you need to move”
•patient can be positioned with uninvolved side to wall and have them lean onto the wall
•if cane is used it can be shortened to encourage weight shift to stronger side
•an environmental boundary such as a doorway or corner may be used to achieve symmetrical standing

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38
Q

Homonymous hemianopsia

A
  • same side as the hemiplegia
  • need to scan environment prior to moving and affected extremity position because they are at increased risk of self-injury and unilateral neglect
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39
Q

Anticoagulants, thrombolytics, anti-platelets AE

A

AE: bleeding, hemorrhaging, bruising, hematomas

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40
Q

Anticholesterols (statins), anti-hypertensives, anti-spastics AE

A

AE: Dizziness

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41
Q

anti-convulsants, anti-spastic, antispasmodics AE

A

AE: drowsiness

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42
Q

secondary impairments that may occur with CVA

A 
decreased sensation leads 
to:
•PI
•unilateral neglect
•decreased motor learning

DVT, PE, osteoporosis, pneumonia, atelectasis etc…

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43
Q

L CVA

A
  • aphasias
  • apraxias (L more often than R CVA)
  • slow and cautious
  • hesitant
  • R hemiplegia
  • R sensory loss
  • R homonymous hemianopsia
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44
Q

R CVA

A
  • visuospatial issues
  • quick and impulsive- need to be told to slow down
  • overestimate their abilities and deny their problems= increased safety risk
  • short attention spans
  • easily distractable
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45
Q

Brunnstrom vs. Bobath

A

Brunnstrom:
•use synergies and associated reactions
•6 stages of recovery
•synergy patterns

Bobath:
•3 stages of recovery
• does not use synergies or associated reactions
•does use automatic righting and equilibrium reactions
•does not use resistance or excessive effort because that leads to increased tone
•does use functional strengthening
TX: integrate both sides and influence tone through key points of control through positioning and movement

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46
Q

Synergies: UE flexor

A

Scapula: retracted

Shoulder: abducted, ER, and hyperextended

Elbow: flexed* and supinated

Wrist/fingers: flexed

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47
Q

Synergies: UE extensor

A

Scapula: protracted

Shoulder: adducted*, IR, extended

Elbow: extended and pronated*

Wrist/fingers: flexed

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48
Q

Synergies: LE flexor

A

Hip: flexed*, abducted, ER

Knee: flexed

Ankle: DF and IN

Toes: extended

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49
Q

Synergies: LE extensor

A

Hip: extended, add*, IR

Knee: extended*

Ankle: PF, IN

Toes: flexed

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50
Q

Associated reactions

A
  • Homolateral synkinesis
  • Raimeste’s
  • Soque’s
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51
Q

Associated reactions: General

A
  • resist flex/ext of UE produces the same in the other UE

* resist flex/ext of LE produces the opposite in the contralateral LE

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52
Q

Associated reactions: Homolateral Synkinesis

A

resisted flexion of UE produces increased flexor tone in the LE on the same side of the body

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53
Q

Associated reactions: Raimete’s

A

ABD or ADD of UE or LE produces the same tone on the contralateral side

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54
Q

Associated reactions: Soque’s

A

raising the arm above horizontal produces finger extension and abduction

55
Q

Brunnstrom stage I

A

Flaccidity
•PROM
•sensory input to affected
•decrease incidence of PI and contractures
•begin bed mobility, especially rolling, initially towards affected side
•positioning: common deviations to avoid= side bent towards and rotated away from affected side, trunk shortened on affected side, unequal WB towards unaffected side, thoracic and lumbar flexed, posterior pelvic tilt (sacral PI), hips abducted and ER, unequal WB on feet, UE is abducted and hanging

56
Q

Supine post CVA positioning

A

neutral head and trunk, scapula protracted, UE abducted, elbow extended and supinated, wrist and fingers are extended and abducted, pelvis protracted or neutral (not retracted), hip neutral rotation, knees extended, ankles neutral

57
Q

Sidelying on affected side post CVA benefits

A

benefits: increased sensory input

•elongation of the side= decreased spasticity, because it’s a prolonged stretch

58
Q

Brunnstrom stage II

A
  • spasticity and associated reactions begin but they’re still mostly flaccid, often have a “catch” in PROM shoulder abduction and elbow flexion
  • TX: same as stage I, but then additionally begin transfers towards unaffected side
59
Q

Benefits of transfer to affected side

A
  • direct attention and increase sensory input to affected side
  • increase WB appoximation of affected leg to facilitate cocontraction
  • work on dynamic balance to affected side
60
Q

Brunnstrom stage III

A
  • spasticity, associated reactions, and synergy patterns dominant and obligatory, can only move in synergy
  • treatment should incorporate tecbniques to inhibit while performing functional activities
  • while sitting emphasize equal WB
  • work on transfers and gait
  • affected UE- ER and ABD, hand flat on plinth=prolonged stretch, pressure on flexor tendons to decrease tone
61
Q

Brunnstrom stage IV

A
  • spasticity begins to decrease

* continue to progress: transfers and gait

62
Q

Brunnstrom stage V

A
  • able to work out of synergy patterns
  • increase endurance
  • work on balance and coordination
63
Q

Brunnstrom stage VI

A
  • nearly normal except with tasks requiring increased speed and coordination
  • community reintegration: walking outside on all surfaces, grocery shopping etc.
  • advanced balance and gait
64
Q

NDT progression

A
  • roll
  • sidelying to sit
  • STS
  • gait
65
Q

prone NDT progression

A
  • prone
  • prone on elbows
  • quadruped
  • tall kneeling
  • half kneeling
  • modified plantigrade: go from kneeling to standing while partially WB through UEs on surface
  • standing
  • walking
66
Q

Bobath/NDT

A

Principles of tx:
•cannot superimpose normal movement on abnormal tone
•this method does not use abnormal movements, synergies, or associated reactions, which is why it’s often used in pediatrics
•facilitate normal tone through normal movement-which involves inhibiting abnormal movement patterns
•CNS mirrors changing state of body musculature, normal stimuli=normal output=normal kinesthetic input to CNS=normal tone=normal movement patterns. The reverse is true with abnormal movement patterns.
•influences tone through key points of control. A change at these points induces pattern of posture which is opposite that of hemplegia.
•Handling: tx should be active and dynamic instead of static posturing.
•facilitate automatic reactions of righting, equilibrium and protective extension
•all movements should be done without effort- increased tone in one extremity increases tone throughout the body.
•don’t use associated reactions
• treat pt as a whole, integrate both limbs

67
Q

Bobath stages

A

3 stages:

1) flaccidity (brunnstrom stages I and II)
2) spasticity (brunnstrom stages III and IV)
3) relative recovery (brunnstrom stages V and VI)

68
Q

Automatic postural reactions

A

•used with Bobath method to provide background for normal movement
•3 large groups of automatic postural reactions:
1) righting
2) equilibrium
3) protective extension

69
Q

Automatic postural reactions: righting

A

automatic reactions serving to maintain and restore normal position of head in space (face vertical, mouth horizontal) and its normal relationship with the trunk, and the normal alignment of the trunk and limbs

70
Q

Automatic postural reactions: Equilibrium

A

automatic reactions serving to maintain or restore balance during all activities

71
Q

Automatic postural reactions: protective extension

A

2nd line of defense when equilibrium reactions are insufficient. Arms and hands are used to pretext the body when at the point of falling

72
Q

Brunnstrom

A

principles of tx:
•governed by primitive reflexes and synergy patterns
• uses associated reactions
• basic limb synergies are primitive spinal cord patterns. Patients must rely on lowest motor centers which are relatively automatic in movement post neuro incident
* because they naturally occur synergies and reflexes are encourages in this approach as a normal part of sequence of return to function.
•6 stages of recovery (UE and LE may be at different stages)
•try to get movement of the distal muscles by including them in a synergy and then working out of synergy

73
Q

Brunnstrom stages of recovery overall

A

1) Flaccidity
2) Limb synergies, associated reactions, and spasticity begin
3) Increased spasticity. Cannot move out of synergy.
4) Gradual control of movement out of synergy, decreased spasticity.
5) Synergies lose dominance. Can perform out of synergy with concentration.
6) Coordination and speed are near normal, but might still not be PLOF

74
Q

Stages of motor control

A

1) Mobility
2) Stability: (2 types)
•tonic holding: ability of muscle to hold a contraction in shortened range against resistance
•cocontraction: simultaneous static contraction of antagonistic muscles around a joint to provide stability in WB or maintain midline posture
3) controlled mobility:
•occurs in extremities when in WB postures, the distal segment is fixed, while the proximal component moves over the distal part (i.e. WEIGHT SHIFTING)
4) Static dynamic activity:
• intermediate stage between controlled mobility and skill. In WB one of the previously supporting limbs is lifted
5) Skill:
• highest level of motor control-includes 2 functions:
- manipulation
- exploration of environment
•in skilled activities- distal component (i.e. hand, foot) is mobile, while the proximal musculature provides the dynamic stability to guide limb

75
Q

ROOD

A

Principles of tx:
•This technique uses sensory stimulation (vibration, quick icing, tapping, slow rocking etc…) more than any other technique in rehab
•goals: to activate postural responses at an automatic level while following the normal developmental sequence
•superimpose mobility on stability (phasic movement only accomplished after tonic control develops
•progress is cephalo to caudal/proximal to distal

76
Q

A & O x3

A & O x4

A

x3: oriented to person, place, and time
x4: oriented to person, place, time, and situation

77
Q

Pupil: size and equality

A

pupil size is normally 2 to 4 mm or 4 to 8 mm in diameter in the light and dark, respectively. The pupils should be of equal size ( less than or equal to 1 mm difference is normal)

78
Q

Pupil: shape

A

pupils are normally round but may become oval or irregularly shaped with neurological dysfunction.

79
Q

Pupil: reactivity

A
  • constrict with light and focus on a near object
  • dilate with dark
  • constriction and dilation should occur briskly.
  • pupil reactivity can be tested by shining a light directly into the patient’s eye.
  • dilated, nonreactive (fixed0, malpositioned, or disconjugate pupils can signify very serious neurologic conditions especially occulomotor compression, increased ICP, or brain herniation
80
Q

Sensory tests:

A
  • light touch
  • pain
  • pressure
  • proprioception
  • vibration
  • temp
  • stereognosis
  • two-point discrimination
  • graphesthesia
  • double simultaneous stimulation
81
Q

Sensory tests: light touch

A

apply light touch with the finger, a cotton ball or washcloth over the extremities or trunk. The pt is asked to identify if there is a stimulus present and the location of the stimulus.

82
Q

Sensory tests: pain

A

touch a pin or pen cap over the extremities or trunk. Ask the pt to distinguish btw dull and sharp

83
Q

Sensory tests: pressure

A

using the therapist’s fingertip, apply pressure on the skin surface that is firm enough to indent the skin and stimulate the deep receptors. The pt is then asked to identify if there is a stimulus present.

84
Q

Sensory tests: proprioception

A

lightly grasp the DIP joint of the pt’s finger or great toe and move the joint slowly up and down. Ask the pt the direction the joint moved. Test distal to proximal.

85
Q

Sensory tests: vibration

A

activate a tuning fork and place on a bony prominence. Ask the pt to state when the vibration slows and stops. Proceed distal to proximal.

86
Q

Sensory tests: temp

A

place test tubes filled with warm or cold water on the area of the pt’s body being tested. Ask patient to state the temp.

87
Q

Sensory tests: stereognosis

A

place a familiar object in the pt’s hand and ask the pt to identify it.

88
Q

Two-point discrimination

A

place two-point caliper or drafting compass on area to be tested. Ask the pt to distinguish whether it has one or two points

89
Q

Sensory tests: graphesthesia

A

trace a letter or number in the pt’s open palm and ask pt to state what was drawn

90
Q

Sensory tests: double simultaneous stimulation

A

simultaneously touch two areas on the same side of the pt’s body. Ask patient to locate and distinguish both points.

91
Q

Spinal tracts: Ascending/ Afferent tracts

A

Bring sensory info from body to the thalamus and then to the sensory cortex
•lateral spinothalamic: pain and temp
•anterior spinothalamic: touch and pressure
•spinocerebellar tract: unconscious proprioception
•dorsal columns: conscious proprioception
-fasciculus cuneatus: arms
-fasciculus gracilis: legs

92
Q

Spinal tracts: Descending/Efferent tracts

A

Motor command for movement, inhibition, or facilitation of tone in preparation of or through movement
•Lateral Corticospinal: (pyramidal) motor commands
•Vestibuluspinal: (extrapyramidal) balance, coordination, postural changes
-Rubrospinal
-Tectospinal
-Reticulospinal
* these 3 extrapyramidal tracts influence tone, posture, and balance

93
Q

W/C positioning post CVA

A

head: neutral (if tipped make sure it’s towards unaffected), no forward head or flexion
neck: “
trunk: extended, back against chair
scapula/shoulder: protracted STA, approximated shoulder
elbow/forearm: supported on lap by pillow
unaffected UE: stroking affected
pelvis: neutral ant. tilt, equal WB on isch. tub.
hip: 90° flexion with neutral rotation
knee: 90° flexion
ankle: neutral, feet flat, =WB

94
Q

Supine positioning post CVA

A

head: neutral, not fwd, if tilted make sure it’s towards unaffected
neck: “
trunk: neutral, not shortened on affected, not rotated, or alternatively elongate the affected side
scapula/shld: protracted STA, shld ABD and ER
elbow/forearm: extended and supinated
wrist/hand: extended and abd, slightly elevated
pelvis: neutral, not retracted, pelvis can be in slight protraction
hip: neutral rotation and extension
knee: extension but not hyperextension
ankle: neutral no pressure on heels
unaffected UE: relaxed

95
Q

Sidelying on affected side post CVA

A

head: neutral, or tilted towards unaffected, no fwd head
neck: “
trunk: extended and neutral
scapula/shld: protracted STA, flexed shoulder
elbow/forearm: extended
wrist/hand: extended and abducted
pelvis: neutral or slight protraction, no retraction
hip: flexed
knee: flexed
ankle: neutral pillows supporting inside of legs
unaffected UE: stroking

96
Q

Sidelying on unaffected side post CVA

A

head: neutral, no fwd head, if tilted make sure it’s towards unaffected
neck: “
trunk: extended
scapula/shld: protracted, affected arm on pillows forward flexed
elbow/forearm: extended
unaffected UE: relaxed
pelvis: neutral to slight protraction
hip: slightly flexed, neutral rotation, pillow btw knees
knee: flexed
ankle: neutral, supported- to prevent inversion

97
Q

Asthenia

A

generalized muscle
weakness
TX: STS, stair and curb navigation, lifting and carrying

98
Q

Dysarthria

A

disorder of motor component of speech

TX: communication with family, communication at work, talking on the phone

99
Q

Dysdiadochokinesia

A

impaired ability to perform rapid alternating movement

100
Q

Dysmetria

A

inability to judge distances or range of a movement

101
Q

Dyssynergia

A

movement performed in a sequence of component parts rather than as a smooth, single activity

102
Q

Asynergia

A

loss of ability to associate muscles together for component movements

103
Q

Rebound phenomenon

A

inability to stop forceful movements after resistive stimulus removed

104
Q

MCA

A
  • branches of the internal carotid
  • supplies the entire lateral aspect of the cerebral hemisphere (frontal, temporal, and parietal lobes) and subcortical structures including the internal capsule, corona radiata, globus pallidus, most of the caudate nucleus, the putamen, and portions of the basal ganglia
  • the more proximal the occlusion (i.e. the closer to its point of origin, the IC) the more extensive the damage and significant the cerebral edema.
  • MCA is the most common site of occlusion in CVA
  • the most common symptoms are contralateral spastic hemiparesis and sensory loss of the face, UE, and LE, with the face and UE more involved than the LE
  • other symptoms include: aphasia (L hemisphere), perceptual deficits (R CVA), unilateral neglect, depth perception, spatial relations, agnosia (loss of ability to identify objects or people), anosagnosia (person unaware of their disability), and apraxia (inability to perform movements on command) and contralateral homonymous hemianopsia
105
Q

ACA

A
  • first and smaller of 2 branches off of the IC (2nd is MCA)
  • supplies the medial aspect of the frontal and parietal lobes, subcortical structures including: internal capsule, portions of the basal ganglia, and most of the corpus callosum
  • more distal lesions produce more significant deficit, because the anterior communicating artery allows perfusion of the proximal ACA
  • common symptoms include contralateral hemiparesis and sensory loss with more involvement of the LE than the UE or face
  • symptoms also include urinary incontinence, apraxia (problems with imitation and bimanual tasks), abulia/akinetic mutism (slowness, lack of spontaneity, motor inaction, delay, and contralateral frasp reflex and sucking reflex
  • can display flat affect due to prefrontal involvement
  • can be asymptomatic if the circle of Willis is competent
106
Q

PCA

A
  • the 12 PCAs arise as terminal branches of the basilar artery
  • each PCA supplies the corresponding occipital lobe, medial and inferior temporal lobes, upper brainstem, midbrain, and posterior diencephalon including most of the thalamus
  • occlusion proximal to the posterior communicating arteries typically result in minimal deficits due to collateral blood supply.
  • symptoms can inlclude: contralateral homonymous hemianopsia, B homonymous hemianopsia with some degree of macular sparing (due to collateral blood from the MCA), visual agnosia (trouble recognizing objects), prosoagnosia (difficulty naming people on sight), dyslexia, memory defect (due to temporal lobe ischemia), topographic disorientation (difficulty finding their way around environment), central post-stroke thalamic pain syndrome, involuntary movements choreoathetosis (involuntary movements in a combination of chorea- irregular migrating contractions- and athetosis- twisting and writhing), intention tremor, hemiballismus (flailing, ballistic, undesired movement of th elimbs, contralateral hemiplegia, Weber’s syndrome (occulomotor nerve palsy and contralateral hemiplegia), blindness, miosis, ptosis, slugish pupillary response
107
Q

Vertebrobasilar artery

A
  • the vertebral arteries arise from the subclavian arteries and travel into the brain along the medulla where they merge at the inferior border of the pons and form the basilar artery
  • the vertebral arteries supply the cerebellum (via posterior inferior cerebellar arteries and the medulla (via medullary arteries)
  • the basilar artery supplies the pons (via pontine arteries), the internal ear (via labyrinthe arteries, and the cerebellum (via the anterior inferior and superior cerebellar arteries)
  • occlusions of the vertebrobasilar system can produce a wide variety of symptoms both ipsilateral and contralateral signs, bexause some of the tracts in the brainstem have crossed and others have not. Numerous cerebellar and CN abnormalities are also present.
  • Locked in syndrome (LIS) occurs with basilar artery thrombosis and B infarction of the ventral pos With sudden onset the patients develop acute hemiparesis rapidly progressing to tetraplegia and lower bulbar paralysis (CNs V-XII are involved). Initially patients are dysarthric (slurred speech due to muscular weakness) and dysphonic but rapidly progress to mutism (anarthria) . There is preserved consciousness and sensation and alertness and orientation but the pt cannot move or speak. Horizontal eye movement is impaired but vertical eye movement and blinking are intact
  • Extracranial injuries to the vertebral arteries as they travel through the cervical spine can also produce vertebrobasilar s/s. Forceful neck motions (i.e. whiplash and neck manupulations are common causes
108
Q

agnosia

A

inability to interpret sensory sensations (though sensory receptors intact) many different types (visual, auditory, tactile etc..)

109
Q

anosognosia

A

person unaware of their disability

110
Q

apraxia

A

inability to perform movements on command

111
Q

abulia/akinetic mutisim

A

slowness, lack of spontaneity

112
Q

visual agnosia

A

trouble recognizing objects

113
Q

prosopoagnosia

A

difficulty naming people on sight

114
Q

dysarthria

A

dysfunction of motor component of speech

115
Q

Common postural deviations with CVA: pelvis

A
  • Asymmetrical WB with majority of WB on stronger side.
  • In sitting: post pelvic tilt (sacral sitting)
  • In standing: unilateral retraction and elevation on more affected side
116
Q

Common postural deviations with CVA: trunk

A

With sacral sitting: a flattened lumbar curve with exaggerated thoracic curve and forward head, lateral flexion of trunk shortening on affected side.

117
Q

Common postural deviations with CVA: shoulders

A

unequal height with more affected shoulder depressed, humeral subluxation with scapular downward rotation and lateral flexion of the trunk, scapular instability (winging) may be present

118
Q

Common postural deviations with CVA: head/neck

A

protraction with lateral trunk flexion, lateral flexion of the head with rotation away from the more affected side

119
Q

Common postural deviations with CVA: UE’s

A

more affected UE typically held in a flexed, adducted position, with IR and elbow flexion, forearm pronation, wrist and finger flexion; limb in NWB, stronger UE used for postural support.

120
Q

Common postural deviations with CVA: LE’s

A
  • In sitting: more affected LE typically held in hip abduction and ER with hip and knee flexion (flexioni synergy pattern)
  • In standing- more affected LE typically held in hip and knee extension with adduction and IR and ankle PF, unequal WB on feet
121
Q

R CVA

A
  • L side hemiplegia/paresis
  • L side sensory loss
  • Visual: L side unilateral neglect and agnosias, visuospatial disorders and distrurbances of body image and scheme, as well as difficulty processing visual cues.
  • Behavioral deficits: quick and impulsive behavioral style, poor judgement, unrealistic, inability to self correct, poor insight, unawareness of impairments, denial of disability, increased safety risk.
  • Intellectual deficits: difficulty with abstract reasoning and problem solving, difficulty synthesizing info and grasping whole idea of tasks, rigidity of thought, memory impairments, typically associated to spatial perceptual info.
  • Emotional deficits: difficulty with ability to perceive emotions, difficulty with expression of negative emotions
  • Task performance: fluctuations in performance.
122
Q

L CVA

A
  • R sides hemiplegia/paresis
  • R side sensory loss
  • Speech and language: aphasia, difficulty processing verbal cues.
  • Behavioral deficits: slow and cautious behavioral style, disorganized, very aware of impairments and extent of disability
  • Intellectual deficits: disorganized problem solving, difficulty initiating tasks, processing delays, highly distractable, memory deficits- typically related to language preservation.
  • Emotional deficits: difficulty with expression of positive emotions
  • Task performance: apraxia common- difficulty planning and sequencing movements, ideational or ideamotor.
123
Q

deficits of either R or L hemisphere

A
  • Visual field: homonymous hemianopsia
  • Emotional: lability, apathy, irritability, low frustration levels, anxiety, depression
  • Cognitive: confusion, short attention span, memory loss, executive functions
124
Q

simple progression of CVA treatment

A
  • demonstrate
  • instruct pt to look at their unaffected UE and do the motion
  • instruct pt to look at their affected UE and PTA guides the motion
  • symmetrical B UE movement
  • asymmetrical B UE movement
125
Q

Facilitation techniques

A

•General: fast, irregular
-rocking, swinging, rolling, spinning
•Visual: lights, bright colors, lots of objects
•Auditory: irregular rhythm
• more than body weight joint compression and approximation (telescoping)
•minimal resistance during motion (tracking)

126
Q

Local facilitation techniques: quick icing

A

3 quick strokes over muscle belly, distal to proximal, quick icing before movement

127
Q

Local facilitation techniques: vibration

A

75-150 cycles per second vibration on muscle belly while moving

128
Q

Local facilitation techniques: tapping

A

on muscle belly while moving

129
Q

Local facilitation techniques: quick stretch

A

in the opposite direction of motion desired before movement

130
Q

Inhibition techniques

A

•General: slow, repetitive, reciprocal, rotatory
- neutral warmth, slow rocking, rolling
• Visual: low/dim lights, pastels, not many objexts, no clutter
•Auditory: low voice, melodious, monotone, regular beat
• cold 10 min
•slow stroking down posterior rami
• maintained pressure
•vibration under 75 cycles per second
•maintained pressure on tendons
•isometric/max contraction
•prolonged stretch
•FES of opposite muscle groups
• less than or equal to body weight joint compression (equal WB or less than WB = inhibition)

131
Q

primary sensory cortex receives

A

pain, temp, pressure, touch, proprioception and vibration

132
Q

sensory association area/secondary/somatosensory area

A

2 point discrimination, stereognosis (identify by touch), graphesthesia (writing on skin recognition), barognosis (discriminate weight), figure ground discrimination (ability to separate objects from background)

133
Q

balance grades:

A

0 absent: unable to maintain balance
1 poor: patient requires HH support and mod to max assistance to maintain upright position (static). Patient unable to move or accept challenge without LOB
2 fair: patient able to maintain balance with HH support; may require occasional min A (static). Patient able to accept min challenge, able to maintain balance while turning head and trunk (dynamic).
3 good: patient able to maintain balance without HH support, min postural sway (static). Patient accepts mod challenge, able to maintain balance while picking up objest off of floor (dynamic).
4 normal: pt able to maintain steady balance without HH support (static); patient able to accept max challenge and can shift weight easily within full range of LOS in all directions (dynamic)

Neurology (9 decks)

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