Chapter 2: Cerebrovascular Accident (CVA Stroke)

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  1. CVA Definition
    Sudden, focal neurological deficit resulting from ischemic or hemorrhagic lesions in the brain
  2. Etiological Categories: Cerebral Thrombosis
    Formation or development of a blood clot or thrombus within the cerebral arteries or their branches
  3. Etiological Categories: Cerebral Embolism
    Traveling bits of matter (thrombi, tissue, fat, air, bacteria) that produce occlusion and infarction in the cerebral arteries
  4. Etiological Categories: Cerebral Hemorrhage
    • Abnormal bleeding as a result of rupture of a blood vessel 
    • Extradural, subdural, subarachnoid, intracerebral
  5. Risk Factors
    • Atherosclerosis
    • HTN
    • Cardiac disease (rheumatic valvular disease, endocarditis, arrhythmias, cardiac surgery)
    • Diabetes, metabolic syndrome
    • Transient ischemic attacks (brief warning episodes of dysfunction (<24 hours); a precursor of major stroke in more than 1/3 of patients)
  6. Pathophysiology
    • Cerebral anoxia: lack of O2 supply to brain (irreversible anoxic damage to brain begins after 4-6 minutes)
    • Cerebral infarction: irreversible cellular damage
    • Cerebral edema: accumulation of fluids within brain; causes further dysfunction; elevates intracranial pressures - can result in herniation and death
  7. Neurovascular Clinical Syndrome
    Characteristic signs and symptoms associated with occlusion of specific cerebral vessels 

    • Internal carotid artery (ICA) syndrome
    • Vertebrobasilar artery syndrome
  8. Internal Carotid Artery (ICA) Syndrome
    • ICA arises off common carotid artery 
    • Gives off opthalmic branch
    • Terminates into ant cerebral artery (ACA) and middle cerebral artery (MCA)
    • Occlusions - produce s/sx of MCA involvement with reduced levels of consciousness
    • ACA may also be affected
    • Lesions involving ACA and MCA distributions may produce massive edema, brain herniation, and death
  9. ACA Syndrome
    • ACA: supplies anterior 2/3 of medial cerebral cortex
    • Occlusions proximal to ant communicating artery produce minimal deficits due to collateral circulation (circle of Willis)
  10. MCA Syndrome
    MCA: supplies lat cerebral cortex, basal ganglia, and large portions of internal capsule
  11. Vertebrobasilar Artery Syndrome
    • 2 vertebral arteries arise of subclavian arteries and supply ventral surface of medulla and post inf aspect of cerebellum 
    • Then joint to form basilar artery at junction of pons and medulla
    • Basilar artery: supplies ventral portion of the pons and terminates in the post cerebral artery (PCA)
  12. Vertebrobasilar Artery Syndrome: Syndromes
    • Medial medullary syndrome
    • Lateral medullary (Wallenberg's) syndrome 
    • Basilar artery syndrome
    • Medial inferior pontine syndrome
    • Lateral inferior pontine syndrome
    • PCA syndrome
  13. Medial Medullary Syndrome
    Occlusion of vertebral ant branch of lower basilar artery
  14. Lateral Medullary (Wallenberg's) Syndrome
    Occlusion of vertebral, post inf cerebellar, or basilar artery
  15. Basilar Artery Syndrome
    • Produces brainstem signs/symptoms and PCA signs and symptoms
    • Locked-in syndrome = basilar artery occlusion at the level of the pons
  16. Medial Inferior Pontine Syndrome
    Occlusion of paramedic branch of basilar artery
  17. Lateral Inferior Pontine Syndrome
    Occlusion of ant inf cerebellar artery
  18. PCA Syndrome
    • PCA and post communicating arteries supply the midbrain, temporal lobe, diencephalon, and post 1/3 of cortex
    • Occlusions prox to post communicating artery produce minimal deficits owing to collateral circulation
  19. Sequential Recovery Stages
    • Stage 1: initial flaccidity, no voluntary movement
    • Stage 2: emergence of spasticity, hyperreflexia, synergies (mass patterns of movement)
    • Stage 3: voluntary movement possible, but only in synergies; spasticity strong 
    • Stage 4: voluntary control in isolated joint movements emerging, corresponding decline of spasticity and synergies 
    • Stage 5: increasing voluntary control out synergy, coordination deficits present
    • Stage 6: control and coordination near normal
  20. Examination
    Signs of increased intracranial pressure

    Level of consciousness, cognitive function

    • Speech and communication:
    • Aphasia with lesions of parieto-occipital cortex of dominant hemisphere (typically L hemisphere) 
    • Perceptual deficits with lesions of parietal lobe of non dominant hemisphere (typical R hemisphere)

    • Behaviors:
    • L hemisphere lesions (R hemiplegia) = slow, cautious, hesitant, and insecure
    • R hemisphere (L hemiplegia) = impulsive, quick, indifferent, often exhibit poor judgement and safety
  21. Sensory Deficits
    • Superficial, proprioceptive and combined sensations of contralateral extremities, trunk and face
    • Hearing, vision - examine for homonymous hemianopsia
    • CN function with brainstem, vertebrobasilar strokes (psudobulbar palsy)
  22. Gait: Typical Deficits at the Hip
    • Poor hip position (retracted, flexed)
    • Trendeenburg limp (weak abductors)
    • Scissoring (spastic adductors)
    • Insufficient pelvic rotation during swing
    • Weak hip flex during swing -- may yield circumducted gait, ER with add, backward leaning of trunk or exaggerated flex synergy
  23. Gait: Typical Deficits at the Knee
    • Weak knee extensors (knee flexes during stance) 
    • May result in compensatory locking of knee in HTN
    • Spastic quads may also yield a hyperextended knee
  24. Gait: Typical Deficits at the Ankle
    • Footdrop
    • Equinus gait (heel does not touch down)
    • Varus foot (weight on lat side of foot) or equinovarus position
  25. Fugl-Meyer Assessment of Physical Performance (FMA)
    • Provides objective criteria for scoring of movements 
    • 0 = cannot perform → 2 = fully performed

    Includes subtests for UE function, LE function, balance, sensation, ROM and pain
  26. NIH Stroke Scale
    Provides measurements of acute cerebral infarction
  27. Postural Assessment Scale for Stroke Patients (PASS)
    Standardized assessment of postural control and balance in its recovering from stroke
  28. Stroke Impact Scale
    Brief assessment of physical and social functioning after stroke
  29. Functional Independence Measure (FIM)
    18 items of physical (functional mobility and basic ADL) psychological and social functioning
  30. Functional Assessment Measure (FAM)
    • Additional functional measures from FIM
    • Community access
    • Instrumental ADL
    • Safety
    • Employability
    • Adjustment
  31. PT Goals, Outcomes and Interventions
    • Monitor changes associated with recovery and inactivity
    • Promote awareness, active movement, and use of hemiplegic side (remediation-facilitation approach)
    • Improve postural control, symmetry, balance
    • Task-specific training
    • Respiratory and oromotor function
    • Functional cardiorespiratory endurance 
    • Isokinetic training
    • Locomotor training using body weight-support (BWS) and motorized treadmill training (TT)
    • EMG - biofeedback training
    • FES
    • Contraint-induced movement therapy for UE's
  32. PT: Changes Associated with Recovery and Inacivity
    • Maintain ROM and prevent deformity through positioning, PROM, mobilization
    • Maintain skin integrity
    • Avoid traction injuries to arm 
    • Teach sensory compensation strategies for sensory and perceptual losses
    • Strengthen all available muscles
  33. PT: Promote Awareness, Active Movement, and Use of Hemiplegic Side
    • Promote normalization of tone through activities
    • Promote selective movement control (out-of-synergy movements) of involved extremities
    • Emphasize functional patterns of movement
  34. PT: Respiratory, Oromotor Function, Cardiorespiratory Endurance
    • Improve chest expansion, diaphragmatic breathing pattern
    • Oromotor training
    • Aerobic conditioning
  35. PT: Isokinetic Training
    Useful to improve timing deficits, velocity control of movement
  36. PT: EMG-Biofeedback Training
    • Decrease firing in spastic muscles
    • Increase firing in paretic muscles
    • Improve motor control
  37. PT: FES
    • Stimulate muscle action
    • Reduce spasticity
    • Substitute for an orthosis
  38. Patients with L Hemisphere Lesions (R Hemiplegia): Guidelines
    • Develop appropriate communication base (words, gestures, pantomime - assess level of understanding)
    • Give frequent feedback and support
    • Don't underestimate ability to learn
  39. Patients with R Hemisphere Lesions (L Hemiplegia): Guidelines
    • Use verbal cues (demonstrations or gestures may confused pts with visuospatial deficits)
    • Give frequent feedback 
    • Focus on slowing down and controlling movement
    • Focus on safety (may be impulsive)
    • Avoid environmental (spatial) clutter
    • Do not overestimate ability to learn
Card Set:
Chapter 2: Cerebrovascular Accident (CVA Stroke)
2015-03-10 23:04:51
NPTE: Chapter 2
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