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Rehabilitation 國國國 _CVA R 國國國

Rehabilitation國考題 cva

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  1. 1. Rehabilitation _CVA R
  2. 2. Stroke
  3. 3.
  4. 4. 56 (101-2-65,100-2-56) 1. basal ganglion 2. thalamus 3. cerebellum 4. pons
  5. 5. ? (95-1-55) 1. anterior cerebral artery) 2. middle cerebral artery 3. posterior cerebral artery 4. vertebral artery
  6. 6. 55 (95-2-46) anterior cerebral artery internal carotid artery basilar artery middle cerebral artery
  7. 7. ABCD (98- 1-67)
  8. 8. 49 CT (95-1-96) Thalamic hemorrhage Putaminal hemorrhage Pontine hemorrhage Internal capsular hemorrhage
  9. 9.
  10. 10. ? (103-1-70) 1. (Brunnstrom stage) 2. (functional independence measure) 3. (Barthel index) 4. (Kenny self care evaluation)
  11. 11. palmar prehension Brunnstroms stage (96-2- 57) Stage II Stage III Satge IV
  12. 12. (103-2-64) 1. poor sitting balance 2. incontinence 3. mental change 4. spasticity
  13. 13. Poor prognosis associated also with: No measurable grasp strength by 4 weeks Severe proximal spasticity Prolonged flaccidity period Late return of proprioceptive facilitation (tapping) response > 9 days Late return of proximal traction response (shoulder flexors/adductors) > 13 days
  14. 14. Brunnstrom (1966, 1970) and Sawner (1992) also described the process of recovery following stroke-induced hemiplegia. The process was divided into a number of stages: 1. Flaccidity (immediately after the onset) No voluntary movements on the affected side can be initiated. 2. Spasticity appears. Basic synergy patterns appear. Minimal voluntary movements may be present. 3. Patient gains voluntary control over synergies. Increase in spasticity.
  15. 15. 4. Some movement patterns out of synergy are mastered (synergy patterns still predominate). Decrease in spasticity. 5. If progress continues, more complex movement combinations are learned as the basic synergies lose their dominance over motor acts. Further decrease in spasticity. 6. Disappearance of spasticity. Individual joint movements become possible and coordination approaches normal. 7. Normal function is restored.
  16. 16. Upper Lower Hand I flaccid II spasticity developing Associated movement/reaction Little or no active finger flexion III Synergy pattern Muscle tone Triple extension(lock knee tip toe ankle inversion) Mass grasp Use hook grasp but no release No voluntary extension
  17. 17. Upper Lower Hand IV Block synergy pattern Placing the hand behind the body Elevated the arm to supination Ankle dorsiflexed Knee isolated extened Lateral prehension( ) release by thumb movement Semivoluntary finger extension V Block synergy pattern Arm-raised forward and overhead supination- pronation Ankle dorsiflexion Knee isolated flexed Ankle Inversion/eversion Palmar prehension VI RAM o r
  18. 18. 2 spasticity passivedorsiflexion 50% range of motion, ROM modified Ashworth scale (103- 1-55) 1. 1 2. 1+ 3. 2 4. 4
  19. 19. Theories for stroke rehabilitation Brunnstrom theory PNF theory Motor relearning theory Bobath theory: NDT: Neural-Developmental Theory
  20. 20. 06/13/15 Jenny 29 Brunnstrom Theory Aim To encourage the return of voluntary movement in hemiplegia patient through the use of reflex activity and a range of sensory stimulation. The choice of stimulation varies depending on which stage the patient has reached in the recovery process.
  21. 21. Brunnstrom Theory Treatment The process is employed until the primitive synergies are established, then facilitation is used to develop some voluntary control. The preparation for walking should be emphasized early but that extensive walking should be postponed in order to avoid the development of a poor gait pattern
  22. 22. 06/13/15 Jenny 31 PNF Theory Proprioceptive Neuromuscular Facilitation Primary for the patient with neuromuscular dysfunction Aim to promote movement and functional synergies of movement by maximizing peripheral inputby maximizing peripheral input
  23. 23. 06/13/15 Jenny 32 PNF Theory Basis of practice People who move normally have passed through a developmental sequencedevelopmental sequence Diagonal and spiral patternsDiagonal and spiral patterns of active and passive movements are encouraged Treatment Providing appropriate sensory stimulus Following activities in a developmental sequence Patterns and techniques
  24. 24. 06/13/15 Jenny 33 Motor relearning Theory By Carr and Shepherd Aim To enable the disabled person to learn how toto learn how to perform or improve performanceperform or improve performance of actions critical to everyday life. Utilizing theories of learningtheories of learning, in particular the use of practice and knowledge of results to encourage people to learn and self monitor Knowledge of biomechanics for analyzing movements and performance of tasks
  25. 25. 06/13/15 Jenny 34 Motor relearning Theory Basis of practice The motor control of posture and movement are interrelated and that appropriate sensory input will help modulate the motor response to a task The program is based on Elimination of unnecessary muscle activity Feedback Practice The link between postural adjustment and movement Task analysis and measurement are viewed as essential elements of the framework.
  26. 26. 06/13/15 Jenny 35 Motor relearning Theory Treatment Movement analysis and training follow the four steps Analysis of the task Practice of the missing components Practice of the task Transference of training A series of task has been chosen because learning by normal subjects has been shown to be task-specific with minimal carry-over from one activity to another
  27. 27. 06/13/15 Jenny 36 Bobath theory: NDT Aim To improve the quality of movement on the affected sidethe quality of movement on the affected side Key point controlKey point control is to allow patients the experience of normal afferent input Basis of practice The movement will be abnormal if it stems from a background of abnormal toneabnormal tone Performing abnormal movements will reinforce more abnormal movements Tone could be influenced by altering the position or movement of proximal joints of the body
  28. 28. 06/13/15 Jenny 37 Bobath Theory: NDT Treatment Treatment centre around the facilitation of corrected movement by a therapist who handles the body at key points of controlkey points of control In recent years treatment has become more activeactive , dynamic and functionally directed, dynamic and functionally directed.. Movement are not isolated to individual joints but take place in patterns
  29. 29. 06/13/15 Jenny 38 Bobath theory: NDT To help the patient to gain control over the released patterns of spasticity by their own inhibition Auto-inhibition Give patient normal kinematics sensation input to facilitated normal posture and movement Muscle strengthening is notnot viewed as part of treatment There are no set Bobath exercise
  30. 30.
  31. 31. bisection test (100-1-55)
  32. 32. (hypesthetic) (left neglect) (left hemianopia) confrontation test (copy test) spontaneous drawing test behavioral inattention test (line bisection test) (cancel- lation test)
  33. 33.
  34. 34. (pure neglect) (pure hemianopia)
  35. 35. hemineglect (97-1-55) basal ganglion frontal lobe temporoparietal lobe occipital lobe
  36. 36. (96-1-58) left hemianopsia left hemineglect left side apraxia left eye blindness
  37. 37. (100-2-59) 70-80% spastic phase flaccid phase
  38. 38. POSTSTROKE SHOULDER PAIN 7084% of stroke patients with hemiplegia have shoulder pain with varying degrees of severity. The majority (85%) will develop it during the spastic phase of recovery. The most common causes of hemiplegic shoulder pain are complex regional pain syndrome type I (see below) and soft tissue lesions (including plexus lesions).
  39. 39. Reflex sympathetic dystrophy (100-2-57)
  40. 40. Complex Regional Pain Syndrome Type I (CRPS Type I) Also known as reflex sympathetic dystrophy [RSD], shoulder-hand syndrome, or Sudeck atrophy. Disorder characterized by sympathetic-maintained pain related sensory abnormalities abnormal blood flow abnormalities in the motor system and changes in both superficial and deep structures with trophic changes.
  41. 41. Stages Stage 1 (acute): Lasts 3 to 6 months. burning pain diffuse swelling/edema exquisite tenderness hyperpathia and/or allodynia vasomotor changes in hand/fingers (increased nail and hair growth, hyperthermia or hypothermia, sweating).
  42. 42. Stages Stage 2 (dystrophic): Lasts 3 to 6 months pain becomes more intense and spreads proximally skin/muscle atrophy brawny edema cold insensitivity brittle nails/nail atrophy, decreased ROM, mottled skin early atrophy, and osteopenia (late)
  43. 43. Stages Stage 3 (atrophic): pain decreases trophic changes occur: hand/skin appear pale and cyanotic with a smooth, shiny appearance, feeling cool and dry bone demineralization progresses with muscula weakness/atrophy, contractures/flexion deformities of shoulder/ hand, tapering digits no vasomotor changes.
  44. 44. subluxation (99-2-56) internal rotation complex regional pain syndrome type 2 deltoid supraspinatus
  45. 45. Shoulder Subluxation Treatment Shoulder sling use is controversial. Pros: may be used when patient ambulates to support extremity (may prevent upper extremity trauma, which in turn may cause increase pain or predispose to development of RSD). Cons: may encourage contractures in shoulder adduction/internal rotation, elbow flexion(flexor synergy pattern). Other widely used treatments for shoulder subluxation: Functional electrical stimulation (FES) Arm board, arm trough, lapboardused in poor upper-extremity recovery, primary wheelchair users. Arm board may overcorrect subluxation. Overhead slingsprevents hand edema (may use foam wedge on arm board).
  46. 46. hemiparetic gait (101-1-56) genu valgum circumduction co-contraction inversion