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INTRODUCCIÓN

In document FACULTAD DE CIENCIAS DE LA SALUD (página 8-11)

Extremity after Hemorrhagic Stroke

Rene Cailliet

Restoration of function of the hand, fingers, and wrist after completed stroke must take into consideration the neurologic aspect of the distal portion of the upper extremity. The flexor synergy that occurs as com-pared to the extensor synergy of the lower extremity has the follow-ing components.

The shoulder girdle in the hemiplegic spastic phase has been addressed in Chapter 11. As noted, the elbow flexes, the forearm pronates, the wrist flexes, the fingers flex and adduct, and the thumb flexes in conjunction with internal rotation of the shoulder.

Although the flexor synergy is predominant, occasionally, an exten-sor synergy of the upper extremity can occur in which the elbow extends with pronation of the forearm, the wrist extends somewhat, the fingers flex with adduction, and the thumb adducts in flexion. It is apparent that in the extensor synergy only the elbow and forearm varies from the flexor synergy.

On analysis, any treatment approach must address activities of daily living. Thus, therapeutic approaches should consider function rather than isolation of individual muscle groups, although the latter, obvi-ously, must be evaluated in examining the difficulties of the patient performing activities of daily living.

Research in animals who have been selectively impaired from cor-tical ablation have been noted to undergo corcor-tical reorganization. This reorganization originally has been in the sensory sphere, but, more recently, complex reorganization of the motor cortex has been described.1–3

In the subacute stage of the completed stroke, there is a decrease in motor cortex excitability and in the size of the cortical representation area of the paretic muscles in the premotor cortex.4,5This decrease may be the result of disuse but could be due to damage of the neural

structures of the cortex. Constraint-induced (CI) therapy has been shown in controlled studies1to improve function and also increase the area of cortical representation in the premotor cortex.

This does not mean that CI therapy is the only or the best manner of providing functional rehabilitation, but it does open an encouraging aspect of therapeutic involvement, with objective measurement of the size of the active cerebral cortex that has been damaged by stroke. As these studies have been conducted months after stroke, they also lend credence to pursuing treatment for longer periods than is frequently undertaken.

CI therapy involves immobilization of the normal contralateral arm and hand while the patient undergoes rehabilitation treatment for the impaired arm. The patients in the Liepert et al. study,1which lasted 12 days, were able to extend their wrists 20 degrees and their fingers 10 degrees, and they were able to walk during the period of shoulder and arm immobilization. Excluded from the study were patients with seri-ous medical problems, global aphasia, cognitive impairment that pre-cluded the ability to comply with instructions in motor testing, and epilepsy and those wearing a cardiac pacemaker. The latter was because these patients were being studied with magnetic resonance imaging instruments.

The patients were immobilized comfortably with a shoulder, arm, and hand-finger splint for 9 hours a day. They were released only dur-ing sleepdur-ing hours. Durdur-ing their immobilization, they underwent sev-eral periods of occupational physical therapy in hand-finger activities.

The type of therapy was the standard.6–8

Rehabilitation modalities of hand function vary regarding “exercise therapy,” which aims at restoring individual hand-finger function.

Many evolved in treatment for cerebral palsied children but ultimately were applied to adults and stroke patients.

Fay9suggested the use of pathologic and unlocking reflexes. The Bobaths10also developed a neurodevelopmental treatment program in which they postulated that normal motor performance was inhibited by sensory disturbances, spasticity, disturbances of postural reflex mechanisms, and loss of selective movement patterns. Brunnstrom11 proposed muscle re-education using reflex training. She defined the associated reactions of hemiplegia as involuntary limb movements revoked by yawning, sneezing, and coughing, and used the labyrinthic and tonic neck reflexes. She also used resistance to the “normal”

extremity and tapping and stroking for sensory stimulation.

Knott,12quoting Kabat, developed the neuromuscular facilitation system in which the total (synergistic) patterns were invoked and resistance given to the portion of the extremity desired. These techniques included maximum resistance, repetition, traction, and 144 TREATMENT OF OUTPATIENTS

use of verbal commands. Basic spiral diagonal patterns of movement were used.

Rood stressed sensory input to enhance motor response.13She stim-ulated skin receptors by ice application, stroking, and brushing. Bas-majian14used biofeedback. All of these techniques are described in Chapter 4 of Basmajian’s text.15

Stern16studied the value of facilitation techniques versus a tradi-tional type of exercise program and showed that either or both bene-fited the patient equally. Basmajian15summarized the value of exercise programs as “Most current hemiplegic exercise programs tend to be an eclectic combination of traditional methods, neuromuscular facilitation techniques, biofeedback training and sensorimotor therapy.” With magnetic resonance imaging PETY studies, as stated by Liepert et al.,1 differentiation may evolve that will standardize and equate benefit from one of the current programs.15

Immediately after the “completion” of a stroke, there is paralysis or paresis of the upper extremity musculature, with initial weakness noted in the distal musculature, especially the intrinsics of the hand. Gradu-ally, the weakness occurs in the forearm, arm, and then shoulder, in that order. The deep tendon reflexes are lost, and hypotonia occurs.

Sensory dysfunction of pain sensation, proprioception, light touch, and vibration occurs. Two-point discrimination, stereognosis, and graphesthesia are lost, which makes the hand and fingers nonfunc-tional. If there are perceptual and visual dysfunctions, they also adversely affect the hand. Spontaneous motor recovery occurs chiefly within the initial 2–3 months after the stroke, with the first voluntary movements noted 6–33 days after onset. Recovery at first is that of flexor synergy, which then leads to return of voluntary control of the components or all of the synergy. The intent of therapy is this return from involuntary synergy on stimulus to voluntary control.

Return of meaningful, voluntary control of hand function varies from 20% to 40% of patients having total recovery to the remainder having no functional recovery.17Carroll18stated in 1986 that if there was no motor functional return in the first week, it was considered unlikely that the patient would regain full use of the involved hand.

More recent studies have not refuted this opinion, but from review of plasticity in recent neurophysiologic studies, this pessimistic prognosis may change.

REFERENCES

1. Liepert J, et al. Treatment-induced cortical reorganization after stroke in humans. Stroke 2000;31:1210–1216.

FLEXOR SYNERGY OF THE UPPER EXTREMITY 145

2. Merzanich NM, et al. Somatosensory cortical map changes following digital amputation in adult monkeys. J Comp Neurol 1984;224:591–605.

3. Weiller C, et al. Functional reorganization of the brain in recovery from stria-tocapsular infarction in man. Ann Neurol 1992;32:463–472.

4. Cacinelli P, et al. Post-stroke reorganization of brain motor output to the hand:

A 2–4 month followup with focal magnetic transcranial stimulation. Elec-tromyogr Clin Neurophysiol 1997;105:438–450.

5. Rossini PM, et al. Hand motor cortical area reorganization in stroke: A study with iMRI, MBG, and TCS maps. Neuroreport 1998;9:2141–2146.

6. Duncan PW. Synthesis of intervention trials to improve motor recovery fol-lowing stroke. Top Stroke Rehabil 1997;3:1–20.

7. Twitchell TH. The restoration of motor function following hemiplegia in man.

Brain 1951;74:443–480.

8. Bard O, Hirschberg GG. Recovery of voluntary motor recovery in upper extremity following hemiplegia. Phys Med Rehabil 1965;46:567–572.

9. Fay T. The use of pathological and unlocking reflexes in the rehabilitation of spastics. Am J Phys Med 1954;33:347–352.

10. Bobath B. Treatment of adult hemiplegia. Physiotherapy 1977;63:310–313.

11. Brunnstrom S. Movement Therapy in Hemiplegia. New York: Harper & Row, 1970.

12. Knott M, Voss DE. Proprioceptive Neuromuscular Facilitation. New York: Harper

& Row, 1968.

13. Stockmeyer SA. An interpretation of the approach of Rood to the treatment of neuromuscular dysfunction. Am J Phys Med 1967;46:900–956.

14. Basmajian JV. Biofeedback in rehabilitation: A review of principles and prac-tices. Arch Phys Med Rehabil 1981;62:469–475.

15. Basmajian JV. Therapeutic Exercises, fourth edition. Baltimore: Williams & Wilkins, 1984.

16. Stern PH, et al. Effects of facilitation exercise techniques in stroke rehabilita-tion. Arch Phys Med Rehabil 1970;51:526–531.

17. Lieberman JS. Hemiplegia: Rehabilitation of the Upper Extremity. In: Kaplan PE, Cerullo LJ (eds), Stroke Rehabilitation. Boston: Butterworth, 1986;95–117.

18. Carroll D. Hand function in hemiplegia. J Chron Dis 1986;18:493–500.

146 TREATMENT OF OUTPATIENTS

14 Lower Extremity

In document FACULTAD DE CIENCIAS DE LA SALUD (página 8-11)

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