Las entrevistas a dos profesores y matrices DOFA

The pathogenesis of pain occurring in the hemiparetic shoulder are all the factors that cause pain in the normal mechanically injured shoul-der. This includes tendonitis, bursitis, partial tear of the rotator cuff, complete tear of the rotator cuff, adhesive capsulitis (the “frozen shoul-der”), and reflex sympathetic dystrophy, currently termed complex regional pain syndrome,⁶which is discussed further in Chapter 12.

REFERENCES

1. Davis PJ. Shoulder Problems Associated with Hemiplegia. “Steps to Follow Guide to the Treatment of Adult Hemiplegia.” New York: Springer-Verlag, 1985;206–240.

2. Clark FJ, et al. Proprioception with the proximal interphalangeal joint of the index finger. Brain 1986;19:1195–1208.

3. Johnsson H. Role of knee ligaments in proprioception and regulation of mus-cle stiffness. J Electromyogr Kinesiol 1991;1:158–179.

4. Johansson H, et al. Receptors in the knee joint ligaments and their role in the biomechanics of the joint. Crit Rev Biomed Eng 1991;18:341–368.

5. Brumagne S, et al. The role of paraspinous muscle spindles in lumbosacral posi-tion sense in individuals with and without low back pain. Spine 2000;

25:989–994.

6. Cailliet R. Shoulder Pain, third edition. Philadelphia: F.A. Davis, 1991.

128 TREATMENT OF OUTPATIENTS

12 Complex Regional Pain Syndrome

Rene Cailliet

One of the ominous causes of painful shoulder is shoulder-hand-finger syndrome, which is a variant of complex regional pain syndrome (CRPS). The relationship is arbitrary, because CRPS is a neurologic syn-drome of the autonomic nervous system, and shoulder-hand synsyn-drome is a secondary complication of painful hemiplegic shoulder, which is considered to be reflex sympathetic dystrophy (RSD), as it has responded to sympathetic nerve blocks and has many manifestations of CRPS.

The shoulder-hand-finger syndrome occurs in an estimated 12.5%

of post-hemiplegic patients with painful shoulders.¹The relationship to the shoulder is that most patients who develop the RSD syndrome have a residual hemiplegic shoulder that is dependent and unable to be elevated above heart level. These patients also have a paretic hand that remains flexed with inability to extend wrist and fingers (Figure 12.1), but there are other pathoanatomic factors that occur.

This syndrome can be over- or underdiagnosed in any painful shoul-der from whatever cause. What must be ascertained is the presence of objective neurovascular changes that are noted rather than merely relying on symptomatology.

This syndrome usually has its onset between the first and third month after the onset of stroke. In the medical literature, the onset of shoulder-hand syndrome has time factors as shown in Table 12.1.^2,3

The patient’s hand suddenly becomes swollen, with marked limita-tion of range of molimita-tion. Pain, at first, is not prominent, if at all present, and therefore the swollen hand is often ignored. In the 60–80% of patients who develop a painful shoulder after a hemorrhagic stroke, the hand swelling painlessly appears in only 12.5% of patients.

The shoulder-hand syndrome was initially considered a variant of RSD when, in 1958, the symptoms were relieved by a sympathetic stel-late nerve block, implicating the autonomic nervous system.⁴These blocks relieved the hand findings but had no effect on the symptoms and findings of the shoulder. There were few well-controlled and

blinded studies, therefore leading to empirical treatments. Oral steroids did have a beneficial effect when combined with physical therapeutic modalities.¹

It is safe to this point in time to say that the cause of CRPS and hence the shoulder-hand syndrome remains unclear. Its objective diagnosis 130 TREATMENT OF OUTPATIENTS

Figure 12.1 Shoulder and hand

“pumps.” The shoulder action pumps arterial and venous blood as well as lymph. The hand also “pumps”

arterial and venous blood and lymph toward the heart.

(Reprinted with permission from Cailliet R. The Shoulder in Hemi-plegia. Philadel-phia: F.A. Davis, 1980;108.)

Table 12.1 Time to Onset of Shoulder-Hand Syndrome Months Percentage of Patients

0–1 0

1–2 28

2–3 37

3–4 16

4–5 17

5–6 2

also remains unclear. Merely the dependency of the hand cannot be the etiology, as many patients who sustain this hand dependency do not have residual symptoms of the syndrome, but it remains a factor that must be addressed.

The hand, which remains in the palmar flexed position, undergoes venous obstruction. This has been verified by contrast medium injected into the hand veins and x-rayed in neutral and forcefully flexed posi-tions. The wrist position and not the spasticity of the upper extremity muscles must be considered a causative factor, as often there is no sig-nificant spasticity at this stage of the syndrome and in fact the extrem-ity may still be in the flaccid stage.

The presence of Raynaud’s vasculitis, systemic lupus erythematosus, and other neurovascular entities must be considered and differentiated.

STAGES

The early stage of shoulder-hand syndrome is acute swelling of the hand, usually on the dorsum of the fingers where the creases of the fin-gers at the metacarpal phalangeal and proximal interphalangeal joints is initially noted. The original edema is soft and can be indented by pressure from the examiner. The normally visible extensor tendons are no longer seen. The edema is localized and ends just proximal to the wrist.

The venous supply of the hand is on the dorsum, and lymph that exudes from obstructed veins fills the space between the extensor ten-dons and the bones, initially being responsible for the limited flexion (Figure 12.2).

The collateral ligaments of the metacarpal-phalangeal joint normally are slack when the fingers are extended to their physiologic limits to permit full flexion of that joint (Figure 12.3).

The edema under the extensor tendon also extends under the col-lateral ligaments, thus extending them before there is full flexion of the joint and maintaining some flexion.⁵The edema contains protein that converts into a cobweb-like scar tissue that adheres the tendons to the joint capsules. As gradual adhesive limitation of joint movement occurs, the nutrition to the cartilage is diminished, causing atrophic degenerative changes.

Hyperesthesia appears early in the onset of CRPS. In fact, it may be the original symptom and sign that indicates its advent. As the shoul-der-hand (CRPS) syndrome progresses, the skin changes to a pink color, indicating vasomotor dilation. This is particularly noted when the hand is held dependent for prolonged periods and diminishes when elevated. The skin feels warm and is moist (hyperhydrosis). Joint range

COMPLEX REGIONAL PAIN SYNDROME 131

132 TREATMENT OF OUTPATIENTS

Figure 12.3

Collateral ligaments of the metacarpal-phalangeal joints.

A. With the joint extended, the col-lateral ligaments are slack and become taut at full flexion (F) (B). C. In the edematous hand, the fluid migrates between these col-lateral ligaments and prevents full extension of the ligaments and thus decreased flexion of the finger.

(ET = extensor ten-don; MC = metacar-pal; PP = proximal phalanx.)

Figure 12.2 Venous supply to the hand. The veins are on the dor-sum of the hand, and the edema that forms is under the extensor tendons as well as over them. (DP = dorsalis pedis; MC = metacarpal; MP = metaphalangeal; PP = proximal phalanx.)

of motion, passive and active, is initially noted in supination of the wrist and forearm and metacarpal-phalangeal flexion. Gradually, the limitation occurs in distal phalangeal flexion and abduction of the fingers (Figures 12.4 and 12.5).

In evaluating this impaired joint function, it must be noted that the metacarpal-phalangeal joint is an incongruous joint and that flexion is not around a fixed axis but rather is a downward glide that precedes flexion (Figure 12.6). This is important in evaluating range-of-motion testing and, ultimately, in treatment.