Neurologic Impairment and Recovery
Infarction of the cerebral cortex in the region of the brain supplied by the middle cerebral artery (MCA) or one of its branches is most commonly responsible for stroke. It supplies the area of the cerebral cortex responsible for hand function; the anterior cerebral artery supplies the area responsible for lower extremity motion (Figure 12–11). The typical clinical picture following MCA stroke is contralateral hemianesthesia (decreased sensation), homonymous hemianopia (visual field deficit), and spastic hemiplegia with more paralysis in the upper extremity than in the lower extremity. Because hand function requires relatively precise motor control, even for activities with assistive equipment, the prognosis for the functional use of the hand and arm is considerably worse than for the leg. Return of even gross motor control in the lower extremity may be sufficient for walking.
Cerebral artery circulation.
Infarction in the region of the anterior cerebral artery causes paralysis and sensory loss of the opposite lower limb and, to a lesser degree, the arm.
Patients who have cerebral arteriosclerosis and suffer repeated bilateral infarctions are likely to have severe cognitive impairment that limits their general ability to function even when motor function is good.
After stroke, motor recovery follows a fairly typical pattern. The size of the lesion and the amount of collateral circulation determine the amount of permanent damage. Most recovery occurs within 6 months, although functional improvement may continue as the patient receives further sensorimotor reeducation and learns to cope with disability.
Initially after a stroke, the limbs are completely flaccid. Over the next few weeks, muscle tone and spasticity gradually increase in the adductor muscles of the shoulder and in the flexor muscles of the elbow, wrist, and fingers. Spasticity also develops in the lower extremity muscles. Most commonly, there is an extensor pattern of spasticity in the leg, characterized by hip adduction, knee extension, and equinovarus deformities of the foot and ankle (Figure 12–12). In some cases, however, a flexion pattern of spasticity occurs, characterized by hip and knee flexion.
Equinovarus deformities of the feet in a patient with spasticity.
Whether the patient recovers the ability to move one joint independently of the others (selective movement) depends on the extent of the cerebral cortical damage. Dependence on the more neurologically primitive patterned movement (synergy) decreases as selective control improves. The extent to which motor impairment restricts function varies in the upper and lower extremities. Patterned movement is not functional in the upper extremity, but it may be useful in the lower extremity, where the patient uses the flexion synergy to advance the limb forward and the mass extension synergy for limb stability during standing.
The final processes in sensory perception occur in the cerebral cortex, where basic sensory information is integrated to complex sensory phenomena such as vision, proprioception, and perception of spatial relationships, shape, and texture. Patients with severe parietal dysfunction and sensory loss may lack sufficient perception of space and awareness of the involved segment of their body to ambulate. Patients with severe perceptual loss may lack balance to sit, stand, or walk. A visual field deficit further interferes with limb use and may cause patients to be unaware of their own limbs.
Medical intervention in the treatment of a stroke is most effective when initiated within 3 hours from the onset of symptoms. However, pharmacologic intervention may play a role, although limited, if administered within 24 hours of onset.
Tissue Plasminogen Activator (t-PA) (Also Known as Recombinant t-PA or Recombinant Tissue-Type Plasminogen Activator [rt-PA])
The efficacy of intravenous t-PA was established in two randomized, double-blind, placebo-controlled studies published in combination by the National Institute of Neurological Disorders and Stroke (NINDS). At 3 months after stroke, approximately 12% more patients in the t-PA group experienced a cure of symptoms relative to those who did not receive it. The risk of intracerebral hemorrhage in the t-PA group was 6% (50% of which were fatal), compared to 0.6% in the placebo group. Despite the differences in hemorrhage rates, there were no differences in mortality (17% in the t-PA group versus 21% in the placebo group).
Key points about the administration of thrombolytic agents include the following:
They must be administered within 3 hours of symptom onset. The time of onset in patients who wake up with symptoms or those who cannot describe accurately the time of their symptom onset is when they were last known to be well.
An imaging study of the head (CT scan or magnetic resonance imaging [MRI]) must be performed prior to treatment to rule out hemorrhage as a cause of symptoms.
Blood pressure should be lower than 185 systolic and 110 diastolic. Agents such as labetalol may be used to lower the blood pressure for the purposes of treatment.
Blood must be tested for platelet count (should be >100,000), international normalized ratio (INR) (many recommend it be <1.6), partial thromboplastin time (PTT) (many recommend <40), and glucose (should be 50–400). INR has particular relevance because individuals properly treated with warfarin to diminish the incidence of stroke (eg, those with atrial fibrillation) may not be candidates for thrombolytic treatments.
Prourokinase (Also Known as Recombinant Prourokinase, or r-pro-UK)
This intraarterial therapy requires the involvement of a skilled interventionist. The time window is 6 hours from symptom onset. In addition, and in contrast to the NINDS t-PA study, patients with a CT scan showing over a third involvement of the MCA territory as seen on CT scan are not eligible for treatment. The absolute percentage increase in patients with slight or no disability at 3 months was 15% in the prourokinase group compared with the placebo group. The hemorrhage rate in the prourokinase group was 10% versus 2% in subjects who received placebo. No difference was noted, however, in mortality (25% in the prourokinase group versus 27% in the placebo group).
This therapy may be especially useful for patients who arrive later than 3 hours from symptom onset and who have less than a third involvement of the MCA territory on initial scan.
The Chinese Acute Stroke Trial (CAST) and the International Stroke Trial (IST) are two large studies evaluating the use of aspirin (160–300 mg/day) within 48 hours of ischemic stroke symptom onset. Compared to no treatment, there was approximately a 1% absolute reduction in stroke and death in the first few weeks. At further time points (eg, 6 months), there was a similar absolute reduction of approximately 1% in death or dependence.
An ongoing phase III study of the efficacy of abciximab (ReoPro) in acute stroke is being conducted. A phase II study of 400 patients found an 8% absolute reduction in poor outcomes at 3 months (P < 0.05). Symptomatic intracranial hemorrhage occurred in 3.6% of patients on abciximab and in 1.0% of patients on placebo.
No studies have evaluated use of warfarin for the acute treatment of stroke.
At this time, only one randomized trial showed benefit for heparins or heparinoids in acute ischemic stroke. In that study, no benefit was seen at 10 days or 3 months, only at 6 months. Other large studies failed to find benefit of heparin or heparinoids, either intravenous or subcutaneous, at 3 months. An exploratory post hoc analysis of one intravenous low-molecular-weight heparin randomized study suggested benefit in patients with severe large vessel (eg, carotid) atherosclerosis; however, the authors conclude that these findings need to be properly evaluated in a prospective randomized trial.
To walk independently, the hemiplegic patient requires intact balance reactions, hip flexion to advance the limb, and stability of the limb for standing. If a patient meets these criteria and has acceptable cognition, the clinician can restore ambulation in most cases by prescribing an appropriate lower extremity orthosis and an upper extremity assistive device such as a cane. Orthopedic surgery to rebalance the muscle forces in the leg can greatly enhance ambulation.
Except for the correction of severe contractures in nonambulatory patients, surgical procedures should be delayed for at least 6 months to allow spontaneous neurologic recovery to occur and the patient to learn how to cope with the disability. After this time, surgery may safely be performed to improve usage in the functional limb.
In the nonfunctional limb, surgery may be performed to relieve pain or correct severe hip and knee flexion contractures caused by spasticity. Most severe contractural deformities in the nonfunctional limb, however, are the result of an ineffective program of daily passive ROM, splinting, and limb positioning.
Most hemiplegics with motor impairment have hip abductor and extensor weakness. A quad cane (cane with four feet to provide more stability) or a hemiwalker is prescribed to provide better balance. Because of paralysis in the upper extremity, the hemiplegic patient is unable to use a conventional walker.
Scissoring of the legs caused by overactive hip adductor muscles is a common problem. This gives the patient an extremely narrow base of support while standing and causes balance problems. When no fixed contracture of the hip adductor muscles is present, transection of the anterior branches of the obturator nerve denervates the adductors and allows the patient to stand with a broader base of support. If a contracture of the adductors occurs, surgical release of the adductor longus, adductor brevis, and gracilis muscles should be performed (Figure 12–13).
Release of the hip adductor tendons and neurectomy of the anterior branches of the obturator nerve to correct the problem of limb scissoring. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Patients with a stiff-knee gait are unable to flex the knee during the swing phase of gait. The deformity is a dynamic one, meaning that it only occurs during walking. Passive knee motion is not restricted, and the patient does not have difficulty sitting. Usually the knee is maintained in extension throughout the gait cycle. Toe drag, which is likely in the early swing phase, may cause the patient to trip. Thus, balance and stability are also affected. The limb seems to be longer than the other side, but this is only functional. Circumduction of the involved limb, hiking of the pelvis, or contralateral limb vaulting may occur as compensatory maneuvers.
A gait study with dynamic electromyography (EMG) should be done preoperatively to document the activity of the individual muscles of the quadriceps. Dyssynergic activity is commonly seen in the rectus femoris from preswing through terminal swing throughout the gait cycle. Abnormal activity is also common in the vastus intermedius, vastus medialis, and vastus lateralis muscles. If knee flexion is improved with a block of the femoral nerve or with botulinum toxin injection of the quadriceps, the rationale for surgical intervention is strengthened. Any equinus deformity of the foot should be corrected prior to evaluation of a stiff-knee gait because equinus causes a knee extension force during stance. Because the amount of knee flexion during swing is directly related to the speed of walking, the patient should be able to ambulate with a reasonable velocity to benefit from surgery. Hip flexion strength is also needed for a good result because the forward momentum of the leg normally provides the inertial force to flex the knee. In the past, a selective release of the rectus femoris or both the rectus femoris and vastus intermedius was done to remove their inhibiting knee flexion. On average, a 15-degree improvement in peak knee flexion is seen after surgery. Transfer of the rectus femoris to a hamstring tendon not only removes it as a deforming muscle force, it also converts the rectus into a corrective flexion force. This procedure provides improved knee flexion over selective release. When any of the vasti muscles are involved, they can be selectively lengthened at their myotendinous junction (Figure 12–14), and knee flexion improves.
Selective lengthening of the rectus femoris tendon to correct a stiff-knee gait abnormality.
A knee flexion deformity increases the physical demand on the quadriceps muscle, which must continually fire to hold the patient upright. Knee flexion often leads to knee instability and causes falls. It is most often caused by spasticity of the hamstring muscles. A KAFO can be used to hold the knee in extension on a temporary basis as a training aid in physical therapy. Such an orthosis, however, is difficult for the stroke patient to don and wear for permanent usage.
Surgical correction of the knee flexion deformity is the most desirable treatment. Hamstring tenotomy (Figure 12–15) eliminates the dynamic component of the deformity and generally results in a 50% correction of the contracture at the time of surgery. The residual joint contracture is then corrected by serial casting done weekly after surgery. Hamstring function posterior to the knee joint is not necessary for ambulation. In fact, ambulation may only be feasible in patients with knee flexion deformities of greater than 30 degrees if a hamstring release is done.
Distal release of the hamstring tendons to correct a knee flexion contracture. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Equinus or Equinovarus Foot Deformity
Surgical correction of an equinus deformity is indicated when the foot cannot be maintained in the neutral position with the heel in firm contact with the sole of the shoe in a well-fitted, rigid AFO. Despite a wide variety of surgical methods designed to decrease the triceps surae spasticity, none is more effective than Achilles tendon lengthening. In this procedure, triple hemisection tenotomy is performed via three stab incisions, with the most distal cut based medially to alleviate varus pull of the soleus muscle (Figure 12–16).
Hoke triple hemisection Achilles tendon lengthening to correct an equinus foot deformity. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
An anesthetic block of the posterior tibial nerve can be a valuable tool in preoperative assessment of the patient with equinus deformity because it demonstrates the potential benefits of Achilles tendon lengthening if the deformity is a result of increased muscle tone.
Surgical release of the flexor digitorum longus and brevis tendons at the base of each toe (Figure 12–17) is done prophylactically at the time of Achilles tendon lengthening because increased ankle dorsiflexion following heel cord tenotomy increases tension on the long toe flexor and commonly leads to excessive toe flexion (toe curling). The flexor hallucis longus and flexor digitorum longus tendons can be transferred to the os calcis to provide additional support to the weakened calf muscles.
Release of the flexor digitorum longus and brevis tendons to correct the problem of toe curling. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Surgical correction of varus deformity is indicated when the problem is not corrected by a well-fitted orthosis. It is also indicated to enable the patient to walk without an orthosis when varus deformity is the only significant problem. The tibialis anterior, tibialis posterior, extensor hallucis longus, flexor hallucis longus, flexor digitorum, and soleus pass medial to the axis of the subtalar joint and are potentially responsible for varus deformity. EMG studies demonstrate that the peroneus longus and peroneus brevis are generally inactive, and the tibialis posterior is also usually inactive or minimally active.
The tibialis anterior is the key muscle responsible for varus deformity, and in most patients, this can be confirmed by visual examination or palpation while the patient walks. A procedure known as the split anterior tibial tendon transfer (Figure 12–18) diverts the inverting deforming force of the tibialis anterior to a corrective force. In this procedure, half of the tendon is transferred laterally to the os cuboideum. When the extensor hallucis longus muscle is overactive, it can be transferred to the middorsum of the foot as well.
Split anterior tibial tendon transfer to correct a spastic varus foot deformity. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Treatment of equinovarus deformity consists of simultaneously performing the Achilles tendon lengthening procedure and the split anterior tibial tendon transfer. At surgery, the tibialis anterior is secured and held sufficiently taut to maintain the foot in a neutral position. After healing, 70% of patients are able to walk without an orthosis.
The first objective in treating the spastic upper extremity is to prevent contracture. Severe deformities at the shoulder, elbow, and wrist are seen in the neglected or noncompliant patient. Assistive equipment can be used to position the upper extremity, to aid in prevention of contractures, and to support the shoulder. Positioning extends spastic muscles but does not subject them to sudden postural changes that trigger the stretch reflex and aggravate spasticity. Brief periods should be scheduled when the upper extremity is not suspended and time can be devoted to ROM therapy and hygiene.
Most hemiplegics do not use their hand unless some selective motion is present at the fingers or thumb. Thumb opposition begins with opposition of the thumb to the side of the index finger (lateral or key pinch) and proceeds by circumduction to oppose each fingertip. In most stroke patients with selective thumb–finger extension, proximal muscle function is comparatively intact. Hence, orthotic stabilization of proximal joints is rarely necessary in the patient with a functional hand.
An overhead suspension sling attached to the wheelchair is used for patients with adductor or internal rotator spasticity of the shoulder. An alternative is an arm trough attached to the wheelchair.
It is usually not possible to maintain the wrist in neutral position with a WHO when wrist flexion spasticity is severe or when the wrist is flaccid. With minimal to moderate spasticity, either a volar or dorsal splint can be used. The splint should not extend to the fingers if the finger flexor spasticity is severe because slight motion and sensory contact of the fingers or palm may elicit the stretch reflex or grasp response, causing the fingers to jack-knife out of the splint.
The hemiplegic shoulder deserves special attention because it is a common source of pain. A variety of different factors contribute to the painful shoulder: reflex sympathetic dystrophy, inferior subluxation, spasticity with internal rotation contracture, adhesive capsulitis, and degenerative changes about the shoulder. If early ROM exercises are performed and the extremity is properly positioned with a sling to reduce subluxation, severe or chronic pain at the shoulder can usually be prevented or minimized.
The classic clinical signs of reflex sympathetic dystrophy (swelling and skin changes) may not be apparent in the hemiplegic patient. If the patient complains that the arm is painful and no cause is apparent, a technetium bone scan assists in establishing the diagnosis (Figure 12–19). Treatment should be instituted immediately, and the patient should be given positive psychological reinforcement. The use of narcotics must be avoided. Treatment options include the use of medications, such as corticosteroids, amitriptyline, or gabapentin (Neurontin), physical therapy, or nerve blocks (stellate ganglion blocks, brachial plexus blocks, or Bier IV regional blocks). Each of these techniques is successful with some patients; however, none is reliable for all patients.
Technetium bone scan showing the periarticular increase in activity characteristic of reflex sympathetic dystrophy.
Contracture of the shoulder can cause pain, hygiene problems in the axilla, and difficulty in dressing and positioning. Shoulder adduction and internal rotation are caused by spasticity and myostatic contracture of four muscles: the pectoralis major, the subscapularis, the latissimus dorsi, and the teres major.
When the deformity is not fixed, lengthening of the pectoralis major, latissimus, and teres major at their myotendinous junction provides satisfactory correction of the deformity. In a nonfunctional extremity, surgical release of all four muscles (Figure 12–20) is usually necessary to resolve the deformity. Release of the subscapularis muscle is performed without violating the glenohumeral joint capsule. The joint capsule should not be opened because instability or intraarticular adhesions may result. A Z-plasty of the axilla may be needed if the skin is contracted. After the wound heals, an aggressive mobilization program is instituted. Gentle ROM exercises are employed to correct any remaining contracture. Careful positioning of the limb in abduction and external rotation is necessary for several months to prevent recurrence.
Release of the pectoralis major, subscapularis, latissimus dorsi, and teres major to correct an internal rotation and adduction contracture of the shoulder. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Elbow Flexion Contracture
Persistent spasticity of the elbow flexors causes a myostatic contracture and flexion deformity of the elbow. Frequent accompanying problems include skin maceration, breakdown of the antecubital space, and compression neuropathy of the ulnar nerve.
Surgical release of the contracted muscles and gradual extension of the elbow correct the deformity and decrease the ulnar nerve compression. The brachioradialis muscle and biceps tendon are transected. The brachialis muscle is fractionally lengthened at its myotendinous junction by transecting the tendinous fibers on the anterior surface of the muscle while leaving the underlying muscle intact (Figure 12–21). Complete release of the brachialis muscle is not performed unless a severe contracture was present for several years. An anterior capsulectomy is not needed and should be avoided because of the associated increased stiffness and intraarticular adhesions that occur postoperatively. Anterior transposition of the ulnar nerve may be necessary to further improve ulnar nerve function.
Surgery of the brachioradialis muscle, biceps tendon, and brachialis muscle to correct an elbow flexion contracture in a nonfunctional arm. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
Approximately 50% correction of the deformity can be expected at surgery without causing excessive tension on the contracted neurovascular structures. Serial casts or dropout casts can be used to obtain further correction over the ensuing weeks.
A spastic clenched-fist deformity in a nonfunctional hand causes palmar skin breakdown and hygiene problems. Recurrent infections of the fingernail beds are also common.
Adequate flexor tendon lengthening to correct the deformity cannot be attained by fractional or myotendinous lengthening without causing discontinuity at the musculotendinous junction. Transection of the flexor tendons is not recommended because any remaining extensor muscle tone may result in an unopposed hyperextension deformity of the wrist and digits. The recommended procedure is a superficialis-to-profundus tendon transfer (Figure 12–22), which provides sufficient flexor tendon lengthening with preservation of a passive tether to prevent a hyperextension deformity. The wrist deformity is corrected by release of the wrist flexors. A wrist arthrodesis is done to maintain the hand in a neutral position and to eliminate the need for a permanent splint. Because intrinsic muscle spasticity is always present in conjunction with severe spasticity of the extrinsic flexors, a neurectomy of the motor branches of the ulnar nerve in the Guyon canal should be routinely performed along with the superficialis-to-profundus tendon transfer to prevent the postsurgical development of an intrinsic plus deformity.
The superficialis-to-profundus tendon transfer to correct a severe clenched-fist deformity in a nonfunctional hand. (Illustration by Anthony C. Berlet. Reproduced, with permission, from Keenan MAE, Kozin SH, Berlet AC: Manual of Orthopaedic Surgery for Spasticity. Philadelphia, PA: Raven; 1993. http://lww.com)
After surgery, the wrist and digits are immobilized for 4 weeks in a short arm cast extended to the fingertips.
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