Upper limb orthoses for the stroke and brain-injured patient

Chapter 14 Upper limb orthoses for the stroke and brain-injured patient

General principles

Stroke and brain injury are often complicated by the development of upper motor neuron syndrome.23,22,39,52 Upper motor neuron syndrome is characterized by impairment of motor control, spasticity, muscle weakness, stereotypical patterns of movement (synergy), and stimulation of distant movement by noxious stimuli (synkinesis). Often the spasticity is severe and prevents adequate range of motion therapy of joints or maintenance of acceptable limb position. Contractures can occur despite the most conscientious and aggressive treatments.

Even when joint motion can be maintained by knowledgeable therapists, it commonly requires much force that is painful for the patient, potentially harmful to limbs, and time consuming for caregivers to provide. Lesser degrees of spasticity can impede a patient’s function or require the use of positioning devices that interfere with the use of an extremity.

Prevention of deformity and myostatic contractures in the presence of severe spasticity is challenging. Splints applied to only one side of an extremity are not sufficient to control excessive spasticity and may result in skin breakdown from motion of the extremity against the splint.5 If used inappropriately, an orthosis may conceal the severity of a deformity or may cause additional deformity. It is important to treat the underlying spasticity in order to utilize orthoses effectively.

Treatment options for temporary control of spasticity

The majority of spontaneous motor recovery occurs within 6 months of stroke and traumatic brain injury. Definitive surgical procedures to reduce spasticity, such as neurectomies, tendon releases, and transfers, are delayed until the patient shows minimal further improvement in motor control.10,36,48

The prolonged period of spontaneous neurologic recovery is further complicated by spasticity (resistance to quick stretch), rigidity (resistance to slow stretch), impairment of motor control, synergistic patterns of movement, synkinesis (involuntary movement in one limb or limb segment when another part is moved [associated distant movement]), and immobility. These phenomena make temporary control of spasticity difficult but essential. Nerve blocks, chemodenervation, and casting techniques are used commonly and aggressively.6,7,9,13,15,17,22,23,26,51

Phenol nerve blocks

When muscle spasticity requires control for an extended period but the patient still has potential for spontaneous improvement, a phenol nerve block may be indicated.6,7,13,19,27,28,35,37,41,44,45,53,54,69 Phenol exerts two actions on the nerves. The first is a short-term effect. The short-term effect is similar to that produced by a local anesthetic and is directly proportional to the thickness of the nerve fibers. The second is a long-term effect that results from protein denaturation.

Phenol, a derivative of benzene, denatures the protein membrane of peripheral nerves when used in aqueous concentrations of 5% or more. When phenol is injected in or near a nerve, it reduces neural traffic along the nerve; hence, it is useful for temporary treatment of spasticity. Onset of the destructive process may begin to show effects several days after injection, but phenol also has a local anesthetic feature that allows a clinician and the patient to see “partial results” shortly after the phenol block is performed. The denaturing process induced by phenol continues for several weeks, but regeneration eventually occurs within 3 to 5 months.

Histologic studies have shown that phenol destroys axons of all sizes in a patchy distribution. The effect is more pronounced on the outer aspect of the nerve bundle, onto which phenol is dripped. When phenol is percutaneously injected, the nerve block likely will be incomplete. This effect is particularly beneficial in situations where a spastic muscle has retained volitional capacity, because under these circumstances it is desirable to reduce spasticity while preserving volitional capacity of a given muscle or muscle group.

The technique of phenol injection is based on electrical stimulation. Nerve branches are injected as close as possible to the motor points of the involved muscle. A surface stimulator is briefly used to approximate the percutaneous stimulation site in advance. A 25-gauge Teflon-coated hypodermic is advanced toward the motor nerve. Electrical stimulation is adjusted by noting whether muscle contraction of the index muscle occurs. As one gets closer to the motor nerve, less current intensity is required to produce a contractile response. The motor nerve is injected when minimal current produces a visible or palpable contraction of the muscle. Generally 4 to 7 mL of 5% to 7% aqueous phenol is injected at each site. As with any injection, care must be taken to avoid injection into a blood vessel; this is accomplished by aspirating prior to the injection.


Use of botulinum toxin also exemplifies a temporary, localized approach to controlling spasticity.15,17,20,22,23,26,29,30,59,61,62,63,66,68 Ordinarily, an action potential propagating down a motor nerve to the neuromuscular junction triggers the release of acetylcholine (ACh) from presynaptic storage sites in the nerve terminal into the synaptic space. The released quanta of ACh, after traversing the synapse and attaching onto receptors located on the postsynaptic muscle membrane, cause its depolarization. This activates a biochemical sequence that ultimately leads to forceful muscle contraction. Botulinum toxin type A is a protein produced by Clostridium botulinum that inhibits the calcium-mediated release of ACh at the neuromuscular junction. Botulinum toxin A attaches to the presynaptic nerve terminal, and a component of the toxin crosses the nerve cell membrane. This component interferes with “fusion proteins” affiliated with vesicles of ACh and thereby prevents release of ACh from their storage vesicles.

Clinical benefit lasts 3 to 5 months but may be more variable. Botulinum toxin is injected directly into an offending muscle. Depending on the size of the muscle being injected, dosing has ranged between 10 and 200 units (U), depending on the size of the muscle. Current practice is to wait at least 12 weeks before reinjection and not to administer a total of more than 400 U in a single treatment session. Because this upper limit of 400 U can be reached rather quickly when injecting a few large proximal muscles or many smaller-sized distal muscles, a different strategy is needed for the limb requiring many proximal and distal injections. In this circumstance, botulinum toxin A and phenol can be combined, with the former injected into smaller distal muscles and the latter aimed at larger proximal ones. A 3- to 7-day delay between injections of botulinum toxin A and the onset of its clinical effect is typical.

The technique of injection varies. Some physicians prefer to inject through a syringe attached to a hypodermic needle that doubles as a monopolar electromyographic (EMG) recording electrode. Patients may be asked to make an effort to contract the targeted muscle, or the muscle may be contracting involuntarily. After the needle electrode is inserted, injection is made when EMG activity is recorded. For deep or small spastic muscles (e.g., tibialis posterior, long toe flexors, or finger flexors), electrical stimulation is preferred as a means of localizing the muscle prior to injection.

Because botulinum toxin is the most potent biologic toxin known and the cost is relatively high, the smallest possible dose should be used to achieve results. Most studies have reported side effects in 20% to 30% of patients per treatment cycle. The incidence of adverse effects varies based on the dosage used (i.e., the higher the dose, the more frequent the adverse effects); however, it has been reported that incidence of complications is not related to the total dose of botulinum toxin used. Local pain at the injection site is the most commonly reported side effect. Other adverse effects (e.g., local hematoma, generalized fatigue, lethargy, dizziness, flulike syndrome, pain in neighboring muscles) also have been reported.

Causes of limited joint motion

The brain-injured patient is likely to have quadriplegic involvement, concomitant peripheral nerve injuries, residual deformities from fractures, and limitation of joint motion from heterotopic ossification.11,47,49 Distinguishing from among several possible causes of decreased range of motion often is difficult in a brain-injured patient. The causes of decreased motion to be considered are increased muscle tone, myostatic contracture, heterotopic ossification, undetected fracture or dislocation, pain, or lack of patient cooperation secondary to decreased cognition.8,10,31 The stroke patient tends to be older. Limited joint motion can be associated with degenerative arthritis. Congenital deformities can be present.

Arthritis, fractures, or dislocations may not exhibit a clinical deformity but can be detected easily by plain radiographs. Early heterotopic ossification is accompanied by an inflammatory reaction, with redness, warmth, severe pain, and steadily decreasing range of motion. Generally a radiograph shows evidence of the heterotopic bone as a hazy area of calcification forming in a periarticular location when it is suspected clinically.

Differentiating between the relative contributions of pain, increased muscle tone, and contracture can be more difficult. Diagnostic blocks using short-acting local anesthetic agents are extremely useful in assessing a spastic limb. The blocks can be performed at bedside or in the clinic setting without the use of special devices. By temporarily eliminating pain and muscle tone, patient cooperation is gained and the amount of fixed contracture can be measured. The strength and control of antagonistic muscle groups can be determined.

When focal intervention (chemodenervation, neurolysis, or surgery) is being considered, differentiating between the resistance to stretch offered by muscle contraction on a reflex basis versus resistance to stretch generated by inherent physical stiffness properties of muscle tissue is extremely important. EMG examination is another tool that can help make this distinction.21,23,43,48

General classification of orthoses

Orthoses can be constructed of different materials, such as plaster, metal, cloth, plastic, and thermoplastic. Thermoplastic materials usually are classified into high- and low-temperature types, based on the temperature at which they become pliable. Many upper limb orthoses are constructed of low-temperature thermoplastics. This material becomes pliable below 180°F, and it can be molded directly against the body. The materials used in orthotic devices include low-temperature thermoplastics that can be custom made for fit and other appropriations. Other materials include casting, metal, strapping, and hook-and-loop closure. Orthotic devices can be divided in two groups:

Exact fit is a key element for many upper limb orthoses. In order to work properly, the orthosis must hold the body part in an exact position. If the orthosis does not fit exactly, it may not work and may actually cause harm.

The patient’s motivation and attitude toward the orthosis are important components of the treatment plan. Most upper limb orthoses are removable, and patients can choose whether or not to use them. Health care professionals must work closely with the patient to ensure that the patient will accept the orthosis and use it properly.

Uses of orthotic devices

Contracture prevention

A combination of peripheral nerve blocks and casting or splinting techniques are commonly used to give temporary relief of spasticity.10,5658 Positioning a limb in the desired position for later function is important. Because the clinical situation may change quickly after a traumatic brain injury, a short-term orthosis such as a cast often is a practical choice.5 Casting maintains muscle fiber length and diminishes muscle tone by decreasing sensory input. Lidocaine blocks are helpful when done prior to cast application, because relieving the spasticity allows for easier limb positioning. Casts are used prophylactically to prevent contracture formation in a nonfunctional position. A well-applied circular cast will protect the skin in unconscious patients. Casts are commonly used to treat pressure sores in these patients. Close neurovascular observation is necessary in head injury patients after circular plaster application because many cannot complain of pain secondary to a tight cast.

Contracture correction

Correction of contractual deformities can be obtained by serial cast application done at weekly intervals or use of dropout casts.5 Serial casting is most successful when a contracture has been present for less than 6 months. The patient is sedated, and an anesthetic nerve block is given if necessary to decrease the spasticity. The limb is manipulated for 10 minutes prior to cast application to gain increased joint motion. A well-padded cast is applied, holding the arm in the improved position. Care must be taken not to exert excessive force while applying the cast. The major correction in joint position should have been obtained by the manipulation.

Dropout casts utilize the force of gravity to passively assist in correction of an early contracture. These casts have be modified to allow motion in one direction while preventing motion in the opposite direction. Because gravity is needed for correction, these casts are used in patients who can be seated in an upright position or who are ambulatory.

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Jul 12, 2016 | Posted by in ORTHOPEDIC | Comments Off on Upper limb orthoses for the stroke and brain-injured patient

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