Upper Limb Orthoses for the Stroke- and Brain-Injured Patient

Key Points

Stroke and brain injury are often complicated by the development of upper motor neuron syndrome.
Most spontaneous motor recovery occurs within 6 months of stroke and traumatic brain injury. Combining the therapeutic interventions of oral antispasmodics, therapy, casting, bracing, and targeted chemodenervation is a first-line measure. Definitive surgical procedures to reduce spasticity are effective and include neurectomies, tendon releases, and transfers. It is important to treat the underlying spasticity to use orthoses effectively.
The prolonged period of spontaneous neurologic recovery is complicated by spasticity (resistance to quick stretch), rigidity (resistance to slow stretch), impairment of motor control, synergistic patterns of movement, synkinesis (involuntary associated movement in a distant limb segment), and immobility.
Orthotic selection heavily depends on the patient's realistic functional goals as well as the severity, type, and distribution of joint range of motion impairment. It is a compromise of immobilization versus function meant to restore normative biomechanics to the upper limb.

General Principles

Stroke and brain injury are often complicated by the development of upper motor neuron syndrome. 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). The type and severity of the upper motor neuron lesion dictates the severity and location of spasticity and muscle weakness. Up to 60% of stroke survivors experience spasticity at 1 year, with 4% severely affected. In the United States alone and likely an underestimation, poststroke spasticity affects 100,000 individuals each year. Predictors of poststroke spasticity include severity of paresis, pain, and sensory deficits. Moderate to severe spasticity is common and decreases joint range of motion, impairs residual antagonistic muscle contraction, and may preclude placing the limb in an acceptable and comfortable position.

Spasticity is initially dynamic, caused by an excessive hypertonic response to stretch in muscles of normal length. Later, if left untreated, it develops into a structural reinforcement, or static contracture, of the shortened muscle position wherein hypertonia plays a minor role and fibrosis a major role. The determination of dynamic versus static contracture is a crucial factor that determines the path of treatment.

Contractures can occur despite the most conscientious and aggressive treatments. Maintenance of preinjury joint range of motion is time intensive and commonly requires application of force that is painful for the patient and potentially harmful to limbs. 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. 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 to use orthoses effectively. Whereas spasticity and hypertonia in the lower extremities may have positive benefits, such as increasing resistance to knee flexion and encouraging bipedal weight bearing, in the upper extremities, spasticity may serve to maintain the arm close the body from a protective standpoint but nearly universally impairs active function.

Treatment Options for Temporary Control of Spasticity

Spontaneous neurologic recovery of motor control is commonly complicated by upper motor neuron syndrome and its constellation of features: 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.

Spasticity can develop as early as 1 week after stroke or brain injury. Early management of spasticity should be introduced gradually in proportion to the severity of the developing spasticity and mainly consists of reversible interventions: physical and occupational therapies, positioning, bracing, and pharmacotherapy (focal and systemic). As the severity and distribution of spasticity declares itself over the course of the next 6 months, focal, titratable, and longer-acting interventions such as nerve blocks and chemodenervation gain relevance. Definitive surgical procedures to reduce spasticity, such as neurectomies, tendon lengthening, and transfers, are reserved for myostatic contractures or delayed until the patient shows minimal further improvement in motor control, typically 6 months to 2 years after injury. Optimal treatment should combine therapeutic approaches and be tailored to meet individual patient needs.

Anesthetic Nerve Blocks

Anesthetic nerve blocks can be used to temporarily eliminate muscle tone. They can be used diagnostically to evaluate what portion of a deformity is dynamic or neurally mediated (caused by hyperactive motor neuron excitation) and what portion is secondary to myostatic (nonneurally mediated) contracture. Repeated blocks of local anesthetics give a carryover effect to decrease muscle tone.

Phenol Nerve Blocks

First used in 1936, phenol is a cost-effective, titratable, and targeted chemical neurolytic agent that causes a temporary reduction in spasticity for up to 6 months. Phenol exerts two actions on the nerves. The short-term effect, similar to local anesthetic, affects small-diameter nerve fibers first, blocking pain before the large, well-myelinated motor and sensory fibers. This short-term effect is useful in the hours to days after injection and allows for patients and clinicians to measure the efficacy of the intervention. Second is a longer-term dose-dependent effect that results from protein membrane denaturation of mixed sensorimotor peripheral nerves. Reinnervation of peripheral nerves generally occurs within 3 to 5 months after injection. Repeated injections result in decreased axonal diameter and patchy myelin. Phenol is typically injected in aqueous concentrations of 3% to 7% with 4 to 7 mL injected at each site. It may be targeted at the peripheral nerve, such as the musculocutaneous nerve, when the intended effect is more generalized or at motor points for more focal targeting of spastic muscles. If phenol is injected perineurally, diffusion of the benzene-derived alcohol diffuses through the epineurium from exterior to the interior. As such, nerve fascicles on the exterior of the nerve have a greater relative concentration compared with interior fascicles and thus a greater effect.

Percutaneous phenol injection is performed predominantly with electrical stimulation. A Teflon-coated hypodermic needle connected to a pulse generator is advanced to the target nerve or motor point. Pulsed cathodic stimulation of the electrically active needle tip produces action potentials in the peripheral nerve and rhythmic contractions in the associated innervated muscles. Index muscle twitches can be palpated or directly visualized. Because a greater proportion of nerve fibers are stimulated with increasing current or decreasing radius from needle tip to nerve, clinicians can ensure direct perineural placement of the needle. Ultrasound guidance may be used as well, but after repeated phenol injections, differentiation of echotexture becomes more difficult because of soft tissue denaturation and fibrosis.

Potential drawbacks of chemical neurolysis include fibrosis of the target nerve (making repeated subsequent injections difficult to locate) and fibrosis of the target tissues, occasionally resulting in loss of manual dexterity in the distal upper extremity. Additionally, nonselective destruction of mixed sensory, pain, and motor fibers may result in insensate skin patches and the emergence of neuropathic pain, especially dysesthesia. Because phenol also causes sclerosis of vessels, special care must be taken to avoid intravascular injection; this is accomplished by aspirating before injecting.

Chemodenervation

Botulinum toxin (BT) has garnered strong evidence and broad clinical use in the treatment of localized spasticity. Its widespread adoption is the product of its low side effect profile, nondestructive reversible therapeutic effect, and superior ability for specific muscle targeting. Ordinarily, an action potential propagating down a motor nerve to the neuromuscular junction triggers the presynaptic release of acetylcholine (ACh). Released quanta of ACh traverse the synapse and bind to receptors located on the postsynaptic muscle membrane, causing depolarization of the muscle. This activates a biochemical cascade that ultimately leads to forceful muscle contraction. BT type A is a protein produced by Clostridium botulinum that inhibits release of ACh at the neuromuscular junction. BT attaches at the presynaptic nerve terminal and then is partially translocated into the cell cytoplasm. A component of the toxin then cleaves the SNAP-25 fusion protein, a member of the greater family of SNARE proteins integral for vesicular fusion and ACh release. Without functional fusion proteins, ACh vesicles remain sequestered and inactive until the BT dissociates from the nerve and the proteins are regenerated. There are a number of botulinum toxin variants approved by the U.S. Food and Drug Administration (FDA), including abobotulinumtoxinA (Dysport), incobotulinumtoxinA (Xeomin), oncabotulinumtoxinA (Botox), and rimabotulinumtoxinB (Myobloc). These variants all block the presynaptic release of ACh through loosely related mechanisms. BT injection has the advantage of inducing 3 to 4 months of focal dose-dependent attenuation in neuromuscular signaling in the injected muscle with little to no effect on distant muscles. It can also obviate the need for oral muscle relaxants and their associated systemic side effects. Botulinum toxin has a limited number of adverse events, including temporary pain in the injected limb, rash, flulike symptoms and, far less commonly, generalized weakness.

Causes of Limited Joint Motion

Nonprogressive brain lesions such as stroke and brain injury contribute to limited joint motion in various ways. In stroke, paresis, spasticity, and contracture cause most joint immobility. Because the stroke-injured population is often older, rheumatoid arthritis and osteoarthritis can exacerbate joint-protective behaviors and decrease range of motion. In brain-injured patients, in whom the inciting event often carries more distributed energy, there are more quadriplegic involvement, concomitant peripheral nerve injuries, residual deformities from fractures, and limitation of joint motion from heterotopic ossification. Distinguishing from among several possible, even potentially compounding, causes of decreased range of motion often is difficult in a patient with a brain injury. The causes of decreased motion are paresis, increased muscle tone, myostatic contracture, heterotopic ossification, undetected fracture or dislocation, pain, or lack of patient cooperation related to decreased cognition.

Imaging and other forms of diagnostic investigation can untangle the differential diagnoses that may contribute to decreased range of motion. Arthritis, fractures, or dislocations can easily be detected by radiographs. Early heterotopic ossification is accompanied clinically by inflammatory reaction, redness, warmth, severe pain, and steadily decreasing range of motion. Heterotopic ossification can be first seen with three-phase bone scintigraphy, but the sensitivity of ultrasonography is improving. Radiographs, magnetic resonance imaging (MRI), and computed tomography (CT) have low specificity, and there are no reliable serum markers for screening in the early stages of heterotopic ossification. Pain and muscle tone, as independent contributing factors to decreased joint motion, can be assessed with diagnostic nerve blocks using short-acting local anesthetic. By temporarily eliminating pain and muscle tone, static contracture can be measured. Nerve block can also help uncover antagonistic muscle strength and coordination when previously obscured by spastic tone. Electromyography (EMG) is a more sensitive measure of spasticity than typically used clinical measurements; it can also determine whether peripheral nerve injury is contributing.

General Classification of Orthoses

The use of orthotics is one set of tools in the effort to restore homeostatic range of motion, soft tissue flexibility, agonist–antagonist muscle balance, and ultimately function of the upper extremity. As a result of restoring these balances, secondary improvements to pain, balance, hygiene, and task-oriented function occur. Orthotic designs span a continuum from robust immobilization to incremental liberalization of range of motion on a joint-by-joint basis. Dependable, robust immobilization, such as casting, is used early and has the benefits of overcoming severe spasticity and decreasing the amount of user error by the wearer or caregiver. Later on, as the emphasis on function increases and spasticity wanes, it is important to liberalize joint movement where possible for a user to perform functional tasks. This process of liberalization is implemented by limiting how many degrees a joint may range, by isolating joint movement to one plane, or mechanically defining the trajectory of movement. As a reflection of this continuum, orthotics can be divided into four types:

1
Static orthoses: These devices rigidly immobilize one or more joints and do not allow any motion. They are most commonly used for fractures and nerve injuries in the postsurgical phase. By nature, they have the ability to overcome severe spasticity and to distribute pressure equally along all contact points. Attachments for assistive devices (eating utensils, pens) may be grafted onto static orthoses.
2
Dynamic or functional orthoses: These devices allow a prescribed amount of motion across one or more joints. Designs are typically hinged and may or may not have a spring or elastic force encouraging rotation about the joint. They are used to assist movement of relatively weak muscles where there is either inadequate force generation by one muscle or too much force generation by its paired antagonist. They can provide a corrective force across a joint to encourage normal movement patterns and agonist–antagonist balance. Multiplanar joint motion (i.e., the wrist) is usually simplified to one plane to support vulnerable structures or to encourage a specific movement trajectory. Use of a dynamic orthosis allows a patient left with residual volitional movement of a joint to use it functionally while still providing adequate focal immobilization where needed. Functional orthoses are not categorically as strong as static orthoses, require care to appropriately don and doff, and unevenly distribute contact forces on the skin and soft tissue. Dynamic splinting, in which a force is applied to oppose a spastic muscle, has a very limited role in treating spastic contractures because it may trigger increased muscle tone if not used carefully. Bilateral tension-providing mechanisms ameliorate this risk and better accommodate for spasms and avoidance of soft tissue injuries.
3
Progressive orthoses: These devices incorporate nonelastic components to apply force across a joint to hold it at its end range position to improve passive joint range of motion. They allow incremental changes in joint position as the end range of the affected joint improves over time.
4
Serial orthoses: These devices accomplish similar goals to those of progressive devices but are static casts or splints applied over time. Every 5 to 7 days, the cast is refit and the joint is repositioned at the maximum tolerable end range position. This accomplishes a prolonged passive stretch over time and blends the durability and reliability of casting.

Upper limb orthoses can be commercially premade out of laminates, plastics, or metal. Most often they are custom fabricated with thermoplastics, plaster, or fiberglass casting with a hands-on manually contoured technique. Newer developments in organic computer-aided design modeling, three-dimensional scanning, and additive 3D printing have increased the range of feasible geometries and will likely continue to expand if the same comfort and fit can be achieved as conventional methods.

Exact fit is a key element of upper limb orthoses. Proper anatomical relationship to the patient is critical to maintain an ideal joint position, evenly distribute contact pressure, and prevent uncomfortable potentially injurious movement of the orthosis on the body. A patient's motivations and attitude toward the orthosis are important components of the treatment plan. Considerations of comfort, cosmesis, independent donning and doffing, and ergonomics in the prescription and the design phases can greatly improve patient compliance. Because most orthoses are removable and transiently uncomfortable, some patients may not wear them consistently enough for adequate treatment effect. As such, it is incumbent upon health care professionals to educate patients and their caregivers to understand the aims and rationale for orthotic use. Health care professionals must work closely with the patient to ensure that the patient and potential caretakers will accept the orthosis and use it properly.

Uses of Orthotic Devices

Contracture Prevention

As discussed previously, the progression of contracture develops over time, typically weeks to months. Neurogenic shock often occurs directly after stroke or brain injury. Over the following few weeks, spasticity develops in parallel with neurologic recovery. In this period, a combination of oral antispasmodics, peripheral nerve blocks, and casting or splinting techniques are commonly used to give temporary relief of spasticity. Positioning a limb in a desired position for later practical function is important. A short-term orthosis such as a cast is often a practical choice, especially for patients with a brain injury whose insight and cooperation may wax and wane initially. Casting maintains muscle fiber length, protects the limb, and diminishes muscle tone by decreasing sensory input. As a general rule of thumb, temporary nerve blocks should be performed before the cast is applied to ease positioning and decrease pain. Experienced health care professionals should apply the cast to avoid pressure hotspots. A well-applied circular cast can protect the skin of unconscious patients and is commonly used to treat pressure sores. Close neurovascular observation is necessary in cognitively impaired patients after circular cast application, because many cannot complain of pain caused by a tight or ill-fitting cast. In stroke that mostly affects the distal upper extremity, a static removable resting wrist–hand splint can prevent contracture and provide comfort. Because of the heterogeneity of neurologic injury and associated recovery, orthotic intervention type, indication, duration, and construction vary by geography and practice. Rigorous standardization of spasticity measurement and these components of orthotic intervention is ongoing and needed.

Orthoses as Reinforcements After Chemodenervation

An orthotic device can augment the treatment effect of targeted chemodenervation with BT, phenol, and others. Combining these two modalities, health care providers can leverage passive stretch and attenuate tonic activation of motor units. Serial orthoses are changed weekly to gradually increase the amount of stretch over the next 3 months, the duration of BT's effects. In many patients this level of treatment is sufficient; however, with more severe spasticity a patient may need surgical correction. Ensuring ideal positioning in the postsurgical phase is also critical.

Contracture Correction

Restoration of joint range of motion or contracture correction can be achieved with serial casting at weekly intervals. It is often most successful when a contracture has been present for less than 6 months. Surgical management entails manipulating the joint under anesthesia beyond soft tissue endpoints. After this, a cast may be applied to allow the limb to heal in its new position. A major correction in joint position can be achieved directly through manipulation. A dropout cast may be used instead of serial casting. The uses and limitations of a dropout cast are discussed later in this chapter.

Maintaining Limb Position

Maintenance of limb position after achieving a desired position is not trivial and must continue on a regular basis for months after contracture correction. If ideal limb position is not maintained, affected joints will regress over time, losing as much as 50% of the gains in a month. For these reasons, using a bivalved cast or splint is important because it is more comfortable than a traditional circular cast and can be removed several times a day to perform joint range of motion and skin care. Bivalved casts or splints are inadequate for severe spasticity because they do not have enough inherent stability and may increase the risk for skin and soft tissue injury.

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