© Springer International Publishing Switzerland 2017
Alexios Carayannopoulos DO, MPH (ed.)Comprehensive Pain Management in the Rehabilitation Patient10.1007/978-3-319-16784-8_66. Pain in the Spasticity Rehabilitation Patient
(1)
Department of Brain Injury Medicine, Northwestern Medicine: Marianjoy Rehabilitation Hospital, 26W171 Roosevelt Road, Wheaton, IL 60187, USA
Keywords
SpasticityStrokeBrain injuryTraumatic brain injuryCerebral palsySpinal cord injuryMultiple sclerosisBotulinum toxin injectionPhenol injectionBaclofen pumpSplit anterior tendon transfer (SPLATT)CordectomyMyelotomyIntroduction
Spasticity is an unmasked reflex that occurs when there is a lesion in the central nervous system (CNS) , a type of upper motor neuron (UMN) sign, first described by nineteenth century neurologist Hughlings Jackson [1]. Clinicians identify it as a velocity dependent increase in muscle tone when a particular muscle is stretched through its full range of motion. It can also be described as “muscle over activity.” Injuries to the CNS that can lead to spasticity include stroke, brain injury, spinal cord injury (SCI) , multiple sclerosis (MS) , and cerebral palsy . Prevalence varies from each condition: 28–38% in stroke patients, 60–80% in SCI patients, 41–66% in MS patients, and 13% in traumatic brain injury patients [2].
Pathophysiology
Spasticity is mediated through monosynaptic and polysynaptic spinal reflexes that are unmasked after injury to the CNS. There is reduced cortical inhibition of UMN spinal reflexes, which leads to a decreased threshold for reflex firing, and subsequent emergence of spasticity [3]. Spasticity emerges in SCI patients after spinal shock resolves.
Symptoms
There are characteristic spasticity patterns that can emerge in the upper and lower extremities. Upper extremities often will present with a flexor synergy pattern of finger flexion, wrist flexion, forearm supination or pronation, elbow flexion, and shoulder internal rotation [4]. The lower extremities often will present with an extensor synergy pattern of plantar flexion, toe flexion, knee extension, and hip extension [4]. Spasticity may also present with abnormal posturing of the trunk. Spasticity can often be made worse when the body perceives a noxious stimulus, such as bladder retention, urinary tract infection, pressure sore, ingrown toenail, constipation, occult fracture, excessively tight clothing, pulmonary embolus, or any other illness (e.g., syringomyelia).
Functional Limitations
Not all spasticity needs to be treated, and some spasticity may create a functional advantage that helps with gait mechanics, bed mobility, transfers, and general maintenance of muscle bulk. In other instances, spasticity is often associated with pain and discomfort when affected limbs are moved or stretched against the increased tone.
Many functional limitations can occur with both upper and lower extremity spasticity. Upper extremity spasticity can lead to an impaired ability to perform self-care, hygiene, grooming, feeding, and dressing. Lower extremity spasticity can impact gait, thereby increasing risk of falls and/or inability to tolerate braces.
Skin breakdown can occur in areas with joint tightness, which can limit the ability to maintain hygiene, such as cleaning the hands, genitals, or axilla. Skin breakdown can also occur with abnormal pressures across exposed joints.
Spasticity can also affect impact bladder and bowel management, as well as sexual activity.
Poor posture due to increased spasticity through the trunk can affect transfers, bed mobility, sleep, hygiene, and positioning while in the seated or supine position.
Spasticity, when sustained for an extended period of time, can lead to muscle and tendon shortening, ultimately leading to a functional state of contracture formation.
Treatment/Common Techniques
Initial
It is important to rule out other organic causes that may be exacerbating and contributing to spasticity, such as a urinary tract infection, constipation, and bladder retention. Although some clinicians opt to initiate treatment of spasticity with oral medications, localized injection therapy with botulinum toxin is considered an appropriate first-line treatment. Oral medications include baclofen, dantrolene, diazepam, clonidine, and tizanidine. Tizanidine may have the dual ability to treat both spasticity and pain.
Rehabilitation
Physical and occupational therapy , that incorporates stretching, offers an important adjunct to both oral and injectable medication. Both can help to maintain range of motion and to determine appropriate splinting strategies for the upper and lower extremity. More than 40% of SCI-associated spasticity responds to stretching and should be performed twice daily. Stretching helps to maintain numbers of sarcomeres, reduces buildup of connective tissue, and thereby maintains muscle bulk and length [5]. Serial casting is an option for allowing sustained stretch across a muscle longer than could be offered with splinting alone [2]. Strengthening exercises can help to reduce spasticity by improving both strength and motor control.
For postural management , use of a standing frame can be helpful in allowing patients to remain in an upright position, which allows full weight bearing across extended hips, extended knee, and dorsiflexed ankles. Electrical stimulation may be used to reduce spasticity although its benefits tend to be temporary [6].
Procedures
Injection therapy is an effective way of treating localized spasticity. Phenol injection s cause tissue destruction or nerve lysis, thereby reducing spasticity. Onset of action for phenol is within minutes and can last up to 6–9 months. Botulinum toxin injection s prevent pre-synaptic release of acetylcholine at the neuromuscular junction, leading to temporary denervation, thereby reducing muscle contraction that contributes to spasticity. Onset of action for botulinum toxin is within 5–10 days and lasts up to 3 months.