Medical Conditions Related to Brain Injury
Spasticity Symptoms and Treatment
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Spasticity, also known as hypertonia, is an involuntary increase in muscle tightness (tone), and is seen often in traumatic brain injury that is associated with paralysis (loss of voluntary strength). Because a person with spasticity cannot voluntarily relax their limbs, voluntary movement of an affected limb may be impossible. Spasticity can be seen as early as a few days after brain injury or may take up to 3-6 months to develop. In as little as two weeks, spasticity may cause muscles to shorten permanently, which in turn causes joints to lose motion. The condition of permanent shortening is called a muscle contracture. It is critically important in the early stages of recovery to stretch a muscle to its full length in order to maintain normal joint motion.
Families should be alert for signs of contracture, such as: feet pointing downward and turning in, forearms drawing up, or fingers curling into the palm. If the person is hospitalized, in a coma or unable to move, families may want to ask:
- What plan is in place to address the issues of spasticity? Often a combination of physical therapy and drug interventions may be needed to manage spasticity.
- What medical person(s) will be addressing the spasticity? A physiatrist or neurologist? Does the hospital have a department specializing in brain injury to manage spasticity?
- How many times a day is the person receiving physical therapy? Usually muscle stretching and joint movement two or three times a day is needed from the onset of the injury to prevent contractures.
Many hospitals, while prepared to handle the initial trauma stage, provide only minimal treatment of spasticity. They may not be equipped to offer the proactive therapy (both physical and pharmacological) needed to keep spasticity from causing irreparable damage to muscles and joints. In cases of severe injury where extensive medical attention still is required, it may be necessary to find a brain injury specialty program that can both deal with the medical issues as well as spasticity caused by brain injury. Later in rehabilitation, spasticity is reassessed to determine how it interferes with voluntary arm and leg movement, or activities such as performing self care activities.
Spasticity is caused by a lack of control of reflexes originating in the spinal cord. Normally, the brain controls the spinal muscle (motor) nerves; however, when the brain is damaged, these normal spinal reflexes frwequently become overactive, causing muscle spasticity. Loss of voluntary muscle strength, called paralysis, usually occurs along with spasticity.
Spasticity treatment is divided into two phases: an early, acute phase (usually the first 6-18 months), and a long term phase (beyond 6-18 months). Recovery of movement control can take up to 18 months, during which time spasticity lessens as voluntary movement improves. After approximately 12-18 months, it is possible to determine how much spasticity will remain permanent. In the acute phase, treatment focuses on maintaining muscle length and joint motion while maximizing normal control of the arms and legs and improving mobility and self care abilities. Beyond 18 month, treatment is directed toward more permanent control of hypertonia.
The most important goal in the acute phase is to preserve passive range of motion or movement of the muscle and joint. If the joint tends to position or posture itself abnormally, then splinting or casting may be needed to hold the muscles and joints in their normal positions. If this is inadequate to prevent contractures, then oral medications may be employed. These medications include Dantrium, Baclofen, Zanaflex, and Valium. Unfortunately these medications cannot completely control spasticity and in some patients may be very sedating. The next step in acute management involves anesthetic, alcohol, and botulinum toxin injections to the nerves and muscles. These agents act as blocks that temporarily paralyze nerves and muscles for durations of a few hours (anesthetics) to up to 3-6 months (alcohol and botulinum toxin), allowing for improved passive range of motion, and for splinting or casting to be more effective. The goals of all these treatments are to preserve joint and muscle motion until the point of maximum voluntary movement recovery is reached.
After about 18 months, if spasticity persists, long term options for permanent control of spasticity will be considered. The two most commonly used treatments are the intrathecal Baclofen pump and orthopedic surgical tendon lengthening and tendon transfers. The intrathecal Baclofen pump administers the anti-spasticity medication, Baclofen, directly onto the spinal cord nerves where the spastic reflexes originate. Often, this dramatically decreases muscle tone and improves movement without sedation. Orthopedic surgery can be used to lengthen muscle tendons that are shortened to improve positioning or to transfer tendons to other bones to allow for more normal positioning.
In summary, spasticity management occurs throughout the recovery process. It can be divided into two phases: an acute phase when treatment focuses on preventing deformities, such as muscle shortening or loss of joint movement, and a long term phase when more permanent treatment options are considered to produce the best level of function in mobility and self care.
Alan M. Harben, MD, PhD is a Fellow of the American Academy of Physical Medicine and Rehabilitation and has completed doctoral training in the field of Biomechanics. He is Medical Director of the Restore Neurobehavioral Center located in Roswell, Georgia, a rehabilitation program for persons with behavioral disorders due to acquired brain injury. He also serves as the medical consultant for The Bridge, an adolescent psychiatric program located in Atlanta, Georgia. He is a past Chair of the Brain Injury Resource Foundation. His private practice in Roswell, Georgia specializes in neurological and musculoskeletal rehabilitation.