Consider this scenario: You work in a spa, and your client has come for a day of pampering that you are pleased to be part of. There’s a catch—this morning she had Botox injections to her forehead. Do you know what kinds of adjustments you need to make to keep her healthy and happy?

Or this one: You work in a clinic. A new client has a condition you’ve never heard of, called cervical dystonia. It causes painful and uncontrolled muscle spasms of the neck. His neurologist has recently given him injections of Botox, and now he would like to receive massage. Are you sure that’s a good idea?

The chances are, typical massage therapists know little or nothing about how best to help their clients who use Botox for therapeutic or cosmetic purposes. Indeed, little research has been published about the interface between these two interventions. But these clients come to us for care and depend on us to work for their best interests. In this article, we will try to map out enough information for readers to be able to ask the right questions when clients who use Botox come their way.

Anatomy Review—Muscle Contractions

Readers will probably remember that muscle contractions begin with a signal in the movement centers of the brain. The signal travels down the descending tracts of the spinal cord. A synapse links the impulse to the motor neurons that form the outgoing section of the spinal nerves at the correct levels. Ultimately, peripheral motor neurons deliver the stimulus to the targeted muscle cells at the motor end plate—the connection site between the myofiber membrane and the motor neuron. The electrochemical signal jumps from motor neuron to muscle cell with the help of acetylcholine, the neurotransmitter that tells muscle cells to begin the process of ratcheting actin and myosin molecules together. Then, the muscle cell contracts.

Obviously, this happens in hundreds or thousands of locations simultaneously in order for muscles to do the work we ask of them, and the coordinated movement that results can be a thing of beauty. Sometimes glitches occur, though—muscles contract more often or for longer periods than we would like, or stray neurological signals cause them to contract painfully and involuntarily. Alternatively, a central nervous system disruption, like stroke or cerebral palsy, can cause some muscles to stay in permanent contraction—this is spasticity that can be painful and even debilitating.

 If somehow the secretion of acetylcholine at the motor end plates could be stopped, the muscle would no longer be able to contract. Could this be a solution to some muscle contraction problems?

Botulism—A Brief History

The first recorded case of botulism was in 1735, when a German physician documented an outbreak of dangerous, even deadly, paralysis that accompanied the consumption of a particular batch of contaminated sausages. He named this phenomenon, which turned out to be related to a bacterial infection, from the Latin botulus, which means “sausage.”

Clostridium botulinum is a rod-shaped bacterium that doesn’t need oxygen to thrive, and it creates an environment-resistant shell called a spore. This allows it to be dormant for prolonged periods until it finds a friendly growth medium. These bacteria, which have several subtypes, secrete a substance that seeps into motor neurons at the motor end plate, and it blocks the secretion of acetylcholine altogether, leading to flaccid paralysis of the affected cells. The action of this toxin is permanent. The motor axon branches that are exposed will never secrete acetylcholine again, and the affected muscle cells are effectively out of commission until the neuron regenerates new terminating axons—a process that can take weeks or months.

A botulism antitoxin has been developed and can be used in cases where accidental botulism toxin exposure occurs. This can stop the progression of nerve damage, but not reverse it—whatever muscle power is lost will not be regained until the affected neurons regenerate their axon terminals. Advances in the understanding of this pathogen and its toxin, along with better attention to careful hygiene in food storage, means that botulism poisoning has become rare in this country, but about 100 cases of accidental poisoning are still reported annually.

Botulism to the Rescue

The neurotoxin that causes the paralysis associated with botulism was first isolated in 1944. While it has been considered as a possible biological weapon, other uses have prevailed. A diluted and purified version of it was first used therapeutically in 1980 for strabismus—a condition involving the muscles that control eye movement. In 1989, the US Food and Drug Administration (FDA) approved the use of botulinum toxin for several muscle problems of the face and neck. In 2002, the FDA approved the use of botulinum toxin for some other conditions, as well as for cosmetic uses—it can temporarily paralyze the muscles of facial expression that cause wrinkles. From that time, the industry grew fast, and some subtypes of the laboratory-prepared material have now become available. The most common trade names are Botox, Botox Therapeutic, Dysport, and Myobloc. Some preparations of botulism toxin have slightly different effects for different conditions, and the dosing guidelines are unique to each brand—they are not interchangeable. Consequently, in 2009, the FDA issued “black box” label warnings so that professionals would use these products with great care.

What Is It Used For?

Botulinum toxin is used cosmetically to address glabellar lines (those are formed by forehead muscles that pull the eyebrows together in a frown), and to reduce tone in other facial muscles, specifically the corrugator and procerus muscles. The net result is a face with a reduced appearance of wrinkles, brought on by induced flaccid paralysis of the key muscles. It typically takes three to six months for the affected neurons to grow new axon terminals, at which time control of the muscles is restored.

In addition, the toxin is approved for use to treat the following conditions.

• Strabismus. This condition involves asymmetrical tone in the muscles that move the eyeballs. The result is sometimes called “lazy eye” or “crossed eyes,” and the pupils are not parallel. Botulinum toxin can equalize the muscle tone between the eyes.

• Blepharospasm. This is a condition in which the orbicularis oculi muscle involuntarily contracts. It may be a part of several different types of dystonia, and it can lead to functional blindness, even though the eyes themselves are not affected.

• Hemifacial spasm. This unilateral involuntary contraction of the muscles of the face can be related to a cranial nerve irritation, a tumor, or unknown factors. Botulinum toxin prevents the contractions.

• Cervical dystonia. Also called spasmodic torticollis, this condition involves painful unilateral involuntary contractions of the sternocleidomastoid and other neck rotators.

• Vocal dysphonia. This involves involuntary contractions of the muscles that control the vocal cords, leading to problems with speech.

• Migraines. Chronic migraine appears to respond well to injections of botulinum toxin. It has also been studied for chronic tension-type headache, but the results were not consistently better than alternative options.

• Axillary and palmar hyperhydrosis. Multiple tiny injections to the skin where sweat glands are overactive can reduce sweating for several months at a time.

• Muscle-related pain. People who have pain related to involuntary spasm can benefit from injections that limit muscle tone. New research and manipulation of the toxin holds promise for other pain-related applications as well.

Other applications are common but less well-studied, including its use for spasticity related to cerebral palsy, Charcot-Marie Tooth syndrome, multiple sclerosis, stroke, and others. One generous person shared his experiences with me—while he found some relief from leg spasms with his injections, the trade-off was intense muscle weakness.

Botox and Massage— Allies or Adversaries?

Most applications of botulinum toxin occur without major adverse effects, but while complications are rare, they are not unheard of. According to the FDA, symptoms of botulism poisoning can occur if the treatment protocol is wrong, or—and here is where massage therapists should be alert—if the solution seeps out of the intended treatment area.

The promotional material distributed for cosmetic applications of Botox suggests that the full effect of cosmetic injections may not be achieved for several days after treatment. The patient is encouraged to gently exercise facial muscles immediately, but not to touch, compress, sleep on, or otherwise disrupt the injection sites for a minimum of four hours after treatment, in order to avoid spreading the toxin to unintended areas. This includes facial manipulation with massage as well, and massage elsewhere on the body must be conducted without putting the client face down in the cradle—otherwise the postmassage “table face” that many of us experience may last a lot longer than usual.

So it seems clear that massage and Botox are not good partners, because manipulation of treated areas may decrease the desired action at the targeted spot and increase undesired action in surrounding tissues. This makes sense for cosmetic applications. However, some research suggests that the toxin, when injected into deeper muscles, may work better if the tissues are carefully manipulated to improve its uptake. For our clients who use Botox for therapeutic rather than cosmetic purposes, this could be very significant. Unfortunately, this also appears to be the situation with the highest chance of adverse effects. The people documented to be most at risk have been children with cerebral palsy and other patients who use the toxin for deep muscle applications at the extremities, rather than for head and face issues. Some patients with cervical dystonia or vocal dysphonia also experience problems with swallowing after treatment. This can be dangerous, because it allows the aspiration of material into the lungs that can lead to life-threatening infection.

Where does all this leave the massage therapist in the spa and the other one in the clinic?

The spa therapist has guidelines that are fairly clear: no facial massage on the day of injections, and no prone work either—any massage must be conducted without putting pressure on the face. That client can receive massage as usual when the full effect of the Botox treatment is achieved, which may take several days.

For the clinical therapist, the guidelines are murkier. Questions that need to be answered include: Where was the injection, and what condition was it for? How recent was the treatment? Should she work deeply on the injection sites to help the toxin be more effective? Should she avoid the area to reduce the risk of an adverse reaction? What kinds of adverse reactions are possible?

 In this situation, we are in largely uncharted territory, but we are not here alone. With the client’s permission, it is possible to work closely with the neurologist or other specialist who administers the injections and to follow up with the client to track results.

Ruth Werner is president of the Massage Therapy Foundation. She is a writer and NCBTMB-approved provider of continuing education. She wrote A Massage Therapist’s Guide to Pathology (Lippincott Williams & Wilkins, 2009), now in its fourth edition, which is used in massage schools worldwide. Her latest book, Disease Handbook for Massage Therapists (Lippincott Williams & Wilkins, 2009), is also available at www.lww.com. Werner can be reached at www.rutherwerner.com or wernerworkshops@ruthwerner.com.

Author’s note: several people shared their Botox stories with me to assist with this piece, and for them I am immensely grateful. We all benefit from such generosity. My thanks to you all.