Residual Effects of Bell’s Palsy
by H. Jacqueline Diels, Occupational Therapist
Most people who develop Bells palsy will recover completely and spontaneously (i.e. without any physical therapy) within 3 months. The following discussion is intended to review and clarify the possible residual effects that can be present in cases where recovery from Bell’s palsy is delayed beyond the 3 months point. Generally, the longer the recovery takes beyond the initial three months, the more severe the residual effects.
Residual effects can include eye problems (decreased lid closure / increased lid closure, dryness / excessive watering / watering during eating [crocodile tears]), nasal problems (running nose, dryness, collapsed nostril), and others. This discussion will focus primarily on the residual effects as they pertain to facial movement.
For the person who has facial paralysis after Bell’s palsy there are typically 2 stages of recovery. In the first stage (first 3 months) there may be no facial movement at all. In this phase, nerve healing is taking place as the inflammation caused by the virus subsides. The affected side of the face may droop. The eye may be unable to close or blink and tearing may be decreased. There can be corneal dryness due to decreased lubrication coupled with exposure to air. There is risk of corneal damage. Patients should be followed by an ophthalmologist during this period to ensure a healthy eye. Weakness of the mouth muscles may cause difficulty with eating, drinking and speaking. The face may pull uncontrollably toward the unaffected side.
As nerve recovery takes place you may notice small facial movements beginning. People recover at different rates, but generally this process will be complete in the three months after onset. If recovery is delayed you may begin to notice movements in areas of the face that you are not even trying to move. For example, when you smile the eye may close or twitch or when you close you eye the corner of your mouth may pull up or out to the side. This condition is known as synkinesis. It is characterized by uncoordinated or unsynchronized facial movements that occur along with normal movements. Synkinesis varies in severity from mild to severe. In its worst form, mass action, it can result in uncontrollable movement of the facial muscles on the affected side during any attempted expression. The affected side of the face may feel tight as the result of the uncontrolled muscle contractions (spasms).
Many people, when describing their history of facial paralysis after Bell’s palsy describe it something like this: “I had no movement for about 3 months and then it started to come back. It was getting better and better and then suddenly it started getting worse again”. So what happens in this transition between getting better and getting worse again? Specific areas of synkinesis can sometimes be difficult to identify, because in a severe form it can result in what appears to be no active facial movement. So how do you differentiate this condition from the first phase of facial paralysis when you have no movement? It is the difference between lack of muscle function resulting in no movement and too much muscle contraction resulting in completely restricted movement.
Synkinesis is theorized to be the effect of abnormal nerve regeneration, where some of the healing facial nerve fibers can actually implant themselves into the wrong muscles. Think of the facial nerve as a telephone cable. If you cut through a telephone cable you see many different color-coded wires. The telephone repair person can repair the broken cable by reconnecting the wires according to their color. The facial nerve cable is about the diameter of a strand of thin spaghetti. Within that strand are between 6000-7000 different nerve fibers (wires) which conduct the electrical signal from the brain to the facial muscles causing them to contract. They are very delicate and obviously have no color-coding. Inflammation from the Bell’s palsy can harm, or “break” some of these very frail fibers. In time the damaged fibers heal. They regenerate at the rate of about 1-2mm per day. But there’s no mechanism that directs these fibers back into their original muscles. The brain sends the signal for the muscle to contract thinking the nerve fiber is still connected to the original muscle, but instead, the nerve may be lodged in an entirely different muscle, which then contracts at the same time.
Synkinesis can affect any of the facial muscles, in any imaginable pattern. An easy to see example is eye closure during a smile. When the person tries to smile the eye twitches or closes. We could speculate that some of the nerve fibers that used to go to the smile muscles (zygomaticus) got rerouted during recovery and implanted in the muscles that close the eye (orbicularis oculi). Other synkinetic patterns may be more difficult to observe, but can be much more limiting to facial movement. Let’s consider one of the most common: The inability to smile. First we need to acknowledge that there is a distinct difference between inability to smile just after onset (flaccid paralysis) and in the synkinetic face. On casual observation, it can appear that the smile muscle is simply not working because the corner of the mouth does not go up during a smile. There’s an easy way to determine whether the smile muscle is “working” or not. Please refer to the muscle diagram as you read this. Most of us think we smile with our mouths because the corner of the mouth moves. In actuality the smile muscles reside in the cheek. The bottom end of the muscle implants near the corner of the mouth. When the muscle contracts the cheek lifts, pulling the corner of the mouth “along for the ride”. Look in the mirror at your cheek on your unaffected side and smile. Watch for the “apple” of the cheek as you smile and you will see it “bulge” as you smile and then flatten out again as you stop smiling. Don’t watch the corner of your mouth. Do the same movement now and watch the affected side cheek. In most cases you will also see the “apple” of the cheek bulge up and then release. The shape of the two cheeks may be similar or different. So now you see that the smile muscle is working (even if it’s not exactly the same as the other side). So now the question is: If the smile muscle is working why doesn’t the corner of the mouth go up?
To answer that question we need to go back to basic facial anatomy and high school physics. The facial muscles are designed differently than other muscles in the body. Their only purpose is to move the skin of the face. The facial muscles don’t move bones around joints like leg or arm muscles. They don’t carry heavy loads or provide postural support. They simply move skin. Different combinations of muscle contractions move the skin in various directions (more than 2000 distinct facial expressions have been catalogued!). Going back to physics we can describe the movement produced in a specific direction as a vector, or a directional movement. The vector of the smile muscle generally pulls the corner of the mouth up toward the cheekbone. What if another muscle is contracting out of sequence and pulling the skin along a vector in an opposite direction? Which way will the skin move? Can it possibly move in a normal pattern? Let’s go back to the smile example. Assuming that the smile muscle is contracting based on our previous mirror observation, why doesn’t the corner of the mouth go up? Try smiling again and this time watch your neck in the mirror. Do you see cords or bands “pop out” on the affected side of the neck? This demonstrates synkinesis or abnormal contraction of the platysma muscle. This is a superficial muscle on the neck that is innervated by the facial nerve. We can speculate that some nerve fibers abnormally regenerated into the platysma (since it doesn’t contract during the smile on the unaffected side). The normal action of the platysma muscle is to pull down the corners of the mouth. If the smile muscle is pulling up the corner of the mouth and the platysma is pulling it down, where does it wind up? Usually stuck, going nowhere. It is totally restricted from performing normal movement and expression. Think of it as being comparable to a tug of war. Typically, you have two very strong teams pulling with all their might and yet the rope doesn’t move much- until one team lets go.
So what do we do about it? The first step is to accurately identify which muscles are contracting both normally and abnormally. This usually requires a therapist who is experienced in this fine type of observation. The next step is to learn how to inhibit the activity of the muscles that are contracting out of sequence. For example, learning how to keep the platysma relaxed while producing a smile will allow the corner of the mouth to begin to move upward. A byproduct of this process is that associated tightness and spasm subsides, leaving the person much more comfortable. The therapy is less like typical therapy and more like athletic or music training. Minimal, successful movements are practiced and then progressed as success is achieved. Electrical stimulation is not helpful. It does not improve coordination of synkinesis and can actually activate already overactive and uncoordinated muscle movements further reinforcing abnormal patterns.
Treatment for residual synkinesis can be effective at any time after it is noticed. There is no time limit. That is because the focus of the treatment is on re-coordinating rather than stimulating muscles. We know that when synkinesis is present the facial muscles are viable, or “alive”. Even an abnormal movement is still a movement! So even many years after synkinesis develops it is possible to restore more normal movement patterns and expression with specific, appropriate training.