Bell’s Palsy: the Full History, the Treatments and Why it Happens
Almost all of us have heard of “Bell’s Palsy”– it’s relatively common. But, luckily, Bell’s Palsy is uncommon enough that most have no personal experience with it. It’s description, especially without any context, can sound worrisome- a disease state caused by a virus, occurring suddenly without pretense within hours to a days, most often affecting those in their 20s to 40s along with the pregnant and chronically ill, deforming half of the face, causing ear pain and affecting hearing and vision and speech.
Those of us that treat facial paralysis know well how it starts - suddenly one side of the face starts to feel sluggish. Or there’s a slight tingle or pressure around the ear. Usually it’s ignored at first, but as the hours pass things worsen. Soon one-half of the face isn’t moving. The facial muscles on the opposite side now pull the nose and mouth away from the midline. The affected eye doesn’t close but just rolls upward when trying to blink. Drinking becomes difficult. It’s hard to articulate clearly.
The experience can be terrifying. Many if not most are convinced they’re having a stroke. Some don’t know how or when the symptoms will stop progressing - will things continue on to their limbs, or lungs, or heart? Have they been exposed to some neurotoxin? In the ER, or in urgent care, or over the phone – we can hear the distress in their voices. So it’s the doctor’s job to slowly, clearly calm things down and provide some context:
To teach these patients about what they’re experiencing, we have to provide the details first about the facial nerve, and next about the virus that’s attacking it. The facial nerve supplies the signals for all our facial muscles. The nerve starts in the brain and runs from deep in the side of the skull through a narrow bony tunnel outward and forward to the muscles that allow us to smile, blink, frown, sneer, and all the rest our face can do. Bell’s Palsy likely occurs when a latent Herpes virus, that normally lives quietly within a nerve bundle, “reactivates” and causes swelling of the facial nerve. The likely culprit, the Herpes simplex 1 virus, is found in roughly half the population (and also causes cold sores). The virus often finds opportunities to flare up when the host’s immunity is down, like after an illness, or when prone to big fluid shifts like during pregnancy. When it does flare up it causes swelling within the nerve right inside that narrow bony tunnel. With all the swelling in that narrow space the nerve is choked off from its blood supply and is unable to send signals out to its recipients – so the facial muscles are paralyzed. As mentioned it also causes pain or pressure within the ear, changes in taste, and hearing sensitivity because of the other duties of the facial nerve.
The History of Bell's Palsy
The scientific explanation of Bell’s Palsy, the pathophysiology, is relatively new knowledge. However Bell’s Palsy itself is not. As a species we’ve been suffering from Bell’s Palsy long before it was given it’s name. In Ancient Greece, for example, they recognized that nerve pathology like paralysis, spasms, numbness, etc. could occur but they didn’t know how or why. Aristotle thought all nerves originated from the heart - he saw the heart as the most important organ of the body, and the nucleus of all movement and sensation. Centuries later, Galen, in Ancient Rome, got a little closer. He recognized that nerves stemmed from the brain, which he assumed was the chief operator of the body. He even noted that some nerves were responsible for sensation while others for specifically for action. However, he also believed that the nerves were hollow tubes that function via the flow of the human energy force, spiritus animalus.
Galen’s way of thinking remained the working theory for centuries. It was not until much later, in 1686, when the Dutchman Cornelus Stalpart van der Wiel was the City Physician of the Hague that we are provided with one of the first clear written descriptions of Bell’s Palsy. He described a patient of his, a shoemaker’s wife, 14 days post-partum, who had made the “reckless and impudent” decision during her recovery to leave the house for church to thank God for her safe childbirth. Suddenly and quickly her mouth became twisted, one of her eyes wouldn’t close properly, she drooled and she could no longer “blow or spit”. Stalpart van der Wiel believed that because of her exposure to the cold, her mucous had cooled and became more viscous within that hollow tube that joined the brain to the facial muscles. This obstruction must be inhibiting the spirits from flowing within the tube – and thus causing paralysis. While he was wrong about why this was happening to our impudent shoemaker’s wife, he treated her correctly with what tools he had. He wrote for a concoction of anti-rheumatic therapies – unguentum nervinum, lignum guajacum – among others I’d never heard of. She was better within 3 weeks.
We must jump ahead another 150 years to learn why it’s Bell’s Palsy, not van der Wiel’s Palsy. The eponymous Bell is Sir Charles Bell, a Scottish surgeon, neurologist and artist that was born in Edinburgh two years prior to the Declaration of Independence. He was the fourth of what would become four famous Bell sons, born to a clergyman who died 5 years after Charles’ birth. Of note, his older brother, John, was also a famous surgeon known for his diagnostic skills –he was later the inspiration to Arthur Conan Doyle’s Sherlock Holmes.
Charles Bell was a surgeon, an academic, devoutly religious, a skilled painter and –most of all- an anatomist. In Edinburgh and later in London, he dissected, taught, and painted the intricacies of the human body – especially the nervous system and the emotionality of facial expression. During one careful dissection, he exposed the spinal cord of a rabbit and precisely poked it – discovering that the posterior spinal cord was responsible for sensation and the anterior spinal cord for movement (now called the Bell-Magendie Law). In a human dissection he identified the nerve partially responsible for breathing (respiratory nerve of Bell). He was also one of the first to correctly recognize the function of the facial nerve, and thus the syndrome that results from its injury took his name – Bell’s Palsy.
Prevalence and Prognosis: Bell's Palsy
So fast forward two centuries to today – what do we know? The answer is a lot, but far from everything. One of the most comprehensive summaries we have of the natural course of Bell’s Palsy comes from Dr. Erik Peiterson, a Danish otolaryngologist from Copenhagen. Dr. Peiterson compiled a list of over 1,700 cases of Bell’s Palsy (BP). Looking at these 1,700 cases we learn that BP carries a relatively good prognosis. We also know that relatively is not good enough for the patients that suffer from it.
In Denmark, Peiterson found that BP afflicted 32 people per 100,000 each year. That may not seem like many – but once again this requires some context. For comparison, annual mortality from lightning strikes in the U.S is 0.023 per 100,000 – with most in the South and Midwest. So, with reasonable certainty, you’re probably safe from lightning strikes (but don’t push it). On the other hand, during the 2017-2018 flu season the annual incidence of getting the flu was 14,000 per 100,000, or 14 people in every 100. So – very common.
With these types of statistics I think of Lawrence, KS – a college town near where I grew up. Lawrence, KS has a population of approximately 100,000 people. You’d need 43 Lawrence, KS’s to have one lightning strike mortality in a year. But, by the numbers, 32 citizens of Lawrence, KS are afflicted with BP each year. So it’s not an every day occurrence, but it’s definitely not uncommon.
The 32 citizens of Lawrence, KS that suffer BP each year don’t care whether it’s common or uncommon. It’s happened to them, and it’s undoubtedly a traumatic event. For example, Peiterson asked the patients with new facial paralysis what they thought might be happening to them when the symptoms first started. As mentioned, half of them thought they were having a stroke. Another 25% thought they had a brain tumor! Obviously to walk into an emergency room or doctor’s office believing you’re suffering a stroke or brain tumor is a life-changing event.
Luckily, as mentioned, the data shows that the overall prognosis is a good one. Seventy-one percent of those suffering from BP in Peiterson’s study had a complete reversal of their symptoms – their facial movement returned completely to normal. But what, specifically, do we tell patients when they come to us with new onset facial paralysis? This is why cross-sectional studies such as this is helpful to clinicians - the chief goal is to help us predict whether a new patient with BP will end up in the 71% group, or in the 29% group that don’t have a complete recovery.
To give the most accurate prognosis for a patient, we need a few key pieces of information. These include how bad the facial paralysis was to begin with, the patient’s age, how quickly the nerve shows signs of life afterward, and whether the patient received the right treatment at the outset.
For example, some of those suffering from BP notice that their facial muscles are weakened, or asymmetric, but not completely paralyzed. Others have no movement of the face whatsoever. The patients in the former group, with partial paralysis, did much better – they enjoyed a 94% rate of total recovery. The patients in the latter group, with complete paralysis, didn’t fare as well – only 61% returned to their baseline. Obviously we need to factor these numbers into our discussions with patients to give them the clearest picture of what to expect.
How is age as a predictor?
Luckily, most kids do very well – 9 out of 10 return to normal. For teens and those in their 20s the prognosis is also pretty good – 84%. In their 30s and up to age 44 – 75%. However for those older than 60, about 1/3rd will make a full recovery from BP as the weeks and months pass.
How quickly the nerve starts to recover is also an important factor. When there is a complete paralysis, the faster the nerve shows signs of life, the more likely a better outcome. For those that recognized some facial muscle movement early - in weeks 1, 2 or 3 after the Bell’s Palsy set in - 90%, 88% and 84% ended up back to normal, respectively. So, even if its just a flicker of movement, when you notice some semblance of recovery early on the prognosis is good. The chances of a complete recovery if there’s no movement after 3 weeks is smaller – luckily this was a smaller group, only 15% of those that suffered a complete paralysis.
Using a person’s age, timing of recovery, and other predictors are helpful to tell us what happens during BP. But we also want to know why the facial paralysis occurs as it does. For example, why do 85% of those with complete paralysis notice some movement within 3 weeks after the onset – and most of the other 15% don’t notice any movement until 3-6 months later? Why is there a bimodal distribution to the recovery, rather than a smooth curve? What’s happening after the first 3 weeks but before the 4th month?
The authors of the study believe it has to do with how badly the nerve was injured during those first hours after the BP set in. As mentioned, BP follows a reactivation of a latent Herpes virus that normally resides quietly in a facial nerve bundle in about half of the U.S. population. When the nerve reactivates our immune system responds to this and sends in the troops – causing swelling within the nerve. This swelling occurs in a very poor location for the facial nerve - within a narrow bony tunnel - like the L train tripling in size traveling under the East River. This chokes off the nerve, impairing its blood supply and preventing it from transmitting signals from your brain to the muscles of your face.
If the nerve is just bruised and remains continuous the signal will just be interrupted briefly and the nerve will soon start passing along instructions again. Eighty-five percent of those with BP are in this camp. But if it’s more seriously injured, it has to start again from scratch. The facial nerve is like the copper filament that runs within the plastic insulation of our cable wires. The plastic insulation is like the myelin sheath, a fatty insulation around the nerve that helps to protect the nerve within and send its signals more efficiently. It’s the nerve inside the sheath, like the copper filament, that actually sends the signals via electricity. And when the nerve itself is severely injured during BP, the segment that is “downstream” from that narrow bony tunnel withers away to nothing over the next few days. This is called Wallerian degeneration. Your body has to rebuild this missing nerve segment from that point onward – and it lays down new track at a speed of about 1 millimeter per day. This is the situation in about 15% of those with BP – those that notice their facial muscles perking up 3 to 6 months later. And unfortunately it often doesn’t recover with complete fidelity – those in the delayed group have a lesser chance of a complete recovery in the end.
Treatment of Bell's Palsy
Finally – how do we treat those suffering from Bell’s Palsy? How do we treat BP acutely, right when it starts? And how do we treat the long-term effects for those minority of patients that suffer them?
Luckily for those of use that treat Bell’s Palsy, when trying to answer these questions we have Cochrane Review articles to reference. This is important, because there isn’t always solid evidence to rely on when making medical decisions. Especially in a niche field such as facial plastic surgery. Much of the literature we refer to involves a fellow clinician writing “I’ve tried this new treatment on x number of patients and it was safe and effective for me - consider giving it a try”. And they present their data. These studies are not the most rigorous in terms of scientific evidence – but still invaluable. They present a new idea to the group, they document it’s efficacy, and – if it catches on – they get the ball rolling for more robust scientific comparisons in the future. And, when done correctly, the best scientific comparisons we can hope for are randomized clinical trials – the kind found in Cochrane reviews.
Cochrane is a British charity formed in the early 1990s named for Archie Cochrane – a Scottish physician whose life story is fascinating enough to warrant its own blog post (but I’ll spare you). The charity was founded in response to frustration over the lack of real evidence doctors could find to make decisions. So they set out to help clarify the good research from the not-as-good to make sure patients were getting the best care possible. They do this by picking a subject and summarizing all the randomized controlled trials (RCT) that have been published on that subject. They throw out everything that’s not an RCT - doctor’s opinions, surveys, case reports - and focus on direct comparisons. For example, what happens if you give 100 people this medicine, and another 100 people a placebo, do they get better?
Luckily, there are Cochrane review articles addressing the treatment of BP. One such review, last updated in 2010, scanned all the available RCTs in the literature and concluded that patients should take an oral steroid medication quickly after onset. Intuitively, this makes sense. Steroids are potent anti-inflammatory medications. They’re given for poison ivy induced dermatitis, for rheumatoid arthritis, for tendonitis, for sinusitis, and for countless other “itis”’s because they decrease the body’s inflammatory response. When the facial nerve becomes inflamed within that narrow canal we need to quickly tamp down the swelling, and a burst of steroids help do just that.
Another Cochrane Review studied the use of anti-viral medication. Anti-viral treatment seems to make sense – if we target the Herpes virus that’s causing the swelling then the symptoms may improve. Despite this, the results were mixed. Anti-viral treatment by itself doesn’t seem to be helpful. But it seems to work well along with steroids. In part because of these Cochrane Reviews, doctors treating BP will prescribe both a steroid and an anti-viral medication.
The longterm effects of Bell’s Palsy are very different than what we see in the short term. Immediately after onset, some people’s faces will have no movement or tone at all - complete facial paralysis. But as the nerve recovers, 30% of these people will not have a clean recovery. The muscles in the face will regain their tone, but often it feels too tight and cramped. It pulls against the healthy side and leads to a sort of grimace. And the muscle doesn’t fire when you want it to. It can twitch. Or fires when you’re trying to move a different muscle in the face. Sometimes when people blink the corner of their mouth twitches. Or when they smile their eye narrows. The neural circuitry has crosswired – this is called facial synkinesis.
Most would agree that facial synkinesis is a better problem to have than true facial paralysis – but most would also agree that “better” doesn’t really matter. It changes the way one interacts with the world. One patient told me that she feels her cheek pulling continually – a tightness, a bulky mass where her smile muscles used to be. When she’s at a cafe ordering coffee, for example, she feels it pulling, and feels her face forming a kind of sneer. She doesn’t want to sneer, she wants to smile, or at least have a neutral expression – she just wants to have control over which emotions she shares and doesn’t share.
Why is this happening?
There are a few theories. The simplest explanation involves inaccurate nerve regeneration. Remember that, in cases of more severe Bell’s Palsy, Wallerian degeneration occurs. The nerve injury occurs upstream and then the roots downstream degenerate and have to regrow one millimeter at a time. This often takes months. While the nerve branches are regenerating many of the rootlets get lost along the way. The tiny nerve branch that operated the muscle around the eye instead travels downward and connects to a muscle near the mouth. Afterwards, whenever the brain sends signals for the face to blink, just like it always has, the lip twitches instead. This could also be true for the muscles in the neck, and the forehead, and below the lip – resulting in facial synkinesis.
Another theory involves the aforementioned plastic insulation around the copper wire. Its possible that the nerve sheath isn’t insulating as well as it should after Bell’s Palsy. If the insulation, the myelin sheath, is injured along with the nerve then we may see cross-signaling from one nerve rootlet to another. If a signal is sent to raise the eyebrow it may sloppily run off to a lower branch at the same time, causing a blink, or a lip twitch, or a neck cramp.
After years of study we’ve come up with a host of different treatments for facial synkinesis - from meditation to surgery and everything in between.
Picture a common facial synkinesis encounter: a young woman is bothered by excessive tightness in her cheek and neck. Her eye on one side is always narrowed, and closes when she eats or talks. The crease between her upper lip and her cheek is deepened, her chin dimples asymmetrically and she dislikes the appearance. Even though she feels an uncomfortable tightness in her face, the muscles around the eye, above the mouth and in the neck don’t function as well as the other side. It’s like they’re frozen, just pulling against themselves rather than allowing her movements of self-expression. And she’s worried – it’s been getting worse since she started feeling the muscles function again 3 or 4 months after the BP.
So where do we start?
As with most treatments, you want to start with the least invasive and work your way up. The first visit, for many patients, is to the acupuncturist. Acupuncture and other Eastern medicine disciplines are finding their niche in the treatment of many chronic conditions, such as back pain, cancer associated nausea or discomfort, abdominal pain, and facial synkinesis. Western medicine has in imperfect track record treating conditions such as these – Eastern medicine can be helpful. I wouldn’t seek acupuncture for an abscess, for example, as surgical procedures and antibiotics are the best treatment. But for a chronic condition like facial synkinesis, in which there is no panacea, acupuncture can play a role.
Many patients early in my career asked me whether I recommended for or against acupuncture as an ancillary treatment. Thus I had to familiarize myself with the practice. I learned the pre-eminent text, Huangdi Neijing, was written more than 2,000 years ago. This alone helps to illustrate the differences between Eastern and Western medical treatments. My Pathology textbook from 1998 is already out of date. The text, and the centuries of study and practice that followed, describe our bodies’ vital energy, qi, flowing in circuits throughout our body called meridians. There are 12 main meridians that run through certain anatomic points, including internal organs. The meridians are divided into yin and yang groups. The path of the energy flow through these structures is of vital importance to an acupuncturist. The yin organs include the heart, pericardium, lung, spleen, liver and kidney and the yang organs include the stomach, gallbladder, large and small intestines, and bladder. An anatomic diagram of the primary meridians looks like a map of the New York subway system.
The flow of qi through these meridians is prone to disruption. Disruption in flow, in turn, leads to sickness and disease. Chinese medicine includes the yin/yang concept, or the mutually opposing forces like heat and cold that can affect the body. It also includes the five elements that structure our universe – earth, metal, fire, water, and wood. Balance, both internal and external, is essential to healthy flow of qi.
The flow of energy within a meridian can be disrupted when an imbalance occurs at a certain anatomic point. With this a dam-like effect can occur within that meridian. For example, with Bell’s Palsy, Chinese medicine practitioners believe that cold air against the face combined with stress at work, amongst other stressors, leads to an obstruction within the meridian that encompasses the face. By inserting a narrow needle into a defined point along the meridian the obstruction can be released and the flow of qi restored.
There are more than 300-400 described key points along the yin and yang meridians (the number varies amongst practitioners). The acupuncturist memorizes which points correspond with each meridian, and thus which points can be treated for nausea vs. fatigue vs. back pain vs. depression vs. headaches, etc.
Does this work?
The answer is complicated. For some conditions, there is some evidence that acupuncture therapy may be helpful beyond placebo. Why this is the case remains unclear. There are obviously no anatomic correlates to the yin and yang meridians within the body. There is no bodily substance that correlates to qi. Acupuncture diagrammatic guides were drawn before we attained a sophisticated view of human anatomy. But Western medicine remains incomplete, as well. Eastern medicine may help to fill in that gap, even if we don’t fully understand the specifics.
For BP, however, no one has yet to show its beneficial. Our friends at Cochrane have done the work for us – they told us in 2010 that acupuncture has no proven benefit – or deficit. So when I’m asked “should I try acupuncture?”, I reply – “sure, it can’t hurt, it just might not help” .
Many patients with BP just need to feel as though they’re trying something. As a physician, asking a “patient” to just be patient is a terrible task. Most of us need an avenue of self-improvement.
But I give very different advice when symptoms of synkinesis kick in. When the face is still paralyzed, allowing time for recovery is often the best we can do. But when the face tightens – it’s time to get to work. My first recommendation is physical therapy. PT is an umbrella term for an assortment of exercises and massages, guided by a physical therapist and practiced at home by the patient.
PT is a one-on-one sport. It’s conducted over multiple sessions with a certified therapist that acts like a trainer – reminding your face how it used to move. It’s difficult work with slow, but real, gains. Prior to BP, when we smile our brain sends a signal to one twig within the bundle of the facial nerve that goes precisely to the smile muscles. Through that tiny nerve branch the brain gives details for how long to smile, how broadly, how sincerely. With facial synkinesis, when the brain sends that same signal the twig doesn’t send it to the smile muscles but rather to the frown muscles, or the blink muscles, or the muscles in the neck. The brain gets that feedback and responds – “what’s going on down there?”
PT works on the brain, on the muscle, and on the person as a whole. A therapist will work on the brain by sitting in front of the person and asking him or her to mirror their facial movements. When the therapist frowns, their client frowns. When the therapist blinks, their client blinks. But if the client tries to blink and grimaces instead, they both work together to practice ways to isolate those blink muscles. Or if the client tries to smile and their neck tenses up – they rehearse firing those smile muscles and relaxing the neck. Sound difficult? It is.
A therapist will work on the muscle directly, too. If a client has a bulk of tight muscle contracting in their cheek rather than allowing them a smile the therapist will provide instruction on how to massage it, elongate it, and tell it to calm down despite the fact that its being told to contract. If the muscle can relax, potentially it provides feedback to the nerve to relax, or the brain to stop sending these errant signals. With a relaxed muscle you’ll find a more relaxed patient. They look more symmetric and they feel more symmetric. With this mindset, progress can be made.
For those in the 30% dealing with facial synkinesis despite having undergone rounds of physical therapy and countless home and YouTube remedies, we still have options. Our next treatment is well known – botulinum toxin A, better known by its namebrand: Botox®. Botox is a truly a toxin. It’s produced by the microbe Clostridium botulinum. The toxin prevents the release of the messenger acetylcholine from the nerve to muscle – thus blocking the signal from your brain to the muscle.
Luckily, despite the connotation of the word “toxin”, Botox has dozens of beneficial effects. Within 50 years of Clostridium botulinum’s discovery by a Belgian scientist Americans had begun to use a synthetic version for medical use. It began with strabismus (an error of the muscles around the eye), then expanding to migraines, sweating, spasms, and – of course it’s most common use – wrinkles. Botulinum toxin is now marketed under brand names such as Botox®, Dysport®, and Xeomin® - providing consistent and safe results in experienced hands. And these safe results extend to patients suffering from facial synkinesis, too.
When I bring this up in my clinic, some patients ask – “I’ve just had facial paralysis - why would I want an injection that causes more muscle paralysis?” This is a valid question. Botox®, Dysport®, Xeomin® do causes paralysis in the narrow area in which they’re injected. That’s the benefit behind its use for facial aging. If the muscle below the skin doesn’t contract, the skin that’s atop the muscle won’t get scrunched up as it does when the muscle shortens. No movement of the muscle = no wrinkling of the skin.
For those dealing with facial synkinesis, flaccid facial paralysis is no longer the problem. The problem is that the facial muscle is firing and tensing when it shouldn’t be. When you treat facial synkinesis often you recognize a pattern. The lip twitches when the eye blinks. The muscles that pull down the lip fire at the same time as the muscles that lift up the lip – and thus there’s no smile. The muscle around the eye fires whenever the mouth whistles or uses a straw, and one eye closes. The muscles in the neck tense during stressful days, causing cramping and frowning. This is not a paralysis issue but a synkinesis issue, where the muscles make up their own rules.
This is where the Botox comes in – to lasso, corral, and bludgeon the facial muscles into submission. In this sense, Botox is only as good as the person injecting it. It’s not like an antibiotic for tonsillitis where we take a pill and wait for things to improve. It’s more like a surgical tool – it needs to be administered precisely and delicately to get the right result. To do so we must treat the face like a game of tug-of-war. For example, take the eyebrow. There’s one muscle pulling it upwards – the frontalis muscle – and three muscles pulling it downwards – the orbicularis oculi, the corrugator, and the procerus muscles. If I paralyze one side, the other side wins. People with synkinesis can often have the eyebrow pulled down, as though they’re persistently suspicious. In this case, I release one side of the tug-of-war with Botox® and let the other side win – injecting the down-pulling muscles to lift the brow and create symmetry.
The smile is the same. At least 4 muscles are pulling up the corner of the mouth when you smile, and at least 3 are pulling it downward. I need to help the muscles lifting upward by injecting the down-pulling muscles to encourage a more symmetric smile. This is also true around the eye. While only one muscle controls the blink, the orbicularis oculi, it’s waging a tug-of-war with itself. It’s closing and narrowing the eye when it shouldn’t, but not closing enough when it should. So we need to walk a tightrope when treating this muscle. With too much of the medicine the eye may close inadequately – causing additional dryness and tearing. With too little the eye muscle remains taut. It requires just the right amount.
One of the benefits, and detriments, of Botox is that is requires repeat injections every 3 months. This transience is helpful if a patient describes too much laxity after the injection in one area following an injection (an unusual occurrence). But the temporary nature of Botox is unwanted if the effect is just right – it may be inconvenient to visit the facial plastic surgeon every 3 months.
In these cases, a final option is a surgical procedure – called selective neurolysis. The goal is to snip the tiny nerve branches that are sending the wrong signals, and leave the tiny nerve branches sending the right signals in place. Under general anesthesia, we utilize an incision that’s hidden in the hairline and around the ears (the same incision we use for cosmetic face and neck lifting surgeries). Then we tunnel carefully under the skin towards the corner of the lip. We then isolate all the pale yellow branches of the facial nerve that are stemming like reeds from behind the ear toward the facial muscles ahead. Sometimes we’ll find up to 10 or 12 branches in all. One by one, we use a handheld device that sends electric impulses to its grounding electrode. We stimulate the small nerve branches individually. For each stimulation we carefully observe and denote the facial movements that’s produced - grimaces, twitches, squinting, and flexes. For the facial movements that are unwanted, like dimpling of the chin, frowning, neck tensing, and others, we precisely remove approximately 1cm of that nerve branch. (We remove a segment rather than just transect the nerve because we want to leave no chance for that nerve to recover). For the desired facial movements, like smiling, dimpling of the cheek, blinking we leave the nerve just where we found it. Then we suture the skin back together with a minimal, well hidden scar.
Right when the patient awakes he or she will notice the change. With an ideal result, the smile looks more symmetric and the facial movements look more natural.
To get the best result we need lots of tools – physical therapy, meditation, botulinum toxin injections, and surgery. All play a role in moving the ball forward. That’s the goal – working to make each month better than the month before. And this is true from the moment BP sets in.
The diagnosis of BP can be feel like a crisis. It’s traumatic, and, despite the fact that the overall prognosis is good, those suffering from BP need reassurance. So we start with steroids and antivirals, we watch carefully for things to improve, and give advice every step along the way. Bell’s Palsy is more than just deficit in the muscle or the nerve. Our faces and its expressions are windows – allowing others to peer in and for us to look out. When this changes, we change. The physician’s job is to both convince our patients they can be resilient, and give them every chance to change for the better.