Peled Migraine Surgery Blog

Ziv M. Peled , M.D. Presents Burning Migraine Questions for April 18, 2019. Dr. Peled discussed he following questions:

0:55 Following an Occipital Nerve Block I ended Up With a Pronounced Dent In the Back Of My Head
3:11 Can the Nerves That You Separate Go Back Together
5:03 My Neurologist Said He Didn't Want to Cut My Nerves Because He Said I Would Have A Burning Sensation All of the Time
7:16 Is it True That Autoimmune Diseases Can Make Occipital neuralgia Worse?
11:18 My Neurologist Says This Is Experimental - I Feel Guilty Going Against Their Best Judgement
19:14 What If Compression Is Done Higher Up On the Scalp?

As many of you are likely aware, there is a general disagreement between plastic/peripheral nerve surgeons and neurologists with regard to nerve decompression or transection and implantation as a treatment for chronic headaches.   The main issue stems from the fact that chronic headaches such as migraines are considered to be centrally-mediated.  What that means is that the headaches arise from any number of complex mechanisms within the central nervous system (i.e. brain or spinal cord). 

From the viewpoint of the neurology community, this concept of chronic headaches (e.g. migraines) accounts for the overwhelming majority of the various headache subtypes recognized clinically (e.g. cervicogenic headaches, new daily persistent headaches, etc.).  In contrast, surgical decompression (e.g. of the occipital nerves) is performed on the peripheral nervous system (i.e. nerves outside the brain and spinal cord). The possibility that peripherally mediated factors can cause or contribute to chronic headaches is relatively new, but has been around for over 20 years. 

Plastic/peripheral nerve surgeons who perform headache operations feel that in some patients (e.g. those that have failed traditional treatment modalities, those that respond to nerve blocks and those that have a specific set of findings on physical exam), peripheral nerve compression is a critical causative factor in headache symptoms.  Historically, these two camps have been at odds, but that dictum may be changing.

In a recent article in a prominent neurology journal (Blake and Burstein, The Journal of Headache and Pain, (2019) 20:76), two prominent neurologists, discuss the concepts and science behind peripheral nerve factors in the generation of headaches.  Furthermore, they elaborate on the fact that some patients who have what they term ‘unremitting head and/or neck pain’ (UHNP) share many clinical features of patients diagnosed with other headache disorders (e.g. chronic migraine, NDPH). 

The authors conclude among other things, that we lack an accurate classification system and nomenclature to describe these patients and that peripheral nerve surgery may be a reasonable treatment option for this subgroup of people.  The scientific possibilities underlying these conclusions are also discussed in some detail. 

I cannot emphasize how critical this paper is to those of us who have been championing the concept of headache surgery as a viable treatment option.  It is also a huge milestone for headache patients themselves.  I believe this manuscript is one of the first cracks in the dam that separates neurologists from peripheral nerve surgeons and might ultimately lead to wider acceptance of peripheral nerve causes for chronic headaches. 

Working together, both neurologists and peripheral nerve surgeons have the best chance of convincing  their respective colleagues that this notion is valid and advocate/work together to lobby for better insurance coverage and more scientific studies to further refine the patient population who would best benefit from surgical intervention as a primary or adjunctive treatment modality.  I applaud Pamela Blake and Rami Burstein for their courage in putting their thoughts to paper in what I am sure will be a somewhat controversial topic amongst their own neurology colleagues, but one which will ultimately benefit millions of headache patients.

There continue to be questions raised both in my office as well as online about the difference between neurectomy/implantation (transection of the nerve and implanting it in the local muscle) and decompression.  Along with these questions come many misconceptions about the advantages and disadvantages to each.  This post hopes to address some of those issues.

To decompress a nerve means simply to remove some form of external compression that is putting excess pressure on that structure.  As has been mentioned previously, compression can be a result of scar tissue, tight muscles, abnormal blood vessel anatomy, connective tissue, etc.  Decompression also means that the nerve is left intact and that hopefully, once the effects of the operation (e.g. swelling) and the effects of the compression wear off, the nerve will function well again.  There are advantages to decompression.  The most obvious advantage is that the nerve is preserved so hopefully sensation to that area will also be preserved.  Secondly, since the nerve is not cut, the chances of a post-operative neuroma are theoretically low.  There also disadvantages to this approach.  First, the surgeon and/or patient make a judgement call that the nerve will recover if simply decompressed, but this doesn’t always occur.  I believe that this is the primary reason some people who have decompression ultimately require neurectomy and implantation Second, just because the chances of a neuroma are low it doesn’t mean that they are zero - you can still get a neuroma-in-continuity, especially if there is a lot of manipulation required to adequately decompress a nerve.  Third, if the compression has been severe and long-standing, the nerve may take many months to fully recover.  Fourth, if recovery does occur, there is no guarantee that sensation to the relevant area will be “normal”.  It may always feel a little bit off.

The biggest misconception with a neurectomy is that it is like pulling the plug out of a wall outlet.  However, the injured nerve is not ripped out of the spinal cord.  A better analogy is that the injured portion of the nerve is identified and the area just upstream where the nerve appears healthier is where the nerve is transected.  This maneuver is just like cutting the central portion of a power cord to a lamp where the wires have frayed.  The downstream part of the nerve (e.g. that which goes to the skin) is now irrelevant just like the part of the cord that is still attached to the lamp.  There is no longer any electricity going though that part so the bulb will not turn on.  However, that upstream cut end is still a live wire as it is still connected to the wall outlet and therefore must be capped. In a human being the “capping” goal is achieved by implanting the upstream (proximal) nerve end (which is still getting nerve impulses from the spinal cord) into the local muscle.  There are advantages and disadvantages to this approach.  One advantage is that you may see immediate improvement in symptoms although not always.  Sometimes, people continue to experience pain in that nerve even though when they touch their skin they are numb.  This situation exists because the nerve that used to go to that area of skin is getting impulses from the spinal cord and brain albeit ending within the muscle and so your brain thinks that part of the skin hurts even though when you touch it, it is numb.  Eventually in most cases, the nerve end in the muscle calms down and the pain improves.  Another potential advantage is less dissection because the downstream area of the nerve doesn’t need to be dissected once transected as it is now irrelevant. There are potential disadvantages as well such as persistent nerve pain if the implanted nerve doesn’t calm down, a neuroma if the nerve comes out of the muscle and the obvious numbness in that nerve distribution. Another misconception is that neurectomy is a guaranteed, home-run result which is not true for those reasons mentioned above.  There are clearly other nuances that exist which is why discussing these issues with your peripheral nerve surgeon is so important.  Just as each patient is unique, each person will have different tolerances for different post-operative outcomes so a good discussion is useful both for the patient and the surgeon.

One of the questions I find myself answering again and again is how I make the decision as to what to do with a nerve once I see it in the operating room.  Do I perform a neurectomy and muscle implantation or do I stop at a decompression?  There are a lot of factors that go into making that decision so I will elaborate on a few of these in the lines that follow. 

To begin, there are certain ultrastructural characteristics that indicate a relatively healthy nerve.  One, you should have an intact vasa nervorum – the blood vessels within the nerve.  These can be seen under loupe magnification as fine red lines and indicate good blood flow to the nerve itself.   Blood flow is usually a sign of life and this nerve should be considered for decompression and preservation.  Another characteristic is the feel of the nerve.  A healthy nerve should feel like a soft, wet noodle.  If a nerve is firm like a banjo string, it usually means that there is at least scarring of the epineurium (the outermost covering of the nerve) and often the structures contained within.  In these cases, an internal neurolysis to separate the healthy from unhealthy fascicles is required and if the scarring affects too many fascicles, a neurectomy with muscle implantation is probably the better part of valor.  Third, the fascicular pattern should be visible.  Think of nerve fascicles like bundles of wire (e.g. the blue one vs the red one in all of those movies in which the hero is trying to defuse a bomb) within an electrical cord.  Stated differently, what you’re looking at when you look at a cord plugged into a wall is a rubber tube - the actual wires are the copper fibers inside that rubber housing.  Those copper wires are analogous to the individual neurons (i.e. nerve cells) and in an electrical wire, are often arranged into bundles.  In a nerve, those bundles of neurons are called fascicles. However, unlike the cord plugged into the wall, in a healthy nerve, the “rubber housing” should be transparent and the fascicular pattern should be visible. If it isn’t, the nerve isn’t completely healthy and those fascicles may be permanently damaged.  Take a look at the attached picture of a recent patient whose supraorbital nerve branches (multiple black lines) and supratrochlear nerve (arrowhead) are visualized.  Notice how white the supratrochlear nerve towards the right of the picture is and the lack of any fascicular pattern.  In contrast, the supraorbital nerve branches towards the left are pink indicating an intact vasa nervorum and the fascicular pattern is visible if you look very carefully (and likely magnify the picture on your computer). Fortunately for this patient, the vasa nervorum re-constituted and the fascicular pattern became more pronounced once the supratrochlear nerve was decompressed and a few minutes were given for the nerve to declare itself – yet another nuance of technique.  Therefore, both nerves were able to be preserved in this particular case.

Yet another factor to consider when deciding what to do with a nerve in the operating room is the actual function of the nerve itself.  For example, the greater occipital nerve, as its name suggests, has the largest area of sensory distribution of any nerve in the occipital region.  Therefore, performing a greater occipital neurectomy would leave the patient with a relatively large area of numbness.  Personally, I have a relatively high threshold for transecting the GON.  By contrast, the third (a.k.a. least) occipital nerve is many times smaller than the GON and has a minimal area of sensory distribution that is often also supplied in a redundant fashion by the GON.  Therefore, if the third occipital nerve is damaged, I have a lower threshold for performing a neurectomy since it is likely the patient wouldn’t have much numbness, if at all, were that nerve to be cut and buried in a muscle.  Lastly, is what I would call the “x factor”, in other words clinical decision making.  I’m often reminded of a saying I heard once that went something like this, “Good judgement comes from experience and experience comes from bad judgement”.  In other words, experience counts and takes into account a myriad of other variables before ultimately making decision A versus decision B.  What was the mechanism of injury and how long ago did it occur?  What other treatments have they had that might have affected the nerve along its length (e.g. RFA or cryoablation) and how many times have those modalities been performed?  How did the patient respond to the numbness from the nerve blocks?  How old is the patient and how likely is it that they would tolerate a repeat procedure if decompression fails? Alternatively, how young is the patient and what is their regenerative potential?  If you cut that young person’s nerve, how would they tolerate 50 years of numbness as opposed to the 70 year-old patient who may only live with it for a few years and has many other medical problems more pressing than a little hypoesthesia.  The take home message is that electing to perform a neurectomy as opposed to a decompression involves a multifactorial decision making process so have a frank discussion with your surgeon about how s/he will decide which path to take.

If I only had a dollar for every time I’ve heard this question…! I think this is a very reasonable and understandable query and gets at the heart of what it truly means to be a plastic surgeon. It reminds me of what one of my mentors once told me, which is: “Ziv, don’t go into plastic surgery unless you want to spend your whole career apologizing for your colleagues.” This mentor is a Full Professor of Plastic Surgery at Stanford University and is a full-time researcher. He has published over 1000 scientific articles in some of the top scientific journals (e.g. Nature, JAMA, Science) and is a member of the National Academy of Science. The problem with this question is that it implies that plastic surgeons are only known for performing cosmetic surgery. However, we do so much more.

If you have breast cancer, it is a plastic surgeon who will reconstruct your breast. If you are shot and have a large hole in your leg that requires tissue be moved from your back to cover the hole in your leg, it is a plastic surgeon who will perform that operation. If you have a cleft lip or palate, it is a plastic surgeon who will repair it. If you have a child born with a prematurely fused skull, it is a plastic surgeon who will fix it. If you need a face or arm transplant, it is a plastic surgeon who will lead that surgical team. If you cut a finger or arm off, it is a plastic surgeon who will replant it.

As you might appreciate given the breadth of these cases, we as plastic surgeons operate all over the body, on both young and old patients alike and on many of the bodily tissues such as skin, muscle, fat, bone, and of course, nerves (e.g. in the replantation of an extremity or face transplant).   Some of us have dedicated the majority of our practices to peripheral nerve surgery and perform operations on hundreds of nerves each year. That background gives us a unique skill set and degree of experience that is shared by few others.

When it comes to headaches and migraines, they are generally considered to be disorders triggered within the central nervous system and many patients are successfully treated in this way. However, for those who have head pain as a result of mechanical compression of nerves, causing occipital neuralgia or trigeminal branch neuralgia, the treatment needs to occur within the peripheral nervous system. Neurosurgeons predominantly operate on the brain and spinal cord. There are exceptions to be sure, but the majority of neurosurgeons have an expertise in the physiology and surgical treatment of the central nervous system. In contrast, many plastic surgeons have significant experience with peripheral nerves, and thus are much better positioned to work in the peripheral nervous system.

Hope that helps clear up some of the confusion. We clearly need to do a better job as a society, telling the world what exactly it is that plastic surgeons really do.

1. One of the first things to assess is whether your surgeon has significant and specific training in peripheral nerve surgery. Since the operations for chronic headaches/neuralgia potentially involve many nerves within the peripheral nervous system, the person performing such operations should have had focused training on the workup, evaluation and management of patients with any number of peripheral nerve problems (chronic headaches included). Because peripheral nerve surgery is performed on all parts of the body (e.g. arms, legs, trunk and head), your surgeon should ideally have experience and training with many of these types of nerve procedures because they provide the procedural foundation now employed in the operations designed for chronic headaches. A sample question that a patient might ask is what percentage of the surgeon’s practice is focused on peripheral nerve surgery.
2. Another important thing to ask your surgeon is how many of these procedures they have performed. In addition to the specific number of cases s/he has performed, the surgeon should also have experience with the wide breadth of peripheral nerves that are known to be potential causes of chronic, severe headaches. These include nerves within the forehead, temple and occipital regions.

3. Is your surgeon and member of the American Society for Peripheral Nerve (ASPN)? This society is the leading academic society for peripheral nerve surgeons. It’s mission is to stimulate and encourage study and research in the field of neural regeneration, to provide a forum for the presentation of the latest research and relevant clinical information and to serve as a unifying authority on all areas of neural regeneration and restorative neuroscience. In order to become a member there are a number of qualifications that a surgeon must meet. For example, a candidate has to be nominated by two of their peripheral nerve surgical peers and have published at least one scholarly, peer-reviewed paper on some aspect of peripheral nerve surgery. Looking for ASPN membership can serve as an objective vetting factor in deciding between several surgeons.  It also demonstrates a true commitment to the study of peripheral nerve problems and a genuine interest in advancing the field.

4. Your surgeon should also be able to provide you with references for the type of procedure(s) he or she is recommending. Not only does this give you the chance to speak with someone who has gone through what you will likely experience, it demonstrates that the surgeon has actually performed the procedure at least once before.

5. Finally, you should choose a surgeon with whom you have the best rapport. This is the hardest concept to describe or discern.  While there are still so few of us who perform these operations with regularity, realize that there still may be several qualified surgeons technically capable of performing the right operation for the correct indications.  However, just like every patient is different, so too is every surgeon.  Is their office staff professional and pleasant?  Does the doctor answer your questions in a manner that you can understand and make you feel at ease that they understand your particular situation?  Do they spend time actually listening to you and your symptoms?  Are they realistic in setting your expectations for what will happen before, during and after your procedure?  These factors can make the difference between simply a good outcome and a good outcome with a good experience along the way.

I hear this question quite often from just about every patient I see, whether for chronic headaches or tarsal tunnel syndrome.  The answers have to do with the technical aspects of the surgical procedure, the physiology of peripheral nerves as well as the wound healing process itself.    As you can imagine, a compressed nerve is usually compressed on all sides because it is a three dimensional structure.  Therefore when decompressing a nerve, it has to be manipulated such that the superficial, deep, medial, lateral, cranial and caudal aspects of the nerve can be examined and released if necessary. In addition, there are often multiple compression points (the GON has up to 6 that have been described and often others that are noted intra-operatively).  Moreover, there are times when there is intra-neural scarring (scarring within the nerve, not just around it) which also requires removal.  Hence, there is a fair bit of manipulation usually required (albeit with microneurosurgical techniques) during any decompression and or neurolysis procedure.

As part of the normal wound healing process, there is swelling.  The more neural manipulation required during the operation, the more swelling of the nerve you’re likely to have post-operatively.  I tell my patients to think of nerves as electrical wires, pure and simple.  All they do is conduct electrical signals back and forth, but it is the brain the interprets these signals as ‘hot’, ‘cold’, ‘painful’, ‘ticklish’ etc.  Therefore nerve swelling after an operation is similar to pouring water into the drywall in your house near the electrical wires – doing so will cause the lights to flicker on and off until the water dries up because the fluid is interfering with efficient electrical conductivity.  In the same way, swelling of the nerve can result in all sorts of “unusual firing” of the nerve and is one reason many patients may experience weird, sometimes painful sensations post-op.  However, if the nerves are going to recover, within a few weeks or months when the swelling has subsided, this “unusual firing” abates and the nerves “calm down”.  Just like with cutaneous scars (which also swell as part of the healing process) the time for swelling to decrease is usually longer than a few days or weeks.

Another reason why nerves may take a while to recover has to do with the severity and duration of compression.  I’m sure everyone has fallen asleep on their arm(s) at some point in their lives.  Sometimes, when you wake up, your hand is just a little numb and it takes about 10 seconds of shaking your hand to restore normal sensation.  Other times, however, when you wake up the entire arm seems paralyzed, weak and numb!  In these cases, aside from some transient agita, it takes several minutes of shaking the arm out for function and sensation to return fully.  Phew!  The difference between these two situations is that in the latter, the compression of the nerves to the arm has been present for longer and may have been more severe as compared with the former.  Therefore, it takes longer for sensation (and function) to return.  Now take that phenomenon and stretch the timeline out months and often years (sometimes decades) - that is how long many peoples’ nerves have been compressed.  Therefore, it can take weeks or months for function to return to “normal”.  Also, since the blood flow to the nerves in the latter scenario has been compromised for a longer period of time, they become more engorged with blood after flow is restored and then that extra blood takes time to return to its baseline levels.  It is for this reason that you often experience that sensation of tingling and pain after you remove pressure from the arm and as blood flow resumes. The same thing happens when blood flow is restored after decompression - (more intra-neural blood flow usually combined with more surgical manipulation).  Finally, we don’t immobilize our heads after surgery because doing so would stiffen all the joints and increase the likelihood that the nerve will become re-entrapped in scar. As a result, the nerves will glide right away after we manipulate them and also likely contributes to the lengthy recovery process. The take home message is that as patients and physicians, we have to be patient in assessing whether or not decompression has been successful as the final results may not be apparent for many months (as noted by many here).  After all, the same would true of a facelift or breast augmentation.

Chronic headaches continue to be a huge burden on the American healthcare system accounting for tens of billions of dollars in both direct and indirect costs annually.  These financial considerations don’t even take into account the psychological and emotional toll that this form of chronic pain has on those who suffer with it. Migraines themselves are felt to afflict as many as 12% of the US population.  As much as 2% of the world’s population suffers from chronic migraines, which by definition, means that traditional treatment modalities have failed. As I sat on the plane coming back from a recent conference, I began to reflect on the fact that we really need to step back and re-think how we approach this problem.

Over the years that I’ve been operating on patients for chronic headaches, a consistent thread is peoples’ frustration with their current care because their symptoms are not under control.  I hear constantly about confrontational patient-physician interactions or negative patient-health system interactions as these patients express that they feel their doctors aren’t listening to them or keep going around in circles with regard to treatment.  The “best” of these interactions seem to be when their doctors plainly tell them they don’t know what more they can do – itself a frustrating and demoralizing thing to hear.  To all of those patients I say that I completely empathize and validate that they have every right to feel as they do.  Having been a patient on several occasions myself, I know what it’s like to speak with a physician or an insurance adjustor and feel like you are talking to the wall - and I’m a healthcare practitioner.

As a peripheral nerve surgeon, especially one that operates on people with chronic, intractable headaches, I have heard criticisms from other doctors whom I don’t feel even understand what it is that I do.  However, I’ve learned that by putting myself into the shoes of that doctor across from me I can almost always find common ground.  Happily, that common ground is as advocates for our patients. After all, we physicians are (or should be) on the same side as our patients in trying to treat any medical condition. Therefore, I believe that teamwork is particularly and practically helpful and there are already paradigms for this approach that work very well.

Breast cancer is sadly a disease that touches too many people throughout the world.  Over the past few decades, the medical profession has made incredible strides in fighting this dreaded disease and we now have cancer remission rates that were once thought impossible.  One of the biggest factors in helping this development along has been the team approach.  In our community, a patient with a new breast cancer diagnosis is immediately given a team of physicians and clinicians to help them navigate the process that is current treatment.  To be sure, there is a “captain of the ship”, usually the breast surgeon or oncoplastic surgeon who is coordinating all of the moving parts, but every member of the team is critical to ensuring success.  The breast surgeon may remove the actual tumor, the plastic surgeon will help reconstruct the resultant defect, a radiation oncologist will ensure that any disease that might have spread locally is controlled and a medical oncologist will determine if the risk of distant disease is high enough to warrant a regimen of chemotherapy or hormonal therapy. There is also often a psychologist and nurse navigator who can help the patient deal emotionally and psychologically with the emotional rollercoaster accompanying a cancer diagnosis.  Only when you put all of these components together, do you get the wonderful results that modern medicine has been able to achieve.

For years I have been hopefully telling my patients that someday soon, we will realize that chronic pain (of which chronic headaches are a prime example) is also best treated with a multi-modality approach.  There are certainly many patients for whom medication works very well.  Those people do not need injections or surgical intervention.  There are those for whom pharmacologic agents are simply ineffective and in those cases, nerve decompression may be a good option.  However, for most, a combination of therapies is necessary to control the underlying symptoms.  I have heard from countless patients who tell me that prior to surgery their medication was inconsistently helpful.  Following operative intervention, their headaches are much less frequent and often much less severe, but what was interesting to me was that they would tell me that when they would get an attack, the medication they’d been using for years was now consistently effective.  “Why is that?” they would ask.  I felt it was likely that they had two problems contributing to their headache symptom complex.  One was a chemical imbalance that medication would treat, and the other was a mechanical compression of a nerve(s).  Only when both conditions were adequately treated, would the symptoms be optimally managed. 

The take home message is that many medical conditions are best managed when we work together.  Not just as patients and physicians, but as physicians and physicians. I have had great success locally with neurologists and pain management physicians as we not only refer to each other, but also actually talk to each other about our shared patients, recognizing that we each have a role in their care. Those that have seen me know that I often like to communicate with the very same such doctors prior to surgery to ensure we can optimize the post-operative recovery period which certainly can have its share of ups and downs. In the end, we all have to partner in this endeavor together as a team if we hope to triumph.

 To learn more about Migraine Surgery and Relief, visit www.peledmigrainesurgery.com today, and follow us on Facebook, Twitter, Instagram, LinkedIn and YouTube for more information.

I have been asked many times about the relationship between whiplash and occipital neuralgia.  First of all, what is whiplash?  Simply put, it is a sudden jerking of the head, usually in a backward/forward direction or sometimes side to side.  Common causes of whiplash include motor vehicle accidents, sports related injuries and any other violent motions such a shaking a baby too hard or even a big roller coaster ride.  Motor vehicle accidents are by far the most common cause with an estimated incidence of over 1,000,000/year although the true number is hard to gauge since many cases of whiplash are not reported. In 2008, the total estimated cost to the healthcare system of whiplash injury was over 40 billion dollars!

One of the most common sequelae (consequences) of whiplash is chronic neck pain/headaches. Why do these symptoms occur?  Likely, because the nuchal muscles will suddenly tighten as the head is rocked violently and the soft structures that pass through and around these muscles are affected. Nerves are like wet noodles - they are soft and pliable, but the neck muscles and fascia that covers these muscles is tough and tight to begin with to allow stabilization and efficient mobilization of those bowling balls we call our heads. If you think about the force it would take to tear a wet noodle, you get a sense for how easy it could be to injure an occipital nerve.

However, as many out there can attest the work up of these patients is often negative.  Why is that?  The answer lies in what I believe to be the underlying cause of this chronic pain/headache which is a traction (i.e. stretch) injury to the occipital nerves.  Even with high resolution MRIs (see previous post on why the MRI may be negative), the relatively small occipital nerves (greater, lesser and third) are hard to image accurately.  Therefore, a negative MRI may rule out an injury to the nuchal ligaments, bones, and/or muscles, but it cannot rule out a small tear to an already tiny nerve(s).  Moreover, since the above-mentioned occipital nerves are purely sensory (i.e. they don’t move any muscles, only provide sensation to the scalp and back of the ears), the primary symptoms tend to be pain which cannot be objectively measured with a CT scan/MRI or blood test.  Since many practitioners don’t recognize the impact of a traction injury to these sensory nerves, management is often empirical.

For these reasons and others, patients are often treated with a combination of pharmacologic agents, PT, chiropractic manipulation, cervical collars, etc.  Certainly, many patients do get better with these conservative modalities, but given the sheer numbers we are talking about, many thousands do not.  However, if you believe as I do that the issue may be a tear within a small nerve causing intra-neural scarring, or a small tear within a muscle surrounding that nerve that causes subsequent scarring and narrowing of the canals through which these nerves usually pass (hence compression), then the above-mentioned modalities will not work for obvious reasons.  If there is mechanical compression on a nerve, that compression must be physically and precisely removed or permanent damage may occur.  The take home message is that when all other potential causes of chronic neck pain/headaches post-whiplash have been ruled out, think of occipital neuralgia as a possible cause.  A consultation with an experienced peripheral nerve surgeon should then follow and ON ruled out as a possible cause.  The good news is that if ON is felt to be the culprit, there are safe and effective procedures that can provide significant relief.

To learn more about Migraine Surgery and Occipital Neuralgia, visit www.peledmigrainesurgery.com today and follow us on Facebook, Twitter, Instagram, LinkedIn and YouTube for more information.

Someone recently asked this question on one of the forums and I thought it was a very good question the answers for which may not be immediately clear. First of all, I think it is important to define exactly what is meant by ‘neuralgia’. The prefix ‘neur’ simply refers to a nerve and the term ‘algia’ means pain. Therefore, simply put, neuralgia means pain cause by a nerve or nerves. The question always becomes which ‘neur’’ is causing the ‘algia’? Then, if you can answer that question, can you then do something about it?

Occipital neuralgia (ON) is a neurological condition in which the occipital nerves are irritated or compressed (i.e. pinched) and hence cause pain. The typical symptoms are episodic (i.e. paroxysmal) bouts of “lightning-like” pain in the back of the head although as many of you know and as I have blogged about many times, the symptoms can vary widely. Because each person is unique, they will each experience pain differently. Similarly, trigeminal neuralgia (TN) is a neurological condition in which the main trigeminal nerve trunk is compressed. Not surprisingly, the classic symptoms are episodic bouts of “lightning-like” pain in the face which are the areas innervated by the various branches of the trigeminal nerve. These sets of nerves are not physically connected so why is it that ON often co-exists with TN? The answer lies in the anatomy. I will have a picture of a peripheral nerve included in this post to help illustrate the points I make below.

Many people don’t know that that the upper-most, neural elements in the neck (e.g. the occipital nerves) have a common connection zone in the medulla (part of the brain stem) with nerve cell bodies that become the trigeminal nerve. This zone is known as the cervico-trigeminal complex and can potentially explain why discomfort from lesser occipital neuralgia may sometimes be referred to trigeminal nerve territories anteriorly. Referring to the image of a neuron (i.e. nerve cell) below, you can see that when the long part (axon) of the nerve is injured (e.g. in a whiplash accident), the whole nerve becomes inflamed including the cell body. This injury is depicted in #1 in the attached image. When the cell body of a cervical nerve (e.g. one that becomes the greater occipital nerve) is chronically inflamed, the adjacent cell bodies (e.g. those that become a trigeminal nerve branch – for example, the supraorbital nerve) also become inflamed. This injury is depicted in #2 & #3 in the attached image. Then the axons of those latter nerves cause pain in their respective nerve distributions (e.g. in the forehead in the case of the supraorbital nerve). This injury is depicted in #4 in the attached image. In this way, an injury to the GON can ultimately result in forehead discomfort. To use an analogy close to home here in California, think of it as a forest fire that has burned too long and the embers from one part of the forest jump the clearing to the adjacent wooded area and cause a fire there.

Hopefully, it now becomes clear why ON and TN often co-exist. It is usually the case that one begets the other and I have seen countless patients in my office whose pain started in the neck area and eventually spread elsewhere. Fortunately, the process can also reverse itself if the inflammation/irritation of the involved nerve branches can be addressed.

A couple of weeks ago, we talked about the definition of a migraine, which in many practical instances is simply a name given to a constellation of symptoms.  We also spoke about occipital (meaning back of the head) and neuralgia (meaning nerve pain). When all is said and done, however, the real question is: “Can you figure out which ‘neur’ (i.e. nerve) is causing the ‘algia’ (i.e. pain)?”  Is occipital neuralgia therefore considered a headache?

Well, yes and no. occipital neuralgia can give you symptoms of a headache because it can cause head pain and any head pain is by definition a “head ache”. Can occipital neuralgia fall under the definition of or be considered a migraine? The answer to that question is also technically, “yes”’ because all the clinician and patient will “see” is the presence or complaints of head pain that is this level of severity, this frequent (often constant), associated with these other sensations (e.g. pulsation/throbbing, light sensitivity, nausea) and this duration (usually several hours or more at least).  These characteristics are now established, but say nothing about the cause of the headaches. Is it a chemical imbalance, an issue of an inflamed blood vessel or a compressed nerve?

The upshot is that so many of the patients who come to see me have been diagnosed with migraines which is not necessarily inaccurate, it’s just not very specific.  Many people who have been diagnosed with migraines do find a conventional treatment modality that works for them (e.g. medication).

However, there are also many millions who don’t have success with these traditional modalities and the reason is because the diagnosis of “migraine” doesn’t tell you what’s causing the problem and therefore how to fix it.  Those people end up being treated “empirically”; in other words, it’s like throwing darts at a dartboard - try this drug, or that drug or these drugs together or these drugs with massage, PT, acupuncture, etc. to see if you can find something that works.

What practitioners are really trying to do is figure out what problem - chemical imbalance, muscle tightness etc - is causing the issue by eliminating factors one by one using trial and error. At its essence, actual occipital neuralgia is the result of pressure on a peripheral nerve(s) in the occipital region.  If you can figure out which nerve(s) is involved, in many cases, the headaches can be significantly improved or completely relieved by surgical intervention.

To learn more about Occipital Migraines or schedule a consult with Ziv M. Peled, M.D. visit www.peledmigrainesurgery.com today.

These days, whenever I read the news or look online, the world can seem like a pretty bleak place. The political divide remains, natural disasters abound, and trade wars are imminent. However, just when things seem pretty dark, little rays of light seem to peak through the clouds. This past weekend, I had the distinct honor and privilege to serve on a panel about migraine/headache surgery at the international meeting of the World Society for Reconstructive Microsurgery in Bologna, Italy. I was speaking and interacting with several esteemed colleagues in this burgeoning field from around the world. Amongst the highlights of this event (and there were many) was the feeling amongst several of my colleagues that a few neurology counterparts in their communities had begun to embrace the idea that surgical intervention might just have a role in the treatment of chronic headaches.

It reminded me of the time Dr. Pamela Blake spoke on our on our panel teaching headache/migraine surgery at the American Society of Plastic Surgeons annual meeting two years ago. Dr. Blake is a board-certified neurologist, an active member of the American Headache Society & International Headache Society and former Director of the Headache Clinic at Georgetown University. She remains active in research in behavioral neurology and cognitive science and served as volunteer faculty at the Cognitive Neurosciences Section at the National Institutes of Neurological Disorders and Stroke at the National Institute of Health. As impressive as this resume is, perhaps the most impressive thing to me, however, is that Dr. Blake is a firm believer in the concept that peripheral nerve pathology is a very under-recognized factor in the generation of chronic headaches for many people. Just last year, she published an article detailing some success with the surgical approach in Cephalalgia, a peer-reviewed journal and the official Journal of the International Headache Society. 

While this fact may seem trivial to many, I cannot overstate what it means to those of us who have been banging on this door for over ten years. Since 2000, there have been over 80 scientific articles from numerous centers across the US, Europe and Asia detailing positive outcomes from nerve decompression surgery for chronic headaches such as migraines. Last year the American Society of Plastic Surgeons issued a formal policy statement that headache/migraine should no longer be considered “experimental” when other treatment modalities have failed.

 If someone with Dr. Blake’s background and training can be convinced by the available evidence and our results with headache surgery patients that we are onto something, then perhaps others can be convinced similarly. In my humble opinion, this change would be nothing short of revolutionary as it would finally give peripheral nerve surgery a seat at the table in the armamentarium of modalities that could be considered in the treatment of chronic headaches in particular and perhaps chronic pain in general. Perhaps in the not-too-distant future we will see positive position statements from various other societies and if things go really well…. a change in the overall medical establishment’s perspective. When I think of the hundreds of thousands of people who may find relief from the scourge of chronic headaches like migraines, a big smile begins to creep across my face. Dare to dream big….. I remain ever hopeful, but more optimistic with each passing day. The longest journeys begin with the smallest steps.

 To learn more about Migraine Surgery and Relief, visit www.peledmigrainesurgery.com today, and follow us on Facebook, Twitter, Instagram, LinkedIn and YouTube for more information.

The title of this post is really the $60,000 question.  I have posted many times in the past about how ON can be caused by compression from spastic neck muscles, compression by tight connective tissue (i.e. fascia) and/or compression from surrounding blood vessels.  Many of the patients I see have had headaches ever since they can remember. However, there are just as many for whom the headaches began seemingly spontaneously one day. The question for these folks remains: What happened?  Why now?

There have been recent articles that hint at possible answers to these questions and they may surprise you. I have attached a link to one of the more interesting ones as part of this post. One of the most surprising comments contained therein was that craning the neck downward only 60º puts as much as 60 pounds of pressure on the cervical spine and neck muscles.  With that kind of pressure, you can imagine that nerves (among other structures) would be compressed. So the explanation as to why you might all of a sudden develop ON can almost be summed up in one word - overuse. This explanation is one of the potential causes of carpal tunnel syndrome, the most common compression neuropathy recognized (even by neurologists). Why could that not be the case for ON?  Nerves are very susceptible to chronic compression (see post - ‘What Causes Occipital Nerves to Malfunction’) even if intermittent. The occipital nerves take very circuitous routes through all of the nuchal soft tissues. When you add to that fact the constant motion of our necks that require the nerves to glide constantly and then compound those factors with an additional 60 pounds of added pressure, there are many things that may occur to those nerves.

One, they may simply get kinked as they make their way through the neck to the scalp.  Not a week goes by when I don’t see a patient in the office who, in describing their headaches contorts their head to recapitulate their symptoms and when they get it just right, it’s like a thunderbolt of pain.  Two, even if not kinked, the pressure will compress the vasa nervorum - the microscopic blood vessels within the nerves themselves that supply blood to those nerves. After numerous episodes of compression, especially if for prolonged periods, these blood vessels can clot and the nerves become ischemic (i.e. choked).  The neurons that comprise that nerve then die off and try to regenerate causing the hyperesthetic symptoms so typical of ON. Three, even if the nerves recover from each successive insult, the additive microtrauma will likely result in some inflammation and the subsequent formation of scar tissue in the surrounding structures, thus closing off already tight corridors through which these nerves must pass - another compressive force. While no one has demonstrated these possibilities in real time, I see the sequelae of them in the OR weekly.

So what do we do?  Good posture, stretching and avoidance of triggering activities seem to make common sense.  In addition, as many of you know and as intimated in the article, steroids seem to be the mainstay of treatment amongst some practitioners, but as also stated, the effects are often not permanent.  The reason is obvious - the compressive forces remain, even if inflammation is temporarily suppressed. Therefore, I continue to believe that decompression (or neurectomy & implantation for permanently injured nerves) are reasonable options as they are safe and effective.  Moreover, they address the underlying problem, the mechanical compression of these poor nerves caused by our ever more technologically demanding lifestyles. So next time you pick up your smartphone, remember to pick up your head as well.

Learn more about Occipital Neuralgia and Migraine Surgery from Ziv M. Peled, M.D. at www.peledmigrainesurgery.com now.

http://gizmodo.com/my-smartphone-gave-me-a-painful-neurological-condition-1711422212

The relationship between diabetes and peripheral nerves is an important one.  As many people already know, diabetes is the leading cause of neuropathy, which in its simplest definition means some pathology of the nerves.  Therefore, diabetes obviously negatively affects nerves, but how? There are a number of ways in which diabetes can affect a peripheral nerve.

In a diabetic, despite the best glucose control there is always more glucose in the bloodstream as compared with a non-diabetic.  This excess glucose is taken up by many cells in the body, among them nerve cells. When inside the nerve cell, the glucose is metabolized into another sugar called sorbitol which then acts as an osmotic load (e.g. as a sponge) , drawing more water into the nerve cell. In effect, because of this excess water in the nerve cells, diabetic nerves are swollen.  When any object swells inside a fixed space which cannot expand, that object is under pressure. This process partly explains why carpal tunnel syndrome is more common in diabetics than in non-diabetics and it stands to reason that the same process would affect the symptoms of another nerve compression problem, ON. Although the correlation between diabetes and ON has never formally been elucidated, several studies have hinted at a causal relationship. Another way in which diabetes can affect peripheral nerves is by causing a low grade inflammation of the blood vessels within the nerves.  With inflammation comes swelling and the process noted above worsens even further.

Two other processes have also been identified, but with very different mechanisms.  Diabetes has been associated with increased molecular cross-linking of certain proteins within the nerve cells walls.  This cross linking effectively makes the nerves “stiffer” than they otherwise would be which causes then to bang around more within their tight spaces and resulting in more micro-trauma.  This process is especially true around joints such as the wrist (carpal tunnel) or at the base of the neck (ON) where all of the structures are moving around, hopefully gliding smoothly past one another. When coupled with an impaired ability to repair themselves secondary to decreased axoplasmic flow, repeated micro-trauma likely results in scar build-up over time thereby decreasing already tight spaces even further. While I’m sure that other processes have also been identified, the bottom line is that diabetes has multiple negative effects on peripheral nerves and is the reason why in a diabetic patient, optimal glucose control is the first line of therapy. Poor glucose control is likely to exacerbate nerve-related symptoms (whether carpal tunnel or ON) for all of the reasons noted above.  Despite tight controls on sugar levels, diabetics still have symptoms and sometimes these even worsen over time. In these cases, I believe that a meticulous search for nerve compression is important because if found, decompression can potentially be very beneficial symptomatically.

To learn more about Migraine Surgery, visit www.peledmigrainesurgery.com today.

A number of patients have come to the office over the years consistently telling me that they had worse pain AFTER their injections with their other doctor.  This phenomenon seems to occur irrespective of what is being injected, whether Botox, a local anesthetic (such as is used in nerve blocks) and/or steroids. Remarkably, despite numerous queries to their treating clinicians, their physicians have never had a good answer for them as to why this problem happens.  Actually, the answers are quite simple. Worse pain after injections such as those done to diagnose ON can occur for several reasons.

One reason is that the injections done for ON are performed within muscle.  Injections into muscle cause a little muscle inflammation/swelling no matter what you inject (even saline) and this inflammation causes discomfort.  Anyone who has ever had a tetanus shot into the shoulder muscle (deltoid) knows exactly what I’m talking about. Their shoulder can be sore for 7-10 days afterwards.  Fortunately, the discomfort is temporary and only lasts a few hours or days as the inflammation/swelling subsides.

Second, these injections, by design, are performed AROUND (not into) nerves which means that you are injecting several mL of fluid around a nerve.  This fluid causes some irritation of the nerve itself because of the mechanical pressure from the fluid, not so much the make-up of the fluid itself and hence theoretically would be equivalent with Botox, local anesthetics or steroids so long as the same volume was used with each. If a local anesthetic is used, the effects of the anesthetic provide relatively immediate, albeit temporary relief when injected properly. Yet when the effects of the local anesthetic wear off, the nerve irritation from the fluid pressure often remains and can cause worse pain for a few hours or days afterward.  Once again, this situation is usually temporary as the residual fluid is absorbed by the body, although the discomfort can last several days on occasion.

A third reason an injection can cause pain afterwards is some complication from the injection itself.  For example, following any violation of the skin (e.g. surgery, injections, IV placement) an infection can occur.  With infection comes the inflammation noted above often causing localized pain from irritation of the nerve endings in the surrounding skin as well as from irritation of the target nerve. A hematoma (a collection of blood) can result from an injection although it is uncommon.  Blood is a great culture medium and can be a factor in promoting infection (see above) as well as a mechanical force impacting the local tissues (e.g. the target nerve). One potential sign of a hematoma is significant bruising following an injection, especially one involving a small needle and a small injection volume.  Finally, and fortunately very rarely, an intra-neural injection (into the nerve itself) can be the culprit. If a significant volume of anything is injected into the nerve itself, it can disrupt the microscopic blood supply to the nerve and cause permanent damage, which can result in permanent problems. However, since nerves are usually quite small, since the injection needles are small and since the required injection volumes are low, intra-neural injections are about as common as finding a needle in a haystack or a four leaf clover.   The take home message for my patients: knowledge is power. If patients are told what MAY happen following their injection, they are much calmer if and when it does occur and hence better prepared to deal with the situation.

To learn more about Migraine Surgery and the treatment of Migraines, visit www.peledmigrainesurgery.com today.

I was recently asked why some people require more than one operation to obtain optimal relief.  As usual, the answer has many components to it so I will try to delineate some of these issues below.  Let me preface these remarks by stating that what I write below is my opinion only and how I approach patients, but should not be considered dogma.  While a number of colleagues also use this approach, it is not necessarily shared by every peripheral nerve surgeon, some of whom will be more aggressive and some less aggressive.

In situations where there are many nerves that will require surgical intervention to achieve an optimal result, there are number of reasons why I prefer to stage the operations.  First, patients often say that one area usually flares up initially and when very severe or uncontrollable, causes the headache and discomfort to spread to other areas. For example, s/he will state that their neck gets tight, they get occipital headache pain and if medication is unable to help, the headache spreads to the temples and forehead.  In these particular cases, there may be a reasonable assumption that the occipital area is triggering the frontal and temporal headaches.  Therefore, theoretically if the occipital nerves are appropriately addressed, with time and healing, those triggering nerves should calm down such that the frontal and temporal areas are only triggered infrequently and hopefully to a much lesser degree.  In other words, if you can remove the fuse, the dynamite stick will never explode and therefore an operation to address the frontal and temporal nerves may never be required. Even if this patient continues to have some degree of headaches, these headaches may be so infrequent and/or relatively mild that they feel the remaining symptoms are easily manageable and don’t want another operation.  As I’ve said in prior posts, no one should tell you whether or not you should live with whatever pain you have. Doing so is making a value judgment - only the patient can and should make that determination.

Second, let’s assume that a person has the appropriate operation over the occipital nerves and has a successful outcome with respect to their posterior headaches, but the temporal and frontal headaches persist even after several months of recovery.  In those cases, while another operation may be required to address the temporal and frontal nerves, there is now good reason to believe that the second procedure is likely to be successful. The converse is also true - if the occipital procedure is performed correctly and for the right indications, but yields no result, I would question whether or not a temporal/frontal procedure would be indicated.  I would be less confident surgical intervention in those areas would be successful since the same approach was unsuccessful over the occipital area, thereby precluding the potential for complications in areas where surgical intervention may not be successful. Therefore, staging an operation has the potential to give you information about whether or not a second procedure will be helpful.

A third reason for staging these operations relates to the safety of an operation.  While I obviously agree that neuralgia (occipital or trigeminal branch) is a significant medical problem, these operations are elective.  Therefore, the most important thing we can do for the patient is give them a safe operation and try to minimize complications while maximizing the potential for a successful outcome.  From a technical standpoint, the longer a surgical procedure takes, the greater the chance for complications or issues arising from anesthesia. While long operations can certainly be done safely, when it comes to elective surgery, the more efficient a procedure can be the better.  Therefore, if I had a choice between one 8-hour operation or two 4-hour operations, I would choose the latter because there is likely a lower risk for deep vein thrombosis (blood clots in the legs that can embolize), the need for an in-patient stay, post-operative nausea and other anesthesia-related issues.

A fourth reason for staging operations has to do with recovery.  In my opinion (and as many of my patients will attest), one of the hardest parts of the surgical experience is the post-operative recovery which often has many ups and downs apart from the immediate, peri-operative surgical discomfort.  With respect to the latter, if you have incisions on the front, the sides and the back of your head bilaterally, I can only imagine how uncomfortable the whole head must feel and I often wonder how these patients rest at night since sleeping on any portion of the scalp is likely to result in discomfort.  Rest post-operatively is critical and lack thereof is potentially problematic. In addition, as decompressed or transected nerves are manipulated in the operating room, the normal, post-operative inflammation can lead to many nerve-related symptoms which, if they occur all over the scalp as opposed to just posteriorly or over the temples, is likely to be quite uncomfortable.  More discomfort often leads to increased opioid use which can lead to a whole host of other issues such as constipation, cognitive impairment (e.g. sedation), nausea etc.

One last comment: I don’t use any one of these contra-indications in isolation.  They are all considered together as part of the overall clinical impression when I go over a patient’s records, examine him/her and perform whatever diagnostic maneuvers are necessary.  It is for these reasons among many others that I always recommend a consultation with a peripheral nerve surgeon when deciding if surgical intervention (whether decompression/neuroplasty or neurectomy/implantation) is appropriate.  

I also believe that among the many questions patients should ask their potential surgeons is how they will approach the surgery. It is important for patients to understand their surgeons’ plan, particularly if their case will involve more than one or two incisions, and make an informed decision about the path forward.

In my humble opinion, the possibility that mechanical compression of a peripheral nerve in the head and neck can cause headaches is vastly underestimated.  I realize this is a big statement, but I think it is legitimate. It is primarily for this reason, that the diagnoses of occipital neuralgia and trigeminal branch neuralgia are not made nearly as often as they should. What is particularly fascinating is that many practitioners will use nerve blocks to provide temporary relief from headaches successfully.  

What do those practitioners think is happening when they temporarily and chemically inactivate a peripheral nerve or nerves and the headache improves significantly or goes away, albeit for a short period of time - usually until the numbness wears off?  What exactly does one conclude from this information? In my mind, the most obvious answer is that the nerve(s) that was blocked must be involved in the generation of headache symptoms. So why is this concept so foreign to so many? I believe there are a number of reasons for this phenomenon and I will delineate some of these reasons below.

The first is that the central concept of chronic headaches has been around a long time.  It is generally widely accepted that most chronic headaches (e.g. migraines) are caused by chemical or vascular imbalances in the brain.  And yet, if we understand the chemical imbalances, how come we not only have dozens of drugs to treat ‘migraines’, but numerous classes of drugs.   Pharmacologic treatment of migraines includes the use of anti-depressants, neuroleptics, serotonin-modulating agents, CGRP-modulating agents, opiates, muscle relaxants, anti-seizure medications, anti-hypertension medicines, anti-anxiety drugs and others.  

If there is a clear chemical problem, how come there aren’t one or two classes of drugs that treat that problem effectively? I will say that these medicines work for many, but the problem is so prevalent (more than 36 million people in the US are diagnosed with migraines), that even if they fail for just 20%, that means more than 7 million people continue to suffer.  The point is that the central concept of chronic headaches is deeply ingrained in medical teaching and hard to overcome. Therefore, the notion of peripheral nerve compression causing these problems would be somewhat of a paradigm shift - something that doesn’t occur easily and without some resistance.

A second issue is that this concept is being championed by primarily plastic surgeons.  One of my mentors once told me, “Ziv, don’t go into plastic surgery unless you are willing to spend the rest of your life apologizing for your colleagues.”  While I disagree with this blanket statement, I understood his point - when most people think of plastic surgeons, they think only of cosmetic surgery.

Yet, plastic surgeons reconstruct breasts after mastectomies, repair difficult lacerations, fix cleft lips/palates, provide coverage for difficult wounds following trauma, do face transplants and replant fingers, forearms and whole arms (including nerves) after accidents.  Some of us have made peripheral nerve surgery a focus of our practices and spend time teaching others what we know, publishing our work for others to read and critique and educating patients so that they can be more informed. Yet I suppose if a neurologist came up to me and told me that I was doing my tummy tucks incorrectly and that they had a better way to do it, I might look at them slightly askance at first. Skepticism is always healthy, especially when it comes to surgical intervention,  so it makes sense that practitioners who care about their patients wouldn’t want them to do something they were unsure of.

Third, we who do these operations need to continue to publish our data, educate other medical professionals (as well as the public) and hopefully build bridges between the various specialties so that ultimately patient care is optimized.  While a reasonable number of surgically-treated patients experience elimination of their headaches, many continue to have symptoms albeit significantly reduced in frequency, severity and duration. So we all still need our neurologists, pain managements docs and physical therapists to help manage the remaining issues.  This multimodality approach remains elusive in headache care, but is a dream of mine before I retire. Because peripheral nerve surgery is the newest and smallest voice at this potential table, the things we have to offer are often not acknowledged.

Despite these hurdles, the shift to wider acceptance of this concept is underway. There are board-certified neurologists now writing about “nerve compression headaches”, which are not currently listed in the International Classification of Headache Disorders as a distinct clinical entity to my knowledge. So while the wheels of change slowly turn, patients have to be advocates for themselves. If the pharmacologic agents, injections and conservative modalities are not giving lasting relief, then seeking a qualified surgeon to test for mechanical compression may be the next course of action…...and the solution.

To learn more about migraine surgery, visit www.peledmigrainesurgery.com today!

Just a few days ago, I read an Instagram post that discussed post-traumatic headaches. There was a description of someone who had suffered a head injury following an assault and suffered a skull fracture that healed without surgery. This person subsequently began to experience headaches that were unremitting. The MRIs of the brain and neck did not identify any pathology and the patient had failed physical therapy and massage treatments. He was diagnosed as having a concussion and treated accordingly, but the headaches persisted.

The remainder of the post went on to detail how, over the ensuing years, he was presumed to have developed ‘migraines’ and tried on various medications, all unsuccessful. There were descriptions of altered brain activity, presumed (but never identified) problems with the blood vessels in the brain and various suspected chemical abnormalities (hence all the drugs). During this entire time, the patient was complaining of consistent pain in a specific area of the head/scalp.

Unfortunately, this story resonated with me because it sounded all too familiar. The remarkable thing for me was that no time during the entire saga did anyone even entertain the possibility that there might be a peripheral nerve in the scalp that had been injured with the fracture and subsequent scarring that occurred. It struck me as odd that if the same thing had happened in the forearm with an ulnar bone fracture and the patient began to experience hand pain in the small finger, the concept of a nerve injury would be at the top of the possible causes. The fact of the matter is that this person might just have an entrapped peripheral nerve in the scalp that is causing the pain.

I wanted to reach into the phone and suggest to this patient that he consider this possibility.  He should have a nerve block and if, successful, perhaps an outpatient procedure might just fix the issue permanently.  This whole scenario also got me thinking about why people don’t consider the peripheral nervous system in these cases. I think there are many explanations for that observation. More about that topic in an upcoming post.

To learn more about migraine surgery, visit www.peledmigrainesurgery.com today!

As with many things in life, there are positive and a negative ways to perceive anything. Just because the MRI was negative, clearly doesn’t mean that there’s nothing wrong. Let me explain why below. First, however, let’s look on the bright side. You don’t have a brain tumor. You don’t have an aneurysm. It doesn’t appear as if you’ve had a stroke. And you don’t have lesions on your brain that might be suggestive of multiple sclerosis, Alzheimer’s or ALS (Lou Gehrig’s disease)….all good things NOT to have.

So what do you have and if it’s so bad, how come you can’t see it. Well, with standard MRI sequences, nerves are often not visualized as well as other structures such as muscle and bone. However, there are certain modifications which the MRI technician and radiologist can perform (if knowledgeable enough) to highlight nervous tissue. There are a special set of MRI sequences collectively called Magnetic Resonance Neurography (MRN for short) that, when combined can produce high resolution images that preferentially highlight nerves and their pathology. Unfortunately, this type of technology is still relatively new and is certainly not available at every hospital. 

There are a couple of technical considerations when deciding whether or not a suspected nerve can be evaluated with MRN. The first is the strength of the coil (magnet) within the MRI machine. Standard MRI uses a 1.5 Tesla (1.5T) coil to image routine structures. More recently there has been a prevalence of 3T coils and these machines are sometimes considered “high resolution” MRI scanners. The images they produce are more refined and specific. Think of it as the difference between the images from a VHS player versus a DVD player. There is even a well-known, local institution that supposedly has a 7T scanner. The image quality will probably be that of a Blue-Ray player. The second issue at play is the size of the nerves being imaged. The larger the nerve, the easier it is to detect any pathology. MRN has been shown to be quite effective and useful in imaging larger nerve bundles such as nerve roots emerging from the spine, the sciatic nerve in the thigh and even the brachial plexus in the neck and upper arm. It has been less well-studied in more peripheral and hence smaller nerves such as those involved in carpal tunnel syndrome and occipital neuralgia. The third, rate-limiting step in imaging the nerves is interpreting the images - this step requires a good radiologist. The more experienced they are in reading such images, the more likely they are to pick up fine details that may represent true pathology.

So if the MRI is “negative”, it may be because the optimal MRI sequences were not used - perhaps the radiologist thought you were really looking for a brain tumor and simply didn’t see one. Make sure the ordering physician specifies that they think you may have ON and are looking for compression of, for example, the greater occipital nerve. If the MRI is “negative”, it may be because the MRI machine is not capable of producing high resolution images that would highlight small nerves such as the greater occipital or supraorbital. If the MRI is “negative”, it may be because the radiologist interpreting the images is not experienced enough in MRN to pick up subtle differences in the appearance of a compressed, small nerve versus a normal one. Knowledge is power in these cases. One final note: given the novel nature of MRN technology, most insurance companies still consider such tests “experimental”. 

To learn more about Migraines and Post Traumatic Headaches, visit www.peledmigrainesurgery.com today.

One of the most common questions that I get from my patients when they come into the office to see if they are a candidate for nerve decompression surgery goes along the lines of, “Gee Doc, I hope you find something! What if you get in there and don’t find anything wrong? What will you do?”

I have never encountered a patient on the operating table where there hasn’t been some element of nerve compression. Sometimes this is seen in the form of how the occipital nerve interacts with the occipital artery where the latter wraps around the nerve a bit like an anaconda. Sometimes, compression can be caused by a spastic muscle and sometimes, compression can be caused when the connective tissue tunnel through which an occipital nerve passes in the neck to the base of the skull is excessively narrow.

While some element of compression has always been present, there are a couple of caveats to these observations:

1. We don’t have an empirical method for measuring occipital nerve compression. If a patient suffers from a critical condition like compartment syndrome in the leg, in which when pressure builds up, there are established tools to measure what critical pressure is and when to operate. A similar baseline has yet to be established for nerve compression causing head pain, so there is no defined way to measure the degree or severity of the compression that we see.
2. Secondly, we also don’t know what degree of compression will cause symptoms of pain. This amount of pressure will likely vary based on a number of parameters such as which nerve is involved.  For example, the greater occipital nerve is a much larger and heartier nerve and therefore is likely to be able to tolerate more pressure before becoming symptomatic as compared with the lesser occipital nerve.  
3. Lastly, we don’t ever operate on people who don’t have symptoms nor where candidacy for surgery has been not been verified via history, physical examination and nerve blocks. In other words, when you only have symptoms on the right side, I’m not going to dissect and open the left side of the neck just to look so that I have a comparison of what “normal” supposedly looks like.  Doing so exposes those left-sided nerves to potential injury unnecessarily. That being said, there was an important study conducted by Dr. Guyuron several years ago to validate the outcomes of headache surgery. It was what was known as a sham surgical trial, 76 patients knowingly participated with 49 patients undergoing the actual nerve decompression procedure and the remainder undergoing what’s called a sham operation. On the day of the surgery, Dr. Guyuron would open an envelope and it would tell him if the patient was having the real surgery or not. The sham surgeries had to seem like they could be real, so these patients were still induced under anesthesia, were cut open and their nerves exposed, but ultimately left alone for a typical time that the operation would take. The patients who had the actual surgery did statistically better in terms of frequency, severity and duration of their headaches when compared to the sham surgical patients. In addition, while there was some placebo effect, none of the patients who received the sham surgery were headache-free, while a statistically greater percentage in the actual surgical group did report this outcome.

The take home message is this:  There is still much work to be done in order to establish a measurable baseline for nerve compression that leads to head pain.  However, in the meantime we can work with what we know and that is if a patient experiences chronic pain, has exhausted all non-surgical methods of treatment and responds well to nerve blocks, they are reasonably good candidates for nerve decompression surgery.