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How Good Is Peyton Manning Going To Be?


Does Muscle Weakness Improve After Disc Surgery?

For an NFL fan arguably the best thing that could happen to your team is to sign Peyton Manning and have him perform at or near his pre-injury level.  The corollary is that one of the worst things to happen to your team would be to take a huge salary cap hit to get a Peyton Manning with such weak throwing arm that even with his experience and determination he is unable to excel or that he is re-injured and unable to play. The opportunity to get a superbowl champion, 4-time MVP, and future hall of fame quarterback who suddenly has become available to lead your team to a championship makes it easy to overlook the nature of spinal nerve injuries and cervical spine surgery.

The excitement and media heyday surrounding Peyton Manning neck surgery and his recent free agency prompted me to post about the nature of weakness from spinal nerve injury, and what can be expected in terms of recovery of strength and function.  The real issues come down to two questions:

  1. Is the nerve injury he has sustained to his cervical nerve root significant enough to cause irreversible weakness that will render him unable to perform at a level close to his previous superstar status. How much more recovery of strength can he expect.
  2. Is he going to be able to hold up to the trauma he will be subject to as an NFL quarterback?

Let’s look at these one at a time.

How much of Manning’s arm weakness can he recover?:   The real key to how successful Mr. Manning is going to be in his comeback hinges on the degree of chronic nerve injury he has sustained.  Most of the time once a spinal nerve had been injured leading to muscle weakness, if the weakness persists for very long the damage is permanent.  It is not clear how long Manning had been having weakness prior to his single-level fusion procedure, but it is certainly concerning that he had undergone at least 2 prior microdiscectomy procedures and that with a player as valuable to his team and generally competitive as Manning it seems unlikely that he chose to stop playing and have surgery at the first sign of weakness.

So what is the chance of a full recovery of motor function, i.e. strength, for Manning and how is this likely to affect his effectiveness as at throwing a football?  I expect it to be more significant than may be widely appreciated. I cannot find it reported anywhere just which cervical level Manning had fused, so I don’t know which cervical nerve root is damaged.  The most common cervical levels for disc injury are the C5-6 and the C6-7 levels.  The cervical discs and nerves are labeled for the two vertebrae they are between.  There are 7 cervical vertebrae, so the C6 nerve root exits

Brachial Plexus Diagram

between the C5 and the C6 vertebrae, and the C7 nerve root exits between the C6 and the C7 vertebrae.  The anatomy is further complicated because the nerves to each muscle in the shoulder and arm get stimulation from several spinal nerve roots.  This is because the cervical nerves come together in a complicated conglomeration of nerves called the brachial plexus.  The nerve roots enter the plexus and fibers from several nerve roots joint to exit the plexus as peripheral nerves.  Each muscle gets stimulation from one of these peripheral nerves.  Key muscles in the throwing process include the triceps, the pectoralis major and minor, the latissimus dorsi, the deltoid, the biceps, the biceps radialis, and others.  Each of these muscles in innervated by a specific peripheral nerve, and most of these receive varying amounts of innervations from the C5, 6, 7 and 8 nerve roots.

Certainly Manning has had access to the best available therapy to try to regain muscle strength.  Still muscles just don’t work without nerve stimulation.  This is called trophy, or trophic stimulation.  Muscles that lose their innervations undergo atrophy (no trophy) and become smaller and lose their function.  (think of polio and spinal cord injury victims) No amount of exercise, therapy or effort can make a muscle without innervations work. So if Manning still has arm weakness six months after his fusion surgery it is likely he will be left with at least some degree of muscle weakness.  Six months post surgery he is not likely to get much more strength back.  Certainly therapy can help other muscles become stronger and assume some of the roll of the muscles that have lost strength, but for Manning to function at a level required of a top level NFL quarterback I predict he will need to be able to throw the a football at very close to his prior strength.

How Vulnerable Is Manning To Recurrent of Further Injury?: How serious are the concerns that Peyton Manning will be at risk of additional levels of disc injury due to already existing disc injuries and the additional stress on the disc levels adjacent to a fusion.  I expect that the fusion is going to hold up pretty well, and not itself be highly vulnerable to becoming unstable.  The issue is really whether he develops disc herniations at the levels above and below the fusion, and whether he develops narrowing of the spinal canal (spinal stenosis) related to scar tissue or exuberant bone growth in the area of the fusion or at adjacent disc levels. NFL quarterbacks are sacked an average of twice a game, an although Manning is very experienced and may be able to minimize the number or sacks and hits he receives, undoubtedly he will be hit and his neck will be put in harm’s way in the course of an NFL season.  I anticipate that these are going to be future issues for Manning, but that they are not likely to be the reason he is or is not successful in his short term comeback.

I anticipate that Peyton Manning’s success or lack of success at his comeback is going to hinge on how much arm strength he has remaining.  This will be apparent to fans by the time the season comes, and he really has had enough time to strengthen his muscles by now.  Teams expecting him to become a great deal stronger than he is right now are likely to be disappointed.

Tony Romo’s Rib Injury

Tony Romo, the star quarterback of the Dallas Cowboys of the NFL sustained a fractured rib and punctured lung in last weekend’s game against the San Francisco Giants. On the way to work today on ESPN sports radio I heard a discussion about a “shot” that Romo might get to allow him to play with less pain this weekend.  There was discussion as to whether a “pain shot” might be something that a quarterback, who presumably needs to play at a higher cognitive level than say the ex-defensive lineman who brought up the subject might need to have to play effectively.

This prompted me to write about what type of shot they are discussing.  The injection likely being considered for Romo is a type of regional anesthesia known as a nerve block.  This type of injection is commonly used in areas where a nerve that gives sensation to an area of the body can safely have an injection of local anesthetic placed near the nerve proximal to an area where pain is experienced or expected to be experienced.  Dental anesthesia is an example of a nerve block that many people can relate to personally.  A broken rib is this type of situation.

The nerve that supplies the rib runs just under the lower margin to the rib, and runs from back to front.  This means that if a local anesthetic is injected near the lower border of a rib well behind (posterior to) the area of the fracture this area will become numb.  The local anesthetic is safely injected just above the rib below the one that is cracked to avoid injury from injection directly into the nerve or blood vessels, and  so that it can diffuse through the tissues up to the nerve just above that area, i.e. the lower margin of the rib above where the never is located.

If Mr. Romo has only one rib that is cracked this type of nerve block, called an intercostal nerve block, could potentially give him excellent anesthesia without interfering with his performance cognitively.  It could also be done relatively safely, as minor movements of the cracked rib though extremely painful are not terribly dangerous.  I expect Romo to have just this type of intercostal nerve block and play effectively against the Washington Redskins on Monday night.  Nothing about an intercostal nerve block is going to interfere with Romo’s play calling, decision making or thought processes.  The duration of the nerve block will depend on the type of local anesthetic used, but will likely be a few hours as one of the longer acting agents like Marcaine is usually chosen.

This type of injection is occasionally administered to patients in a physician’s office when they are experiencing severe pain from a cracked rib, and it can be very effective.

Justin Smoak of the Seattle Mariners and His Jammed Finger

As a Mariners fan I am concerned about Justin Smoak and his jammed finger, specifically his jammed thumb.  It’s certainly possible Smoak has some other type of thumb injury, but if he has a jammed finger type injury it is likely to be very slow to resolve.   Jammed finger is often called basketball finger because of the frequency seen in basketball players, where in trying to catch the ball a finger is accidently hit on the end while held rigidly straight and the first finger joint is jammed.  In the thumb there are only two phalanges so the proximal interphalangeal joint is the only interphalangeal joint.  The thumb is also pretty critical to a baseball player for hitting.  To grip a bat and generate power while hitting the ball the thumb on the upper hand is critical.  I expect if he has this injury that his hitting left handed will be more severely affected than hitting right handed.

The usual treatment of a jammed finger other than the thumb is to support the finger by buddy-taping the finger to an adjacent finger for splinting while allowing pretty normal function of the hand.  With the thumb this is of course not possible.  The natural course of healing of a jammed finger is quite prolonged.  The joint can become swollen and inflamed, and the swelling can last many months.  Good function usually returns in a matter of a week or two, but my prediction is that Smoak will end up on the 15 day DL to recover from this injury if he has a jammed finger.  If it is just a less serious contusion he may recover more quickly.   If he had an ulnar collateral ligament tear it would have been evident by now.  That type of injury seems very unlikely given the nature of the injury but given that it was on his throwing hand, and not protected by his baseball mitt it is possible to get an ulnar collateral tear from being hit by a batted ball.

Hopefully Justin will just need a few days of ice and therapy, but don’t be surprised to see this recover slowly and for him to be put on the DL retroactively to the date of his first missed game.

 

Addendum:  I was wrong regarding the DL for the jammed thumb, but possibly the M’s should have used the DL for that problem.  Smoak had a serious facial injury and was put on the DL for that the first game back after the thumb injury, and since returning and having plenty of time for the thumb to heal much better he is hitting much better.  Let’s hope this is a predictor of a big 2012 for Smoak.

A Fitness Gene?

Our individual genetic makeup seems to play a role in just about everything about us, and so this probably should come as no surprise.  There is proving to be a genetic explanation for why some people seem to get really fit when they exercise, and others just don’t.  An interesting article in the NY Times Health section outlines a recent genetic study of aerobic capacity improvement with exercise.   I found it an interesting read:

March 16, 2011, 12:01 am

Is Fitness All in the Genes?

By GRETCHEN REYNOLDS

Why do some people respond to an aerobic workout routine by becoming incredibly fit, whereas others who exercise just as hard for months end up no fitter than when they began?

That question has bedeviled countless people who’ve started exercise programs. It has also motivated a major new study of the genetics of fitness. Scientists long have known that when any given group of people faithfully follows the same aerobic workout routine, some increase their cardiorespiratory fitness substantially, while an unfortunate few seem to get no benefits at all. But what, beyond the fundamental unfairness of life, makes one person’s body receptive to exercise and another’s resistant? According to the new study, which will soon be published in The Journal of Applied Physiology, part of the answer may depend on the state of specific genes.  Read more

Prednisone Taper

Prednisone Taper – No Longer Needed for Short Course Corticosteroid Therapy: As a medical student and resident I remember hearing all of the attending physicians tell me about the best way to do a prednisone taper.  I still have older patients question why prednisone tapering is not recommended, because their old doctor always did a prednisone taper.  For those of you not familiar with prednisone, or corticosteroid treatment in general, prednisone is a commonly used, inexpensive, and quite potent corticosteroid.  Corticosteroids are distinctly different from the anabolic steroids of the Mitchell Report and Marion Jones infamy.  Corticosteroids are naturally occurring hormones produced by the adrenal cortex that are essential to our wellbeing.  They serve to regulate glucose, protein and fat metabolism and function to reduce inflammation by blocking a key step in the inflammatory process and by inhibiting eosinophil (the primary allergic white blood cell) action, as well as other mechanisms.  Therapeutically corticosteroids like prednisone, dexamethasone, prednisolone, hydrocortisone and others are used in higher than naturally occurring amounts to reduce inflammation.  They are commonly used in attacks of asthma or bronchospasm, in severe acute arthritis, in head trauma or spinal cord trauma with swelling, in acute severe allergic reactions, in severe dermatitis, and for lots of other situations.  They are often injected directly into inflamed areas to reduce inflammation locally.

The big problem with use of high dose corticosteroid therapy is that it eliminates the demand on the adrenal glands to produce cortisol naturally. After the adrenal glands stop functioning to produce cortisol for a period of time, it takes them a while to resume producing normal amounts of cortisol.  It takes even longer to be able to respond to emergency situations where the body requires much higher amounts of cortisol.  In situations like major trauma, surgery, serious infections like pneumonia or pyelonephritis, or really any physically traumatic event the body requires cortisol in higher than usual amounts to cope effectively.  Lack of this adrenal response can lead to shock that fails to respond to fluid resuscitation and death.  This situation is seen clinically in two fairly common situations.  The most common situation is where a patient has been on therapeutic corticosteroid therapy in a dose sufficient to suppress the adrenal glands for a prolonged time and an acute emergent situation develops and the adrenals are not able to respond normally.  The other situation is when a patient has adrenal insufficiency, is on standard daily doses of corticosteroid replacement therapy, and becomes acutely ill or has major trauma.  In either of these situations it is critical to treat the patient with high dose corticosteroids, usually IV if the need is emergent, or orally if it surgery or acute illness is anticipated in order to prevent critical illness-related corticosteroid insufficiency.

Medrol Dose-Pak Seldom Needed Anymore

In order to prevent this situation for years we were taught to taper corticosteroid treatment after short term “burst” course treatments of prednisone.  Typically we would start moderately high dose of prednisone, say 60 mg for 3 days, then 40 mg for 3 days, then 20 mg for 3 days, then 10 mg for 3 days, then 5 mg for 3 days.  You can imagine there are innumerable variations on this theme.  A product is marketed to make this taper simple, the “medrol dosepak”  (see photo above). The dogma was always taper steroids to allow the adrenal gland to recover from the high dose therapy.  As with many things this was done because everyone knew it was the right thing to do, but nobody looked at it critically.  We have learned that the key to avoiding adrenal suppression prednisone side effects after a short course of prednisone therapy is not tapering corticosteroid therapy, but to keeping the course of therapy as short as possible.  Now we will often use 6o mg of prednisone daily for 7 days, and stop.  This is really safer than taking 10-21 days to taper off the high dose.

DO NOT MISREAD THIS DISCUSSION.  IF YOU HAVE BEEN TREATED LONGER THAN ABOUT 2 WEEKS WITH PREDNISONE DISCUSS STOPPING WITH YOUR DOCTOR! YOU MAY NEED A TAPER!

It seems that the taper itself is mostly treatment at much higher than natural corticosteroid needs (roughly 5 mg daily of prednisone, or 20 mg daily of hydrocortisone).  For some illnesses even shorter bursts of treatment are effective.  In croup, a viral illness of young children a single IM dose of dexamethasone, or a 3 day burst of high dose prednisone is quite effective.

In conditions where longer term treatment with corticosteroids is needed, a slow taper is critical.  Examples are many rheumatologic disorders like systemic lupus erythematosis, polymyalgia rheumatica, and other autoimmune disorders like Crohn’s disease and Ulcerative Colitis.  In these cases gradual tapers over weeks to months are needed, and patients are at risk of adrenal crisis for some time after stopping therapy.

The key to understand is that in burst courses of prednisone treatment unless there extenuating circumstances like diabetes or major psychiatric disorders, shorter courses at higher doses are much safer than longer courses or longer tapers.  Now instead of hearing every attending and senior resident preach their favorite way to taper burst courses of steroids, they should be debating how short a course of high dose prednisone they can use and still get a good response.

Concussions: Brains are Important

With all the press and controversy of the NFL crackdown on helmet to helmet hits this week, I thought I’d repost this as relevant.

Originally posted May 7, 2010.

We finally understand that the brain is an important organ to protect, especially in young athletes.  For those of you who have been around long enough to watch any of the Mohammed Ali boxing matches with Joe Frazier or George Foreman, it may have come as no surprise when Ali developed post-consussive brain complications.  At that time concussions were considered a minor inconvenience.  Since then we have learned a great deal about traumatic brain injury.  Professional championship boxing matches were routinely 15 rounds, but now are limited to 12 rounds.  Even in the Mixed Martial Arts (UFC)  competitions that are so popular now referees seem to be fairly quick to end matches when a competitor appears to be about to be concussed severely.   We have learned about the risk of life-threatening cerebral edema when a second concussion follows the initial injury without time for the brain to recover.  We have also learned post-concussive syndrome, when there can be persistent poor cognitive function  as well as depression and mood problems for longer periods of time after concussion.  In addition there is evidence of  late risks of Parkinson’s disease and dementia.

In the state of Washington this has become even more of an issue because of a bill now signed into law that mandates school age athletes receive specific care prior to return to sports participation.  The Washington Interscholastic Athletic Association (WAII)  has a web site that gives excellent guidelines to coaches, parents, athletes, schools and health care providers on the expected management.

The highlights of the guidelines and regulations are stated:

  • On a yearly basis, a concussion and head injury information sheet shall be signed and returned by the youth athlete and the athlete’s parent and/or guardian prior to the youth athlete’s initiating practice or competition.
  • A youth athlete who is suspected of sustaining a concussion or head injury in a practice or game shall be removed from competition at that time.
  • A youth athlete who has been removed from play may not return to play until the athlete is evaluated by a licensed health care provider trained in the evaluation and management of concussion and receives written clearance to return to play from that health care provider.”

Fortunately we now have consensus tools for coaches and trainers to use in the evaluation of athletes.  The Sport Concussion Assessment Tool 2 (SCAT2) algorithm) gives clear guidance for management of athletes with concussion.

Most importantly we as a medical community and the coaches and trainers caring for athletes at practices and competitions now are aware of the need to treat concussions as a serious problem, and we have protocols in place to appropriately manage these athletes.

Do Women Sweat Like Men?

Research shows that women do of course sweat, and like men sweat more with exercise.  The difference is in volume of sweat.  A recent study in the Journal of Experimental Physiology found that women, whether fit or not, are less able to use sweating to get rid of body heat than men.  This is expecially true of unfit women.  An article in the NY Times by Gretchen Reynolds discusses the results of a simple but interesting study where fit and unfit men and women are evaluated for their sweat production, body temperature, and physiologic responses to exercise in a hot environment.  It shows once again that men and women are different. 

October 20, 2010, 12:01 am

Do Women Sweat Differently Than Men?

By GRETCHEN REYNOLDS

Carlos Silva and Endocardial Ablation for PSVT

In the sports news this week was Carlos Silva, the pitcher traded from my local MBL team the Seattle Mariners to the Chicago Cubs last winter, who had to leave a game with what is reported to be supraventricular tachycardia.  This type of very rapid heart rate comes intermittently in paroxysms, therefore the common name Paroxysmal Supraventricular Tachycardia (PSVT).  In the normal heart the electrical conduction of the heart travels through the atria, pauses momentarily at the tiny bundle of tissue called the atrio-ventricular node (AV node), and then travels through the specialized conduction system of the ventricles to cause the ventricles to contract.  In the normal heart this AV node is the only place that has tissue able to conduct the electrical signal from the atria to the ventricles.  In patients with PSVT there is usually an abnormal area of heart muscle fibers through the fibrous separation of the atria from the ventricles.  This allows the electrical impulse of the heart to race in a circuit from the atria to the ventricle then back to the atria and to the ventricle leading to paroxysms of very rapid heart rate.  The heart rate in this condition can get to over 200 beats per minute in young healthy people, and can be very uncomfortable, at times going so fast that there is not enough time for the heart to fill well with blood between heartbeats and leading to reduced circulation.  The rapid heart rate in older patients with a degree of coronary artery blockage can lead to ischemia of the heart muscle, with angina and even a myocardial infarction.  Non-surgical treatment for PSVT includes use of medications to slow the maximum heart rate like beta-blockers or calcium channel blockers.  Procedures like carotid massage and holding one’s breath and bearing down (Valsalva maneuver)  that increase the activity of the vagus nerve, which slows heart rate have been used to interrupt paroxysms for years.  More recently use of IV adenosine has been used in emergency room settings very successfully to convert PSVT to a normal rhythm

Carlos Silva had a fairly new surgical treatment for PSVT called radiofrequency ablation.  In  this procedure a cardiac catherization is done, the abnormal segment of conducting tissue is located by a procedure called endocardial mapping, and the ablation is done through the catheter to destroy the abnormal myocardial cells and prevent the circuit rhythm from occurring.  This procedure has a high success rate and is well tolerated in most patients. 

Silva may be able to return to baseball in a very short period of time if the procedure goes as well as it often does.  Even if the procedure is not completely successful most patients with PSVT have fairly infrequent episodes, and full recovery from a cardiac catheterization is usually quick.  I predict Silva is back on the mound before Sept 1.

Prescription Opiates Connect the Two Biggest NFL Busts

Ryan Leaf and JaMarcus Russell have many things in common.  They are arguably the two biggest busts in recent NFL Draft history, were top ranked collegiate quarterbacks who never lived up to their potential in the NFL, but when you think about it the most telling thing they have in common is arrests for abuse of prescription opioids.

On July 5, 2010 Russell joined Leaf in the fraternity of prescription opioid users who have been busted for their illegal opioid use.  Russell was arrested after an investigation for use of codeine cough syrup, likely being used as an ingredient of the popularly abused purple drank.  In 2009 Leaf was indicted for burglary and theft of hydrocodone, a prescription semi-synthetic opioid.

Few argue that either of these athletes lacked the physical tools needed to be top NFL quarterbacks. In 1998 Leaf was the second overall NFL pick, right after Peyton Manning, one of the best all-time NFL quarterbacks.  In 2007 Russell was the #1 overall pick in the NFL draft by the Oakland Raiders.  Somehow both of these players became remarkable flops at the professional level.

Pain is a part of being a football player.  At the professional athlete level access to opioids is unlikely to be difficult.  They are probably available from trainers, physicians and less legitimate sources.  Some people use pain medications appropriately, and simply don’t fall into the trap of abuse.  Others seem to fall into the downhill spiral of continued use, misuse, and abuse that ends in addiction and in the cases of these two athletes, legal trouble.

Star athletes are pampered, sheltered, and are likely to feel invincible; above the risk of opioid addiction.  Clearly they are not.  Youth in general are at higher risk of misuse and addiction to opioids, and we as physicians need to be diligent in not facilitating the addiction of our young patients.  In the case of these two athletes I have no way of knowing if their addiction problems started with the use of opioids to treat football related painful injuries, but it seems likely that is the case.  Obtaining opioids is very easy for anyone who wants them badly without the help of a physician or athletic trainer.  In sports like the NFL where saying no to star athletes may not be the easiest thing to do for trainers and physicians, and where access to drugs through friends, agents and handlers may be painlessly easy, teams would be well served to be extra diligent to teach their prized property, the players, to avoid opioid misuse.

Would just saying no to opiates have kept these two incredible athletes from becoming dismal failures in the NFL?  Is the fall into opioid addiction just a sign of some character weakness that itself prevented them from succeeding as NFL quarterbacks?  Which came first?  All of these are questions without answers, but one thing is clear.  Neither of these athletes, nor any of the rest of the huge numbers of Americans currently abusing prescription opioids, have come out ahead because of their drug use.

Previous posts on Oxycontin and the epidemic of abuse of prescription drugs on this blog have discussed these issues in detail.  It’s such a problem that finding a physician to prescribe opioids for chronic pain is difficult because of our skepticism over anyone using opioids.  Abuse and diversion is such a problem it’s impossible not to see any new patient who tells us they need opioids as a potentially abusing or selling the drug.

Could a High Ankle Sprain nix the M’s and Yankees Cliff Lee Trade?

David Adams, a New York Yankees Double A infield prospect has been out of action with a high ankle sprain.  You may wonder what the devil a high ankle sprain is anyway.  The ankle is pretty low on the leg, so what does this mean?  The two bones of the lower leg, the tibia and the fibula, are connected by a membrane called the interosseous ligament or syndesmosis.  When it is damaged it allow abnormal movement of these two bones, and makes the ankle joint unstable. It takes far longer to heal than a typical lower ankle sprain, and therapy is less helpful. Still it generally fully heals with time, and it’s hard to imaging this being a deal breaker for the Seattle Mariners in their prospective trade with the Yankees.  My guess is that other teams are making better offers.  See this more complete article on high ankle sprains on the Children’s Memorial Site.