Hello everybody, welcome to the talk on brachial plexopathy. Before I begin, I want to acknowledge the pandemic and the current situation globally that we face at this time. I hope that we are able to turn the corner sooner rather than later. I also want to take this opportunity to thank the American Academy of PM&R for organizing this lecture series and extending an invitation for us to do this talk. And also want to thank all of you to take the time out of your busy professional and personal lives to attend to this lecture series. Today's talk is demystifying brachial plexopathy. My name is Dr. Neenath Karandikar. I'm the assistant chief of PM&R at the VA hospital in Palo Alto and affiliated to Stanford Department of Orthopedic Surgery as clinical associate professor. The other presenter on this talk is Dr. Robert Rinaldi, the chief division of pediatric rehab at the Children's Health Hospital. He's also a professor of pediatrics and PM&R at UT Southwestern in Dallas, Texas. Thank you, Dr. Karandikar. We have no disclosures to make. So our objectives for this talk really are going to be, number one, analyze brachial plexus anatomy. Number two, develop a systematic approach to lesion localization. Number three, differentiate common clinical presentations, including anatomic, clinical and electrodiagnostic correlations. And four, review the necessary principles of brachial plexus management. So starting off with the anatomy, I'm going to provide a quick overview of the brachial plexus itself. It basically is comprised of the ventral rami of the spinal cord segments C5 through T1. If you look at the diagram of it, you'll see that the dorsal root emerges from the dorsal aspect of the spinal cord, and the dorsal root ganglion is comprised of the cell nerves for the sensory cells. On the opposite side is the ventral root, which emerges from the anterior horn of the spinal cord gray matter, and is comprised of the alpha motor neurons or the anterior horn cells. These then combine to create the spinal nerve, which is a mixed nerve, and then the spinal nerve breaks off into the dorsal ramus and the ventral ramus. Now the dorsal ramus is mixed as well as the ventral ramus in terms of carrying both sensory and motor components. You can then split the anatomy of the proximal plexus into preganglionic and postganglionic, and this is important in regard to localization of lesions. Preganglionic lesions are really those that occur prior to the takeoff of the ventral and dorsal ramus. These typically are considered radiculopathies. Postganglionic lesions are those that occur past the level of the dorsal and ventral ramus and are typically considered more plexopathy in terms of pathology. As mentioned previously, if you take a look at the microanatomy of the root levels, the dorsal root ganglion is comprised of the dorsal sensory nerves and the ventral root is comprised of the anterior motor nerves. The dorsal root ganglion, as mentioned previously, is purely sensory in nature, and the anterior ventral root is purely motor in nature. Likewise, as previously mentioned, the ventral ramus is mixed, as is the sensory ramus. So I'm going to discuss pre- and postganglionic lesions and compare these two levels of lesion to look at some key differences. When there's no lesion to the plexus or the pre- and postganglionic regions of the anatomy, you really will have no changes in your sensory nerve action potential. You're going to have normal sensation clinically, and that just makes sense. With the pre-ganglionic lesion, however, where the lesion is between the spinal cord and the dorsal root ganglion, you're typically going to have normal sensory nerve action potentials and a loss of clinical sensation. With postganglionic lesions, where the lesion is occurring distal to the dorsal root ganglion, electrodiagnostically, you will have a loss of your sensory nerve action potentials and a loss of sensation clinically. So the distinction between maintenance or loss of the sensory nerve action potentials can help you delineate whether or not it's a pre- or a postganglionic lesion. Some key considerations with pre-ganglionic lesions are that they typically do have a worse prognosis in regard to recovery. Electrodiagnostically, your sensory nerve action potentials will be normal, but you will demonstrate paraspinal denervation. Depending upon the level of injury, you can see scapular winging. This is typically seen with upper trunk or C5, C6 level injuries, or Horner syndrome, which we typically see with lower trunk or C8, T1 level injuries. Many people will get an MRI scan to assess level of injury in plexopathies. A key finding that can be seen on an MRI scan that's considered a classical finding for root avulsions is what's called a pseudomeningocele. This is typically noted as swelling and enhancement, contrast enhancement at the root level. It appears kind of as a ballooning of the root with that noted enhancement. Interestingly, many people consider this to be pathognomonic for a root avulsion or rupture, but I've seen many cases clinically where that's not been the case. The root has actually been intact to some extent because we see clinical innervation and clinical activation in the muscle served by that spinal cord segment. So again, pseudomeningocele can be seen on MRI scan. Again, many people do consider that pathognomonic for rupture avulsion, but really all it indicates is a root level injury and nothing more. Let's talk about the nature and severity of peripheral nerve injury. There are two common classification systems that are utilized when describing degree of injury, and these are important to understand because of the prognostic value of these. There's the Sedan classification and the Sunderland classification. They're very similar in terms of how they are defining their different classification levels based upon the actual anatomic injury. So with the Sedan classification, the first classification is considered a neuropraxia. The affected structures involved in neuropraxia basically just include the myelin. So you have some demyelination around the nerve itself, and that creates a localized conduction block. This is considered Sunderland classification number one. Sedan classification axonotmatic involves injuries to the axon, however, the endoneurium is intact. So this is an axonal injury with local demyelination, but intact endoneurium. This is considered Sunderland classification score two. Sunderland classification score three is also axonotmatic in the Sedan classification. But now you have axonal and endoneurial damage with an intact perineurium. So a little bit more damage, and then Sunderland classification four extends that damage to include the perineurium, but the epineurium is intact around the around the nerve. And again, these are, if you compare that to the Sedan classification, Sedan basically classifies all three of those levels of Sunderland classification as axonotmatic. So the Sunderland classification scale is a little bit more detailed in terms of the actual neuroanatomy and the degree of injury. And then finally, there's neuromedic injury based upon the Sedan classification, that's a complete nerve transection, that's considered a Sunderland classification score of five. Now, why is it important to understand these different classification scales? Well, the basic reason to understand these is because they are fairly prognostic. And they do exemplify different courses of recovery. So with a neuropraxic injury or Sunderland classification score of one, recovery typically occurs within the first 30 to 60 days, this is just a local conduction block due to demyelination, as I'd mentioned. With axonotmatic injuries, you typically will have a much slower progression of recovery. And typically, these are folks who will go on to improve, and they're demonstrating recovery, but not complete recovery by that 30 to 60 day timeframe. So they're improving, but they don't demonstrate full recovery. So you know, it's not a neuropraxic injury. Again, the Sedan classification scores of two, three and four define a further degree of injury or a more extensive degree of injury. And you can typically correlate those to worsening or not worsening necessarily, but a much slower recovery or less complete recovery of the nerve injury itself. And then finally, neuromedic injuries, those are injuries where you're not seeing any improvement at all, you're not seeing any muscle function, you're not seeing any sensory reinnervation. 30 to 60 days goes by, and you're not seeing anything four months, five months, six months goes by, and you're not seeing any recovery at all. That's neuromedic. And again, those that's that's no recovery at all, because there's typically complete transection of the nerve in those cases. So it's important to understand the definitions and the classification scores in regard to potential prognosis and degree of injury. I'm going to go into a little bit more detail on the clinical anatomy now. And as mentioned previously, the brachial plexus is comprised of the C5 through T1 cervical and upper thoracic roots. These roots then combine to create the upper, middle and lower trunks, which then head into the anterior and posterior divisions, which then combine to create the medial, posterior and lateral cords. The individual peripheral nerves split out at different levels of the plexus, however, they don't all emerge at the cord level. For example, the dorsal scapular comes off at the C5 root level versus the musculocutaneous nerve, for instance, which comes off the lateral cord level. So the peripheral nerves come off at different portions of the plexus. And this is an important concept to understand, because this can help you define the location of the actual lesion. Dr. Karandikar is going to go into fairly extensive detail on how to utilize this understanding of the plexus anatomy to localize lesions. There are also basic descriptions of the intraclavicular portion of the plexus and the supraclavicular portion of the plexus. Clinically, I've not found that to be really a relevant distinction. I think that's more for operative purposes. These two photographs demonstrate the actual anatomy of the plexus. I'm going to talk about this briefly, because I think this is important to understand. So the plexus itself emerges between the anterior and middle scalenes and behind the clavicle and pec minor. The so-called scalene triangle, through which it emerges, is made up of an anterior border that includes the anterior scalene, a posterior border that includes the middle scalene, and an inferior border that includes rib number one. The contents of the scalene triangle include the brachial plexus plus the subclavian artery. The subclavian vein emerges in front of the scalene, so it comes through outside of the scalene triangle. Both photographs on this slide demonstrate that anatomy very nicely, and you can see on the bottom photograph clearly the brachial plexus coming out between the anterior scalene and the middle scalene. Now this relationship between the scalenes and the plexus is important from a clinical perspective, as we'll talk about when we go through some of the clinical correlations towards the end of the lecture. With that, I'm going to hand the lecture back to Dr. Karandikar to talk about clinical considerations for treatment. With the background information presented by Dr. Rinaldi in the previous slides, let's now look at some clinical considerations for treatment. When approaching a patient with brachial plexopathy in the electrodiagnostic clinic, one consideration is lesion localization. The other consideration is assessing for the severity of the lesion. In terms of lesion localization, the first question is whether the lesion is preganglionic versus if it's postganglionic. And remember, this has some implications with respect to prognostication as well as with treatment. If the lesion is indeed postganglionic, the next level that we need to define is whether the lesion is supraclavicular, specifically belonging to the roots or the trunks of the brachial plexus, versus if it is infraclavicular, meaning the lesion is distal involving the cords or the branches of the brachial plexus. An additional consideration is whether the brachial plexus is prefixed with a contribution from C4 versus postfixed with a contribution for T2. This really has more relevance when addressing from a surgical standpoint and not so much for us as PM and our physicians in terms of diagnosis and localization. In terms of assessing the severity, the clinical exam gives us some really valid indicators to assess the severity of the lesion. We are all aware of the clinical exam features, including atrophy, lack of reflexes, and other additional features that help us determine the severity. And again, this goes back to the electrodiagnostic exam being an extension of the history and the physical exam. From an electrodiagnostic standpoint, the nerve conduction study, specifically the sensory and the motor nerve conduction studies that we perform, gives us information with respect to latency and amplitudes. And the amplitudes are a really good indicator in terms of quantification of the lesion. If the amplitude on the symptomatic side is lower by a certain magnitude compared to the asymptomatic side, that is an excellent indicator of the severity of the lesion. Last but not the least, the EMG portion of the electrodiagnostic study, including EMG of the paraspinals, helps us assess the severity of the lesion. The most important of this being the evidence of axonal continuity. If there is evidence of voluntary motor units being recruited on a regular electromyography, then that shows evidence of axonal continuity. If there are no voluntary motor units recruited, that is evidence of lack of axonal continuity, indicating a very severe or neuroautomatic type of injury. Okay, let's get started with the case example. Left hand weakness, post-operative day 10, status post-CABG surgery. On examination, weak long finger and thumb flexors, intrinsic muscles, decreased sensation in the left medial hand and forearm, nerve conduction velocity, right side is normal on the symptomatic left side, the median snap is normal, radial snap is normal, and there are some abnormalities in the left ulnar C-map, left ulnar snap, left median C-map, left median antebrachial cutaneous. If you look at the EMG, a lot of abnormalities in certain muscles and some muscles are normal. Now as we look at this data set, there are certain findings that give us localizing value. First, just the history of the physical exam tells us this is primarily involving the hand muscles, maybe somewhere along the median on the ulnar nerves, or maybe the medial cord, the lower trunk, or the C81. The medial antebrachial cutaneous, which comes off of the medial cord here, is also of immense localizing value. And then last but not the least, the EMG abnormalities in this specific distribution helps us localize the lesion further and helps define the nature of the injury. Paraspinals being normal helps us localize this at distal to the root level. So each of these findings helps us in some way either localize the lesion or help us assess the severity of the lesion. Let's look at this and how it helps us assess localization and severity in a brachial plexopathy over the next few slides. Let's start with the basic foundation of the anatomy of the brachial plexus. And for the purpose of the slide here in the demonstration, I'm just going to simply draw out the brachial plexus and illustrate some points that are of critical importance in terms of localization and in terms of remembering the anatomy of the plexus. As we know, the brachial plexus is formed by the ventral rami from C5 through T1. And I've illustrated those here from proximal to distal. As we start looking at the anatomy of the plexus, the ventral ramus of C5 and the ventral ramus of C6 come together to form the upper trunk. The ventral ramus of C7 continues on as the middle trunk. And the ventral ramus of C8 and T1 come together to form the lower trunk. So if you were to consider the anatomy of the upper trunk, the root value of the upper trunk is C5 and C6. The root value of the middle trunk is C7, it's a direct continuation of C7. The root value of the lower trunk is C8 and T1. There are two branches that come off of the plexus at this level. One is the dorsal scapular nerve that comes off of C5 that innervates the rhomboids. The importance of understanding this is that if we do an EMG of the rhomboids and the rhomboids is abnormal, that localizes the legion to the level of the C5 root or a C5 motor radical apathy. So again, this is the dorsal scapular nerve that's coming out off of the C5 root. The other branch that comes off at the root level is from the C5, C6, and C7 ventral ramus forming the long thoracic nerve, which supplies the serratus anterior. Again, the same localizing value as in the case of the rhomboids. If either the rhomboids or the serratus are abnormal on an EMG examination, that localizes the legion either to the C5 root or the C5 through 7 motor roots in the case of the serratus anterior. The last branch that comes off of at this level is a suprascapular nerve that comes off the upper trunk. The suprascapular nerve supplies the supraspinatus and the infraspinatus. The suprascapular nerve is the branch of the upper trunk. The upper trunk is formed by C5 and C6. The root value of the suprascapular nerve is C5 and C6, and both the muscles that supply supraspinatus and infraspinatus are consequently at level C5 and C6 as well. The localizing value from the suprascapular nerve comes in assessment of upper trunk lesions. If you are looking at either an upper trunk or a distal problem, we can assess either the supraspinatus or infraspinatus, and if the supra or infraspinatus is abnormal, that tells us the legion is proximal to the takeoff of the suprascapular nerve in the upper trunk. That being said, now let's proceed. The upper trunk then divides into anterior and posterior divisions. This is the anterior division. This is the posterior division. The middle trunk divides into anterior and posterior divisions, and the lower trunk then divides into anterior and posterior divisions. Again, each of these trunks is going to divide into the anterior divisions and posterior divisions. In this schematic, I've made the anterior divisions with straight lines and the posterior divisions with these broken lines. The anterior divisions of the upper and the middle trunk combine together to form the lateral cord. So the lateral cord is formed by the combination of the anterior fibers, anterior division fibers, so the upper trunk and the middle trunk. The upper trunk again is 5 and 6, the middle trunk is 7, and so the lateral cord is really a combination of 5, 6, and 7. But remember, these are only the anterior division fibers of the upper trunk and the middle trunk. Let's look at the lower trunk. The lower trunk is a direct... The lower trunk is anterior fibers continue directly to form the medial cord. Since the medial cord is a direct continuation of the lower trunk, the root value of the medial cord is going to be CA21. And then here in the middle of the schematic, we have the posterior divisions of the upper trunk, the middle trunk, and the lower trunk that come together to form the posterior cord. Since it is formed by all the three trunks, it goes without saying that the posterior cord actually has contributions from all the way from C5 through T1. So again, upper trunk, 5-6, middle trunk, 7, lower trunk, 8-1, medial cord, direct continuation of lower trunk, 8-1, lateral cord, anterior divisions of upper and middle trunk, 5-6-7, posterior cord, all three, C5 through T1. Let's progress further. The posterior cord ends by dividing into two branches. The axillary nerve that supplies the deltoid and the teres minor, and the radial nerve. The lateral cord gives off a branch called the musculocutaneous nerve. The musculocutaneous nerve is a direct connection or continuation of the lateral cord. And so the root value of the musculocutaneous nerve is 5-6-7. The musculocutaneous nerve supplies the biceps, the brachialis, and the coracobrachialis, most of which are innervated really by the 5-6 level. A direct continuation of the musculocutaneous nerve is the lateral antebrachial cutaneous nerve. The lateral antebrachial cutaneous nerve coming off of the musculocutaneous nerve is another important sensory nerve conduction study that has localizing value to the lateral cord as well as the 5-6-7 roots and the upper and middle trunks. The lateral cord gives off branches and the medial cord gives off branches together that form the median nerve. And then the medial cord gives out a series of branches. It ends with the ulnar nerve, but it also gives off the medial brachial cutaneous nerve and the medial antebrachial cutaneous nerve. Almost similar to the lateral antebrachial cutaneous nerve, which comes off of the lateral cord, the medial antebrachial cutaneous nerve gives us some localization value to the medial cord of the brachial plexus. In addition, we have the lateral pectoral that comes off of the lateral cord and the medial pectoral that comes out of the medial cord. Most of the times, the lateral and medial pectoral nerves supply the pectoralis major and minor, and this is not really tested from an EMG standpoint. The ulnar nerve is a direct continuation of the medial cord and the lower trunk. And so all the ulnar nerve muscles are going to be C8-T1 muscles. This includes the flexor carpi ulnaris, the flexor digitorum profundus, as well as the muscles in the hypothenar group and the interossei and the ulnar tulumbricals. All of those muscles are innervated by the ulnar nerve with the root value of C8-T1. If you look at the median nerve, the median nerve is formed by the combination of the lateral cord, which is 5-6-7, and the medial cord, which is 8-1. And so the median nerve actually has all fibers from C5-T1. The last but not the least, the posterior cord. The posterior cord is fibers from C5-T1. It gives off three branches here, the upper and the lower subscapular nerves, which supply the subscapularis and the teres major, and then the thoracodorsal nerve that supplies the latissimus dorsi. In addition to the two terminal branches of the axillary and the radial. This is one area of the brachial plexus where the fiber distribution is a little unique. The subscapular nerves supply the subscapularis and the teres major, which belong to the shoulder. The shoulder is primarily a 5-6 area, and the subscapular nerves are also C5 and C6. The thoracodorsal nerve supplies the latissimus dorsi and is a 6-7-8 nerve, and the latissimus dorsi is a 6-7-8 muscle. The axillary nerve supplies the deltoid and the teres minor, again going to the shoulder area. The shoulder area again is 5-6. The axillary nerve is also 5-6, and the deltoid and the teres minor are 5-6 level as well. And then the radial nerve actually has a combination from C5 through T1. The most proximal muscle that it supplies is the triceps, which is a 6-7-8 muscle. The last thing I want to point out is that just at the beginning, we talked about the C5 through T1 being the ventral ramus that contributes to the formation of the brachial plexus. And again, just a reminder, the dorsal ramus that comes out from the spinal canal in the brachial ramus innervates the paraspinals. And so in the EMG lab, if you have any paraspinal abnormalities, that indicates involvement of the dorsal ramus and localizes the legion to the level of the root or a radical apathy. The electrodiagnostic definition of radical apathy proposed by Dillingham includes two or more peripheral muscles innervated by the same nerve root and different peripheral nerves. And so that becomes really applicable here in terms of the brachial plexus lesions. So a few rules of the plexus. These nerves, dorsal scapula, long thoracic, along with paraspinal muscles, localize the legion to the level of the root. The supraspinatus infraspinatus EMG, lateral antebrachial cutaneous nerve, and medial antebrachial cutaneous nerves help us to localize the legion to the appropriate chords of the brachial plexus. Next, the upper trunk has a branch, the suprascapular nerve, which helps us localize the legion, but note there are no branches from the middle trunk and there are no branches from the lower trunk. Next, the shoulder or the proximal limb, mainly the shoulder and some part of the elbow is primarily a 5-6 innervated area, whereas the hand distally in the upper limb is primarily a C8-1 innervated area. The final thing I would like to point out here is as we start looking at the brachial plexus, we need to remember what we learned about the sensory and motor levels of injury in the ASIA exam and correlate that information with that of the peripheral nerve. So think about merging those two data sets together. A prime example of that would be looking at the thumb. If we look at the sensory innervation to the thumb, that comes from the C6 level based off of the ASIA exam. And so if you wanted to look at that level and assess it from a sensory nerve conduction standpoint, we would need to assess a C6 sensory level of the C6 DRG, the dorsal root ganglia. On the other hand, the thenar muscles that constitute the musculature of the thumb are primarily innervated by the median nerve at the C8 and T1 levels. So the sensory innervation and the motor innervation at the thumb are at C6 levels for the sensory innervation and C8 and T1 levels for the motor innervation, again illustrating the importance of separating the sensory levels and the motor levels of the injury and the peripheral innervation for each level to most optimally localize lesions in the brachial plexus. In the next few slides, let's revisit the schematic from the previous slide and then highlight some important points to help localize the lesion in brachial plexopathy. As we discussed, the brachial plexus is formed from the ventral ramus from C5 through T1. The dorsal ramus supplies the paraspinal muscles and helps EMG in the paraspinal muscles as important localizing value, as we discussed earlier. The C5 root gives off the dorsal scapular nerve that supplies the rhomboids. And the C5, 6, and 7 together form the long thoracic nerve that provides innervation to the serratus anterior. Localizing values on EMG in either the rhomboids supplied by the dorsal scapular at C5 level or the long thoracic nerve in serratus anterior give us localizing value in terms of either the C5 motor root or C5 through C7 motor roots, respectively. The C5 and the C6 roots combine to form the upper trunk. So the root value of the upper trunk is C5 and 6. The upper trunk gives off the suprascapular nerve that supplies the supraspinatus and infraspinatus, again, providing localizing value to at or proximal to the takeoff of the upper trunk suprascapular nerve, if there are abnormalities in the supraspinatus or the infraspinatus. The C7 root continues as the middle trunk. So the middle trunk has C7 root value, and then the C8 and T1 roots combine to form the lower trunk. Again, remember, this is before the plexus has divided into the anterior and posterior divisions. The upper trunk is of one branch, the suprascapular again to the suprascapular infraspinatus. The middle trunk has no branches, and there are no branches from the lower trunk. Just to consolidate this information, the C5 and C6 forms the upper trunk. The upper trunk gives off the suprascapular nerve, which supplies the suprascapular infraspinatus. The C7 forms the middle trunk. The C8 and T1 together form the lower trunk. In terms of root values, the upper trunk, 5-6, suprascapular, 5-6, supplies the supra and infraspinatus, which are consequently 5-6 root level innervated muscles. The middle trunk, C7, lower trunk, C8 and T1. And again, there are no branches from the middle and the lower trunk. Adding the plexus up further from where we left off, the upper trunk divides into anterior and posterior divisions. The middle trunk divides into anterior and posterior divisions, and the lower trunk divides into anterior and posterior divisions. The anterior divisions of the upper and middle trunk combine to form the lateral cord. What would be the root value of the lateral cord? It's a combination of upper and middle trunk. Lower trunk is 5-6, middle trunk is 7, and consequently the lateral cord is C5, C6, C7. The medial cord is a direct continuation of the anterior fibers of the lower trunk. The lower trunk is C8-T1, the medial cord consequently is C8-T1 as well. And the posterior cord is formed by the posterior divisions of all three trunks, the upper trunk, the middle trunk, and the lower trunk. And consequently, the posterior cord has a root value of C5-T1. So again, the C5-6 forms the upper trunk, the C7 forms the middle trunk, the C8-T1 forms the lower trunk. The anterior divisions of upper and middle trunk combine to form the lateral cord. The anterior division of the lower trunk continues as the medial cord. And the posterior divisions of all three trunks, upper, middle, and lower trunk, combine to form the posterior cord. The lateral cord gives off the lateral pectoral nerve. The posterior cord gives off the upper and lower subscapular nerves and the thoracodorsal nerve. The thoracodorsal nerve supplies the latissimus dorsi. The upper and lower subscapular nerves supply the subscapularis and the teres major. The medial cord gives off the medial pectoral nerve, the counterpart of the lateral cord and the lateral pectoral nerve. In addition, it gives off the medial cutaneous nerve of the arm and the medial antebrachial cutaneous nerve, which has some localizing value in terms of doing nerve conduction studies of the medial antebrachial cutaneous nerves when looking at either medial cord or lower trunk brachial plexopathies. The lateral cord ends with the musculocutaneous nerve. And again, important to remember, the musculocutaneous ends in the lateral antebrachial cutaneous nerve. We can perform a sensory nerve conduction study of the lateral antebrachial cutaneous nerve when assessing for lateral cord brachial plexopathies. The medial cord also gives rise to the ulnar nerve, which innervates all the muscles in the hand on the hypothenar side. In terms of root values, the musculocutaneous nerve is a direct continuation of the lateral cord. The lateral cord is formed from the upper and the middle trunk anterior fibers. So the musculocutaneous nerve is 5, 6, 7. The ulnar nerve is a direct continuation of the medial cord in the lower trunk and consequently has a root value of CA21. The upper and lower subscapular nerves innervate the subscapularis and the teres major, the shoulder muscles, and belong to root value C5 and C6, whereas the thoracodorsal innervates the latissimus dorsi with a root value of C6, C7, C8, which has some special significance when considering spinal cord injury at that level. The final concluding parts of the brachial plexus, the lateral cord gives us the musculocutaneous nerve. The medial cord gives up the ulnar nerve as we looked at the earlier slide. The posterior cord ends by dividing into the axillary and the radial nerves. The axillary nerve supplies the deltoid and the teres minor, they're both shoulder muscles, and the axillary nerve has a root value of C5 and C6, and therefore the deltoid and teres minor also belong to the root level of C5 and 6. The radial nerve has a root value of C5 through T1, and finally the lateral cord and the medial cord give branches to form the median nerves. Again the axillary, shoulder muscles, 5, 6, the radial nerve C5 through T1, and the median nerve has fibers from C5 through T1 as well, depending upon the innervation in the forearm versus the hand. With that background in the anatomy of the brachial plexus, let's now jump to our second goal, legion localization. To me, legion localization always begins with the clinical interview and exam. The history and physical exam help us understand the mechanism, the duration since injury, the level of functional and neurologic impairments, the comorbidities that might be existent, and give us a sense really of the level of the nerves or the legions being involved and the level of current deficits. This will help us customize or individualize the electrodiagnostic study. The three components of the electrodiagnostic study include sensory nerve conduction studies, motor nerve conduction studies, and the actual EMG portion. And as we think about this, as discussed in the previous slides, we need to consider the root level innervation and the peripheral nerve supply to design most optimally which sensory nerve conduction studies to perform, which motor nerve conduction studies to perform, and lastly, which muscles are we going to sample from an EMG standpoint. Again, remember most of the shoulder weakness stems from either a lateral cord, upper trunk, or C5-6 level legions, whereas most of the hand weakness typically tends to stem from medial cord, lower trunk, or C8-T1 level. And while this is not really a talk on electrodiagnostics, one thing to keep in mind is a statistical policy that is created by multiple tests. Every test has a false positive and a false negative. And the more tests that we perform in terms of sensory and motor nerve conduction studies, it increases the cumulative false positive rate, which we want to consciously avoid. As we start looking at legion localization and which nerves or which muscles we need to test in order to localize the legion, often we come across some atypical nerve conduction studies and muscles to be sampled. Most of us are familiar with the median sensory and motor studies, ulnar sensory and motor studies, and radial sensory and motor studies. But for the world of brachial plexopathy, often we'll end up testing the axillary nerve, and that would include an axillary C-MAP with pickup at the deltoid, musculocutaneous nerve testing with a C-MAP to the biceps, or testing the lateral antebrachial sensory study in order to assess the integrity of the musculocutaneous nerve or the lateral cord and more proximal elements. The medial antebrachial cutaneous nerve, which helps us assess the integrity of the medial cord or the proximal elements. And in terms of the radial, the superficial radial sensory study, or the sensory study to the thumb, also called as the numb thumb sensory study. Let's start with looking at the sensory nerve action potentials. Again, when approaching brachial plexopathy, it is best to approach that by merging two data sets of information. One is the levels, the sensory levels, based on the ASIA exam, the C5 sensory level, C6 sensory level, C7 sensory level, C8 sensory level, and the T1 sensory level in the upper limb, and which peripheral nerve innervates that specific sensory level. As we alluded to earlier, the lateral antebrachial cutaneous sensory nerve innervates this part of the forearm and belongs to the C5 and C6 dermatomes. C7 is the middle finger, which is innervated by the median nerve. The C8 level is innervated by the ulnar nerve, and the T1 level is innervated by the medial antebrachial cutaneous nerve. So to assess the C5 DRG, some people would use the lateral antebrachial cutaneous because there's some overlap, but there's no reliable SNAP study to assess the C5 DRG. The C6 dorsal root ganglion is this area here as illustrated in the diagram to the left. And the sensory nerves that we can use to assess this particular dermatome involves the median study to digit 2, the median SNAP to digit 1, the radial studies, which involve either superficial radial sensory study or the radial study to the thumb, often known as the numb thumb, and the lateral antebrachial cutaneous sensory study. To assess the C7 DRG, the only study that helps assess this sensory level at C7 would be the median sensory study to digit 3. To assess the C8 dorsal root ganglion, we can do the ulnar sensory study to digit 5. This is a very commonly performed sensory study that most of us are familiar with. And then to assess the T1 dorsal root ganglion, as shown here, we need to look at the medial antebrachial cutaneous sensory study, which is not one of the commonly performed sensory studies in the electrodiagnostic lab. So as we just discussed, the C5 DRG has no reliable sensory study. For the C6 DRG, we can use median to digit 1 or 2. We can use the superficial radial or the radial to the thumb or the lateral antebrachial cutaneous. And for the C7, we use the median to digit 3. Once we have these levels, we can build up the rest of the brachial plexus distally into the trunks and the cords. As we know, the upper trunk is a combination of C5 and C6. And so to assess the integrity of the upper trunk, we can use the lateral antebrachial cutaneous sensory study, the median to the thumb, or the superficial radial sensory study. To assess the middle trunk, we can use median to digit 3. And to assess the lateral cord, we can use any of the sensory studies that we have looked here since the lateral cord is a combination of 5, 6, 7. We can use any sensory study for the 5, 6 or any sensory study for 7. The most common one that would be performed in this situation would be the median to digit 2. Continuing on, to test the C8 DRG, we can do ulnar to digit 5 sensory study. And to test for the T1 DRG, we can do the medial antebrachial cutaneous sensory study. And to further trace that out distally, the lower trunk is formed by the combination of C8 and T1. So we can assess lower trunk integrity by using either of those two sensory studies, ulnar to digit 5 or medial antebrachial cutaneous. And consequently, the medial cord is a direct continuation of the anterior fibers of the lower trunk. And we can assess integrity of the medial cord of the brachial plexus using those same two sensory studies, namely the ulnar to digit 5 or the medial antebrachial sensory study. So now let's go to the posterior cord. The posterior cord gets a little tricky to test using sensory nerve action potentials. These branches of the posterior cord, the upper and lower subscapular, the thoracodorsal and the axillae supply motor innervation to all the muscles. And so there is not a good way to test the integrity of the cord, posterior cord, using sensory nerve action potentials in these particular nerves. The radial nerve does supply sensory innervation and we can assess the posterior cord integrity using the radial nerve, specifically the radial sensory study to the thumb, digit 1, which is part of the numtum sensory study or the superficial radial sensory study. So as we have seen in these last few slides, the sensory nerve conduction studies and the resulting sensory nerve action potentials help us not only to localize the lesion, but also give an idea as to the nature of the nerve injury, specifically whether it's a demyelinating type of injury, an axonal type of injury, or a combination of both. And again, most of these sensory nerve conduction studies are standard and performed as part of most routine evaluations. However, some of the sensory nerve conduction studies that we have talked about are really unique to the world of brachial plexopathy. More specifically, we talked about the medial antebrachial cutaneous, the lateral antebrachial cutaneous, which are not commonly performed nerve conduction studies. And so in the next few slides, I'm going to list out some of the less commonly performed nerve conduction studies. This schematic here illustrates the setup for the medial antebrachial cutaneous sensory study. These are the recording electrodes. This is the stimulator. This is the ground in between with a distance of 12 centimeters. The details are mentioned in the slide. The one point I would like to make with respect to atypical nerve conduction studies, specifically, is testing the contralateral side, especially if it is asymptomatic. Most of these studies are not commonly performed, and so we have a slightly lower comfort level with some of these studies as compared to the routinely performed nerve conduction studies. While these studies do have normal datasets that have been established in literature, comparing it to the contralateral side, especially if the contralateral side is asymptomatic and not involved in the disease process, serves to establish a perfect baseline for that individual patient. I would recommend strongly that we consider doing the medial antebrachial cutaneous sensory study on the contralateral side to compare the values before calling it as an abnormal medial antebrachial cutaneous sensory study. The same principle holds true for most of the less commonly performed sensory nerve conduction studies. This is the setup for the lateral antebrachial cutaneous sensory study on the other side of the forearm with the stimulator placed 12 centimeters approximately and the ground in between. This is the superficial radial sensory study setup with the active electrode over the palpable portion of the superficial radial nerve as it runs over the extensor tendons to digit 1. The distance is 10 centimeters. This is the reference 4 centimeter distally, the stimulator 10 centimeters approximately, the ground in between. The one point I would like to make here is with respect to neuromuscular ultrasound. With the increasing availability and use of neuromuscular ultrasound, the superficial radial sensory nerve is fairly easy to trace on ultrasound under the cover of the brachioradialis all the way down through the forearm into the wrist as it goes over the first dorsal compartment. And if you have trouble finding the superficial radial sensory study, then it might be worthwhile to consider using an ultrasound if you have it available to localize the superficial radial nerve and then help that to set up the study. Okay, let's turn our attention now to motor nerve conduction studies and the resulting compound motor action potentials. There's a fair amount of data that's established in terms of the root level innervation for the specific muscles that are commonly tested in the upper extremity, as shown in this illustration here, which has been taken from this paper, Electrodiagnosis of Cervical Rhealty from the Physical Medicine Rehab Clinics of North America, published in 2013. The rhomboid muscles are primarily a C5 muscle. The supraspiratus, while C5 and C6, is primarily C5. The biceps is equal for C5 and C6. The triceps is a C6 through 8 muscle, but it's predominantly innervated by the C7 level, and so on and so forth. Based on the earlier history, the examination, as well as the sensory nerve action potentials, and using this data, we can then think about, number one, which peripheral nerves are involved. Number two, what is the root level that we need to assess? And based on that information, we can then tailor our motor nerve conduction studies. This is another paper and data published by Levin in Neurology in 1996, which specifically lists the approximate yield in radiculopathy at a specific level. The consensus of opinion based on the published data is that for the C5 root, for assessing the C5 motor root, we can use the motor nerve conduction study and a C-MAP either the deltoid or the biceps. More people use the biceps because they're more familiar with that, but we can also do an axillary C-MAP to deltoid. The same thing applies for the C6 root. For the C7 root, we don't really have a reliable motor nerve conduction study. We could use the radial motor study to the extensor indices properties or the EIP. The EIP is a C7-8 muscle, often a very small muscle, often involved in atrophy, and so it's not the most reliable motor nerve conduction study. But if you're able to obtain a reliable radial motor study to the EIP, especially in comparison to the contralateral side, that may be a good indicator for assessing the C7 motor root. For the C8 motor root, we can do the ulnar motor study to the abductor digitiminimi or the first dorsal interosseous. These are both commonly performed studies that most electromyographers are fairly familiar with. Most people prefer the FDI over ADM. And then for the T1 root, we can assess the median motor study to the abductor pollicis brevis. Again, a very commonly performed study in the EMG lab. Once we localize the motor nerve conduction studies at each individual root level, then we can then plan out the rest of the distal brachial plexus using the same information. The upper trunk is a combination of 5-6 and can be assessed using the CMAP to deltoidal biceps. There's really not a good indicator study for the C7 root other than maybe radial to EIP if we can attain a reasonably good study and compare it to the contralateral side. And for the lower trunk, we can use the ulnar motor study to the abductor digitiminimi, the first dorsal interosseous, or then the median motor study to the abductor pollicis brevis. The same muscles can be used to assess the integrity of the medial cord. For assessing the integrity of the lateral cord, the lateral cord is a combination of 5-6 and 7 and upper and middle trunk anterior fibers. And we can use the CMAP to the deltoidal biceps to assess the integrity of this piece of the lateral cord. For assessing the integrity of the posterior cord, the two motor nerve conduction studies that can be performed are the CMAP of the axillary muscle, particularly to the deltoid, or we can perform a radial motor conduction study either to the extensor indices proprious. And if we find that technically challenging, we can always perform a radial motor study using a proximal muscle for pickup, specifically the brachioradialis or the triceps. And again, for a lot of these atypical nerve conduction studies, I would recommend comparing it to the contralateral side. And a further reminder to use neuromuscular ultrasound as is applicable for some of these motor nerve conduction studies, especially for the proximal motor nerve conduction studies. And lastly, just like in sensory nerve conduction studies, some of the motor nerve conduction studies are not routinely performed. And so let's review that quickly in the next couple of slides. This is the setup for the muscular sputaneous CMAP to the biceps, the active recording electrode or the biceps maximum muscle bulge just destroyed to the midpoint. The reference is distally or something inert. The stimulation is at Earp's point and the ground is in between. And again, I would recommend comparing it to the contralateral side and just be aware that supramaximal stimulation may be technically difficult with Earp's point stimulation. This is the setup for the axillary study to the deltoid. And again, the pickup is from the middle of the deltoid maximum muscle bulk. The reference is distally or something inert. The stimulation is at Earp's point. The ground is in between. And again, the same two caveats compared to the contralateral side ensure supramaximal stimulation, although that may be technically difficult. So again, legion localization and brachial plexopathy often require some atypical nerve conduction studies. For the sensory nerve conduction studies, we talked about the medial and the lateral antebrachial cutaneous sensory study that has localizing value for the lateral chord and proximal and medial chord and proximal respectively. We talked about the superficial radial sensory study and the use of neuromuscular ultrasound in terms of motor nerve conduction studies. We talked about muscular cutaneous to biceps, axillary to deltoid, and occasionally the accessory study to the trapezius. And that really has some significance in Parson-Asterner syndrome, which we're going to discuss in the next few slides. And last but not the least, really for a lot of these atypical nerve conduction studies, I would recommend side-to-side comparison as being very critical before calling it as an abnormality rather than relying on the established data normals. Okay, now we have talked about the sensory nerve action potentials, nerve conduction studies, and the motor nerve conduction studies. Let's now look at EMG using the different muscles for lesion localization. And again, the two data points that we need to understand is one, the root level of the muscle under consideration and what is the peripheral innervation of the muscle under consideration. And we could either take it at the root level and then trace it out distally or go through the peripheral nerve and then trace it out proximally. My personal bias here is to go from distal to proximal. Start from the nerve under consideration and then work your way proximal to the root level. And that's really helpful as we start thinking about the EMG lab. So let's say you're in the EMG lab and looking at a person with a wrist drop. Well, then at that point, we want to start at the radial level and then march our way up more proximally. Is it a radial neuropathy? Is it a posterior cord brachial plexopathy? Or is it further proximal involving multiple trunks and multiple root levels? So let's look at the most commonly tested muscles in the upper extremity. I've listed most of them here. Let me go through and trace a few of these muscles to make a point of distal to proximal versus going the other way around. Let's start with the deltoid. So in order to trace the deltoid, the two points that we talked about, one, it's supplied by the axillary nerve and two, it is of C5-6 root level. And so if you are looking at the deltoid innervation, it starts from the axillary, it goes through the posterior cord, then comes through the upper trunk and then goes to the level of C5 and C6. And that would be how we would trace the axillary. Let's look at the pronator teres. It gets a little tricky here. With pronator teres is really a 6-7 muscle and it is supplied by the median nerve. And so once we have those two data points, what I would recommend is going from distal to proximal. So how do we get from median and go to C6-7? Well, it goes from the median through the lateral cord, through the anterior divisions. And again, since it involves C6 and C7, now we are looking at two trunks. We are looking at the upper trunk and we are looking at the middle trunk and that's how we land up at C6-7. The ulnar or the median hand muscles are relatively straightforward. So whether it's the abductor pollicis brevis or whether it's the abductor digitae minimae, we are looking at either a median or ulnar innervated muscle. And as we go more proximally, we're going to go straight through the medial cord, straight through the lower trunk, and then we are going to look at either the C8 or T1 levels. And last but not the least, triceps. To look at the triceps, the triceps is a 6-7-8 muscle as we know, and it's supplied by the radial. And so in order to look at the triceps and trace it from distal to proximal, we are going to go through the radial nerve, through the posterior cord, through the posterior divisions. Now 6 comes from the upper trunk, 7 comes from the middle trunk, and 8 comes from the lower trunk posterior divisions, and then goes back to then go through 6-7-8. And again, doing this from distal to proximal helps us understand if you are looking at a patient with a wrist drop, and we have tested peripheral radial muscles, and the radial muscles are abnormal and show signs of denervation, what would be the next logical muscle to test? Well, we want to make sure it is not a posterior cord breakout like sapathy, and so the next proximal muscle to test would be an axillary innervated muscle, so we could do the deltoid. And if the deltoid was abnormal, that would then localize the lesion to the posterior cord as against being just a radial neuropathy. Okay, let's put this together with the case. We are looking at a right wrist drop, day 14 post-injury, so there has been enough time for valerian degeneration to occur and for denervation potentials to be demonstrated in some of the abnormal muscles innervated by that nerve. This is a 24-year-old healthy male status post-motor vehicle collision with some bony fractures, a T10 fracture, neuro intact, but does have a right wrist drop and the right brachioradialis reflex is absent. And this is the EMG. So let's look at the different muscles in the EMG. Extensor indices proprius, extensor digitorum, communis, brachioradialis, triceps. All of the radial innervated muscles are abnormal. So we are looking at either a radial cord, radial nerve problem or a posterior cord problem or something more proximal. Well the deltoid here is normal. Furthermore, the latissimus is normal as well and so we are looking at the axillary nerve being normal and the thoracodorsal nerve being normal. And what this does is it helps us localize the level of the legion from high radial proximal to the takeoff of the triceps to where it comes in and meets the axillary nerve. So from here distal on downwards. And this is the benefit of using the muscle innervation at the peripheral nerve level and the root level to help localize the legion when we are looking at brachial plexopathies. This is a schematic of what we drew out in the previous slide. So if you are looking at the deltoid, we are looking at axillary nerve and 5-6 and so if we were to trace it back, we would go from the axillary nerve through the posterior cord, through the upper trunk and then go through 5 and 6. Same thing with the pronator teres. If you are looking at the pronator teres, it's a median nerve and c6-7 muscle. So how do we get from the median to c6-7? Well it goes from the median through the lateral cord, through the anterior divisions, through the upper trunk and the c7 contribution comes from the middle trunk and from the upper and middle trunk we go to the c6 root and then we go to the c7 root. Lastly, the hand muscles. The hand muscles are innervated by both the median nerve as well as the ulnar nerve. If you are looking at the abductal pollicis brevis, that's a median c8-t1 muscle and so when we trace that from distal to proximal, you go through the median nerve, you come through the medial cord, you go through the lower trunk and then you trace it back proximal through c8 and then t1 and the same thing with the ulnar nerve. If you're testing any of the ulnar innervated muscles, you're looking at ulnar nerve, direct connection of medial cord, lower trunk and then goes back to c8 and t1. All right, now let's put all of this in the clinical context. While this is a question that often turns up on the boards or the SAE exams for the residents, this is not an uncommon situation in the electrodiagnostic lab as well. And while there is a clear giveaway here with the cervical paraspinals being abnormal, remember we talked about cervical paraspinals or any level paraspinal muscles coming from the dorsal ramus and indicating that to be primarily root level pathology, let's look at the peripheral extremity muscles and use some of the knowledge that we looked at in the previous few slides to help localize lesion. The abnormal muscles are triceps, brachioradialis and pronator teres. While triceps and brachioradialis would point to a radial neuropathy, however, the extensor digitorum communis, which is also supplied by the radial nerve, is normal. The pronator teres is supplied by the medial nerve and is a c6-7 muscle. However, the biceps, which is lateral cord, upper trunk, 5-6, is normal. The flexor carpi ulnaris and the first dorsal interosseus are both ulnar innervated c8-t1 muscles, so that tells us that the ulnar nerve, the medial cord, the lower trunks, the c8-t1 roots are normal and further the supraspinatus is normal, which tells us the suprascapular nerve, the upper trunk and the 5-6 levels are normal. So where does that leave us? Well triceps is a 6-7-8 muscle, brachioradialis is a 5-6 muscle and then pronator teres is a 6-7 muscle and we know based on this that it's a root level problem and it does not fit the distribution of either a trunk pathology or a cord pathology. So with this particular distribution of EMG abnormalities, the most common factors would be a c6 and a c7 involvement and so the correct answer to that would be a c6 radiculopathy. Again, this is just to demonstrate lesion localization principles. The preferred approach is distal to proximal and then again know two data points, know the nerve supply, the peripheral innervation and the root level to help with lesion localization. Let's now put it together with the case that we introduced at the beginning of this talk. Left hand weakness post-operative day 10 status post-CABG, week-long thumb and finger flexors, intrinsic muscles, decreased sensation left medial hand and forearm indicates primarily that an ulnar nerve or a median nerve problem together versus something more proximal. In looking at the nerve conduction studies, the left median snap is normal, which we anticipate that's a c6 level. The radial snap is normal as well, also c6 level. The left ulnar is abnormal, which is corresponding to the ulnar problem, a medial cord or a lower trunk or a c81 problem. Same thing with the left median CMAP, but the giveaway here is the left medial antebrachial cutaneous. Since the left medial antebrachial cutaneous is abnormal, that localizes the level of the lesion to proximal to the left medial antebrachial cutaneous takeoff, which is either in the medial cord or the lower trunk. Furthermore, sensory studies are typically abnormal in a process that is at or distal to the dorsal root ganglion, and so it helps us understand that this is unlikely to be a c81 root problem, but it's somewhere between the lower trunk or the medial cord. And then let's look at the EMG. If we look at the EMG, the first dorsal interosseous, the abductor digiti minimi, the flexor digitorum profundus, these are all ulnar c81 muscles, so they are ulnar, medial cord, and lower trunk. But now the abductor pollicis brevis is abnormal as well, so it's just not ulnar, there's median involvement. Furthermore, the extensor indices proprius is abnormal as well, which is a 7-8 muscle supplied by the radial nerve. And so at this point, we have evidence of medial cord involvement, median nerve involvement, ulnar nerve involvement, and radial nerve involvement. And then looking at the normal muscles, the biceps proarterterius is normal, which we anticipate. The triceps is a radial posterior cord muscle, which is normal. And most importantly, the paraspylons are normal, which we also expected based on a sensory study being abnormal, which localizes it to at or distal to the DRG. And so putting this all together, where do we localize the lesion? Well, we know it's proximal to the medial antebrachial cutaneous. So it's either a medial cord problem or it's a lower trunk problem. But remember, the extensor indices is abnormal, and the extensor indices actually comes from the radial nerve. And so then the radial nerve then localizes that problem to the lower trunk. So this is a lower trunk brachial plexopathy based on all the data that we gathered from the nerve conduction study and the EMG. All right, before I hand it back to Dr. Rinaldi to go over a couple of common clinical conditions that we encounter in the EMG lab, let's consider some common clinical scenarios and how we might problem solve through those scenarios, using the information that we have learned in the previous slides. The first is high ulnar neuropathy versus a more proximal lesion. How do you differentiate whether this is high LNAR versus something more proximal? One, we could do the medial antebrachial cutaneous sensory study. If it's abnormal, it will localize the lesion proximal to the takeoff of the medial antebrachial cutaneous. Second, we could use EMG of the abductor pollicis brevis. The abductor pollicis brevis is a median C8 T1 muscle. And so if the abductor pollicis brevis is abnormal, that tells us that it cannot be an isolated LNAR pathology. We are either looking at a medial cord or a lower trunk problem or something more proximal involving the roots. Then we could test the extensor indices proprius and see if there are denervation potentials in the EIP that is a radial 7-8 muscle. And so if the EIP is abnormal, that localizes it to the lower trunk and we can rule out a medial cord problem. And last but not the least, we can use the C8 T1 paraspinals. And if the C8 T1 paraspinals are abnormal, that localizes the lesion to the C8 T1 roots. Second, if you are looking at a wrist drop, well, how do we localize that to a radial neuropathy versus something more proximal, especially a posterior cord breakout laxopathy? First, we could use the axillary C-MAP to the deltoid. And again, the axillary C-MAP to the deltoid comes from the posterior fibers of the upper trunk at 5-6. And so if you're a radial neuropathy, it should not affect the axillary C-MAP to the deltoid. Again, I would recommend comparing it to the contralateral side. And then from an EMG standpoint, you could do an EMG of the deltoid, which is again supplied by the axillary nerve, or you could use one of these muscles. So you could EMG the latissimus dorsi, which is supplied by the thoracodorsal nerve. And abnormality in the deltoid or in the latissimus dorsi will localize the lesion to a posterior cord and proximal to the radial nerve. However, median neuropathy versus something more proximal to that. So here now we are looking at the upper part of the plexus. And so we could use the lateral antebrachial cutaneous sensory study for the upper part. And we could use the medial antebrachial cutaneous sensory study for the lower part of the brachial plexus. If you are looking at median motor abnormalities in the abductor pollicis brevis and thinking a median mononeuropathy, we could do the first dorsal interosseous EMG, which is an ulnar muscle, which would localize it either to the medial cord or the lower trunk. Similarly, we could use the extensor indices proprius to help us localize it to the lower trunk. And last but not the least, we could use the C81 paraspinals to further localize it at the root level. Lateral cord versus upper trunk. So again, we are in this part of the plexus here. For lateral cord versus upper trunk, we can utilize the suprascapular nerve and we can do an EMG of the supraspinatus to help determine if the lesion is proximal to the takeoff of the suprascapular nerve. And then we could also do an EMG of either the rhomboids or the serratus anterior or the paraspinals to then localize it to the root level. Next, preganglionic versus postganglionic. We talked about it in the earlier part of the lecture. A clinical exam often reveals some clues if there is medial scapular winging or evidence of Horner syndrome at the right clinical level that points to a preganglionic lesion. Again, just a reminder that the sensory nerve conduction studies and SNAPs are normal in a preganglionic lesion. Paraspinal involvement is often seen in a preganglionic lesion and MR imaging might show evidence of pseudomeningocele with a preganglionic lesion. And lastly, Parson-Ashterner syndrome and thoracic outlet syndrome are often things that come up in the discussion of brachial plexopathy. And I will hand it over to Dr. Nardi to talk about some of these conditions. Thank you, Dr. Karandikar. I'd like to now cover a couple of specific cases of clinical correlations and the brachial plexus involvement. The first case I want to talk about is neurogenic thoracic outlet syndrome. This is something not infrequently seen by PM&R physicians, but it's probably more frequently seen by vascular surgeons and in vascular clinics. It's something we all learn about in residency. I'm certainly aware of this as a clinical entity. So neurogenic thoracic outlet syndrome is due to compression of the brachial plexus within the scalene triangle. As I talked about earlier in the lecture, and as you'll recall, the scalene triangle is made up of the anterior scalene, the middle scalene, and the first rib. And it's a small area through which the brachial plexus emerges. Causative factors for neurogenic thoracic outlet syndrome typically include trauma to the scalene. This can be acute trauma, or it can be cumulative trauma over time. This leads to swelling and scarring of the scalenes, which then leads to subsequent compression of the brachial plexus itself. There are some associative factors that have been described operatively in patients who have undergone surgery for thoracic outlet syndrome and that are commonly seen. The first is narrowing of the scalene triangle. There are some reports of about a 10% area loss within the scalene triangle. So it's a much narrow scalene triangle in patients with thoracic outlet syndrome. The other finding that's been described in the literature includes interdigitating fibers between the anterior and middle scalenes. This has been seen in a significantly greater population of individuals with thoracic outlet syndrome versus those without thoracic outlet syndrome. The presenting symptoms of thoracic outlet syndrome include focal neck pain with associated neuropathic quality pain radiating down into the arm. This can be exacerbated by abduction and extension of the arm, and in some cases, by rotation of the head to the contralateral direction. On nerve conduction study, what commonly is seen is normal median sensory nerve action potentials within the C6-C7 dermatome. Now, neurogenic thoracic outlet syndrome typically and preferentially involves the T1 level, so that would make sense then as to why your medial sensory nerve action potentials in many cases are normal, because those are served within the C6-C7 dermatome. With regard to ulnar sensory nerve action potentials, however, these are abnormal because they serve a C8 dermatome, so they will be affected typically in thoracic outlet syndrome. The most affected sensory nerve study is going to be that of the medial anabrachiocutaneous nerve because it serves the T1 dermatome. On EMG, typical abnormalities will include denervation potentials or increased spontaneous activity within the median and ulnar innervated muscles because these are C8-T1 innervated muscle groups. The second condition I'd like to talk about briefly is Parsonage-Turner syndrome. This is another condition not uncommonly seen by physiatrists, especially if you're in neuromuscular practice or running an EMG lab. So Parsonage-Turner syndrome also goes by a number of different names that might seem more familiar to people, and that includes brachial plexitis, idiopathic brachial plexopathy, brachial amyotrophy, and neurologic amyotrophy. It typically presents in an upper unilateral upper plexus distribution, so you'll have asymmetric paresis of the periscapular and perigalinal humeral muscles, and it's typically preceded by a viral illness, immunization, or even surgeries in some cases. It commonly presents first with fairly intense upper extremity pain. This can be severe and it typically is early and subsides after about one to two weeks, so it presents before the actual weakness presents. Following the pain and typically following resolution of the pain will be noted onset of weakness. In cases that are long to recover, significant atrophy can be noted in the muscles served by the affected portions of the plexus. It does also commonly affect the long thoracic and anterior interosseous nerves, so it's important to assess for muscle function within the distribution of both of those nerves, and recovery can certainly be guarded in cases of Parsonage-Turner. It can take months to years for these to completely recover or to reach maximum recovery. Clinically there really is no significant single test that's pathognomonic for diagnosing Parsonage-Turner. Things that typically are done, however, include electromyography and imaging, and these really serve mainly to exclude other disorders such as cervical disc herniations, neoplasms, and such. So nerve conduction study and EMG can play an additional part in the workup, however. They're most important in estimating axonal damage and re-innervation patterns of the involved portions of the plexus, and on nerve conduction study you can also note patchy sensory involvement. That's not that uncommon to see. Treatment typically consists of steroids. That's been debatable, however, over the years as to whether or not they are necessarily effective in treating Parsonage-Turner. So some individuals will not utilize them in the treatment of this condition, and will treat more symptomatically in regard to pain management initially. A Cochran review in 2011, however, did demonstrate that steroids were somewhat useful for management of pain and overall recovery. I'm going to shift gears and talk about principles of management now for plexus injuries. This is a fairly important area to discuss, particularly when it comes down to severity of injury and consideration for involvement of other professionals in the management of the patient. So the first step is to combine your clinical and electrodiagnostic information to one, localize the lesion, and two, determine the severity of the insult. An important consideration in the management is to know when to refer the patient for surgical evaluation, and it's important to know that and understand that timing, because that timing for successful surgical intervention is crucial. So really it comes down to one, understanding the severity of the injury that you're working with, two, whether that injury is recovering, and three, whether there are surgical options for further management of that injury. It's important to always assess rotator cuff status, because the rotator cuff stabilizes the shoulders, most of us know, and for upper extremity function stabilization of the shoulder is critical. And it's also important to know that the best chances of improvement from an injury are within the first three months. So if three months have gone by during conservative management of the injury and you're not noticing much significant improvement, you probably aren't going to notice that much further improvement over time. So when to refer for surgical consultation, as I'd mentioned, it's critical to have the timing down for this and to understand appropriate timing so that optimal outcomes can be achieved through surgical intervention. With open clean injuries, such as knife edge lacerations or glass lacerations of the nerve, referrals to the surgeons for evaluation should be as soon as possible. We do know that earlier surgical involvement in these cases is important for effective outcome. This also includes vascular injuries, where referral should be as soon as possible, because outcomes can be affected by earlier interventions versus later interventions. For preganglionic lesions, such as nerve root avulsions, we also recommend as early as possible referral for surgical consultation. These tend to be more complex types of surgical interventions to take care of root avulsions and can take longer to heal. So the earlier that surgical intervention ensues, the better the outcome. For postganglionic lesions that are outside of the realm of clean injuries, vascular injuries, and vascular injuries, we typically recommend waiting about three to four months to observe clinical recovery and the natural history of the injury itself. As I mentioned earlier with axonotic medic injuries, you may not see much movement or innervation or motor activation in the involved spinal segments for the first two or three months. So it behooves one to wait at least three to four months before making a surgical referral with regard to postganglionic lesions that you know are not ruptures or avulsions. Most individuals will assess for spontaneous recovery every three to four weeks. That can be done through electrodiagnostics as well as clinical evaluation. And then as I mentioned, surgical referral is recommended if no recovery is seen, and then surgical referral is recommended for more severe lesions as noted above. It's important to remember, again, that your best chances of improvement to our surgical intervention is done within the first three months. And again, it's also important to note that a significant amount of recovery will occur within the first three months of time. So the surgeon has an array of options at their hands that they can entertain utilizing, and these are based upon the type of injury, the location, and degree of injury noted. Typically what will occur is when the surgeon takes the individual to the operating room, electrodiagnostic studies will be performed in the OR to assess the status of the conduction across the site of lesion. This is typically done through nerve-to-nerve conduction studies across the lesion, and sometimes can also be done with conduction studies proximal to the lesion and then EMG recording within the compound motor action potential recording within the muscles themselves. So the first surgery that typically can be entertained is end-to-end repair. This is typically done with sharp laceration injuries, where you have a proximal stump and a distal stump that are in fairly close proximity, so you can bring them together and suture them together. The advantage of this is that it does allow for improved regenerative axonal mapping to the distal segment if done early enough, and this is particularly true if these are clean injuries, again such as a knife edge laceration. Neuralytic procedures are done by peeling away scar tissue to relieve any compression and enhance regeneration across the site of lesion. These do not entail any type of cutting of the nerve or removing of an injured segment in the nerve. This is simply stripping away any type of fibrotic tissue or scar tissue that's developed around the site of injury. Nerve grafting can be done as well, and this is used in cases of non-conducting neuromas or large areas of injury that have significant separation of the intact distal and proximal ends. You can do grafts up to a maximum of about six to eight centimeters distance, so you've got a significant amount of gap that you can utilize a graft across. As mentioned, these are done with non-conducting neuromas and typically are post-ganglionic. The next level of surgery includes transfers, nerve transfers, or neuratization procedures. These are done by taking fascicles of the intact nerve and co-opting these distally to the damaged nerve close to its site of innervation. So, for instance, a very common neuratization procedure that's done in brachial plexopathies, at least in the pediatric realm, is by taking a fascicle from the ulnar nerve and co-opting it to the musculocutaneous nerve just before entering the bicep. This is called an Oberlin procedure, and again, as I mentioned, is done fairly commonly in pediatric plexopathies. These neuratization procedures can be also used in late repairs, where you have less length or distance of axonal regeneration required for re-innervation. It can also be done for proximal injuries, such as root avulsions, where you do not have adequate proximal stump segments available for grafting. And then finally, there's tendon transfers, and these are typically done through rerouting of strong muscles to compensate for weaker muscle dysfunction. So, the surgeons will essentially transect the muscle insertion into the bone and then reroute that muscle and reinsert it into another muscle or to the bone itself in a different location to create different function. A very common tendon transfer procedure done in pediatric brachial plexopathy is a several episcopal transfer, in which the latissimus dorsi and teres major transected from the bone. These are typically internal rotators, and the muscles are rerouted to the teres minor, so you've taken two internal rotators and converted them into external rotators. It's a fairly successful surgery and can certainly increase external rotation across the glenohumeral joint in individuals who undergo it. So again, tendon transfers are typically done where you've really kind of run out of options or with regard to nerve grafting and end repair transfers, and you're now looking at really kind of letting muscles do different functions. So, a diagram demonstrating some of the concepts that we just talked about, particularly this diagram, particularly demonstrates harvesting the sural nerve in the leg, which is purely sensory, and utilizing that for your grafting segment in the area of injury. And then a diagram of the neurotization procedure, where a fascicle, the ulnar nerve, is tied into the musculotaneous nerve to provide a late proximal reinnervation. Other transfers that can be done include spinal accessory nerve to the suprascapular nerve, tricep muscle or medial pectoral to make up for axillary dysfunction, and then, as I mentioned, the ulnar nerve to musculocutaneous nerve, or the so-called Oberlin procedure. In regard to overall management planning, several algorithms do exist and have been published. This is one common example. This basically takes you down through the thought process and the steps of evaluation and management. So, you have brachial plexus closed traction injury. Your initial evaluation includes your clinical evaluation, electrophysiologic studies, myelography, or MRI scan, if so deemed. And if it demonstrates a preganglionic, then immediate neurotization procedure and referral to surgery should be considered. If it's a postganglionic lesion based upon your clinical evaluation and studies, then you can observe it for three months, as I mentioned previously. And if it's improving, then you can continue to monitor with conservative management and evaluation. If you don't demonstrate any improvement through observation, then we typically will refer to surgery for exploration and potential neurotization or nerve grafting procedures, depending upon what is seen operatively and what the most appropriate route of management is felt to be. Now, again, as I mentioned, different algorithms do exist. Most of them fall along the same lines of this type of thought process and logic, however. So finally, to wrap things up, there are a number of take-home points to be made. One is the preganglionic versus postganglionic plexopathies are important to understand. Electrodiagnostics can aid in the localization of your injury and determine whether it's preganglionic and postganglionic and can help determine severity of the injury as well. Two, look for associated rotator cuff injuries. This can tip you off to not only level of injury, but also management strategies because of the importance of stabilization of the rotator cuff to further upper extremity function. Three, referral to hand surgery. Timing is crucial, as we just talked about. And early surgical intervention can be important for ultimate outcome and function in more severe injuries and specific types of injuries, as we talked about. The goal with any type of surgery is shoulder stabilization first. Again, as mentioned, that helps with further function in the upper extremity. Then shoulder abduction and external rotation through activation of the rotator cuff, and then elbow flexion. Functional restoration operatively below the elbow is quite challenging, however, because of the distances required for muscle re-innervation. As we're taught, nerves regenerate at a pace of about one millimeter per day. So the distance of re-innervation from the site of injury in the plexus down to the distal intrinsic muscles in the hand or the forearm can take a significant amount of time if surgery is not done early. And while you're waiting for that re-innervation to occur, as time goes by, what's happening is that muscle is becoming more atrophic and more fibrotic. So by the time that re-innervation occurs, the end organ itself is not very healthy anymore. So really time is really of importance when determining surgical intervention for these more complex injuries. And finally, prognostic factors include age. Young children tend to improve rapidly versus older individuals. Time, since the point of injury is important, as we've mentioned multiple times in the talk. And then level of severity of the injury is important. This is particularly true with regard to surgical intervention, as we were just discussing. So a number of key things to take home. Again, pre-ganglionic versus post-ganglionic plexopathy. Whether or not there's associated rotator cuff injury involvement. And then crucial considerations for the timing of referral to hand surgery, so that early surgical interventions can be entertained.

brachial plexopathy

clinical considerations

treatment

anatomy

pre-ganglionic lesions

post-ganglionic lesions

Sedan classification

Sunderland classification

lesion localization

severity assessment

hand surgery

surgical goals