Hi, this is Alex Donahay, and today I'll be talking about Parsonage-Turner syndrome, otherwise known as idiopathic brachial neuritis or neuralgic amyotrophy. We'll start with the case history. This was a patient that we saw in our peripheral nerve injury clinic. So this was a 45-year-old man, otherwise healthy, presenting with about three months of right arm weakness with no signs of improvement. He said it started with severe shoulder pain in the upper trapezius radiating into the scapular area about three months ago, but did seem to resolve without any specific intervention after about two to three weeks. During that time, he did note progressive weakness as well as some visual changes noted in the muscles of the right arm, and his partner also noticed some visual changes around the scapular region. With explicit questioning, the patient did report that there was an upper respiratory illness going around about a week prior, but didn't think much of it at the time. On examination, we were able to appreciate significant atrophy throughout various regions in the upper shoulder region, especially the biceps on the right as compared to the left. We did note some medial scapular winging when we had the patient elevate and protract the shoulders. He had no palpation throughout. On strength testing, he was about a grade four of five with right shoulder abduction. Grade two, so quite weak with shoulder external rotation as well as elbow flexion when he was in a forearm supinated position, so he was really recruiting that bicep alone. In a more pronated position of the forearm, he did have more strength with elbow flexion. His full strength throughout the right arm and hand, including grip, finger abduction. On sensory testing, there was a diminishment of light touch just in the lateral forearm. Elsewhere, he had normal sensation throughout the hand. On reflex testing, it was slightly diminished at the biceps, but elsewhere equal to the contralateral side. Negative Sperling's test, he did have a positive empty cans test, which may suggest some supraspinatus impingement. The differential at this point, and I think clearly this patient has quite a textbook presentation for Parsonage-Turner syndrome, so that's at the top of my differential. Also strongly considering a cervical radiculopathy, probably of the C5 to C6 region, and one could also consider a more central pathology including a cervical myelopathy, however the unilateral nature of this makes that a bit less likely. One could consider rotator cuff tears given his early pain, and some provocative maneuvers, however it wouldn't necessarily explain some of the atrophy that we saw. And one could certainly consider motor neuron disease, flail arm variant of ALS can present in a similar fashion. So we went on to perform electromyographic testing. So on nerve conductions, largely normal, including median ulnar and radial motor and sensory studies of the affected side, we were unable to get a lateral antebrachial cutaneous. We did, but it was quite small as compared to the contralateral side, which was normal. We tested given that he had some numbness descriptors in that region. Unneedle EMG testing is really where we found the bulk of the abnormalities, as would be expected. As you can see, we saw florid fibrillation potentials and sharp waves in a variety of the affected regions, including the biceps, supra and infraspinatus, and the serratus. We also saw that recruitment was down in a few of these regions quite substantially in the serratus anterior. Motor unit morphology, outside of some sort of early polyphasia, was largely pretty normal. All of this to indicate some fairly recent acute to subacute denervation with sort of some early reinnervation findings. Also notable, but not in the chart, was that his cervical paraspinals on that side were normal. So we'll talk a bit about classic symptoms in Parsonage-Turner syndrome in kind of an overview fashion here. Our patient was quite textbook, so typically presents with acute onset of severe shoulder pain followed by muscle weakness, atrophy, and sensory changes. In our peripheral nerve injury clinic, we see quite a few Parsonage-Turner syndrome almost weekly, and it follows a fairly textbook presentation quite often. Something to know about Parsonage-Turner syndrome is that it really results in this sort of patchy distribution of weakness and atrophy that you may not expect to find in something like a cervical radiculopathy, where you'd see more of a predilection to a certain myotome or dermatome. Here it really is quite patchy. The most commonly affected nerves include the suprascapular, the long thoracic, the anterior interosseous spinal accessory, and from a sensory standpoint, the lateral antebrachial cutaneous nerve. Although other nerves may be affected. The cause is considered idiopathic, though we think autoimmune in nature, and it's sometimes associated with infections, vaccinations, trauma, which might include surgery. The treatment is primarily supportive and includes pain management potentially early. Physical therapy should be hit early as well and should definitely include range of motion to maintain that active or passive range of motion and to prevent contracture. And then as you go, you want to incorporate more strengthening, and there's some good evidence for neuromuscular electrical stimulation in any peripheral nerve injury. Early on, there's some evidence that a short course of high-dose steroids may be effective, at least with pain management and potentially longer-term strength and function. Talk a bit about imaging. So imaging may sort of enhance your diagnosis here. MRI may show hyper-intense signal changes in the plexus or the affected nerves. And you may see muscle edema or atrophy in those affected regions, and I'll show that here in a minute. MRI alone can reveal hourglass-like constrictions, which is pathognomonic for this condition, and it will certainly show muscle atrophy as well. Here's an example of an MRI from our patient. This is an axial-cut T2-weighted image through his infraspinatus on his right side, which is your left. You can see that infraspinatus with the arrow sign there indicating muscular edema, increased T2 signal, and you can compare it to the left side, which is a normal finding. Here we can see on high-resolution ultrasound, you can see an hourglass-like constriction. Clinical pearls. So Parsonage-Turner syndrome is largely a clinical diagnosis. It's supported by history, exam, and most certainly electrodiagnostic studies, which help really in identifying this patchy distribution and ruling out some competing diagnoses, like cervical radiculopathy, potentially motor neuron disease. Imaging can aid with the diagnosis, but it's certainly not definitive. Treatment again is primarily supportive, may include early steroids if caught early enough. Potentially surgery down the line, if you do identify an imaging hourglass-like constrictions, which may be amenable to decompression, nerve grafting or nerve transfers, if the targets are identified, and or if there's a lack of reinnervation, you know, probably by that six-month to nine-month mark. Most patients do recover over time, and it takes a long time. We counsel patients on this quite often. Typically we allow for two to three years before we close the window and say this is what you've got is what you've got. But many patients do end up having at least some subtle residual deficits. And here are my references, and thanks for listening.

Parsonage-Turner syndrome

brachial neuritis

shoulder pain

electrodiagnostic studies

physical therapy