Case conference: Shoulder pain and weakness

[PMR 4 MSK]

I haven't posted any cases in a while. Saw this one last week.

Pt is a 52 yo female with about 3 months of shoulder pain and weakness. Symptoms started suddenly one day while watching TV. No injury. Pt did have an URI shortly before this. Pt was sitting there, noticed some left shoulder pain and then the inability to raise her left arm. An hour later the right became involved. Went to ER, ruled out acute neuro event such as CVA, D/c'd home to PCP.

Pt initially treated with muscle relaxors and vicodin, which did not help much. Pt sent to pain management, variety of meds tried, without success. No Dx given.

Pt sent for EMG 2 months ago. Done by someone else in town. NCV of the bilateral median and ulnar motor and sensory reported as mostly normal, except slightly low amplitudes of the median sensories bilaterally. #'s not given. Needle exam of deltoids, biceps, triceps, PT, FDIM and APB reported as normal. No dx given. No treatment, advice or f/u recommended.

Pt sent for MRI of the left shoulder, shown to have supraspinatus tendonitis with small partial-thickness tear, pt sent to one of our ortho's. He, in turn, recognizing the probable Dx, sent her for repeat EMG. Pt also had MRI C-spine with multilevel DDD and mild stenosis C5-6 without cord abnormalities.

PMH only significant for high cholesterol, stable for a few years on Lipitor. Pt also on Vicodin and gabapentin. has been on gabapentin x 5 years for a chromic left sciatica, 300 mg TID. Allergy to codeine (N/V), surgeries - lumbar lami, lap choly. FHx - multiple members with various cancers (unknown types) and heart problems. Never smoked, does not drink alcohol, non-diabetic. ROS benign.

PE - atrophy of the deltoid noted. AROM shoulders only about 50 - 60 degrees abduction, 70 - 80 of flexion. MMT - about 2/5 bilateral shoulder abduction, 2/5 left ext rotation, 3/5 right ext rot, 4/5 int rot bilat, 4/5 elbow ext bilat, 5/5 elbow flexion, wrist and hand lfex and ext bilat.

Paresthesias to touch in bilaterally deltoid areas and 1st dorsal webspace on the left, otherwise sensory testing normal distally. Reflexes absent in the triceps, 1+ biceps, 2 + brachiorad bilat.

Neck exam normal - full pain-free ROM, negative Spurling's bilat. Shoulders non-tender to palpation. Impingment bilaterally to Hawkins > Neer. No instability. No winging.

EMG as follows:
Low amplitude of the left axiallary to deltoid (1.5), radial to triceps, (2.7) musculocutaneous to biceps (2.1) and suprascapular to supraspinatus (0.6), normal distal latecies except suprascapular 5.2 (nl < 3.7). Right side similar except musculocutaneous normal.

Bilateral median motors and sensories normal distal latencies, amplitudes and NCVs.

Needle exam showed serious denervation of deltoids bilat with diffuse PSWs and fibs, increased IA, and no active MUAPs. Biceps mildly affects with scattered fibs and PSW's. Triceps, PT, FDIMs and APBs normal bilaterally. Supraspinatus and infraspinatus bilat 2+ PSWs and fibs, increased IA, 25 - 50% reduction in recruitment. Motor units rather large in the SS and IS. Right rhomboid 1+ PSWs, left normal.

What's your primary Dx? DDx? How would you treat this? My Dx and Tx plan after others have answered.

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[LordArius]

Did she have any abnormalities in the cervical paraspinal muscles?

Since the deltoids, SS, and IS are involved it points to a trunk lesion but the adition of the rhomboid abnormalities, makes it more proximal, like a C5 root lesion. cannot r/o Ca with famHx but less likely due to being bilat.
My two cents says its a far lateral disc herniation due to her DDD.

I remember reading about a case in which a pt. had very enlarged lymph nodes that caused a compressive plexopathy but less likely in this case due to bilateral.

I would give a Prednisone taper, redo a cervical or plexus MRI with and without fat suppresion.

I hope I'm not tooooooo faroff track...

 

[SSdoc33]

the bilaterality of the findings make a c-spine problem less likely, although not impossible. also, sensory NCS essentially normal with a radic. i have a feeling that we got thrown a bone with the h/o URI. i dont want to spoil the diagnosis so ill keep my mouth (fingers) shut for the time being.

question, why do you think the other EMG was negative? too early, or was the guy just a *******?

 

[LordArius]

I believe it was too early to see any changes in the case of the first EMG.
The URI did make me think of a Viral neuritis/plexopathy.

idiopathic brachial plexopathy (well, in this case viral induced)?

 

[DistantMets]

Sounds like bilateral C5 radics vs upper trunk plexus. The paraspinals would definitely help. It certainly sounds infectious, especially being bilateral...with normal imaging, spinal tumor or infection pretty well ruled-out. I would check an HIV, Lyme's (if in an endemic area), inflammatory markers, CBC. She might need an LP(?) Especially if the HIV is + to check for CMV. One textbook mentioned zoster can cause weakness too...any rash? Bilateral zoster would raise suspicion for immune deficiency. The same book also mentioned, of course, neurosyphilis....so I'll throw an RPR in there. I'd probably get an MRI of the plexus to see if anything lights up. Plus, they're pretty cool to look at.

Good case!

 

[PMR 4 MSK]

Paraspinals were normal - left that off, sorry. MRI C-Spine just showed mild stenosis.

LordArius' Dx is the same as mine - classic Parsonage-Turner Syndrome (PTS). The tip-offs here are the URI prior to onset, sudden onset without injury, mainly proximal symptoms and significant neurologic signs - weakness and atrophy. Being bilateral reduces the likelyhood of a focal lesion.

As to the previous EMG, it was done approximately a month after onset of symptoms, and with a proximal lesion, should have been picked up. The EMGer ignored the low amplitude sensory nerves with a shrug of "I don't know" instead of reasoning that proximal symptoms + sensory axonal loss = proximal lesion. Often, the only distal findings in an upper or middle trunk lesion (upper trunk is most common in PTS, with some middle trunk involvement, less common lower trunk) are axonal sensory loss.

The etiology of PTS is not known, but there are many possible explanations, including post-viral.

Treatment is symptomatic and functional. There is no specific Tx for PTS. I have started the pt in PT for strengthening and pain reduction. I have also started her on gabapentin for neuropathic pain. Steroids are not considered effective for this. Recovery can be several months to a few years.

DistalMets' work-up suggestions are reasonable as well.

 

[DistantMets]

My point was that you have to prove that it's not something else to call it idiopathic.

Thanks for posting this case, MSK!

 

[topwise]

Great case! I'm actually learning a lot from these cases and I hope people keep posting.

I thought Parsonage-Turner immediately too, based on the history and the abnormal sensory studies. The only thing that throws me for a loop is that the rhomboids are abnormal. Doesn't the dorsal scapular nerve come off the C5 root?

 

[PMR 4 MSK]

Great case! I'm actually learning a lot from these cases and I hope people keep posting.

I thought Parsonage-Turner immediately too, based on the history and the abnormal sensory studies. The only thing that throws me for a loop is that the rhomboids are abnormal. Doesn't the dorsal scapular nerve come off the C5 root?

Yes, but realize PTS is not a focal lesion, but likely an immune-mediated one, that somehow has a prediliction for the proximal nerves. Why doesn't affect distal nerves too? No one knows.

 

[axm397]

one of my attendings does ultrasound guided steroid injections around the brachial plexus upper trunk for this - haven't seen GREAT results but have seen some relief of pain (just no help with strength)

 

[neurodoc]

What about early motor neuron disease. PTS seems most likely, given the history, but this could be primary spinal muscular atrophy (SMA).

 

[Ludicolo]

What about early motor neuron disease. PTS seems most likely, given the history, but this could be primary spinal muscular atrophy (SMA).

The onset of pain, as well as sensory abnormalities (reduced median sensory amplitudes on the first EMG, and paresthesias to touch on physical exam) would argue against MND. Plus 52 yo is a bit old even for adult onset SMA.

 

[neurodoc]

The onset of pain, as well as sensory abnormalities (reduced median sensory amplitudes on the first EMG, and paresthesias to touch on physical exam) would argue against MND. Plus 52 yo is a bit old even for adult onset SMA.

Agree with your comments about the pain and the SNAP abnormalities. Pain is a symptom that more folks should consider in their DDX of weakness. I'm always surprised when pain (besides headache pain) is a predominant feature of weakness that people want to attribute to stroke or some other central cause. That being said, I have seen several cases of MND that were attributed to spinal stenosis, radiculopathy, and even CTS, and which presented with neuritic pain, and were initially treated with surgery before it became apparent that something else was going on.

While we're on this subject, I have seen a few cases where radiculopathy, Bell's Palsy, and even CTS were treated with thrombolysis in the apparent belief that the symptoms were due to stroke. In these cases a preliminary CT of the brain was obtained and showed no "contraindication" to thrombolysis (such as hemorrage or edema).

This points out the need for a competent neurological exam prior to thrombolysis for presumed stroke.

Nick

 

[PMR 4 MSK]

Agree with your comments about the pain and the SNAP abnormalities. Pain is a symptom that more folks should consider in their DDX of weakness. I'm always surprised when pain (besides headache pain) is a predominant feature of weakness that people want to attribute to stroke or some other central cause. That being said, I have seen several cases of MND that were attributed to spinal stenosis, radiculopathy, and even CTS, and which presented with neuritic pain, and were initially treated with surgery before it became apparent that something else was going on.

While we're on this subject, I have seen a few cases where radiculopathy, Bell's Palsy, and even CTS were treated with thrombolysis in the apparent belief that the symptoms were due to stroke. In these cases a preliminary CT of the brain was obtained and showed no "contraindication" to thrombolysis (such as hemorrage or edema).

This points out the need for a competent neurological exam prior to thrombolysis for presumed stroke.

Nick

How many times have you heard a CTS or similar pt say "When it first started, I thought I was having a stroke!" Had one today.