An easy EMG question !

[Mohd]

Hi every one!
here is a part of an EMG report I've been reading:
"Needle examination:
left biceps: high frequency polyphasic repetitive discharges at rest, decreased recruitment pattern.
Left FDI, left brachioradialis: normal study.
Left triceps, left supraspinatus: repetitive discharge with full recruitment pattern"

I have been reading about EMG and NCS for hours now! and I could only figure out that there is an evidence of denervation of the biceps but I can't tell what's wrong with the triceps and supraspinatus! Could some one help?

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[Ludicolo]

Sounds like the EMGer is describing CRDs (complex repetitive discharges). Can be seen in either neuropathic or myopathic processes. Based on the reduced recruitment in the biceps, sounds neuropathic, but looking at the findings in the other muscles, kinda hard to localize. CRDs in isolation tell me nothing. What are the patient’s symptoms/exam findings?

 

[Mohd]

Thanks for the reply!
The patient has sever atrophy of the deltoid, biceps, supra & inraspinatus his for arms and triceps seem preserved.
Hypotonia around the shoulder and the elbow
Muscle power: shoulder abduction & elbow flexion 2 wrist flexion 5, elbow and wrist extension 4 (or 4-)
Hyperactive reflexes in all limbs, +ve Hoffman's & Babinski signs with spastic gait. constipation and incomplete urine emptying (detrusor insufficiency)
Lower limbs normal (other than the hyper active reflex)

Cervical MRI C4 lesion, non enhancing post contrast, degenerative changes in the spine with disk protrusions

Brain CT & visual evoked potentials are normal

In short: Man-in-the-barrel syndrome due to central cord lesion of > 10 years duration exacerbated hyper extension neck trauma 3 months ago

 

[Ludicolo]

One possible interpretation of the EMG findings: The central cord lesion caused UMN weakness. If the lesion also affected the anterior horn cells in the spinal cord, you could see reduced recruitment along with fibs, polyphasic MUPs, etc. in affected myotomes. But recruitment can be difficult to assess in the presence of UMN weakness (poor activation), and you generally don’t see CRDs in motor neuron/anterior horn cell disease. The atrophy is more than likely secondary to disuse, given the >10y history. Chronic, severe, disuse atrophy can sometimes appear myopathic on needle EMG, and you could see CRDs in this situation. Doesn't explain what's happening in the triceps though. Did the EMGer check any other muscles?

EMG dogma also says that you can also see CRDs in asymptomatic muscles, i.e. a normal variant. However there have been at least a couple studies challenging this.

Not an easy EMG question! Thanks for the case.

 

[Mohd]

I'm glad it's not an easy case! I though that I just couldn't understand it !!

other than what I mentioned above it was mentioned that the NCS study was normal.

And forgive my inaccuracy: this EMG is from the admission 10 years ago the findings above are from this admission (no great difference, however)

Here is a summary for my 10 page report:
The case is really complicated! neurological complaints date back to 1981 (left facial pulsy, quadreplegia with sensory symptoms in all limbs, more severe on the left, however. Recovery in 20 days with no sequele. Labeled as MS)
The bilateral upper limb weakness started at the early 90's, more severe around 1998 and hyperextension neck trauma 3 months ago

And thanks for you interest!
P.S. I have a newer EMG report but it's not typed so I'm still trying to "decode" the handwriting

 

[ben3133]

Which other muscles were seen to be normal? How about FCR, PT, infraspinatus?

I'm thinking it could be related to the C4 changes causing anterior horn cell damage at C5/6, patchy because of the pathophysiology of the process.

 

[Mohd]

This is the only EMG I've got for now!

I attached an MRI section too!

Here is a summary of the neurological examination of the upper limbs, the lower limb were normal except for hyperactive DTRs and upgoing plantar reflexes, the gate was spastic with loss of arms swinging.

Upper limbs (motor)
·Inspection:
.o.Wasting of the bisceps, deltoid, and prominent scapulae. Fasiculations are visible at the deltoid, supraspinatus & infraspinatus.
The forarm flexors and extensors seem normal

.o.No pronator drift (equivocal since the patient can't fully outstretch his arms)
·power :
.o.Tone: normal at the wrist but decreased at the elbow and shoulder.
.o.Power:
§Grip: 5 Rt, 4 Lt
§Wrist flexion: 5 Rt, 4 Lt
§Wrist extension: 5 Rt, 5 Lt.
§Elbow extension: 4 Rt, 4 Lt.
§Elbow flexion: 3- bilaterally.
§Shoulder flexion: 2 bilaterally.
§Shoulder extension: 3 bilaterally.
§Shoulder abduction: 2- Rt, 2 Lt
§Shoulder adduction: 4 Rt, 4- Lt
§Shoulder shrugging: 5 bilaterally
§Fingers: adduction and appostion were weak at the left hand

​

.o.Reflexes:
§DTRs are hyper active bilaterally
§Hoffman: +ve

Upper limbs (sensory)
Position: intact

Vibration:
Rt: decreased distally to the level of the elbow.
Lt: decreased distally to the level of the acromion.
Pain & light touch were decresead from C5 to T1 bilaterally
2 point discrimination: Intact
Sensory inattention: None
Astereognosis: None

 

[ben3133]

Mohd - no EMG is attached!

 

[Mohd]

Thanks for your interest Ben!
The handwriting of the EMG I have is some what ineligible, I can scan it and post it here, but I believe it will be more effective to ask the EMGer to read it for me, when I do that I'll notify you!