AANEM Connect

Which test is more accurate in the diagnosis of an injury to the Brachial Plexus, an MRI  of the Brachial Plexus or a EMG Nerve Conduction study of the Brachial Plexus?
 
I have a patient who has atrophy of the muscles innovated by the upper trunk of the Brachial Plexus clearly shown by the EMG Nerve Conduction study, however the MRI did not show any damage to the upper trunk.
 

Dr. Herbison, great teacher in electrodiagnosis and rehabilitation always said there is a difference between old and chronic. He defined chronic as something that is ongoing but has changes of longstanding neurophysiological changes. Old as something that has neurophysiological changes but has no ongoing pathology. I would appreciate other opinions as to how neurophysiologists use the term chronic and if they use the term old any time.
Thanks

Hi all,
I am wondering if you all have seen a C8/T1 radic present with sudden severe hand weakness.  I did an EDS study for 2 -week history of dominant hand weakness.  Motor nerve conduction studies showed no response in the median and very low amplitude response (0.3mV) at the ulnar recorded at the ADM. Sensory studies of median, ulnar, radial, MABC, and LABC were all normal.  MRI of c-spine shows moderate to severe central and foraminal stenosis at multiple levels without cord signal change.  Postive sharp waves with only one very small motor unit in the FDI and APB with reduced recruitment.  Positive sharp waves in the EIP, PQ as well. Normal deltoid, biceps, triceps an pronator teres.  My diagnosis is a severe C8/T1 radiculopathy but also seems more severe than I have typically seen. Contralateral side was normal. I would think chance for recovery after decompression is not great.  Any thoughts?  Thank you.

Hi all,
I've had a fair number of patients recently with primarily sensory signs and symptoms of ulnar neuropathy at the elbow but normal nerve conduction studies (ADM, FDI, antidromic D5, DUC) and EMG (typically just FDI). Occasionally I have included proximal sensory stimulation below and above the elbow (recording D5), but I have a hard time trusting the conduction velocities due to variable onset latencies. 

My question for this community: While the studies above can exclude motor/sensory axon loss and motor conduction block, I don't know of a reliable way of assessing sensory conduction block at the elbow. Has anyone figured out how to do this? I realize that you can't rely on change in SNAP amplitudes because of physiologic temporal dispersion and phase cancellation, but perhaps with a side to side comparison or an index value?

Would appreciate any insight into this. 

I am working up a man with a slowly progressive (over 5 years) axonal neuropathy with some 'red flag' features (asymmetry, non-length dependent) and have discovered he has an elevated CK (2.5 x ULN) which has remained elevated despite stopping his statin therapy and abstaining from exercise prior to testing.

Neuropathy is often listed as a possible cause in guidelines on assessment of 'asymptomatic hyperCKemia', but I can't find any guideline on how high one would expect the CK to be due to this cause. He has minimal motor involvement both clinically and on NCS. His needle EMG was limited to deltoids and showed possible mild myopathy changes (short duration, early recruitment) without inflammatory features.

His chief complaint is of pain and numbess, so wondering how to decide on the utility of muscle biopsy and/or additional blood work looking for myopathic disorders.

Any advice or references for my own reading much appreciated.

The other thread on warming mechanisms got me thinking. Which product do you all use for skin temperature reading?
thanks in advance
-gautam

I had a 2nd case (in 2-3 years) of monomelic amyotrophy, this one a 67 y/o female, 4 month onset of weakness and wasting in her left hand - no numbness, tingling or pain, and minimal chronic neck pain (non-radiating).  Totally normal sensory studies but low amplitude (ulnar worse than radial) or unobtainable (median) motor responses, and marked denervation in T1>C8>C7 (and paraspinals).  Awaiting C&T spine MRIs.  Is anyone else seeing these kinds of cases? 

There is an article in Muscle & Nerve from January 2008 about this, authored by Patel, Knepper, and Jones.  Volume 37; pp115-119

I evaluated a 45-year-old mechanic with neck pain and was impressed that all of his median and ulnar sensory amplitudes were unexplainably low (all < 10 µV), with borderline-prolonged distal latencies. He had no clinical evidence of a polyneuropathy or mononeuropathy, and no medical conditions aside from neck pain. He was muscular with very large hands. I know that height and BMI adversely influence sensory measures, but I’m wondering if his large hands explain the low sensory response amplitudes?

I was wondering if you could please help me understand the value of doing the paraspinal muscles in patients who have undergone previous lumbar laminectomies and now return with recurrent back pain? Should I do a needle EMG on the lumbar paraspinal muscles following back surgery in that region?

SFEMG, stimulation. I have tried stimulation SFEMG, 3Hz but I cannot see any decrementing response, even in a case of clear myasthenia. Why?

In a patient with severe chronic polio who demonstrates decreased insertional activity, no fibrillation potentials, and no recorded voluntary motor unit potentials in all lower limb muscles, is there a specific EMG term to describe the findings?

I am looking for validated scores or scales that I can use in the clinic for providing objective evidence of treatment reponse in small fiber and autonomic neuropathies. I have found reference to COMPASS-31 but cannot find a version I can use. Practicing in Australia and need to provide evidence of improvement to have continuing access to IVIg.

29 years old male presented with weakness in his right ankle dorsiflexion after releasing a cast in his right lower limb

NCS: peroneal -EDB
normal amplitude of CMAPs ( 3 mV ) for distal & below fibular head stimulation sites with normal distal latencies
decreased amplitude of CMAP above fibular head  stimulation ( 1.3 mV )

peroneal -TA
decreassd amplitude of CMAP for distal & proximal stimulation
tibial & sural NCSs : normal

EMG study
TA,PL : active denervation , unstable MUs with decreased receuitment
EDB : No active denervation with normal duration of MUs and deceeased recruitment
Short head of Biceps femoris,GN :  Normal EMG study

Q: may a compressive  neuroparhh show double abnormal NCS patterns to different muscles ( ex. in this case : axonal loss to TA & partial conduction block to EDB ! )
 

I saw a 45 year-old colleague who became aware of calf fasciculations and was anxious that he may have ALS. He exercised regularly and his fasciculations seemed most prominent after exercise. He was otherwise asymptomatic, and his clinical and EMG examinations were unremarkable aside from calf fasciculations. How can I be confident that his fasciculations fall into the category of benign fasciculations, as opposed to early ALS?

I am hopeful that I can obtain some insight regarding a particular finding in the evaluation of carpal tunnel evaluations that I am seeing from time-to-time.  Specifically, I perform a 14/7 cm antidromic SNAP study and obtain a mid-palm latency of 1.9 ms with an amplitude of 20 uV and a 14 cm SNAP with a latency of 4.4 ms and amplitude of 15 uV. I am comfortable with an assessment of focal slowing of the median sensory fibers to the third digit across the wrist consistent with the diagnosis of the patient’s clinical symptoms of CTS. However, when performing the median CMAP evaluation, I obtain a 8 cm wrist value of 3.8 ms with an amplitude of 7 mV and an antecubital fossa result of  7.7 ms, with a resulting conduction velocity of 46 M/s.  The median motor DML appears fine as does the amplitude, but the NCV is low. The temperature over the APB is 34 degrees C, and I have checked and re-checked my distance. What is going on?

 
Nerve Conduction Studies
Anti Sensory Summary Table
 

Stim Site	NR	Onset (ms)	Peak (ms)	Norm Peak (ms)	P-T Amp (µV)	Norm P-T Amp	Site1	Site2	Delta-0 (ms)	Dist (cm)	Vel (m/s)	Norm Vel (m/s)
Left Lat Ante Brach Cutan Anti Sensory (Lat Forearm)
Lat Biceps		1.3	1.9	<2.5	10.3	>6.0	Lat Biceps	Lat Forearm	1.3	10.0	77
Right Lat Ante Brach Cutan Anti Sensory (Lat Forearm)
Lat Biceps		1.4	1.9	<2.5	41.9	>6.0	Lat Biceps	Lat Forearm	1.4	10.0	71
Left Med Ante Brach Cutan Anti Sensory (Med Forearm)
Elbow		1.3	1.8	<2.6	4.7	>3.0	Elbow	Med Forearm	1.3	10.0	77
Site 2		1.7	2.2		3.7
Right Med Ante Brach Cutan Anti Sensory (Med Forearm)
Elbow		1.8	2.2	<2.6	16.3	>3.0	Elbow	Med Forearm	1.8	10.0	56
Left Median Anti Sensory (2nd Digit)
Wrist		2.1	2.8	4.0	58.2	19	Palm	2nd Digit	1.0	7.0	70
Palm		1.0	1.5	2.3	54.5		Wrist	Palm	1.1	7.0	64
Right Median Anti Sensory (2nd Digit)
Wrist		2.0	2.6	4.0	135.0	19
Left Radial Anti Sensory (Base 1st Digit)
Wrist		1.8	2.2	<2.8	47.1	>11	Wrist	Base 1st Digit	1.8	10.0	56
Left Ulnar Anti Sensory (5th Digit)
Wrist		2.2	2.7	<4.0	41.9	>13	Wrist	5th Digit	2.2	14.0	64

 
Motor Summary Table
 

Stim Site	NR	Onset (ms)	Norm Onset (ms)	O-P Amp (mV)	Norm O-P Amp	Neg Area (mVms)	Site1	Site2	Delta-0 (ms)	Dist (cm)	Vel (m/s)	Norm Vel (m/s)
Left Median Motor (Abd Poll Brev)
Wrist		3.0	4.5	4.6	5.0	15.46	Elbow	Wrist	3.3	18.0	55	>49
Elbow		6.3		4.8		16.99
Right Median Motor (Abd Poll Brev)
Wrist		2.3	4.5	10.5	5.0	31.14
Left Ulnar Motor (Abd Dig Minimi)
Wrist		2.6	3.7	8.1	7.9	21.79	B Elbow	Wrist	2.4	18.4	77	>52
B Elbow		5.0		6.9		17.27

 
Comparison Summary Table
 

Stim Site	NR	Onset (ms)	Peak (ms)	Norm Peak (ms)	P-T Amp (µV)	Site1	Site2	Delta-P (ms)	Norm Delta (ms)
Left Median/Radial Dig I Comparison (Digit 1 - 10cm)
Median		1.6	1.9		46.4	Median	Digit 1 - 10cm	1.9	<0.5
Radial		1.4	1.8		4.7	Radial	Digit 1 - 10cm	1.8

 
F Wave Studies
 

NR	F-Lat (ms)	Lat Norm (ms)	L-R F-Lat (ms)	L-R Lat Norm	M-Lat (ms)	FLat-MLat (ms)
Left Median (Mrkrs) (Abd Poll Brev)
NR		<33		<2.2
Right Median (Mrkrs) (Abd Poll Brev)
	21.27	<33		<2.2	2.34	18.93
Left Ulnar (Mrkrs) (Abd Dig Min)
	26.23	<36		<2.5	1.93	24.30

 

 
EMG
 

Side

Muscle

Nerve

Root

Ins Act

Fibs

HF

Fascic

Amp

Dur

Poly

Recrt

Config

Comment

Left

Deltoid

Axillary

C5-6

Incr

2+

None

None

Nml

Nml

Nml

Reduced

Nml

Left

Biceps

Musculocut

C5-6

Incr

4+

None

None

Absent

Absent

Absent

Absent

NA

Left

Triceps

Radial

C6-7-8

Incr

3+

None

None

Absent

Absent

Absent

Absent

NA

mepps present

Left

PronatorTeres

Median

C6-7

Incr

4+

None

None

Absent

Absent

Absent

Absent

NA

Left

1stDorInt

Ulnar

C8-T1

Incr

4+

None

None

Nml

Nml

Absent

Reduced

Nml

single mup

Left

Opp Pollicis

Median

C8-T1

Incr

4+

None

None

Absent

Absent

Absent

Absent

Nml

Left

Infraspinatus

SupraScap

C5-6

Incr

4+

None

None

Nml

Nml

Incr

Reduced

Unstable

Left

Cervical Parasp Low

Rami

C7-8

Nml

Nml

None

None

NA

NA

NA

NA

NA

 
 
30-year-old patient referred for an electrodiagnostic study to evaluate left arm weakness and numbness.
Medical history significant for a left clavicle fracture in 2017 with malunion.  On January 28, 2019, the left clavicle fracture was treated with open reduction internal fixation.  Patient received regional anesthesia prior to surgery.
When patient woke from surgery, she complained of left-sided lateral neck pain.  She complained of numbness and weakness of the left arm after completion of regional anesthesia. 
Patient completed electrodiagnostic study on February 25, 2019.
Prior to the study, patient completed MR left brachial plexus.  The study indicated normal signal within the plexus, no obvious compression of the plexus, soft tissue edema below the fracture site/surgery consistent with postoperative change.
No other medical history.

Examination
Spurling sign absent
Motor: Right upper limb normal.  Left shoulder abduction 1, external rotation 1, elbow flexion, wrist extension, finger extension, finger abduction, thumb opposition absent.
Sensory: Light touch decreased throughout left upper limb and extremity with painless paresthesia over left medial forearm.
Reflexes: Right/left biceps 2/absent, brachial radialis 2/absent, triceps 1/absent, patellar and Achilles 2/2.
Hoffman sign absent.  Plantar responses flexor and no clonus.
Gait and balance normal.

The tabular data included in the post is the patient's nerve conduction and electromyography results.
The left upper limb sensory and motor responses are preserved but abnormal when compared to right side responses.
Significant active denervation of multiple left upper limb muscles.
Normal left cervical paraspinal examination at rest.

I felt the abnormal findings were best explained by an acute to subacute severe left brachial plexopathy based on the abnormal left upper limb sensory responses, denervation of multiple upper limb muscles and normal paraspinal examination.

I was surprised by the preservation of the left upper limb sensory responses  with the degree of denervation on needle examination.  I have studied a number of traumatic and nontraumatic brachial plexopathies.  The preservation of the left upper limb sensory responses is not characteristic of prior experience.
Stimulation of the brachial plexus at Erb's point to look for conduction block across the clavicle would have been helpful.  The patient recently completed left shoulder surgery and would not tolerate that examination.
Needle examination of the left serratus anterior would help determine whether there was involvement of the cervical nerve roots.

Has anyone had a similar experience with brachial plexopathy?
I was concerned there could be a coexisting cervical radiculopathy or polyradiculopathy.
I requested cervical spine MRI for additional evaluation.
I am concerned about the patient's prognosis for recovery.  Typically, preserved sensory and motor responses indicate a better prognosis.  The degree of denervation and lack of motor unit activity on electromyography concerned me (realizing the injury is less than 3 months duration).

Thanks for your assistance.

David Speach
    
 
   
 
   
 
   
 
   
 
 

SFEMG, stimulation. Sometimes I see one spike occurring with two distinct latencies, particularly when I increase and decrease the stimulation strength when testing for threshold stimulation. What is this?

We recently purchased a Cadwell Summit EMG machine with US. We find the resolution using the US probe very poor for most structures except for the median nerve at the wrist in a thin patient. We have tried changing US frequency, depth, gain and other parameters without much improvement.

In contrast, we have Sonosite free standing US machines that provide better US quality.

Has anyone experienced this difficulty and recommend a solution?

Thanks

David Speach

Failure of an ulnar nerve transfer

 

When I do EMGs and NCVs in my office, I have quite a bit of artifact that I am pretty sure is 60 Hz.  Unfortunately, it is so strong that a fair amount persists even when using the 60 Hz filter.  Does anybody have suggestions on how to reduce this artifact or identify the source of it so that I can remove it?

I'd be very grateful for any experience or advice in this situation.

Young male body builder with suspected but undisclosed anabolic steroid abuse. Initially seen for left foot drop and sensory disturbance in fibular distribution and found to have fibular neuropathy with block and slowing across fibular head. Represents several months later with patchy sensory disturbance over right hand (radial and median nerve distribution) and pain at biceps insertion and in to forearm. Reports some wrist extensor weakness when it first occurred but now has pain with giveway weakness in right deltoid, biceps, wrist extensors and finger extensors. Reflexes all in tact.

UL studies: normal radial SNAPs, both median SNAPs borderline small with no slowing, right ulnar SNAP small but not slow, left ulnar SNAP normal. Median motor studies - normal DMLs, but CV 45 and 44m/s in R and L forearms respectively. Median F waves prolonged at 30ms on both sides (height 172cm). Ulnar motor studies normal (no slowing around elbow on right, left only stimulated below elbow) but F waves both prolonged for height (R 32.34ms, L 31.09ms). Radial-EIP motor studies difficult - unable to elicit response in EIP with elbow stimulation, but response present with stimulation at spiral groove. Amplitude 3mV on right but CV (forearm-spiral groove) slow at 33m/s. Left radial-EIP CMAP 3mV at forearm but then 6.6mV at spiral groove. Suspect submax stimulation in forearm due to muscle.

EMG: slow very sparse fibs seen in right triceps, biceps and EDC. Reduced recruitment in triceps, but others normal. some long duration units in right FDI but recruitment normal and no spontaneous activity. Long, large units seen in right APB. Deltoid and EIP normal.

Could his body building be causing chronic compression of his nerves in his forearms leading to the small sensory responses and slow motor velocities? Does (extreme) body building or anabolic steroid use give you sparse fibrillations on EMG without other features of denervation (i.e.reduced recruitment)?

Any comments/insights very appreciated!

I am occasionally asked to evaluate a patient for myasthenia gravis. I typically evaluate some combination of the ulnar, spinal accessory, deltoid, or facial nerves using a train of four 3 Hz stimuli. I have been surprised by the variability of the results I obtain during individual examinations, not only in the magnitude of decrement but also by the pattern of the decremental response. Sometimes only one or two of the responses show a decrement, whereas other times all responses are smaller than the initial response. Is this variability expected and if not, how do I know the abnormality I find is “real?”

I recently saw a patient with numbness and tingling in the right hand that was sent to “rule out carpal tunnel.” The patient was a 36 year old female office worker that had a rather standard complaint of about a 3 week history of numbness and tingling in the third and second digit with a “feeling” of finger swelling and hand heaviness. She denied dropping objects but did state that she was beginning to have some trouble buttoning clothes with the right hand. The sensations in her right hand were beginning to occasionally wake her up at night. 
 
On physical examination her hand appeared symmetric to the contralateral hand. There was no obvious or subtle swelling, muscle asymmetry, or skin abnormalities. Manual muscle testing revealed a grade 5 to all of her hand intrinsic muscles bilaterally. Sensation was mildly reduced in the classic median nerve distribution on the volar aspect of the right hand with no abnormalities noted in the ulnar, superficial radial, or dorsal ulnar cutaneous distributions on the right. A Tinnel’s sign was present at the right wrist region, but otherwise no other provocative maneuvers caused the patient any discomfort.
 
I thought this was going to be a typical CTS assessment, but I found the motor NCV data to be unexpected and somewhat confusing. I am hoping you can shed some light on the patient’s findings.  Specifically, I performed a median sensory 14/7 cm study using an antidromic ring finger technique with ring electrodes on the third digit. Her mid-palm sensory peak latency was 1.9 ms while her 14 cm peak latency was 4.4 ms thereby yielding a trans-carpal latency of 2.5 ms. I thought, Okay, this makes sense given the symptoms: so far, the SNAP findings are suggestive of a focal median sensory neuropathy at or about the wrist region. I then performed a routine median motor study with the wrist stimulation at 8 cm resulting in a latency of 3.9 ms with a CMAP amplitude of 7 mV. No worries I thought, the median motor study is looking good at this point. But, when stimulating at the elbow, the CMAP displayed an initial positive deflection with a CMAP amplitude of 10.5 mV. This sure looked like a typical Martin-Gruber anomaly regarding the two CMAPs. I made sure the CMAP from the wrist had an abrupt negative deflection, and so I was convinced I was on the APB’s motor point. What is going on?

Is it acceptable to include brief suggestions for management based on the EMG/NCS results?
 
For example in a case of carpal tunnel syndrome: (Suggest: refer to a Hand Surgeon)

Tim Lachman, MD

We have a new EMG doc joining the lab who suggested premedicating patients with Xanax.  I have not used this approach as I never thought it was necessary or indicated, and wondered if anyone else was doing it or had any experience to share.  Our lab only receives EMG referrals (on adults, no peds), and typically we would not have seen the patient before the visit, so we would need to rely on the referring physician for any prescribing.