AANEM Connect

Hello,

I was trained using nautus concentric 30 guage needles and used them the last 7 years of practice. At my new location they are purchasing concentric 30 guage needles from AMBU. I have noticed that patients seem to be complaining more about pain during EMG testing than in the past. I have not changed my technique.

Have others noted improved patient comfort with a particular brand of EMG needle?

Hello EMG colleagues.

Do you plan to attend the A conference in Orlando?

We have an opening for an EMG small group teacher at the AAP's Resident workshop.

If you are interested, please reach out to me at davidhausteinmd@gmail.com.  Thanks!

Details:

• Date: Thursday, March 5, 2020 in Orlando, Florida. 

• Time: 8am to noon

• Conference website: https://www.physiatry.org/general/custom.asp?page=AnnualMeeting

• Course overview: we will have four separate 45-minute sessions of hands-on procedural demonstrations and education for residents and medical students

• Audience: MS1-MS4 medical students and PGY1-PGY4 PM&R residents

• Instructor Preparation: None

• What to bring: just yourself. No need for powerpoints, equipment, or anything else.  It will all be provided.

I am a PM&R physician and a member of the AANEM Program Committee.  Our Committee would love some input from our PM&R colleagues.  We want to make sure that we are meeting your educational needs, particularly at the AANEM annual meeting.  What topics would you like to see at the AANEM meeting that would make you want to come to the meeting? We have lots of different sessions on ultrasound, EMG, and neuromuscular therapies.  What else would you like to see covered?  Thanks.  We look forward to your feedback and making sure we have great sessions at the meeting!  See you in Orlando!
Earl Craig

I saw a 64 year old male for suspected ALS. Among others, his neurological examination and needle EMG were noted for more atrophy and denervation of the abductor pollicis brevis (APB) and first dorsal interosseous (FDI) muscle more than the rest of the hand muscles. I know this has been named split-hand syndrome by the late Asa Wilborun, MD. I wonder if this is specific to ALS, and if so what is the mechanism or explanation for this phenomenon?. Is it that we use these two muscles more often than other  hand muscles, more metabolic demand or is it something related to innervation ratio or type?

Many authors use the term “complete axonal loss” when they don’t obtain a CMAP from either distal or proximal sites on NCS when assessing a focal mononeuropathy, regardless of needle EMG findings. For example, if there is no ulnar CMAP recorded but a few MUPs are recorded from the ADM, can we use the term “complete axonal loss?”

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?

Does anyone have a policy regarding monitoring of blood pressure  before performing EDX testing?  I only ask because I did not see it in our 'Safety and Pain in Electrodiagnostic Studies' paper (published Feb 2017 in M&N) or the prior 'Risks in EDX Medicine' publications.  This may become an issue with new Medicare guidelines where Blood Pressure is required to be monitored and recorded at all E/M visits, so if an EMG doc does an E/M visit same day, they need to document BP, and make a referral if it is elevated.  But what if the BP is high enough to be of concern - should we have a threshold above which the test is not performed?

Thanks for any comments or suggestions.

Is there a software or app catering specifically for NCS/EMG database for Neurophysiology Lab? 

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?