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It has been said that EMG/NCS is a mature specialty, but many of the things we see every day are not adequately explained ,as Dr Albers' post shows. Fairly common but incompletely explained phenonema arise every day. We may be so used to seeing them that they are ignored ! During the open sessions of EMG talk at our annual meetings many of these have been brought up and an explanation sought, in a " Have you ever seen this " format. Surprisingly some "pearls" were well recognized by the audience,but a few of our experts had never heard of them. One that comes to mind is the patient with symptoms confined to the ulnar distribution of his hands, but the nerve conduction studies show only unequivocal , classical carpal tunnel syndrome. After convincing the surgeon to do CTS release, the patient's symptoms completely clear.Many theories are expressed, but no hard evidence given.
Perhaps we could compile a list of these "gems", both for showing trainees that these things do occur, and as a list of research projects...... something for us to do while we're sitting around.
My practice is 100% office based and 100% EMG/NCS. I have cancelled all patients until March 30, but have not decided about after that. I am over 65 and could just retire,but I love my work and feel like I would be abandoning my patients and employees. I have read the AANEM statement,which like most others, is equivocal. Unfortunately,my referral sources all seem to have difficulty telling me how urgent are their patients problems. How are the rest of you planning for the future?
Hi all, I am planning to purchase a new EMG machine in the next few months since my old VIking Quest is >12 years old and can't be updated. I am thinking of replacing it with a newer Viking Quest ( since I am used to it ) but am also looking at the Viking Edx. Does anyone have advice on choosing one of these or other machines to consider? I do standard NCS/EMG, no single fiber. Thank you.
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?
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?
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?
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.
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?
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 enjoy participating in the AANEM Connect Forum for a number of reasons. There are very fundamental questions posed on a frequent basis that cause me to pause and ask myself, ‘Why didn’t I think of that?’ Also, I continue to learn
new things when others contribute their thoughts and experiences. Connect is an excellent opportunity for members to interact and to address any topic, including those that may not be discussed
at an annual meeting or journal article.
