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I would greatly appreciate any comments or thoughts regarding the further management of a patient who has given me permission to present his case in this forum.
He is a 66yo male who underwent a liver transplant for alcoholic cirrhosis complicated by hepatocellular carcinoma in February 2018. He noted difficulty walking immediate post transplant with progressive sensory loss and imbalance. In early 2021, this became signifiantly worse and culminated in a fall with an ankle fracture. During admission, I was consulted and he was noted to have a sensory > motor polyneuropathy with lower limb predominance and nerve conduction studies confirmed a generalised demyelinating polyneuropathy. This was in the context of being on tacrolimus and mycophenolate therapy. Initial consideration was given to the possibility of a tacrolimus associated neuropathy given the onset at the time of transplant with possible worsening in the setting of dose escalation.
He was subsequently found to have IgM kappa paraprotein (3g/L) and positive high titre MAG antibodies on both ELISA and Western blot.
He had significant but incomplete clinical response to IVIg therapy with improvement in balance and distal strength. He remains on mycophenolate and a reduced dose of tacrolimus. He is on maintenance IVIg and notices his foot "slapping" more when walking in the week prior to his 4 weekly infusions.
Is there cause to push to switch his tacrolimus to an alternative - such as cyclosporin which will put him at risk of developing diabetes? Would anyone consider rituximab therapy for MAG neuropathy given persisting gait dysfunction - taking into account he is already immunosuppressed for his liver transplant? What are your thoughts on the development of a presumably autoimmune neuropathy in the setting of immunosuppression?
Today I saw a 25-year-old woman complaining of generalized numbness, tingling and itching over her trunk, extremities and scalp. This started a year ago , and she was treated as if this were an allergic reaction since she had severe allergic reactions to medications in the past. She was treated with antihistamines, IV steroids, etc. with only temporary improvement. She was seen by several dermatologist and neurologists , initially without change in her symptoms. She was started on gabapentin for the possibility that this was a neuropathy. This finally did markedly improve her symptoms . Most of the paresthesias in her trunk and extremities cleared, although they are still present over her face and scalp. Her physical exam today was essentially normal. The electrodiagnostic studies done today showed normal electromyography of all extremities. The nerve conduction study showed normal motor and sensory conduction studies in the distal extremities. Median and ulnar sensory amplitude's were 60 to 80 µV, and sural amplitude's were greater than 30 µV. Medial and lateral plantar sensory studies were easily obtainable and also showed large amplitudes. However, when testing proximal sensory conduction, a completely different picture arose. I was unable to obtain medial or lateral antebrachial cutaneous sensory studies in either arm. I have always found these easy to obtain in young patients who have large distal sensory responses. Since I began doing the procedure for lateral antebrachial cutaneous sensory conduction in 1978, I was sure I was performing this correctly. In the lower extremities, I could not obtain a response in the lateral femoral cutaneous nerve, although it too is usually obtainable in thin patients with large distal sensory responses.
My question is has anyone seen a picture like this before with reduced to absent proximal sensory amplitudes but normal distal responses. Could this be a proximal sensory neuronopathy ? This young, otherwise healthy , slim young woman is very concerned about taking gabapentin on a continued basis since she hopes to become pregnant in the future. Should we pursue a work up for possible Sjogren's disease or occult malignancy in this young woman? I would greatly appreciate any responses from the audience.
Motor artifact can be an annoy to SNAP (antidromic sensory study). It was told that moving the recording electrode away from the muscle would minimize it. This worked when possible.
I wonder if longer stim duration ( say 0.2 ms instead of default setting of 0.1 ms) while lowering the stimulation intensity (60% perhaps) would stimulate sensory fibers preferentially to motor fibers, hence lesser motor interference?
I'm wondering if anyone believes neurapraxia can give small distal motor amplitudes.
We recently had a case of ulnar neuropathy at the elbow with distal CMAPs of 0.7 mV to ADM and 0.2 mV to FDI with only 1/5 strength in those 2 muscles. She had surgery which released marked compression under the FCU and only 2 months later she had 4/5 strength. I think it's too early for axon regrowth (she's 65 y/o and diabetic) so I'm wondering if the neurapraxia somehow affected the axons distally, giving small CMAPs?
I am considering buying my new sierra summit from current practice to use in a new job. Is there an additional cpt code or tech fee for owning the machine?
Does anyone have any experience of using simulation in training? I am aware of Dr Nandedkar's website, but are there any limbs or programmes that have been developed for use in training?
I did an emg on a patient that has had three thoracotomies, The last one included and a Lat Dorsi and serratus ant transfer. Post of pt had some scapular winging. No change with shoulder abduction or protraction. NCS of the LTN was compared side to side. There was a decreased amplitude of the NCS and normal latency. EMG MUAPs showed small polyphaisc potentials, and reduced recruitment or poor activation without large MUAPs. There were no fibs or positive waves. I thought there were a few CRDs. With the previous surgeries a dn msucle flaps , I am reluctant to call this a LT neuropathy as there is signifciant anatomical changes with the previous surgery. I am not confident that this is a LT neuropathy. Perhaps the CRDs and small polyphasic MUAP were false postives becuase of muscle damage from the surgeries.
I was wondering how many of our members have been monitoring or requiring their staff members to receive COVID-19 vaccination.With regard to patients, we have been administering antigen rapid testing in the office to all the unvaccinated . While this is not as accurate as laboratory PCR testing, at least it gives us some information. Regardless of the patient's vaccination status, we still require masking of all staff members and patients.
59 yo female with numbness on the the thenar eminence following a repeat CTS release in 01/2021 (first release surgery was in 2005). Both open release. The numbness pre-op was on the median fingers. NCS (median SNAP with mid palm stim, median CMAP, median-radial thumb comparison) and EMG (including APB, OPPONENS) are normal. Suspecting damage to the palmar cutaneous branch of the median nerve. I do not know how to assess this branch. Help me please.
I was hoping to get some input on this interesting EMG case that I saw the other day. The patient is 65 year old female who was referred for an electrodiagnostic study to evaluate the bilateral lower extremities. Patient presented to the hospital on 4/19/21 s/p being down for 2 days secondary to shock requiring intubation and pressor support. She had a complicated hospital course and ultimately was suspected to have an acute spinal cord process causing paraplegia, however, MRI C/T/L-spine was unrevealing (MRI limited by motion artifact, body habitus, and body wall edema). There were no sensory or motor impairments in the bilateral upper extremities. She was referred for EMG of the bilateral lower extremities due to concern for critical illness neuropathy vs. spinal cord infarct.
EMG of the bilateral lower extremities was performed on 8/16/21.
Physical exam: 0/5 strength in the bilateral lower extremities (hip flexors, hip adductors, hip abductors, knee flexors, knee extensors, ankle dorsiflexors, ankle plantar flexors), absent sensation to light touch distal to the groin bilaterally, and absent patellar and achilles reflexes bilaterally. There was significant pitting edema in the bilateral lower extremities to the knee bilaterally.
NCS: Sural and superficial sensory responses were unobtainable bilaterally. Fibular and tibial motor responses were unobtainable bilaterally. Right median sensory, ulnar sensory, and superficial radial sensory responses were normal. Right ulnar motor and median motor responses were normal. Right ulnar F wave was slightly prolonged at 33.2ms.
Needle EMG: There was active denervation in proximal (TFL) and distal lower extremity muscles (vastus lateralis, tibialis anterior, fibularis longus, medial gastrocnemius, and short head of biceps femoris) bilaterally with no evidence of axonal continuity in any sampled muscles of the bilateral lower extremities. There was active denervation in the right middle/lower lumbar paraspinal muscles. The left middle/lower lumbar paraspinal muscles were normal. The right first dorsal interosseous and right deltoid muscle were normal.
Conclusion:
Abnormal study. Technically challenging study due to significant bilateral lower extremity edema and limited mobility due to bilateral paraplegia.
Bilateral lower extremity sural sensory, superficial fibular sensory, fibular motor, and tibial motor nerve conduction studies showed no response. Needle EMG examination of the bilateral lower extremities showed diffuse active denervation in proximal and distal muscles with no evidence of axonal continuity in any sampled muscles. Taken together, these findings localize the pathologic process distal to the level of the dorsal root ganglion, and could be explained by severe bilateral lumbosacral plexopathies vs. a severe axonal, sensorimotor peripheral polyneuropathy.
There is a possible superimposed right lumbosacral radiculopathy that is non-localizable.
There is no electrodiagnostic evidence of a superimposed left lumbosacral radiculopathy.
There is no definitive electrodiagnostic evidence of median neuropathy, ulnar neuropathy, or myopathy in the right upper extremity.
My practice is devoted exclusively to EMG/NCS testing. I do not provide ongoing care for any patients and all my testing is non-urgent. During this time of the delta variant surge, and in the interest of the safety of my vaccinated patients and staff, I am considering limiting my practice to vaccinated patients.
What are the thoughts in the AANEM community regarding this? Has anyone limited their practice in this way?
Do we have a consensus for the standard of practice for IVIg treatment small fiber neuropathy?
Some insurers will cover, others not. I understand the literature, such as it is, does not clearly support IVIg one way or the other.
I would like to open a discussion about the p-value fallacy.
As a preface – The p-value fallacy has been known and discussed for many years. Yet, little to no change seems to be happening in the medical sciences with regards to how we use and interrupt p-values (though alternate solutions have been proposed). I have only recently read into this topic and feel the implications for medical research are large and unpromising (hence my desire to hear the community’s opinion on the matter).
My understanding is such:
The common way (in medical sciences) p-value is taught/understood is categorically wrong. P-value was developed as part of significance testing. However, it has been erroneously applied to represent a type I error rate (or alpha level) in hypothesis testing. In hypothesis testing - null and alternative hypothesis are developed. Then an alpha level is set (usually and arbitrarily set at .05 or 5%) and an experiment is done. If the observed difference between the null and alternative hypothesis meets or exceeds a p-value of 5%, we reject the null hypothesis in favor of the alternative hypothesis (with the understanding that there is a 5% chance that the observation we made was by chance alone).
The problem is that assumptions made in significance testing (p-value) cannot be seamlessly transitioned to hypothesis testing (type I errors). Yet, this is exactly how it is taught and what is routinely done in medical sciences. Specifically, the null hypothesis in significance testing is assumed to be true. Therefore, it is categorically incorrect to apply it to hypothesis testing where the null hypothesis can be rejected. To bridge the p-value of significance testing with the type I error rate of hypothesis testing, and to mathematically quantify the p-value fallacy, researchers have used a Bayesian framework. Conclusions resulting from Bayesian analysis are multifold with two notable issues, 1) p-values routinely (and at times wildly) underestimate the false positive rate, and by extension, 2) p-values cannot give a specific percentage to uncertainty without considering priors (i.e., if we reject the null hypothesis, we cannot say there is a 5% probability what we are seeing is from chance alone without considering the prior probability the hypothesis was true pre-experiment).
Taken together this would argue the p-value is widely misunderstood and misused with one corollary being we are routinely reporting “statistically significant” findings when none exist. This problem is superimposed on a myriad of other potential problems in medical research – some related to p-values (the reproducibility, or lack thereof, of p-values under theoretically identical experimental conditions) and some not (wide-spread bias, confounding, small sample sizes, lack of reproducibility of new research findings, conflicts of interest, etc).
Below are some resources that have shaped my view. I am very interested to hear the community’s thoughts and the possible implications for medical research.
Colquhoun, D. (2017). The reproducibility of research and the misinterpretation of p-values. Royal society open science, 4(12), 171085.
Gao, J. (2020). P-values–a chronic conundrum. BMC medical research methodology, 20(1), 1-8.
Wasserstein, R. L., & Lazar, N. A. (2016). The ASA statement on p-values: context, process, and purpose.
Goodman, S. (2008, July). A dirty dozen: twelve p-value misconceptions. In Seminars in hematology (Vol. 45, No. 3, pp. 135-140). WB Saunders.
Hey all, I'm in the process of starting up a PM&R EDX Lab in the context of an existing academic EDX lab and I would like to set things up so that patients can electronically enter their history information prior to the visit to help with clinic flow. Does anyone have a patient intake form that they really like that we can use as a template that they would be willing to share? We are also giving a talk on Building a Successful Neuromucular practice at the fall meeting and would love to share it there as well or share a composite of the ones that we find. Thanks everyone and happy Friday! JWN
Hi all,
I wanted to ask for community/expert input on how you approach interpretation of distal latency with regards to demyelination, in the setting of severe axonal loss and muscle atrophy?
I believe it’s generally accepted that distal latency can be prolonged up to about ~130% of the upper limit of normal in the setting of axonal loss (without implying superimposed demyelination)-- largely due to loss of the fastest fibers. For more proximal conduction velocities, ~75% of the lower limit of normal is used, which seems roughly commensurate.
However, when amplitudes are extremely low (e.g., 0.1 mV for a motor NCS), it seems plausible that other factors (beyond loss of fastest fibers) could cause further latency prolongation (without implying demyelination). Some of these include:
(a) distal collateral sprouting: increased NMJ transmission time
(b) distal collateral sprouting: more slowly conducting immature myelin (and decreased spacing of nodes of Ranvier)
(c) increased electrical transmission time through muscle due to atrophy
(d) inability to accurately measure motor onset latency (only seeing "tip of the iceberg" of the motor response
Importantly, it seems to me that all of these factors would affect the terminal portion of the study (distal latency) disproportionately (relative to the more proximal conduction velocity measurements)-- without implying demyelination-- and that these mechanisms bring us beyond what's expected for loss of the fastest fibers. In this context, 130% of the upper-limit-of-normal as a threshold seems too low/lax (might overcall demyelinating disease in the setting of end-stage axonal loss?). I don't know if this has systematically been explored: the range of latency prolongations expected in extreme axonal loss.
In this context, do you have a threshold for assessing distal latencies potentially concerning for focal demyelination in the setting of extreme axonal loss? (A relevant clinical application would be looking for evidence of superimposed ulnar neuropathy at the wrist in a patient with established ulnar neuropathy at the elbow with severe and chronic end-stage axonal loss).
Sandra
I am curious if anyone in the audience is a Medical Director of all Electrodiagnostic Services at a large hospial system (preferably academic medical center), particulary where neurology and PM&R labs are combined under this Medical Director? What are the job responsibilities of the Medical Director in this situation, who do they report to in the hospital? Do they receive any compensation for their time? What has been some of the pros/cons of this arrangement? Thanks for your help!
Hi my name is David Phrathep and I'm a second year medical student that just recently became a member of the AANEM. I'm currently looking for research opportunities involving neuromuscular medicine and PM&R. I'd be appreciative of any opportunity and I'm eager to learn. I'm able to start assisting immediately and I'm enthusiastic about the field. Thank you.
A young male (well...my age of 46) body model and actor came to me for electrodiagnostic testing that revealed a fairly textbook left sided C8 radiculopathy. Imaging revealed single level severe neuroforaminal combined spondylotic and discogenic stenosis. cervical injection improved pain but he was not recovering sufficiently and opted to single level neuroforamenotomy.
All of his symptoms resolved and his strength has improved to a self-reported 80%.He is still fasciculating in those C8 muscle groups.
Prior history of healed triceps rupture but with residual loss of muscle bulk many years ago. This has compromised his ability to sculpt his left pectoral muscles to the same degree as the right.
He is looking to get as close to 100%. I already explained to him that collateral sprouting has a timeline and that he should keep working out (without overdoing it) to optimize recovery.
Is there anything else you would recommend? I was considering functional neuromuscular electrical stimulation but i'm not optimistic that it will help.
A patient recently reported that immediately following NCS performed for neuropathy that he suffered severe constipation and then an inability to distinguish between the need to defecate and urinate. He attributed this to the "amperage" used during the study and that these symptoms continue (two months). I indicated I had not heard of such a thing but would inquire of my colleagues.
How do paralytic meds (in the ICU for example) stay in the body and what is the effect on the EMG and NCS? And how soon can you do a SFEMG or rep stim after the patient is given a paralytic?
I came across the above normative values (see hyperlink above) and appreciate the new acceptable CV drop for the Ulnar nerve across the elbow as at least 15m/s or 23% drop in CV. This was introduced in the Spring meeting.
However,
Is the absolute value of less than 43m/s across the elbow significant as quoted in the normative value chart ? Even if there is no significant drop in CV in comparision to below / above the elbow (i.e. a drop of less that 15m/s) ?
I have seen three people in the past couple weeks who believe their acute neurological symptoms in the upper limbs were related to the vaccines with onset within a few days. One had profound denervation consistent with a plexopathy, but he also had significant cervical spondylosis.
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.
