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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 just had 28 year old man referred for an EMG. Symptoms started about 6 months ago. Numbness in arms and legs . All the same. He was much worse at the beginning and was unable to walk. He uses a cane currently. Poor historian. 2+ upper and absent lower. Full strength.
All thought to be alcoholic. He was a heavy drinker for few months per his report???
could not get any sensory in 4 rextremities. LE motor, very low amplitude or absent. Upper motor is normal. No delayed latency or slow conduction velocity.
No pain at the onset.
EMG is the confusing part. Quads with 3+ fibs. Legs with no fibs but slightly large and polyphasic units. Upper is ok. Lumber paraspinal with no fibs.
I was thinking sensory neuronopathy until I stuck the needle in the quads.
My emg machine finally died, so I borrowed my friend's Cadwell Sierra Ascent. Works great besides for a phantom waveofrm with sensory studies. It always occurs around 1.2 ms at 8 cm or 1.5 ms at 10 cm. I think it's shock artifact but I'm not sure. I have the notch filter on, exam table unplugged, use a shielded shuttle cable, keep the electrode and stimulus cables away from each other, tried using the machine in different rooms, etc.
I attached the waveforms below (or at least I hope I did).
Does anyone know what this wavefore is and how I might get rid of it?
Hi there. I run a quite busy EMG lab that is accredited and I am employed under a huge medical system. I am wondering about venturing to establish my own independent EMG lab. Are there any guidance or resources out there that can help me? Thank you in advance.
Does anyone have any experience with ultrasound billing? Is anyone doing it as an extension to the NCS/EMG?
Can you still do Ultrasound when a primary asks for NCS/EMG only?
How should increased ulnar distal sensory latency, with normal sensory nerve action potential and normal ulnar motor NCS, and otherwise normal NCS of the median and radial nerves, be interpreted?
There have been references to "muscle pairs" for example in the Peripheral Nerve questions (question 3 on my set), it said that fibularis brevis and fibularis longus (peroneus brevis and peroneus longus) are a muscle pair.
There was another question suggesting that coracobrachialis and pectoralis are another muscle pair. Also, extensor pollicis longus and latissimus dorsi as another pair.
Please can anyone explain the defintion of a muscle pair.
hi
we know that Hx , clinical features & temporal course are important integral parts in EMG report , but i wonder if EMG could easily differenciate between two conditions ( AIDP & CIDP ) depending on EDX findings only away from Hx ! ?
I'm seeing a 50 y/o man with painful asymmetric polyneuropathy whose exam suggests severe weakness and sensory loss involving left median and left tibial myotomes/dermatomes. Very weak DIP flexion in left hand digits 1-3 suggesting AIN involvement. Only significant past medical history includes heroin use. Negative or normal: anca, esr, crp, hiv, hep Bs Ag, hep c ab, Ana, sjogrens abs, cryoglobulins, CBC, cmp. Last reported use of heroin February 2020, symptom onset September 2020. Nerve and muscle biopsy planned. Has anyone ever seen mononeuritis multiplex without any abnormalities on the serum lab tests? NCS/EMg confirms asymmetric polyneriopathy with subacute denervation in left APB, left FCR, left gastric. Chronic denervation in left TA.
Is swelling and blisters can be a side-effect after NCS?
I did NCS of both lower limbs to my 68 y/o woman lasts Wednesday, possibly poly neuropathy. She didn't complain of any untowards pain during the test.
Today, Saturday the patient came back and she had right foot swelling and blisters. Are these a side effects of NCS?
Blisters location are not on the stimulation site.
I was reading about the the new bill being introducecd into the house of repersentatives. I am excited there is action being taken to ensure EMG quality. I was suprised to see a requirement of 3 months of EMG during trianing. Where I trained EMG was only one month, does this mean the average neurlogist would no longer be able to perform EMG's upon graduation? I am fellowhip trained so I dont have to worry but it made me wonder, how this effects the average resident going into practice?
Also as somone not in a large hospital system the prospect of accreditation is worrisome from a financial perspective. Has this been taken into consideration?
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.
