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-A patient who was referred to me for a deficit in the left hand with numbness of the inner side of the forearm….
Motor Amplitude of median nerve with wrist stimulation was 3.5mV, at the palm stimulation amp 7.5mV (simultaneous recording of the first interosseous, there is no diffusion) a block at the wrist, palm stimulation in the other side was 14.
- Motor ulnar amplitude at the wrist was 10 and symmetrical to the contralateral without any conduction bloc (wrist, below and above elbow and axilla), the sensory D1, D3 and D5 are normal and symmetrical, the left cutaneous brachii medialis 20uV and hard to get it and on the other side at the first attempt I get 34, mixed cubital 45 and 65 on the other side….
The Needle electromyography: Was neuropathic: The abductor digiti minimi detection poor to intermediate recruitment (accelerated trace) same for the 1st interosseous, abductor policis brevis simple reduced recruitment too, only a single MUAP that was firing, the flexor carpi radialis and flexor carpi ulnaris were in good strength (5/5).
-History: Stress and important weight loss according to the patient, He is a smoker
-Cervical MRI: Degenerative changes, uncarthrosis C5 and C6
---> What are your opinions dear colleagues about this presentation? Are we allowed to consider it as postganglionic rather then preganglionic lesion because the cutaneous brachii of the affected limb is significantly reduced compared to the contralateral?
What about the distal bloc in the wrist? Could this be the onset of neuropathy with conduction bloc, proximal and distal?
I plan to retire in a year or so. I have two EMG machines, one a Natus Quest, the other a Nicolet Viking, both working fine. I would like to give these away to a "worthy cause" at retirement, but do not know of any such that could use these machines. Please help me identify potential recipients.
a 45 y.o. woman with a past medical history significant for hypothyroidism presented for evaluation of episodic muscle weakness. Patient reported 3 episodes of severe weakness of her legs. She describes this as feeling her legs like jello. Her 1st episode was in 2017 and lasted for 6 months. It usually starts in the legs then progresses all over. All her symptoms resolved and she was fine until 2019 when the same exact thing happened. All her symptoms resolved again after 3 days per her report. About a month ago, the same thing started again . She has difficulty getting upstairs. She has difficulty walking and is currently using a walker. She denies any weakness in the arms at the current time.
She had a muscle biopsy. It was read as showing myopathic changes including lipid accumulation consistent with lipid storage myopathy (That is all). She also had an EMG on 02/27/2019 that was read as diffuse myopathy with fibrillation potential.
On Exam: Normal exam except for hypertrophy of her calves.
Her son is autistic and while he was having some medical treatment, he, his sister and mom (patient) had whole exome sequencing. All had mutation in the TMEM43 gene, heterozygous for arrhythmogenic right vent dysplasia-5 and Emery-Dreifus muscular dystrophy-7.
EMG yesterday: Myotonia most prominant at TA, M Gastroch and thoracic paraspinals with other areas of denervation and myopathic units. Myotonic discharges were breif and fading.
I sent the comprehensive NM panel to Invitae yesterday which has EDMD
The fact that it comes in spells (not exclusively in the winter), she is completely normal and able to exercise in between is buzzling to me. She has never had any physical restriction.. She denies any physical restriction in her children, or weakness.
What do you think? We are in Greater Philladelphia area. She was seen before at U Penn. The initial EMG and muscle biopsy were done there.
My future employer is designing a new EMG/EEG shared space and is asking me if a "chair bed" would work for EMG. My employer's goal is to have a single unit rather than having a separate recliner for EEG placement/sleep and a bed cart for EMG. The chair bed can convert from a flat bed to an upright chair and everything inbetween. Max pt weight is 385 lbs, length while flat is 74" (6' 2").
Have any of you done EMG on a motorized chair bed? Any advice/"lessons learned" on the patient surface for doing EMG?
My biggest worries are the lack of bed rails and thinking of a large patient lying in the fetal position for back muscles, but I'll be doing outpatient only for a community practice. I currently do EMG on patients in a Stryker hospital bed or a patient transport cart, which have been fine.
Store link: https://www.source1beauty.com/Radi-Fully-Electric-Treatment-Table-2246B-Grey-p/2246b-g.htm
What patterns/studies on EDX are helpful in differentiating between the two ?
There is suggestion of non length dependent non entrapment sensory neuronopathy could suggest a neuronopathy.
One study mentioned absent blink reflex in the setting of activated masseter reflex suggests a neuronopathy.
Can I request opinions re EDX findings to differentiate between the 2 or any recommended resources to differentiate between the two ? Also I'm not sure what an activated masseter reflex EDX testing involves, any leads ?
I recently evaluated a 25 year old woman for a question of thoracic outlet syndrome, who was found to have a cervical rib on an X-ray. Her nerve conduction studies showed a median CMAP amplitude of 8 mV, ulnar CMAP amplitude of 7 mV, and normal median and ulnar SNAP amplitudes. However, her medial antebrachial sensory response was 7 uV but 18 uV on the other side. Is this consistent with true neurogenic TOS?
Has anyone had a patient with Cervical Dorsal Arachanoid Cyst and positive EDX changes?
Case is 55 yo 4 years well controlled diabetes, but 8-10 years progressive ataxia. Widespread upper and lower extremity sensory symptoms. MRI shows extradural dorsal arachnoid cyst and cord atrophy over the same segements. NCS in feet looks like sensory motor axonal polyneuropathy but UL SNAPS are all single digits (6-12uV). In theory could be sensory ganglionopathy + diabetic polyneuropathy but I was wondering if the dorsal arachnoid cyst/ cord atrophy could result in low SNAPS (by affecting the DRG?) Has anyone seen these cases and had similar results?
In the last 3 years, in two different patients, we have found during the EMG the activities shown in the attached images. The first time in the Gastrocnemius medialis muscle, while trying to record spontaneous activity; the patient didn’t achieve full relaxation, and the sparse MUPs triggered the activity in question. In the second occasion the activity was recorded in the Deltoid, only triggered by needle movements. I considered these as variants of CRDs/increased insertional activity. Both cases were referred for possible radiculopathies, with findings in the clinical/EDX examination congruent with MRI abnormalities, no other diagnoses suspected or established. The particularity of MUP-triggered CRD have been documented before? Am I right? What other possibilities could there be?
I was wondering if anyone could point me in the direction of literature addressing the phenomenon of pre-fixed and post-fixed cervical spine and cervical level overlap. I have a case this may apply to and would like to be able to read more and present something to my neurology colleague.
I'm curious to learn from others' experience on use of proximal motor nerve conduction studies in assessment of conduction block affecting the upper brachial plexus elements. Do you use motor NCS recording proximal upper limb muscles (e.g., biceps brachii, deltoid, spinati, etc.) specifically to assess for conduction block across the brachial plexus, and if so, have you found some (C5-6) muscles more reliable than others for this purpose? Or, conversely, have you not found this to be a useful diagnostic tool for this particular indication?
I have not personally used these a lot, and I hope to learn from others' experience.
Thanks for any insights from the group. Happy New Year to our EDX/NM community here!
Was hoping to pick the brains of folks who give lots of botox and/or have more experience than me (and what I can find in the literature) in how to interpret rep stim changes in patients who are receiving botox.
I have a patient in her 30s who had a prior C spine surgery for a left C5/C6 radiculopathy and regained 90% of her strength after this surgery. For chronic neck/shoulder pain and migraines she has been receiving botox for migraine and also to the neck and trapezius muscles (around 350-400 units every 3 months). About a year ago she started to develop recurrent left sided weakness and repeat imaging hasn't shown new nerve root compression. I saw her a few months ago and thought she had bilateral proximal arm weakness. Prior EMG in 2023 reported "neurogenic changes" in several muscles in the left arm in keeping with a presumed radiculopathy. I re-studied her and found myopathic units in proximal muscles in both arms and given the relative symmetry decided to also do rep-stim in the hand (assuming that the trapezius and facial muscles would be clearly impacted by botox). This was positive with decrement of 14% at at baseline with repair of decrement and no facilitation with 10-sec and 60-sec exercise with return of decrement at 2-4minutes post-60-sec exercise.
My question is: is this consistent with systemic effect of botox or is it possible that the botox has unmasked another disorder like MG (antibodies negative) or a hereditary condition like a congenital myopathy, myasthenic syndrome or otherwise? The appearance of a more-typical post-synaptic finding on rep stim in a muscle very far away from any botox injection is what has me questioning whether botox can be blamed.
Question for those that use the AANEM 2016 standardized techniques and reference values. I have been using these since shortly after the practice topic review paper was released in 2016. However, the latency suggested as upper limit of normal (97th percentile) often will give calculated conduction velocities in the mid 30s when using the distances described. As an example, the median sensory nerve peak latency upper limit of normal is 4.0ms, but at 14cm distance, this gives a conduction velocity of only 35 m/s. I have had some astute refering hand surgeons ask me why the latency is normal (3.8) but the CV is not (36.8 m/s). I am not sure how to answer this, though I feel I should be able to. What do you all do in these situations? Do you use different latencies or conduction velocity cut offs? Any information and discussion would be much appreciated.
Having recently seen uncommon nerve injuries a few more than I would have, on 30-years past form, expected, I am prompted to share some thoughts.
In headline, here are three:
Man, seventies (intentionally not specific), felt numbness only at the tips of the little and ring fingers straight on coming round after open-heart surgery. He had no impairment of dexterity, ulnar SNAPs only a little reduced, and the referring spinal surgeon “struggling to think that the cervical spine is likely to be the cause of polyradiculopathy like this”. Cannulation through veins on the back of the ulnar side of the wrist is likely the culprit.
Man, forties, felt numbness and dull pain in the little and ring fingers and on the ulnar side of the hand and forearm immediately after – for anaesthesia for surgery on the knee – cannulation, inserted into a vein on the back of the ulnar side of the wrist. Symptoms lasted over two years.
Woman, fifties, felt numbness and pain in the middle finger straight after trapeziectomy. Few days later, the surgeon decompressed the carpal tunnel, with no benefit. SNAPs from index, middle and little fingers and APB’s amplitude severely reduced, with no slowing. Injury to the median nerve is likely to have resulted from regional nerve block anaesthesia.
These nerve injuries are unique for several reasons:
Pain (“neuropathic”) alongside numbness is a distinctive feature.
In most, the referring clinician is not only not considering what the culprit might be (as transpires – on the balance of probabilities – only at the end of the examination) but thinking along what might prove red herrings: mal-positioning of the elbow or neck, aggravation of pre-existing cervical radiculopathy, injury to the brachial plexus, and other. These red herrings may all too easily be “supported” by confirmation bias. The commonest is “compression” at the elbow, likely to be followed by another surgery, for “release”, not infrequently making matters worse.
As the patient may not know or recall (having been anaesthetised), history may need digging out from records, or talking to the anaesthesiologists – as I have on numerous occasions and always found invaluable.
Sometimes already, or become litigious, they are uniquely educational, demanding relearning (and illustrating) minutia of anatomy beyond what us called for in academic tests. They can be fiercely contested – by lawyers and doctors, necessitating exclusion and inclusion in rigor beyond what is needed in routine clinics.
Demonstrate the importance not only of detailed history but of comprehensive examination that includes both sides. To make a conclusion on a 45m/s across the elbow, wrist, or knee without knowing the asymptomatic side’s, is to court (as an “expert witness”) discredit – or worse.
Two references worth considering:
Nerves and Nerve Injuries. Sir Sydney Sunderland. Churchill Livingstone. Second Edition 1978. I. Injection injuries. Section 5. Nerve injuries caused by the destructive or toxic action of certain therapeutic agents. Chapter 10. Causative agents. Pp. 173-6. Perioperative Peripheral Nerve Injuries. Abdul Ghaaliq Lalkhen, Kailash Bhatia. Cont Edu Anaesth Crit Care & Pain. 2012;12(1):38-42. 2012 Oxford University.
There are others. From patients I have studied, mechanisms of anesthesia-related nerve injury include:
Cutting action by the tip (crowned, in some designs, by multi-faceted bevel) of the injection needle as it passes through the nerve. Or injury by a cannula that, on being advanced through winding or networking veins at sharp angles, may breach the vein wall and allow extravasation of anaesthetic agents (sometimes containing adrenaline) or antibiotics coming into direct contact with the nerve or with its nutrient blood vessels, resulting in toxic or ischaemic injury.
Volume-expansion effect of infiltration (sometimes inadvertent) of the anesthetic inside nerves.
Tetanic electrical nerve stimulation to monitor neuromuscular block during or after surgery. The stimulator (one lent to me by anaesthesiologists) looks innocuous, hand-held (similar to stimulators on some EMG equipment) with two prongs to be placed on a nerve (commonly the ulnar at the wrist or elbow, on the side opposite to where the blood pressure monitor cuff is). Although AA-battery powered, it can deliver up to 80mA, 0.2ms wide stimuli at up to 200Hz, thus ensuring hand muscles undergo effective tetanic contraction that visibly fluctuates with the depth of the block. At even mid-range setting, such stimulation would be intolerable. But as the patient is anesthetised, and although stimulation trains can be delivered in various modes, stimulation can also be applied continuously (or with little interruption) for long periods. When thus applied, it can (as learned from Professor Erik Stålberg, 25 years ago) generate heat, which might be at least one mechanism of injury. Most cases resolve within few weeks; it is the severe, sometimes irreversible injuries that come to our clinics.
Ischemia to nerves, muscles – and other tissue – from prolonged cumulative constriction of the thigh, leg or foot, from application of inflatable garments (or boots) to prevent deep vein thrombosis. Although inflation of these garments (applied independently on the three sections of the lower limbs) is meant to be programmable – with cycles of inflation and deflation throughout the surgical procedure, operations (on the thorax, for example) may last over six hours, and inflation / deflation may fail to avoid ischemic (segmental infarction) injury to nerves – such as the sciatic or its divisions, right into the sole. Aside from uniform compression within the boot, additional constriction, on nerves or on their blood vessels, may result just under the rims of the boot if close to where nerves are superficial or over bone.
Lithotomy stirrups: in gynecological and obstetric procedures, weight of the legs in the lithotomy position taken largely by acutely flexed knees placed on stirrups. Although stirrups (or knee crutches or loop leg supports) are padded, the fibular and tibial nerves – and their blood vessels – can still be subjected to prolonged external compression especially if the upper rim of the boot or support abuts on the head of the fibula or across the popliteal fossa. In these cases, however, I would exclude epidural first.
Unrelated to anesthesia but sharing mechanism of injury with regional block is venepuncture, which I have described in some detail in relation to the antebrachial nerves under ‘True Neurogenic Thoracic Outlet Syndrome’ – but appending a selection here in a (large) footnote.[1]
Although uncommon (in the severity that persists weeks after operation), these potential nerve injury mechanisms need to be considered notwithstanding the tendency to forcibly contest forcibly – for they may become litigious.
Amongst the arguments for dismissal: These procedures are used in hundreds of operations every day, so how come we do not see nerve injuries more often? The answer: While the argument is (partly) true, such injuries do occur more frequently but remain largely submerged, in the early postoperative weeks, below what the patient – and medical staff – are concerend about most of the various elements of recovery: pain, immobilisation, wound healing, etc. And if patients do point out numbness on, for example, the outer side of the foot, or inner of the hand, or inability to move the foot, they might be reassured ‘it is one of the things not unexpected after such a lengthy operation and will resolve shortly’. By and large, this forecast comes true.
Nerve injuries, however, that come to our attention two weeks or more after surgery are those (tip of the iceberg) that have exceeded injury-threshold (beyond neuropraxia, to infarction) to remain noticeable after the other postoperative concerns have receded.
Nerve injuries I am describing are what have come to my attention, and there might be more I am unaware of, but other colleagues are, and from whom I hope to learn.
For update on devices, procedures, and injuries, I defer to anesthesiologists. Nevertheless, these nerve injuries should be kept in mind amongst what (physician Arthur Conan Doyle’s) to eliminate so that what remains, however improbable, must be (or most likely is) the culprit.
[1] On normal anatomy, the medial antebrachial enters the forearm in two branches: anterior and posterior. Around where the nerve can optimally be recorded, antidromically 7cm distal to the medial epicondyle or elbow crease (stimulated just proximal to the crease), the two branches can be 4cm apart. In most patients I can reliably record only one branch, settling for maximal amplitude (usually 2-3cm medial to the medial border of the forearm) as either representing an undivided nerve or the larger branch. But there is a caveat. The nerve usually divides in mid upper arm, such that unless stimulation is also (separately) applied to the anterior branch (more medial to the posterior and stimulation thus encroaching on the median nerve) the anterior branch cannot be recorded. This may be acceptable in routine practice, although ideally recording the two branches – and adding up their individual amplitudes – allows a more sensitive index of the total axon content of the nerve before it divides. Which means we also need to compare the two arms. While this is perhaps pedantic and beyond the routine, it is worth being mindful of in cases of selective injury to the anterior branch (with division of the parent nerve in mid upper arm). Such injury can result from difficult venepuncture for blood donation: 16G, 75mm long needle, possibly retracted and redirected a few times. While the patient may have numbness and difficult-to-describe ‘strange’ sensation over the medial 2/3 of the front of the forearm including numbness, felt at the same instant of injury, in the little finger. Although the ulnar nerve might be suspected, this is not necessarily: inclusion of the little finger likely mediated by terminal connection of the antebrachial with the palmar cutaneous branch of the ulnar – both zones within the territory of the anterior branch. (Such terminal plexus formation applies to the lateral antebrachial with the superficial terminal branch of the radial nerve, which can be confused with injury to the radial.)
Back to the selective injury to the anterior branch of the medial antebrachial, the posterior branch may have been spared and recording it at ‘normal’ reference amplitude may be confusing – and misleading: if, on symptoms as described above, the medial antebrachial is pronounced normal based on recording its posterior branch only. This is not just pedantic; in litigious cases, it can have grave implications.
A case I have seen included separate selective fascicular injury to the musculocutaneous nerve. This nerve supplies articular branches to the elbow joint, and a branch to the humerus, and injury to the musculocutaneous nerve is thus likely to underlie pain at the elbow – which can be confused with pain directly related to the puncture site and can also be incorrectly considered “tennis elbow”). Nevertheless, pain of musculocutaneous nerve injury is unique and is characteristically relieved by maintaining the elbow in acute flexion.
I use bar electrodes (with shortened – 15mm – felt inserts) as these are easier to slide in small sideways steps, imperative for bracketing variability in the course of nerves and minimising overlap between adjacent nerves. Furthermore, although these nerves (lateral and medial) come from different trunks and have different (but adjacent) root representations, the latter may overlap. Thus, assessing these nerves is enhanced by looking at them together on both sides.
Would appreciate ideas about what is the appropriate way to deal with a bleeding spot at the site of needle insertion. Is taping a cotton ball over it appropriate? Thanks to all.
I have seen 2 cases of sciatic nerve damage following foot/ankle surgery over the past few years. In both cases, the surgery involved popliteal block and tourniquet, with post-op complaints of motor and sensory loss from the knee down. The first case was a few years ago and I don't recall all the Edx details, other than there were abnormalities below the knee c/w tibial/fibular injury. The second case I saw this week 15 y/o with dense sensory loss globally below the knee and global weakness following ankle ligament reconstruction 7 months ago. The patient described some improved sensory in the proximal 1/3 of the leg but no feeling in the distal leg and foot. Motor exam with marked weakness (2/5 DF, toe flex/ext, eversion, PF). NCS with absent superficial fibular, sural and fibular motor. Interestingly, tibial motor WNL and no side to side difference (so tibial weakness seems out of proportion to the motor nerve study). Needle EMG c/w denervation short head bicep, gastroc/soleus, TA and fibularis longus (small amplitude spontaneous activity, long duration polyphasic motor units) and normal EMG quad and proximal hamstring.
Question: Other than the Edx study, does anyone have a take on whether these need to be further worked up? The case I had a few years ago I recall getting MRI of either the femur or leg and then did the other part of the limb when the first study was unremarkable in terms of obvious abnormality around the sciatic (memory not totally clear). However, it was a work comp case and studies were approved, so no issue with $$ for the patient. In the current patient, any thoughts? In the cases that the community has seen, have you figured out etiology?
I am a sports and spine physiatrist that completed fellowship in 2012. When I was in residency, it was common for PM&R graduates to continue practicing EMG. However, I have noticed (anecdotally) that younger physiatrists in my area are no long practicing EMG. They are often part of a ortho, neuro, or multispecialty group so I know that referrals are probably not a factor. The wait time to EMG also seems to be increasing and I'm wondering if there are is a connection here.
Are there more EMG referrals or less people actually performing them?
I know the reimbursement cut several years ago was a major event that signficantly affected EMG practice.
I have also noticed (coincidentally) that there are more PTs now performing EMGs as well. Quite a common practice in the military system but I'm starting to see it more and more in the civilian sector as well.
I would be curious to hear thoughts from the group.
Good morning to all. I will try to present a case as summarized as possible. An 81-year-old woman presented with progressive loss of muscle strength in her left hand, ascending to the shoulder, a clinical condition that began 7 months ago. muscle weakness has compromised the left lower limb to a lesser extent. She has a history of severe left trigeminal neuralgia a few months earlier, which required several interventions, including infiltrations. In June of last year she had an electromyography with a possible diagnosis of C8, T1 radiculopathy. Clinical doctors have dismissed the electromyographic findings, whether due to images of the cervical spine without signs of disc pathology that explains the compression of the lower cervical roots, presence of old infarction in the territory of the left PICA and in brain MRI with small vessel disease Fazekas 2-3. They manage it as sequelae of cerebrovascular disease. an orthopedist requests the examination again. physical examination with signs of upper and lower motor neuron in the left hemibody, the motor conductions of the left median and ulnar nerves are absent, no further striking alterations are evident in the motor and sensory conductions. The study with a monopolar needle shows signs of denervation in the left first interosseous and abductor pollicis brevis, and in the left tibialis anterior with neuropathic units. What do you think, dear colleagues? Do you think it's ALS vs MNN? . What other diagnostic option could I have? I appreciate the attention provided
I have recently been doing EDX studies at our Hand Clinic for several months. We prefer to do the ulnar conduction with the arm "raised", resting on a pillow. Our fellow noticed a device in their clinic that made our ulnar positioning much easier to maintain the limb in a comfortable, fixed position. This is an arm support that the Hand Clinic uses for their purposes, but I think nicely adapts to nerve conductions. This is best shown in the picture provided. The elbow is in a 90 degree position which does not show well in the photo. We also show the picture of the support with arm placed directly on it for clarity- in clinical use the support is placed in a pillow case. The attachment lists a couple of sites where they can be purchased. It goes to show that sometimes a fresh set of eyes sees a better way of doing things! We hope that you may also find this a convenience in your practice.
I like the median D2 or D3 segmental sensory study for the CTS evaluation. I usually measure 14cm to the wrist and 7cm to the palm. It's the only way that I'm aware of to distinguish sensory axon loss from sensory conduction block across the wrist. It also seems to be very sensitive in detecting focal slowing that was diluted over the larger distance. However, it can be technically challenging to produce a flat baseline, especially in the palm. And there is often significant variability in onset latencies with repeated attempts, so I will typically take the average 4-6 responses at each site before looking at the segmental conduction velocities. My question for this group: Why not use the peak latency difference between wrist and palm instead of conduction velocity? It would have to be standardized for distance of course but most hands fit the 7/14cm montage. Does anyone use peak latency difference or know of reference values for this?
I have a question regarding an issue that came up recently and would appreciate any and all thoughts.
We had a consult to perform a bilateral facial nerve study (NCV/ENOG & needle EMG) on a patient with active TB for “immediate surgical intervention purposes” in an isolation negative pressure room. Appropriate medication had just been started but no idea if it is/will be effective or if the patient will be resistant.
The concern is regarding taking our EDX equipment into the room with respect to multiple fans running in the laptop/base unit. Clearly any beasties in the air will potentially be sucked into the machine, possibly become lodged in there for some time; then when we take our instrument out of the room and back to the outpatient clinic there is a potential for blowing out nasties into the clinic. This seems like a setup for a potential “hot zone” of community based contamination.
The hospital’s “infection control” are not concerned in the least and state that “machines” go into and out of those rooms all the time and into an adjacent room or ICU rooms “without issue”. To be sure, this is true. For example those portable X-ray units go all over the hospital from a TB room, to a Covid room, then into an possibly immunocompromised patient’s room without concern. I am not aware if those portable X-ray units have removable HEPA filters or not; I doubt it. It’s the “without issue” that bothers me. There are no studies I am aware of that have swabbed machines or rooms to ensure there is no cross contamination “issues”.
I know our EDX instruments are running fans and there are no filters of any kind on the vents for the base unit or computers. Having changed both batteries and memory drives I know most computers with some exceptions have fans running in them (laptops PCs/Macs) and for sure tower units have fans.
I would have thought with the recent CoVid issues that someone would have a concern or policy regarding this issue. I am not aware of any EDX manufacturer that has a policy or recommendation as to this issue. Also, I do not think the AANEM has a policy or SOP for this type of scenario. It’s probably not a good idea to douse the instrument’s internals with a fluid disinfectant risking electrical issues or voiding the manufacturer’s warranty.
In short given the above scenario and no doubt other scenarios, is there a concern here or is this in the line of what the great Bard once said, “Much Ado About Nothing”? Maybe it is just me that has an unwarranted concern and it is well known and documented that these instruments are NOT a potential source for disease spread. Appreciate any thoughts.
Hi friends, new attending here looking for any advice:
I was asked to do NCS under sedation for a 3 month old with krabbe disease. I have not seen a patient with this diagnosis before nor have I done a NCS on a baby this small. Any suggestions are appreciated! I will likely also bring the ultrasound with me, more out of my own curiousity as I have read that the cross sectional areas of the nerves can correlate with NCS findings and I am working on incorporating NMUS into my practice. Any tips/suggestions for the US part is also greatly appreciated!
Looking for help/thoughts from those in RVU based system that personally perform the nerve conduction portion of studies without a technician.
Essentially RVU targets changed at the beginning of the year by 700+. Some of us in the group do not have technicians but it just does not seem right that we only get the "physician work" portion of the RVU when personally performing the nerve conductions. Thinking that some percentage of the technical component as well would be more fair and act as a "buffer" of sorts.
Have heard of some groups who give flat rates like $55 for each nerve conduction that is physician performed.
Have also heard of other groups that do $35 for the nerve conduction and $35 for EMG and this is with technician performing the NCS.
Anyone have thoughts or willing to describe what is done, if anything, to compensate for the physician performed NCS. Thanks in advance!!
I have a complicated patient, 54 y/o male, diabetic currently under good control. h/o C5/6 ACDF August 2021 with some residual right hand numbness in the thumb/index which interstingly completely resolved following right rotator cuff repair in January 2023. Shortly after the surgery, he started to have left arm and hand paresthesias and subjective numbness radiating from the L neck and shoulder. This was intermittent for a few months but then progressed to both arms and hands, all fingers. constant. Cervical MRI did not show correlating findings but was technically limited from the hardware.
I did EMG LUE in May:
-Absent median sensory studies to index and middle
-normal ulnar and superficial radial sensory
-Median motor, 8 cm, latency 9.5 ms, amplitude 5.6 mv, CV 46 m/s
-ulnar motor, 8 cm, normal except mild decreased CV across elbow 46 m/s
-EMG: ABP with decreased recruitment but no spontaneous activity
CTR done in June with no change in symptoms.
Spine surgery obtained CT myelogram and concluded that neck not causing the bilateral symptoms
Brain MRI was also obtained in May due to these symptoms and development of motion sickness following the shoulder surgery in January 2023 and was read as unremarkable.
Spine surgeon referred him to neurology, who saw him August 31 and did bilateral UE EMG:
LUE:
-absent median transcarpal
-Median motor, 7 cm, latency 8.1ms, amplitude 3.8 mv, CV 46 m/s
Question: Given the CTR was done 3rd week of June and new EMG 9+ weeks post op shows basically no change in motor latency, I can't help but wonder if the CTR was not complete and he still has focal compression. I realize that demyelinting issues can take up to 3 months to recover, but in general I expect the latency to look better this far after CTR. Does anyone have a take/suggestions on what to do with these data?
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.
