AANEM Connect

I recently saw a patient with numbness and tingling in the right hand that was sent to “rule out carpal tunnel.” The patient was a 36 year old female office worker that had a rather standard complaint of about a 3 week history of numbness and tingling in the third and second digit with a “feeling” of finger swelling and hand heaviness. She denied dropping objects but did state that she was beginning to have some trouble buttoning clothes with the right hand. The sensations in her right hand were beginning to occasionally wake her up at night. 
 
On physical examination her hand appeared symmetric to the contralateral hand. There was no obvious or subtle swelling, muscle asymmetry, or skin abnormalities. Manual muscle testing revealed a grade 5 to all of her hand intrinsic muscles bilaterally. Sensation was mildly reduced in the classic median nerve distribution on the volar aspect of the right hand with no abnormalities noted in the ulnar, superficial radial, or dorsal ulnar cutaneous distributions on the right. A Tinnel’s sign was present at the right wrist region, but otherwise no other provocative maneuvers caused the patient any discomfort.
 
I thought this was going to be a typical CTS assessment, but I found the motor NCV data to be unexpected and somewhat confusing. I am hoping you can shed some light on the patient’s findings.  Specifically, I performed a median sensory 14/7 cm study using an antidromic ring finger technique with ring electrodes on the third digit. Her mid-palm sensory peak latency was 1.9 ms while her 14 cm peak latency was 4.4 ms thereby yielding a trans-carpal latency of 2.5 ms. I thought, Okay, this makes sense given the symptoms: so far, the SNAP findings are suggestive of a focal median sensory neuropathy at or about the wrist region. I then performed a routine median motor study with the wrist stimulation at 8 cm resulting in a latency of 3.9 ms with a CMAP amplitude of 7 mV. No worries I thought, the median motor study is looking good at this point. But, when stimulating at the elbow, the CMAP displayed an initial positive deflection with a CMAP amplitude of 10.5 mV. This sure looked like a typical Martin-Gruber anomaly regarding the two CMAPs. I made sure the CMAP from the wrist had an abrupt negative deflection, and so I was convinced I was on the APB’s motor point. What is going on?

Is it acceptable to include brief suggestions for management based on the EMG/NCS results?
 
For example in a case of carpal tunnel syndrome: (Suggest: refer to a Hand Surgeon)

Tim Lachman, MD

We have a new EMG doc joining the lab who suggested premedicating patients with Xanax.  I have not used this approach as I never thought it was necessary or indicated, and wondered if anyone else was doing it or had any experience to share.  Our lab only receives EMG referrals (on adults, no peds), and typically we would not have seen the patient before the visit, so we would need to rely on the referring physician for any prescribing.

I am interested in bringing ultrasound to my electrodiagnostics lab (it would be refreshing not to have to shock and stick every patient that comes in!), but I’m not sure how much I would use it, and I don’t want to invest a bunch of time and money into something I’ll use once a week. Any thoughts on how to know when it’s the right time to bring nerve ultrasound into your practice and how is the best way to transition it into your EDX lab?

electrophysiologically , why sural response is difficult to obtain or even unrecordable in many healthy subjects > 80 years old ??

does this simply imply a subclinical neuropathy ?? or  or it's normal aging loss of axons?? 

      

Recorded this interesting EMG waveform from a patient with distal leg weakness and numbness.  I’m interested in what others would call this discharge.  (I’ll let you know what it is in a followup post).

Here is the link to the video: https://youtu.be/IJrcsX727KA

 

Does anyone have recommendations for specific products to help with warming patients in the lab that are less than $3000?  Open to all suggestions, but also interested in anyone that has experience using a hydrocollator as I think that may work well with our lab set up.  Thanks!

SFEMG, voluntary activation. I sometimes see highly increased jitter (150 µsec), but no blocking is observed. Why?

I would like to hear your opinions on reference values. Which do you use and why?  Do you use age-specific normals?  For median sensory, do you record from D2 or D3 and why?

1) I prefer to be interactive, and therefore, please pose me with questions you would want to ask the patient?

2) What tests if any, you would like to do first apart from the exam?

3) You would like to know my exam findings, but prior to that, what in his history, you would enquire of this patient?

Does anyone know of tendon transfers or other treatments to help with thumb opposition after complete denervation of the abductor pollicus brevis (not motor units seen in APB on EMG) after T1 radiculopathy due to sarcoma resection in T1 vertebra? 

Based on my review of multiple text books, Fibs/PSWs are thought to occur in inflammatory myopathies due to fiber splitting, resulting in essentially denervation of that segment that no longer has access to the neuromuscular junction.

I have often quoted this as the reason for finding abnormal spontaneous activity in muscles that have been injured by direct muscle trauma (either a single severe event or mild repetitive). 
 
A former trainee of mine asked me for a reference for this and i can't find anything about direct muscle trauma. I think i'm right but would prefer if i could quote it.
 

A patient I performed an UE EMG was diagnosed with an UE DVT two days after the exam. I could not identify DVT listed as a risk factor or identify with a (brief) internet search of a DVT as a complication of an EMG. Has anyone had DVT associated to an EMG?

70 year old healthy looking male with a 5 day history of insidious onset of (just below mid inguinal ligament) with mild diffuse discomfort over the left anterior thigh, intermittent, most aware when sitting and not during gym hour. No motor weakness or sensory loss. DTR: 1+ knees. SLR -ve. Exercises regularly 4/wk cardio + weights. Vitals: 160 lbs, 5'8". No medical issues. No prior surgeries of the spine, or iguinal region, or hernia. No unusual activities. Sleep is unaffected.

What are the possible clinical diagnosis? Please do not order tests.

Currently using Biomedix 6' x 30" vertical & tilt powered bed on rolling/lockable wheels) but am relocating to a smaller lab. Online search hasn't turned up any smaller (eg 5' long w/ leg extension) platforms having power & mobility features above. Any suggestions are welcome. Thanks!

In performing an EMG on a 63 year old man, I obtained an absent left peroneal motor response from the extensor digitorum brevis, with a normal response on the right. The tibial motor studies were normal and symmetric and the surals were absent bilaterally (which I interpreted as being age-related). The man had no sensory loss or weakness in his left leg. Does an absent left peroneal motor response, without clinical findings, have any significance?

I was wondering if you could help me understand and localize a lesion so as to explain the findings below in a 42 year old woman who is 1 year s/p a MVC with an associated pelvic ring FX and right foot drop. On physical examination she has a clear inability to dorsiflex the right foot against gravity and similarly can’t evert this foot either. When she tried these maneuvers, I can, however, feel some muscle contraction. She is also numb on the dorsum of her foot, but there is a clear well healed scar 7 cm in length just medial to the lateral malleolus extending from just inferior to the lateral malleolus vertically.  Her sensation along the lateral margin of her foot is relatively intact but decreased compared to the other side. The patient has no difficulty extending her knee and I cannot overcome her ankle plantar flexion.  Hip flexion is normal as is hip extension and leg external/internal rotation.

On needle EMG of the right lower limb, there are PSW/Fibs easily observed in the following muscles with motor units, but displaying a somewhat neurogenic recruitment pattern: gastrocnemius, tibialis anterior, peroneus longus, flexor digitorum longus, short and long head of the biceps femoris, semimembranosus. There were fewer motor units recruited in the fibular compared to tibial innervated muscles. The following muscles revealed no abnormalities at rest with normal recruitment: gluteus maximus, tensor fascia lata, vastus medialis, and adductor longus. At this point, the patient declined any further needle examination.

Of note, the patient had considerable instrumentation of her L/S spine following the trauma and would not permit any needle assessment of her back.

The sural SNAP on the affected limb had a latency of 3.9 ms with an amplitude of 7 uV and the superficial fibular sensory response was absent. The tibialis anterior CMAP revealed a below fibular head magnitude of 2 mV with an above fibular head amplitude of 1.6 mV. The patient now requested termination of any further needle insertions or nerve stimulation.

Some of my colleagues use the terms “demyelinating” or “demyelination” to explain localized conduction slowing associated with conditions such as carpal tunnel syndrome. For example, their interpretation may state that there is a median mononeuropathy at the wrist characterized by demyelination but no axonal loss. Is it appropriate to include this description?