AANEM Connect

In the evaluation of a person with LMN spina bifida (ie S1), who is referred for query S1 radiculopathy, can we be sure that if we see spontaneous activities on needle EMG that there is something acute going on? Or could that be a remnant of the underlying spina bifida? 

Hello colleagues,

I have a 16M patient with complicated history, presumed CIPD but also found to have MFN2 gene mutation. He came to me for PM&R consult, he has persistent distal weakness and atrophy requiring AFOs, hand splints and scoliosis. He has seen multiple neuromuscular specialists over the past few years, but now they are looking for referral to a neuromuscular specialist in CIDP who they can get another opinion regarding his medications (IVIG, rituximab). He likely needs a repeat EMG but I didn't want to do it if he was going to go to a new neuromuscular doctor who would probably want to repeat the study themselves anyway. He lives in central NJ. Any recommendations for a CIDP specialist in this area? Thank you

Hello All,

Looking for input/data for safety of NCSs in cardiac patients with external pacers/ defibrillators/ LVAD. there is plenty of literature on implanted devices, any insight for external devices.

Thanks.

I am requesting all of your help to better define both the audience and outreach for this forum via the AANEM Connect discussion venue.  Would you be so kind as to please give your thoughts on the following:

 

• Continue to keep the AANEM Connect forum open only to the AANEM membership as it currently exists as a benefit of a paid membership only.

Or

• Open up the AANEM Connect forum a bit for viewing purposes only, to Neurology/PM&R residents/neuromuscular fellows who are not members of the AANEM, but without the ability to ask questions or perform searches and free of charge.  A support letter from a program director would ensure the status of the resident/fellow.

 

Greetings EMGers,

 Do you have any old EMG or SSEP equipment or parts?  ASET--The Neurodiagnostic Society (Technologist society) is collecting old EMG and EP parts and equipment for the virtual museum of the  Smithsonian Institute Neurodiagnostic Museum. I'm on the ASET Historical committee for the Smithsonian Institute.  I'm working on the EMG/EP section.  If you have anything that looks like it should be thrown in the trash or old equipment you are trying to get rid of , please consider donating these old items to ASET for the virtual museum. 

I am posting this in part out of frustration, and also to generate discussion regarding training and philosophy on performing history/physical during EDx consult.

I recently saw a 63 y/o male, smoker, with pmxh from pcm note copd/chronic hep c with about 1 year of progressive subjective decreased balance, dropping items, shoulder weakness, numbness/tingling equal bilateral volar forearms into hands d1-3 (constant but improved with gabapentin) night cramps in thighs and calves.  He had seen local neurologist shortly before I saw him (fellowship trained neuromuscular) who did NCS but could not do needle study due to patient refusal.  NCS normal other then ulnar slowing across elbow, felt to be indicental given lack of ulnar symptoms.  This doctor did no history or physical exam, nor did he make any comments regarding potential diagnoses or workup.

My exam notable for deltoid and scapular muscle atrophy and weakness with distal UE muscles and quad/hip flexors normal. Reflexes spastic with Hoffman, no clonus.

I orderd c-spine MRI:  Severe central stenosis C3-5 with cord signal changes.

• I was trained as PM&R to always do H&P; discuss findings with the patient; discuss clinical correlation, need for additional workup/treatment in my report. I will make the surgical referral or order additional workup within my scope of practice because that's how I learned and it's good for the patient and their referring provider.
• However, I have seen many studies over the years, all done by neurologists, where none of the above is done.  The patients have confirmed this as well.  Doctor told them to get on the table, no exam, test was done, no discussion, minimal or no discussion in the report, sent back to PCM so they can try to figure it out.
• I have had neurologists tell me this is how they were taught.
• I struggle with the concept that at least some neurologists don't practice EDx medicine per the guidelines from AANEM, especially considering that the AAN seems to use the AANEM guidelines.
• I'm frustrated:  how can a fellowship trained neuromuscular specialist miss what should be a pretty simple diagnosis?  
• Does anyone in this community also not do H&P as part of the test?  If so, why?
• Can we as a community do anything about this problem?

I've been looking for the ideal pen to use for studies -- a combination of visible, somewhat resistant to electrode gel, and washable.  I've used Zebra Clickart Water-Based Pen Calm Dark 12 Colors Set, Wyss22-12Cdk that has the advantage of being clicked open/closed but does smear a bit when patients sweat or when too much electrode gel is present.  Does anyone else have a product that they are happy with?

Hi all,

I'm interested in your opinion regarding relative sparing of the EDB muscle compared to an atrophic tibialis anterior. I have seen this occasionally in myopathy and dystrophy patients. 

I recently had a very complicated study for left foot drop and bilateral lower extremity numbness/burning in a 77 year old in which the left tibialis anterior muscle was visibly atrophic and bilaterally the TAs had low amplitude CMAPs [1.0;symmetric], yet the EDB were bulky with high normal CMAP amplitudes (left [foot drop side] was 3.6; the other was 8.7). There were not sensory or tibial abnormalities. A very comprehensive EMG Bilateral lower and some uppers) showed no myopathic findings at all. There were very significant, mostly chronic or sub-chronic reinnervation changes in all distal > proximal leg muscles bilaterally and in the left FDI with denervation (PSWs and fibs) in the left tibialis anterior only (the foot drop side).

The lumbar MRI doesn't show anything that would cause multilevel radiculopathy -- it's pretty normal. I feel that the time course (onset of foot drop 7 years ago) and relative paucity of active denervation would be atypical for ALS plus the robustly normal EDB muscles in the setting of ALS with foot drop would also be atypical.

Is this EDB sparing significant? What does it make you think of?

Thanks for your thoughts--

Hello! can anyone give guidance on how to approach a winging scapula case, on exam this appears to be long thoracic neuropathy. Needling Serratus Anterior muscle, is challenging, any suggestions, on the safest technique, I guess the diagnosis will mostly be based on the needle test. Appreciate any guidance!

-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 am looking for a black Neuromax, not a white one, 2 or 4 channel, to buy hopefully with a cart.

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

Youtube: https://www.youtube.com/watch?v=zHfLw6hFMOg&t=128s

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 ?

Thank you

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?

Hello all, 

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!

Hey all, 

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. 

Would appreciate any thoughts!

-Tom Ragole 

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?