Post-op concern

Clint
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Bilateral CTS for >10yrs. Dx NCS (L): severe; (R) moderate but 'complicated' by mild mid-line palmar paraesthesia over thenar / hypothenar eminences. Bilateral open CT release 3/52 previous. Both transverse ligs. demonstrated at surgery to be fully resected prox & dist. Underlying basis of problem: morphological. (R) required dissection through substantial thenar muscles that had crossed the midline. (?bleed) Prompt post-op bilateral resolution of nocturnal Sx. (a real delight!)

Recovery (L): v.nice healing, v.minimal swelling, some incisional tenderness. Grip, excellent; finger pince grip, excellent; wrist mobility and tendon glide full and excellent; mild paraesthesia as before over median distribution but absence of nocturnal sx. Anticipate continued good recovery.
Recovery (R): v.nice healing, mild swelling, incisional and thenar anaesthesia extending to volar pad and lateral aspect of thumb. Grip, poor/moderate; finger pince grip, moderate and weaker at 4&5 with pain in CT. Continual 'squeezing' neuralgic pain felt at wrist, and along course of median n. to medial arm and axilla. Intermittent sharp pain in the deep dorsum of the forearm and hand. Sx markedly > by activity, particularly more static tension eg. playing piano, which results in > neuralgia and profound anaesthesia/dysthesia in the thumb pad and odd swelling sensation. Relieved after a night's rest, though sleep may be disturbed.

I concede I may have been doing 'too much' - eg. mowing grass 2 days after surgery etc.. but based on the superb recovery of the diagnosed worse (L) side, which involved prolonged dissection to release a heavily compressed ribbon like nerve, and which presented no post-op difficulties at all, I pressed on. The (R) side is a frank cause of anxiety with the brachial neuralgia (median n.) varying from a persistent quiet throb to awe-inspiring. It may be brought on by keyboard work (within 1 min or playing piano, within 3 min). It has improved since surgery, when immediately afterward the neuralgia in the arm was truly severe and only relieved by staying completely still. In any event, these are entirely new (R) hand and limb sx since surgery.
Surgeon's comment at suture removal and post-op check was dismissive. He offered no explanation and less interest. I regard the surgery as 'successful' but the development of troublesome and new symptoms in the right extremity are personally concerning.
Due for 6/52 post-op follow-up end Jan.

I would deeply appreciate any insightful comment please. Clinicians make the worst px!
My own feeling is that a cutaneous branch of the (R) median n. may have been injured. This may explain the distribution of the anaesthesia. The (R) brachial neuralgia appears more difficult to explain. Could it have been associated with a bleed? A sense of prognosis (on the R) would also be helpful based on your extensive experience.
Many thanks in hopeful anticipation of your response.
Clint.

jeremydpbland
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The palmar cutaneous branch of the median nerve is certainly sometimes injured during surgery and usually supplies the skin over the thenar eminence and lateral half of the palm but not usually the border of the thumb so there is something a bit odd about that - though of course there is considerable variation in 'normal' human anatomy when it comes to the cutaenous distribution of small sensory nerves. This much pain after surgery is unusual, though it is at least, by the sound of it, improving somewhat. It probably is reasonable to review at 6 weeks as most of the immediate peri-operative inflammation should have settled by then. If it is still very problematic at that point I personally would want to repeat the NCS and look at the operation site with the ultrasound scanner to check that there really has been an improvement in nerve function and that there is nothing structurally untoward. If you have read the sections of this website on severity you will know that the terms 'moderate' and 'severe' can mean very different things to different people when it comes to CTS - do we have the actual NCS rescults from before surgery? JB

Clint
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Thank you kindly JB. Yes, I understand the subjective nature of descriptive terminology and have finally secured the NCS results, below.

Left MEDIAN MOTOR (thenar)
SD left median motor raw data
Distal motor latency 6.1 8.3 MARKED DELAY Lat Amp Area Dur Distance
Distal amplitude(mV) 9.8 0.6 WR 6.05 9.80 46.60 8.85
Distal area 46.6 1.8
Distal duration 8.9 2.5

Left MEDIAN SENSORY digit III - wrist
SD left median sensory raw data
CV onset 34 -6.4 MARKED SLOWING Los Lpk Amp o/p Amp pp Distance
CV peak 26 -7.9 MARKED SLOWING 3.70 4.85 1.70 1.20 124
Amplitude (μV) 1.7 -9.0 MARKED REDUCTION
duration 1.15 10.2

Left MEDIAN SENSORY antidromic digit III
SD
Amp palm-III 12.5 AXONAL LOSS left median antidromic raw data
Amp ratio wr/palm 0.69 -1.3 Los Lpk Amp o/p Amp pp Distance
dispersion 122% -0.7 pa 1.25 2.15 7.10 12.50 67
CV palm - III 54 wr 5.25 6.35 4.00 8.60 85
CV carpal tunnel 21 -8.1
CV diff (normal >-7) -32 -10.0 MARKED SLOWING

Left ULNAR SENSORY digit V - wrist
SD left ulnar sensory raw data
CV onset 59 -0.3 Los Lpk Amp o/p Amp pp Distance
CV peak 42 -1.5 1.85 2.60 5.90 9.60 110
Amplitude (μV) 9.6 -0.4
duration 0.75 3.9

Right MEDIAN MOTOR (thenar)
SD right median motor raw data
Distal motor latency 4.4 3.7 MILD DELAY Lat Amp Area Dur Distance
Distal amplitude(mV) 9.5 0.5 WR 4.35 9.50 37.80 6.70
Distal area 37.8 1.0
Distal duration 6.7 0.7

Right MEDIAN SENSORY digit III - wrist
SD right median sensory raw data
CV onset 40 -4.4 MODERATE SLOWING Los Lpk Amp o/p Amp pp Distance
CV peak 33 -5.3 MODERATE SLOWING 3.10 3.80 1.80 2.00 125
Amplitude (μV) 2.0 -8.5 MARKED REDUCTION
duration 0.70 3.0

Right MEDIAN SENSORY antidromic III

Amp palm-III 25.8 right median antidromic raw data
Amp ratio wr/palm 0.43 -3.2 CONDUCTION BLOCK Los Lpk Amp o/p Amp pp Distance
dispersion 100% -1.5 pa 1.35 2.10 20.70 25.80 70
CV palm - III 52 wr 4.15 4.90 6.50 11.00 83
CV carpal tunnel 30 -6.2
CV diff (normal >-7) -22 -7.0 MODERATE SLOWING

Right ULNAR SENSORY digit V - wrist
SD right ulnar sensory raw data
CV onset 55 -1.5 Los Lpk Amp o/p Amp pp Distance
CV peak 43 -1.4 2.10 2.70 3.20 6.30 115
Amplitude (μV) 6.3 -1.8
duration 0.60 1.6

OTHER RELEVANT INFORMATION: symptoms have been quite marked and unusually seem to include the median palmar cutaneous distribution as well as digital nerve involvement.

PRINCIPAL FINDINGS: marked left median nerve compression at the wrist with moderate involvement on the right.

DETAILS: median sensory amplitudes were markedly reduced bilaterally. This was shown to be due to axonal loss on the left and conduction block on the right. Marked focal slowing was found through the left carpal tunnel in both motor and sensory axons. Mild (motor) to moderate (sensory( slowing was present through the right carpal tunnel. Normal ulnar sensory action potentials were present bilaterally.

jeremydpbland
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If I am interpreting which number is which correctly those show grade 3 left and grade 1 right CTS - on my scale from 1(mildest) to 6 (worst), you might push the right side to grade 2 depending on the local normal values for that lab which are not given. The really key figure is the distal motor latency to APB which I take to be 6.1 msec on the left and 4.4 msec on the right.

From grade 3 you would expect rapid resolution of symptoms after surgery and more or less complete recovery as long as you escape the complications of cutting the ligament, so that side is going according to plan.

With grade 1 changes it is sometimes hard to be sure that the abnormality you are finding on NCS is actually anything to do with the symptoms and a significant number of people with grade 1 do poorly with surgery, probably in at least some cases because CTS was not really the main problem. Our preference is to try grade 1 with splints and steroids first and to be very wary of surgery on patients who show no symptomatic response to steroids. The comment on involvement of the median palmar branch territory is interesting though they did not say which side they were talking about. Anatomically CTS should in theory spare the palmar branch so I would keep an open mind about whether the problem was CTS on the right, though if it felt the same subjectively as the left that is pretty strong evidence. It's also slightly unusual for this to be worse in the left hand unless you are left handed or there is some specific reason for it like an old wrist fracture.

If the right hand problems do persist then repeating the NCS and ultrasound imaging between 6-12 weeks post surgery may throw some light upon it but is not guaranteed to I'm afraid. The palmar cutaneous branch can be imaged as it leaves the median nerve and usually as far as the heel of the hand over the transverse carpal ligament but gets a bit difficult after that. An American colleague has published a paper describing imaging of the recurrent motor branch too but I have had little success with this myself so far. If there has been damage to that branch it should be evident from needle EMG however. That's about as far as I can speculate at this stage. JB

Clint
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My grateful thanks once again for your reply. I will bear your helpful comments in mind and simultaneously hope that with the passage of time the incremental improvement continues.

Clint
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Dear Dr Bland,
By way of up-date.
Now 2/12 since bilateral CT surgery. Bilaterally, healing good and hand function/grip strength good. Some weakness in (L) AbdPB (worst NCS side). (R) seems fair, consistent with pre-surg NCS. Absence of nocturnal paraesthesia relieved by dropping the hands over the edge of the bed is the chief and solitary bilateral improvement post-surgery.

However ...

Intermittent (R) volar forearm pain and accompanying medial arm ache continue though less acutely. These were was truly frightful for 3/52 after surgery! (as mentioned previously). (L) side numbness in thumb and thenar region and to lesser extent 2/3/4 has grown since surgery. All are > by activity and < by rest or by straightening the upper extremities.

These symptoms and a careful rethink about the history suggests an additional site of compression of the median n. at the elbow (bicipital aponeurosis appears possible because of notable > Sx with resisted supination in flexion or simply with sustained flexion and pronation, which engenders a bilateral neuralgic pain at the elbow that radiates distally and proximally from the elbow in the course of the median n. ie specifically, playing piano and and computer mouse use for example, or cutting and peeling fruit).

Not all of these Sx were so obvious pre CT-surgery. The bilateral median n. pain with resisted forearm supination is a very longstanding observation. I can now just tolerate the persistent discomfort in the forearms when I use a gym cross-trainer for a long period of time. However, after prolonged use, nocturnal paraesthesia in the hands (median n. distribution) with profound thumb and thenar numbness is obvious and troublesome and cannot be relieved in any position except standing with arms by the side, so I usually rise and that helps.

On reflection, I anticipated that post-surgery I would be able to maintain a growing level activity on a gym cross-trainer (wrists neutral and low use forearm) generally free of discomfort. I am quite used to an hour or more of intense activity (and the median n. hand numbness that always accompanies this). It maintains fitness well and spares an OA hip.

Post-surgery I found that I could only manage about three minutes before bilateral severe volar forearm pain between the wrist and the elbow precluded any further activity. Presently, this still occurs though less profoundly and is accompanied by bilateral pins & needles and growing intense numbness in the hands of median n. distribution though profoundly so in the thumbs and and thenar region

My question:
In your substantive and substantial experience, could release of a restricted or entrapped median n. significantly aggravate a concurrent median n. restriction at the elbow?

From a mechanical perspective I believe it appears to make reasonable sense. The release of a distal tether might increase the theoretical load on a proximal tether by reducing strain and increasing stress at that point.

I well understand that decompression of the distal CT may serve to reveal concurrent symptoms of entrapment at the elbow. I will see the surgeon again next week and will bring this more coherent symptom picture and history to his attention. I only hope he doesn't think I'm developing either hypochondriasis or Munchausen's syndrome!

This has been and continues to be a euphemistically 'interesting' and salutary experience!

With thanks for your generosity,
Clint.

PS. Is there anything I can do by way of recompense for your time and expertise?

jeremydpbland
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I've met a few patients whose surgeons, having failed to fix the problem with median nerve decompression at the wrist, have then gone on to look for and operate on a pronator syndrome. My impressions of the success rate are probably biassed by the fact that such patients are more likely to be referred to me if they still have a problem afterwards. The situation is not helped by the fact that pronator syndrome is not easy to detect neurophysiologically. The median nerve in that region is just about at its deepest point in the forearm and it is very difficult indeed to carry out short segment conduction studies on a deep nerve so unless the lesion is bad enough to produce denervation in the forearm flexors there may be no abnormality, and even then this has to be differentiated from radiculopathy so neurophysiologically it is a difficult challenge. Ultrasound imaging shows more promise but as this is a quite a rare syndrome experience is limited so far - personally I have yet to see a convincing case.

Whether carpal tunnel release could actually aggravate a more proximal median nerve lesion is an interesting thought. Freeing the nerve at the wrist should make it more mobile at that point and thus reduce stresses from tethering at other sites. On the other hand, increasing the overall mobility of the nerve might increase the sliding movement at another site perhaps. Alternatively the inflammatory response to surgery itself may spread throughout the limb and have remote effects to aggravate an existing problem elsewhere - all very speculative and hard to experiment with given the rarity of more proximal entrapment compared to CTS.

I think there would be good grounds for a careful ultrasound examination of the whole length of the median nerve in your case - but finding someone competent to do that can be difficult I'm afraid.

Regarding the PS - one previous correspondent kindly made a donation to the Kent and Canterbury Hospital League of friends which was much appreciated. There is a link from the 'about carpal-tunnel.net' page. Personally I try to keep the site completely free of financial bias so far as possible.. JB

Clint
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Thank you once again Dr Bland. I will gently pursue the imaging approach (and keep you posted).

Purely as an aside, have you encountered this interesting study?
Incidence rates and determinants in meralgia paresthetica in general practice.
van Slobbe, A.M., Bohnen, A.M., Bernsen, R.M.D. et al. J Neurol (2004) 251: 294. doi:10.1007/s00415-004-0310-x
http://link.springer.com/article/10.1007/s00415-004-0310-x

I mention this because I have bilateral meralgia paraesthetica (MP), which I became aware of in my mid-teens and which now, several decades later has led to complete obliteration of any sensation in the anticipated territory. Never a cause for personal concern merely one of interest, my father also has this but to a lesser degree. The study reported an OR of MP with CTS that is quite striking, although unfortunately the CI is large enough to accommodate a coach and horses (!)/

I speculate whether one day a genotype may be described for a potential for 'tight spaces', or at least linking the various morphological mechanical predispositions (course of nerve in relation to ligament; ligamentous morphology) into a broader anatomical coherence? Who knows.

Thank you kindly once again.
Clint.

jeremydpbland
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The well known inherited disease HLPP, due to a deletion of the PMP22 gene on chromosome 17 (Peripheral Myelin Protein) results in a predisposition to compression palsies. CTS, Ulnar neuropathy and foot drop due to compresion of the peroneal (fibular) nerve are the commonest manifestations but these people are likely to get MP too. Several studies have screened people with more than one peripheral nerve entrapment for HLPP but generally have not found lots of cases so it is likely that that there is also a polygenic predisposition to nerve compression - certainly CTS is strongly genetically determined, with the St Thomas's twin study concluding that it is about 50% genetic in origin, at least in women. JB

Clint
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Good day Dr Bland,

Thank you once again for your previous reply.

I undertook bilateral sonographic imaging of the forearms. Bearing in mind I am now some 10/52 since bilateral CT release surgery, sensory symptoms remain worse than prior to surgery with the exception of an absence of the nocturnal paraesthesia that unfailingly disturbed my sleep. I concede that there might be some quite subtle improvement only.

The imaging report as follows:

Right: There is a waisting (relative thinning) of the Median nerve in the palm with thickening of the
nerve distal and proximal to this.
Left: There is waisting (relative thinning) of the Median nerve in the palm with thickening seen distal
and proximal to this. The Median nerve shows signs of oedema into the mid-forearm. There is
hypoechoic area seen adjacent to the Median nerve in the palmar region may represent granulation/
scar tissue.
The Radial and Ulna nerves appear normal.
Overall Conclusion:
Relative waisting of median nerve in region of carpal tunnel bilaterally with thickening proximal and
distal to this particularly on the left with possible scar tissue adjacent to nerve on left . No extrinsic or
intrinsic compression seen.

My question: Is full sensory recovery likely in your experience? What period of time seems a fair estimation for potential recovery?
Even if I returned to pre-surgical state I think I might be far happier than at present (excluding the noctural symptoms of course), though accept that my judgement is hopelessly impaired in this regard.
Surgeon has refused NCS considering it pointless presently and also considered sonography a waste of time, necessitating that I undertook the latter by self-referral.

I am moderately 'happy' to sit tight for 5 -6 months post-surgery to see how things unfold.

Thank you sincerely you as ever.
Clint.

PS. Sonographic images themselves are available.

jeremydpbland
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Typical surgeon I guess. The ultrasound imaging seems to have been confined to the wrist where, by the sound of it, it shows the typical morphology of carpal tunnel syndrome (which does not necessarily return to normal after surgery). A comment on the division of the transverse carpal ligament would have been helpful. I'm happy to look at any stored images but u/s is a very interactive process and it is rarely possibly to re-report a few still pictures in situations like this. Did they not explore the possibility of a lesion at pronator? Repeat NCS for comparison with the earlier studies would be automatic in my clinic at this point - what more can I say. One of the annoyances of running this forum is that cases come along where I itch to get my hands on the patient so that I can see the problem myself but it is of course impossible. In the absence of further intervention/investigation then I would review the situation again 6m after surgery and if there was no progress then press once again for further investigation. JB

Clint
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Thank you once again Dr Bland. I queried the radiologist further and he was able to add to the report I quoted previously,

"The transverse ligament was visible distal to the decompression site when I scanned and at the site of decompression it appeared ill defined which is what I would expect post op."

As regards the pronator, the sonographer had me pronate/supinator my forearm (elbow flexed at approx 120deg, no resistance) and pronounced that she identified no problem.

I'll press-on and hope that the 6/12 mark is more compelling. If not, I'll do as you suggest.

Thank you again.

jeremydpbland
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The thing to look for specifically at the wrist is usually whether the incision in the transverse carpal ligament extends far enough proximally. When it does not go far enough you can often see a quite sharply defined 'notch' indenting the nerve. I tend to think of this as a 'cheeswire' effect of the undivided sliver of ligament cutting into the nerve, but given the way your symptoms changed I think incomplete section of the ligament is relatively unlikely. "Ill defined" is a fair description of what the actual operation site usually looks like. It tends to be irregularly hypoechoic where the cut has been made. At least they tried to look for pronator - but this is very difficult I think. At some point I'll have to put some example post-operative images in the ultrasound section of the site I think - too many things to do! JB

Tudorsurgeon
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I cannot resist commenting........................

The OP does not give his age. This is significant as the older the patient, the longer the recovery. any other co-morbidities such as Diabetes?

He has had CTS for 10 years and its severe on nerve tests. It will take months to recover and may not return to normal

If the operator had to dissect through a lot of thenar muscle then was the incision too medial? If one has to dissect through muscle then the motor branch is at risk. Moreover, was the surgeon a Hand Surgeon or a GPSI?

If the incision does not cross the wrist crease then certainly its possible for the decompression to be "inadequate" proximally.

I would get repeat nerve tests at 3 months. If no significant improvement, then re-explore under a GA

jeremydpbland
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Nice to have a surgeon's (I presume) comments too. Age and diabetes do impair recovery a little but the effect is not very strong in our multivariate prognostic model so although they are worth bearing in mind I would be careful about blaming a poor outcome whcih could be due to something else on a factor like diabetes.

It wasn't really that severe on NCS - grade 3/6 on one side and either grade 1 or 2 (depending on the lab's normal values - which we do not know) on the other. Up to grade 3 recovery is usually pretty quick if the diagnosis is right and nothing has gone wrong.

I agree about dissecting through a lot of muscle. On ultrasound imaging you can almost always find a point where the ligament is entirely fibrous but I have seen one or two where the thenar and hypothenar muscles meet or overlap. I believe this case is in the USA - not sure whether they have GPSI practitioners - doubtless Clint will tell us.

I'm also glad to see someone agree with me about the NCS, though I reckon one can go as early as 6 weeks if the patient says symptoms are actually worse after surgery, as they often are with incomplete decompression. Most of the incomplete sections I have seen have been proximal rather than distal.

Thanks for commenting. JB

Clint
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If I might ...

dob. 1960. No laboratory or clinical indication of DM. Normal LFT's, thyroid, renal and cardiac indicies. NCS did not indicate any other finding beyond CTS. Axonal degeneration (L) and complete sensory block (R) were reported (see above). At the time of presentation the significant bilateral clinical obs. were:
1. thenar atrophy; 2. palmar trophic change; nocturnal paraesthesia. No clinical sign reliably indicated CTS eg. Phalen / modified Phalen and Tinel were equivocal.

Surgery was conducted nearly 4/12 ago. As a clinician and clinical anatomist I had already 'sensitized' the senior and experienced orthopod (FRACS in NZ) to the concern I had regarding incomplete division. At open surgery under local without sedation, he was keen to and actively demonstrated full division proximally and distally. Subsequent to surgery I reported novel anaesthesia of the substantive portion of the (R) thenar eminence and lateral aspect of the thumb. Presently, this remains largely unchanged. Distressing nerve pain in the (R) forearm developed after syurgery, then largely settled. At times it reminds me of its presence at perhaps 20% of the initial level. I believe it emanates from the region of the carpal tunnel and numb thenar region, though little reproduces it save odd grip/traction movements. On the (L), dysthesias and hypoesthesia abound throughout median distribution, but most unpleasantly pronounced over the thumb and lateral aspect of the 4th finger, medial aspect of the 3rd. On the (R) spontaneous pain in and around the site of the incision and referred pain to the elbow occur intermittently. Bow-stringing is present chiefly on the (L), though this has diminished somewhat.

Sonographic imagining 2/12 after surgery confirmed that the median nerve appeared bilaterally free of entrapment. However, as mentioned previously, nerve enlargement distal and proximal to the site of entrapment was seen, along with significant enlargement, endoneurial odema and scar tissue. This was more extensive on the (L) side, extending proximally a third of the way up the forearm. The (R) appeared less severe. I will repeat the sonographic imaging again in another month to evaluate change over the preceding 2/12.

Formal surgeon prognosis has ranged from being absent to a moveable feast. Presently, the surgeon has suggested a further 6 - 8 months. I have trawled the literature with very limited predictive enlightenment, in the end finding it more illuminating to pursue the subject on the basis of peripheral nerve damage (Menorca et al. 2013. Hand Clin 29(3): 317 - 330. doi:10.1016/j.hcl.2013.04.002 together with the neural obs from sonographic imaging.

So, at 4/12 elapsed since surgery I remain subjectively, considerably worse. Intellectually, I appreciate the value of the division, which has yielded the solitary benefit of diminished nocturnal paraesthesia and the ability to use the hands during the day without aggravating the noctural paraesthesia.

On occasion the (L) hand wakes me when there is persisting lightest pressure of any sort on the palmar aspect (eg. hand resting on mattress). Subtle improvement has occurred with the (L) index finger feeling a mild sense of warmth. The dysthesias are also no longer quite so vicious, though they wax and wane without obvious precipitation and remain somewhat distressing. Grip strength (barring the post-op healing phase) was never a subjective issue. This remains the case. Free body chin-ups on a bar present no difficulty. Subjectively, symptoms are constrained to pure sensory disturbance - something no one appears to have been able to explain adequately to date. In addition, the entire region of the median distribution (L) from the lower third of the volar forearm demonstrates a markedly positive Tinel sign with the lightest of finger percussion, not present on the (R), with the exception of the lateral border of the thumb.

I conjecture that the (L) side is recovering very slowly. It is impossible to predict the extent to which this will occur and anchor this to a time frame. The right side, I just don't know. I speculate a neuropraxic injury to the palmar branch maybe associated with incision retraction or pressure induced ischaemia. In so far as this branch was sonographically imaged, it appeared intact, at least in its proximal branching region.

As an anatomist I am troubled somewhat by relatively unknown extent to which detailed individual variation remains unaccounted for. I would advance the idea (seemingly quite well supported in the literature) that aside from routine NCS prior to CTS release, sonographic imaging is also routinely undertaken to establish a guide to individual neural morphology and condition.

Finally, the GPSI scheme is present in NZ.

Thank you for getting this far!
Clint.

jeremydpbland
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I see I was wrong about the USA - good to have a contribution from NZ - one of the very early postings on the site here came from NZ and was particularly interesting.

Overall I think it does sound as though a complete decompression was achived but in the right hand I think your theory of trauma to the palmar cutaneous branch is plausible, and is a well known risk of carpal tunnel surgery. It's not usually possible to see it on ultrasound much beyond the wrist crease.

A lot of the left hand symptoms sound like nerve hyperexcitability which can be seen while nerve function is improving and which can also, if you are unlucky, be permanent and might require pain clinic management.

In both hands there is probably little one can do except sit tight and wait at this stage, though I would still find it reassuring if the NCS were improving. It might be interesting to experiment and see if something like gabapentin made any obvious difference to the left hand symptoms.

Sonography before surgery is a good idea I think and I try to image as many of the people I am sending for surgery as possible but we are still fighting to get surgeons to accept that NCS before surgery should be routine so giving them another test to think about is probably pushing it a bit at present. JB

Clint
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My thanks once again, Dr Bland. You have been an extraordinarily valuable touchstone through this surprising and unpleasant experience. Your site is an utterly superb resource.

I've been cautious about exploring the effects of a GABA analogue, noting their widespread off-label use for pain and peripheral neuropathy. I take your point well, but have been reluctant to potentially add to the list of woes with which I am coping adequately. Were I not coping, then it may be different.
In the meantime, fingers and toes both fused in cruciform position, and if I sat any tighter I would run the risk of requiring a chairectomy.
Thank you again.

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