Aug. 23, 2024
A Guide to Carpal Tunnel and Other Nerve Conditions
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Ever wondered how to distinguish between peripheral and central nervous system disorders, or what red flag symptoms necessitate urgent medical attention? This episode offers critical insights as Dr Gavin Nimon ( Orthopaedic Surgeon and Host) interviews Dr. Jessica Hafner, a Consultant Neurologist at the Queen Elizabeth Hospital, as she unpacks the complexities of peripheral neuropathy. From common causes like carpal tunnel syndrome and diabetic neuropathy to the nuances of symptom patterns and tempos, Dr. Hafner provides valuable guidance for medical professionals aiming for precise diagnoses and effective management of these conditions.
Explore the world of autoimmune neuropathies, including conditions like Parsonage-Turner syndrome and Guillain-Barre syndrome, which are triggered by immune responses and cause severe pain and motor weakness. Dr. Hafner elucidates the importance of nerve conduction studies for accurate diagnosis, explaining how such tests differentiate between various neuropathies. The episode also covers a broad spectrum of peripheral neuropathy causes, such as diabetes, B12 deficiency, thyroid dysfunction, and alcohol excess, emphasizing the significance of understanding these diverse etiologies.
Finally, get equipped with practical strategies for evaluating and treating nerve entrapments and generalized neuropathies. Learn about the intricacies of diagnosing carpal tunnel syndrome, the utility of clinical tests like Tinel's and Phalen's, and the effectiveness of different treatment methods, including surgical options. Dr. Hafner delves into the multifaceted causes and treatments of generalized neuropathies, discussing the role of chronic conditions, medication side effects, and the necessity of thorough evaluations. This comprehensive discussion is a must-listen for anyone involved in the care of patients with peripheral nerve disorders.
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Have you ever wondered what causes that tingling sensation in your hands or feet, or why some patients struggle with unexplained numbness and pain?
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Peripheral neuropathy is a complex and often misunderstood condition that affects millions of people worldwide.
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In today's episode, we're diving deep into this intricate topic with Dr Jessica Hafner, a neurologist from the Queen Elizabeth Hospital.
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Whether you're a medical student, a seasoned practitioner or someone just curious about the human nervous system, this episode promises to unravel the mysteries of peripheral neuropathy and offer practical insights into diagnosis and management.
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G'day and welcome to Aussie Med Ed, the Australian medical education podcast designed with a pragmatic approach to medical conditions by interviewing specialists in the medical field.
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I'm Gavin Nimon, an orthopaedic surgeon based in Adelaide, and I'm broadcasting from Kaurna land.
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I'd like to remind you that this podcast is available on all podcast players and is also available as a video version on YouTube.
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I'd also like to remind you that, if you enjoy this podcast, please subscribe or leave a review or give us a thumbs up, as I really appreciate the support and it helps the channel grow.
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I'd like to start the podcast by acknowledging the traditional owners of the land on which this podcast is produced.
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Acknowledging the traditional owners of the land on which this podcast is produced, the Kaurna people and pay my respects to the elders, both past, present and emerging.
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Well, it's my pleasure now to introduce Jessica Hafner, a consultant neurologist from the Queen Elizabeth Hospital, working in the public sector.
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She describes herself as someone who's got a strong passion in medical education and teaching.
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She's also Director of Basic Physician Training and she's going to talk to us about neurology and peripheral nerve disorders in general.
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Welcome, jessica.
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Thank you very much for coming on.
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Aussie Med, ed.
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It's great to have you here.
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Thank you.
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Thanks for the invitation.
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Well, peripheral nerve disorders are something I see regularly as an upper limb orthopedic surgeon, but obviously it's more than just a carpal tunnel that can cause peripheral nerve reduction sensation in the hands.
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It's quite a huge area.
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I thought I'd like to ask you about how you consider peripheral nerve disorders when you're actually working someone up.
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What is the thoughts that go through your head when you're assessing them?
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Yeah.
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So I think probably the first question is really around looking at what the pattern of it is, and that's going to be the thing that tells us how worried we need to be about this sensory change and obviously to go even one step back.
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Obviously sensory and motor changes can come not just from the peripheral nervous system but also the central nervous system, and so really when we see a patient who's had sensory and or motor symptoms, that's our first thought as a neurologist is where is the lesion?
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And the trick there is really at looking at the pattern and understanding enough about our neuroanatomy to be able to tell what part of that neural axis is going to be involved.
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So for peripheral nerve disorders, the few main patterns that we see, the most common would be things such as carpal tunnel, where we're just getting symptoms very local in the hands, usually coming on at night time, tingling, waking people up we all know the sort of plastic syndrome but then also tingling in both of the feet would be probably the other really common way that peripheral nerve disorders presents and that sort of symmetrical pattern starting in the feet, because they're the longest nerves and the longest nerves are the ones that are the most vulnerable to the really common things that cause peripheral neuropathy, such as diabetes.
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And so that's my first question really is where are the symptoms?
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Is it just in one side, both sides, starting in the feet, starting in the hands, or is it all of them, hands and feet?
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And then also making sure that when I do an examination I'm really confirming that the signs fit, with the problem being in the peripheral nervous system and not something more centrally.
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So making sure that we don't have any outgoing plantar responses or increased tone or hyperreflexia or anything that makes us think we might be dealing with like a spinal cord issue and bowel and bladder dysfunction.
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That sort of thing would be another thing to really screen for.
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If you've got particularly bilateral leg symptom and then in terms of also the other thing that would be a clue to a central nervous system disorder would be symptoms like down just one side of the body, so an arm and a leg on one side, or the face involved as well.
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Really, then you're thinking about, you know, could be a stroke, or something else in the brain and then I guess, once you've worked out where the problem is and you've confirmed that it's a peripheral nerve problem by looking for, you know, loss of reflexes and loss of sensation, what's the pattern?
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Is this something that's symmetrical on both sides and sort of just coming up the legs, or is it something that's just affecting a particular nerve root or a particular peripheral nerve, and that'll help us really narrow down where the lesion is?
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And then also the tempo of the problem.
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And that's the other thing we really need to pay attention to, because things that come on very slowly and insidiously.
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We've got time to work it out, we can think through it, we can do some tests and sort of really get a picture before we need to worry.
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If something's come on very quickly and there's red flag symptoms, then we might need to move much faster and think much more quickly.
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In terms of red flag symptoms for peripheral nerve disorders, the things that really make us sort of sit up and listen is if it's rapidly progressive.
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So sensation, that sort of oh, I had a tingle in my toes yesterday, but now it's up to my shins and I'm starting to feel like I'm having trouble standing up out of a chair.
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We really need to move quickly.
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We're thinking is this Guillain-Barre, is this spinal cord compression?
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That's the kind of situation that you might need to send someone straight to the emergency.
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Other things that are red flags is asymmetrical symptoms.
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So I've got sort of really severe symptoms in sort of one arm, but not in the other arm.
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You're sort of thinking there's something going on.
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It's not just your average neuropathy.
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Lots of motor involvement early.
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So somebody who's getting lots of it looks like a peripheral neuropathy, but it seems to be just affecting the motor nerves and not really the sensory nerves.
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You start to think is this motor neuron disease or amyotrophic lateral sclerosis?
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And then then also, if it's very painful so someone who develops a foot drop and it's very painful, or a wrist drop and it's very painful then we worry is this vasculitis?
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And that can obviously can be a medical emergency as well.
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And then early autonomic involvement.
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So peripheral neuropathy.
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And suddenly they've also got really bad postural hypotension or something as well as tingling in their toes, a bit of a red flag, could be amyloidosis, could be perineum plastic.
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And then the other thing is someone who's very systemically unwell.
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So as well as having neuropathic symptoms, they've also got night sweats and weight loss and all of those other things that would make us sit up and listen in any circumstance.
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So they're the sorts of things that I'm assessing when I first see somebody with sensory and motor symptoms Where's the lesion and how fast is it moving, and are there any red flag features?
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And it sounds like a lot of them are more central type conditions rather than peripheral type conditions.
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They're really about red flag peripheral nerve disorders.
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So vasculitis affecting the peripheral nerve and motor neuron disease is border zone.
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It's obviously affecting the anterior horn cells which are in the spinal cord and that's the point between the peripheral and the central nervous system and that is why you get a mixture of signs in that condition and then things that give rapidly progressive things.
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I did mention spinal cord, obviously as an emergency, but Guillain-Barre disorder is an inflammation of the peripheral nerve can be a medical emergency as well.
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Are there any central conditions themselves that we need to be watching out for that also have red flags too, then.
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Yes, so similar.
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In things that are rapidly progressive and people have rapidly acquired disability.
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We always have to think carefully, and central things could do that as well.
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So things that come on over sort of seconds to minutes we're thinking about strokes particularly Things that come on over sort of hours to days, particularly if the distribution is suggestive of a central location, so affecting one side of the body or being characterized by ataxia or involving the cranial nerves, double visions, word speech.
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Think about things like demyelination of the central nervous system, so that's multiple sclerosis as opposed to demyelination of the peripheral nerves, which is more Guillain-Barre.
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And then also thinking about other things coming on over sort of weeks to months, Obviously worry about things like brain tumours or space-occupying lesions, people that are getting evolving neurological symptoms over slightly longer periods of time.
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Right, Okay.
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So a question that comes to mind when you're talking about those conditions with Guillain-Barre parsing-neutrality syndrome, where you get peripheral neuropathy secondary to a viral-type causation how does that vary compared to Guillain-Barre, which I thought there was some sort of viral etiology for it or some sort of autoimmune disorder?
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That's a really good question, gavin.
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So both of those conditions are inflammatory.
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So the thing that's causing the problem in the nerves is inflammation and it's being driven actually by the immune system rather than infection.
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So it's an autoimmune type inflammation.
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Parsnage-turner, which we also sometimes call brachial neuritis, is inflammation affecting the brachial plexus and it can be triggered by things such as vaccination or a viral illness.
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But it's not an infection actually causing it.
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It's more the immune response to that insult that then sort of seems to aberrantly attack the nerves in the plexus and cause problems.
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Classically that will present with very severe pain.
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People often end up presenting to emergency services and requiring opiates.
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It's very severe neuropathic pain and then followed up sort of days afterwards by a development of motor weakness.
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Similarly, guillain-barre is also an autoimmune inflammatory condition which is often occurring in the setting of some sort of immune stimulation.
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So it can occur, you know, of some sort of immune stimulation, so it can occur several weeks after a viral infection.
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We do see cases of Guillain-Barre which seems to be linked to having had vaccinations or by other stressors such as surgery.
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Classically in medical school we all learned about Guillain-Barre being triggered by a campylobacter jejuni, and that certainly can be the case or it can actually just occur without any obvious driving factor.
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But both of those conditions are similar in that they are sort of a dysregulation of the immune system causing peripheral nerve damage, one in the brachial plexus and the other sort of more generally, particularly approximately the lumbosacral roots and the plexus and the nerves all being affected in Guillain-Barre.
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Right.
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Obviously, there's such a huge list of causes that can cause tingling and numbness in the hands or in the limbs as well, and weakness in general.
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How do you go about really nutting it down to what actual condition is?
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Yeah, so that's a really good question.
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So I think when you're faced with this person who's presented with sensory symptom and you've done your history and exam and you've worked out that you think it's a peripheral nerve problem and either it's affecting just one nerve or it's affecting sort of all the nerves and particularly the feet, then that helps to focus your investigations.
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So for the most common generalized peripheral neuropathy picture, which would be that sort of, you know, tingling in the feet but sort of slowly spreading up the legs, there are some common and potentially treatable causes of that that are often screened for in the community by general practitioners before patients are referred for non-GP specialist care, and that would include diabetes, followed by diabetes diabetes and then next after that is diabetes Very, very common cause of this problem in the community.
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Other things that are really valuable to check for is B12 deficiency and that can cause various neurological presentations but can cause a peripheral neuropathy.
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Also, thyroid dysfunction both under and overactive thyroid can be attributed to this.
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And the other thing that often actually gets missed in the community is alcohol excess, and excess alcohol consumption is probably one of the more common causes I see for people who have an insidious, slowly progressive neuropathy for which all the other blood tests haven't really shown a cause.
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And then you spot the elevated GGT and ask the right question and it turns out to be related to alcohol.
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So that's the first thing, and then I think the other thing in terms of initial investigations is really some nerve conduction studies, because one of the things that's quite tricky is that there's not really any reliable clinical clues on examination that help you differentiate between a peripheral neuropathy that's due to a sort of a metabolic situation such as diabetes, versus an inflammatory neuropathy where the immune system is actually driving the damage and something that can present Guillain-Barre usually presents more acutely and so that makes it clearer.
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But there is another variant of that which is quite similar, which is called chronic inflammatory demyelinating polyneuropathy, or CIDP, and that presents quite insidiously and slowly and can really clinically look very much like a more sort of common neuropathy.
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And the main way to differentiate those things is with a nerve conduction study.
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So I think anyone who has peripheral nerve symptoms that are disabling enough for them to be presenting to the GP probably does deserve at least a one-off nerve conduction study, just to make sure we're not missing one of those conditions that needs a very different treatment approach.
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Well, now's probably a good time to explain what actually is involved in the nerve conduction studies and when you actually do nerve conduction studies versus an EMG study as well, which I think is slightly different, isn't it?
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Yeah, so they're often done together and it would be very unusual to do an EMG without doing a nerve conduction study.
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But certainly people do do nerve conduction studies without needing to do an EMG and nerve conduction study.
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But certainly people do do nerve conduction studies without needing to do an EMG and these are also a great first-line investigation for something like carpal tunnel, and usually with carpal tunnel you wouldn't necessarily need to go checking for B12 deficiencies et cetera, but you might just go straight to nerve conduction to try and confirm the diagnosis.
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So when we do a nerve conduction study, usually there's a brief history and clinical examination before we start the test, make sure we're testing the right thing, and then what we do is apply small recording electrodes over either the nerve or the muscle and then use a probe to stimulate the nerve by delivering a small electrical pulse and then recording, using the little electrodes we've stuck on the skin, how quickly that impulse travels through the nerve and how large the response is that we're able to record and using that information we're able to get a clue about how well the nerves are conducting electrical impulses and whether the problem is due to the axons themselves not working well or whether there might be the axons intact, but there's a problem with the myelin surrounding the axons, causing slowing or block of the messages going through those nerves.
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So that's the main thing, and the important thing with doing a nerve conduction study is doing the right study.
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So if someone comes with classical carpal tunnel symptoms and I do a study that's really focusing on their ulnar nerve, I'm not going to get the information I need to make the diagnosis.
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So that's why it's important we do a histrion exam before we start and we've got good information on our referral so we know exactly what we're looking for, because we can't do all the nerves for everybody.
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We would be there all week, yeah.
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Can you explain what some of the numbers mean, though on it.
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Yeah.
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So there's a lot of numbers come out, and when you get your nerve conduction study report I'm sure you've received these Gavin where you get this black bit chart with all these numbers in it and very little explanation as to what to make of it all.
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Hopefully there's a good summary at the end.
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But usually we'll do either sensory nerves or motor nerves.
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There are some situations where we record over what we call mixed nerve, where the fibres in that nerve are transmitting both sensory and motor messages.
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But in simple terms, the sensory nerves we're recording over the nerve and stimulating over the nerve, and so what we're recording is very, very small in microvolts, and so it can be quite technical in terms of getting a good response.
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The amplitude is a sort of a surrogate marker for the number of axons that are able to transmit messages.
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So in somebody who has an axonal neuropathy so a neuropathy that is due to loss of axons the amplitude will be smaller because there are less axons translating that message, and so you're getting less of the signal arriving at your endpoint.
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With a motor nerve, we're recording actually over the muscles, so the size of the thing we're recording is actually dependent on the number of muscle fibers that are firing off.
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So that can be small if we've got axon loss, because less axons means less message getting to the muscle and less muscle firing.
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But it can also be small in other conditions, such as if somebody had a severe myopathy and had lost muscle fibers due to that.
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You would also get small amplitudes on your motor studies.
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The velocity I think you've mentioned sort of makes sense.
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It's talking about the speed with which the message is transmitted through the nerves.
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And then there are some other words which kind of sound a little bit more complicated but are simply markers of the same thing.
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So you might see mention of things like distal motor latency or distal sensory latency.
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And the reason we call it that rather than a velocity is that a latency is a time measurement, so it's the time between when the stimulus was sent and when the message was received.
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And the reason that we need to do that with motor studies is that because we're stimulating over the nerve but recording over the muscle, it's not just the message traveling through the nerve that we're measuring.
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We're measuring the signal going through the nerve, through the neuromuscular junction and then through the muscle fibers to our recording electrode.
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And so if we calculated a velocity on that.
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That would be sort of odd, because the speed with which the impulse travels through the nerve, the junction and the muscle is all variable.
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So you'd get this kind of average and it wouldn't really be truly meaningful.
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So we use latency instead, because that's what we are able to measure.
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We're not really able to measure the velocity.
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So that's only when you're measuring motors, is it?
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Yeah, it's only when you're measuring motors.
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People do report digital sensory latencies and all that means is that they haven't converted it to a velocity.
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But if they had taken a distance measurement, they would be able to use the latency to calculate a velocity.
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Right, yeah.
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And what about fibrillation and things like that on the muscle fibers as well?
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Because that's also a sign of something going on as well, isn't it?
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Yeah, so that's in the EMG, so I'll talk a little bit about that as well.
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So you mentioned about having EMG as well as nerve conduction.
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So what I've described so far is really what we call nerve conduction, and then in certain situations it's helpful to also perform a needle EMG.
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And what we're doing in that test is using a small needle that's got a recording electrode in the tip of it and we insert that needle into the muscle and then record the electrical activity that is within the muscle itself.
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So due to the muscle fibers contracting, and so we don't give any stimulation with that, we just sit and listen and we record both while the person is relaxing their muscle as best they can sometimes a bit harder than other times and then also getting them to activate the muscle, and looking at the muscle fibers firing off, and by analyzing that and it's something that's sort of analyzed live by an expert who's been trained in it we're able to get all sorts of information.
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So fibrillations and positive sharp waves are two words for essentially the same thing, and they are generated when small individual muscle fibers have lost their axonal connection and they just sort of fire off on their own, sort of like a kind of like a pacemaker kind of effect if you like.
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The little muscle fiber just fires off on its own when it's lost that input from an axon.
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So if we see that in muscles, that gives us a clue that there's some denervation that's occurred.
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And there's all sorts of timeframes in which if a denervation occurred five minutes ago you might not see fibrillation.
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So that's why we often say send the patient back in six weeks, because then we'll be able to see the fibrillation potentials and it's often a marker of it being a reasonably active or acute process.
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However, that nothing in medicine and certainly nothing in neurology is cut and dry and there are people who have fibrillations present in their muscles for very long periods of time after the insult.
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But it's thought to be primarily a marker of active or acute denervation.
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And then we also can assess the muscle fibers when the patient is trying to activate their muscle.
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We can get information about whether or not the muscle has good axonal inputs or whether there's good messages coming in from the nerve and then also whether the muscle fibers themselves are healthy.
00:21:18.411 --> 00:21:53.226
So in myopathies we also can get abnormalities in the EMG with seeing very small muscle fibers to the motor units, which is the group of muscle fibers that are all talking to the one axon get much smaller and many more of them need to fire off to generate the same amount of muscle strength, whereas in a nerve problem, particularly a chronic nerve problem, where the axon has sprouted and tried to re-innovate the muscle, you can get these very big motor units that fire off very, very quickly and have to work very hard to try and generate force.
00:21:53.226 --> 00:22:05.231
So there's all sorts of things we look at and you get words like recruitment and polyphasia and all that sort of stuff, but it's all just the description of what the motor units look like and that should be.
00:22:05.231 --> 00:22:24.976
Hopefully, when you get those reports synthesized for you and we can come up with things about whether there's active or acute or chronic denervation, re-innovation indicating a nerve process, a neurogenic process, or whether there's features suggesting a primary muscle problem, a myopathic process.
00:22:26.070 --> 00:22:44.001
That EMG actually is really interesting because if you're listening to the muscle tone and you've worked out what different waves represent different conditions, then obviously with this new AI era, being able to analyze all those different measurements with AI, must be able to sort of fine-tune these results even more so I would have thought.
00:22:44.549 --> 00:22:47.494
Yeah, it's definitely an area that there's lots of interest in.
00:22:47.494 --> 00:23:07.855
For some time there's been a sort of computer-assisted interpretation of EMG, which is not used that commonly, but so-called quantitative EMG, where they measure a lot of the parameters of these muscle fibers and try to get sort of more nuanced data than can come from the live human interpretation.
00:23:07.855 --> 00:23:19.800
But yeah, I certainly think that and EEG are the two kind of leading places where AI applications I think are going to be very interesting to watch in the next decade or so in neurology.
00:23:19.800 --> 00:23:21.005
Yeah, Right.
00:23:21.586 --> 00:23:26.431
So in working these patients up, we've taken a good history and we've sorted out the sort of patterns they're representing.
00:23:26.431 --> 00:23:35.458
A couple of blood tests that came to my mind as well were things like VDRL for syphilis, and also I know there's a condition of hypersensitivity to pressure on nerves.
00:23:35.458 --> 00:23:40.881
Is that a blood test that's also done as well as a screen, or is that an expensive test that's too hard to do routinely?
00:23:41.890 --> 00:23:42.351
Oh look.
00:23:42.351 --> 00:23:47.659
So to answer your first question about syphilis, syphilis wouldn't be something I would usually test for.
00:23:47.659 --> 00:23:53.693
If I just had someone with a fairly typical peripheral neuropathy, that would be a very unusual way for that to present.
00:23:53.693 --> 00:24:02.431
But certainly if there were features to suggest some spinal cord involvement as well or other things, then that may be something that we could consider.
00:24:02.431 --> 00:24:16.779
As neurologists we always think of syphilis when we have people with unexplained cognitive problems and then also with myelopathy spinal cord issues In terms of the HNPP, which is hereditary neuropathy with predisposition to pressure palsies.
00:24:17.121 --> 00:24:20.453
That's quite an easy and straightforward blood test to do.
00:24:20.453 --> 00:24:27.582
It is MBS reimbursed, but usually I would only send that off if, after doing nerve conduction studies, I found multiple compression neuropathies.
00:24:27.582 --> 00:24:33.723
And then I would only send that off if, after doing nerve conduction studies, I found multiple compression neuropathies, and then I would consider doing it.
00:24:33.723 --> 00:24:48.039
Obviously, with any genetic testing, it's always important to make sure that your patient is fully counseled and informed before proceeding with any genetic testing, because it can have implications beyond the diagnosis for family members and also for them personally.
00:24:48.580 --> 00:24:50.305
Of course, excellent.
00:24:50.305 --> 00:24:53.099
So we've done our bloods and we've done our nerve conduction study.
00:24:53.099 --> 00:24:54.434
Where do we progress from there?
00:24:54.434 --> 00:24:55.954
What's the next things we're doing?
00:24:55.954 --> 00:24:56.919
And working someone up.
00:24:57.590 --> 00:24:59.910
Well, it really depends on the patient.
00:24:59.910 --> 00:25:27.479
So if the patient has a sort of very slowly progressive, bothersome but non-disabling sensory predominant neuropathy and the initial investigations haven't really revealed a cause and this is not an infrequent situation that we find ourselves in, unfortunately I think in the next decade or so we're going to discover that quite a lot of these sort of slow, insidious, late-onset neuropathies are probably actually genetic in origin, the ones that we sort of can't find the cause for.
00:25:27.479 --> 00:26:04.952
In those situations where it's non-disabling, then usually we do shift to a symptomatic focus and preventing complications making sure people are seeing podiatrists, good footwear, physio if they've got sort of balance issues, falls prevention and making sure that we're avoiding any medications or situations that could worsen neuropathy, so counselling them about alcohol minimisation, making sure they've got good nutrition, not giving them antibiotics that could cause a neuropathy, that sort of thing In someone who's got more disabling symptoms or their symptoms are more progressive and we're much more concerned.
00:26:04.952 --> 00:26:25.494
Then there is a next level of investigation that you can go to with looking for more rare and unusual causes of neuropathies, Looking at things like amyloidosis, HIV, hepatitis C and cryoclobulinemia can give you a neuropathic presentation and that sort of thing.
00:26:25.494 --> 00:26:30.776
That next level would usually be at the level of being in neurology specialist care.
00:26:31.258 --> 00:26:43.278
If you've got somebody who's progressing and the initial screening hasn't worked up and there's a sort of a list of various things that they would go looking for and then also considering you know, could this be a genetic condition?
00:26:43.278 --> 00:26:47.173
And looking for other clues to that, and considering genetic testing.
00:26:47.173 --> 00:26:52.805
We do now have access to really quite affordable, comprehensive genetic panels.
00:26:52.805 --> 00:27:03.439
We can test for 20, 50 genes at a time, and so we'll be guided by the clinical situation as to whether that might be indicated, and then for more focal neuropathies.
00:27:03.439 --> 00:27:32.542
So, coming back to things such as your ulnar neuropathy or your median neuropathy, such as a carpal tunnel, In addition to the nerve conduction studies, the other thing that is increasingly used and, I think, exceptionally useful is imaging and with either ultrasound or MRI depending on the patient and the situation, and that would be something that I might also consider in some of those more progressive neuropathies as well, looking at lumbosacral nerve roots and that sort of thing as well.
00:27:32.542 --> 00:27:33.765
Yeah, Right.
00:27:34.509 --> 00:27:39.682
Obviously I understand the MRIs for cervical or lumbar spine, looking for nerve entrapment there.
00:27:39.682 --> 00:27:48.097
One of the interesting things I've found is the idea that carpal tunnel, where the nerve is supposed to be compressed, the ultrasound shows the nerve actually larger.
00:27:48.097 --> 00:27:49.858
Can you explain why that occurs?
00:27:49.878 --> 00:28:02.117
Yes, so we think that the nerve is actually engorged, so it's compressed and that's disrupting sort of microvascular flow through that nerve, and so the nerve actually becomes edematous and engorged.
00:28:02.117 --> 00:28:20.116
And that's possibly why things like steroid injections work for so long, because even though you think, well, surely the steroid wears off pretty quickly, probably the nerve gets trapped in a bit of a vicious cycle that it swells up and then the more swollen it is, the more compressed it is, the more swollen it becomes.
00:28:20.116 --> 00:28:33.287
And so by just temporarily interrupting that inflammatory swelling situation you can kind of short circuit it and give relief, even for extended periods of time, with a single steroid injection.
00:28:33.587 --> 00:28:37.113
In your area as a neurologist, what are the more common things you would investigate?
00:28:37.113 --> 00:28:40.949
I presume a standard carpal tunnel with a nerve conduction stays, confirming the diagnosis.
00:28:40.949 --> 00:28:44.096
You wouldn't routinely do an ultrasound for that, would you?
00:28:44.096 --> 00:28:44.727
Oh?
00:28:44.948 --> 00:29:16.492
I mean I probably wouldn't, except for various situations, I think, certainly in anybody who you're sort of surprised by how severe the carpal tunnel is or you're not entirely sure that the problem is in the wrist and whether it's somewhere else and you're considering sending someone for surgery, I think it's pretty reasonable to do some imaging just to confirm that there is actually entrapment before you go sending somebody for an invasive procedure such as surgery, particularly if there's atypical features or something about the story that doesn't quite make sense.
00:29:16.664 --> 00:29:26.154
What I would say is what I find really useful when I'm assessing carpal tunnel or alder nerves is something like the simple Tennell's test, which I think is probably my favourite examination technique of the lot.
00:29:26.154 --> 00:29:29.134
And it actually is very, very reliable.
00:29:29.134 --> 00:29:31.344
Am I just biased, or is that actually well-spoken?
00:29:32.006 --> 00:29:37.048
I don't know what the evidence is around a sign in terms of how sensitive or specific it is.
00:29:37.048 --> 00:29:40.674
I certainly do do it and I find it quite useful.
00:29:40.674 --> 00:29:45.642
And, yeah, when I find it I can sort of guarantee that my nerve conductions are going to be abnormal.
00:29:45.642 --> 00:30:03.436
The other one I like to also do is the Phelan's test with putting the hands in a sort of a 90 degrees flexed position and holding them there for a minute, and because sometimes, particularly if your percussion technique's off with your tonnels, you might not get it, but a phalanx will bring out carpal tunnel symptoms in most people as well.
00:30:04.346 --> 00:30:04.586
All right.
00:30:04.586 --> 00:30:09.876
So you've done all these sort of things your area, you say you treat a lot of the steroids and observation.
00:30:09.876 --> 00:30:13.035
What sort of success rates have you found with those sort of scenarios?
00:30:15.964 --> 00:30:16.045
Yeah.
00:30:16.045 --> 00:30:19.815
So I mean, I think really most of this is actually done in the community rather than by me.
00:30:19.815 --> 00:30:21.807
I don't often follow these patients up.
00:30:21.807 --> 00:30:24.794
Mostly my contact with them is in the nerve conduction clinic.
00:30:24.794 --> 00:30:39.900
So for the mild cases and by mild I'm really talking about on the nerve conduction studies, we can just see that the sensory responses are a little bit slowed as they go through the wrist, but there's not really any evidence of axon loss or difficulty with the motor nerves.
00:30:40.404 --> 00:30:47.012
In those situations usually we would suggest splinting conservatively, and for some patients that's really helpful.
00:30:47.012 --> 00:30:53.272
Just wearing a splint that holds the wrist in a slight degree of extension, particularly at nighttime, can be helpful.
00:30:53.272 --> 00:31:02.432
This is a really important strategy, particularly when the cause of the carpal tunnel is something that's reversible, such as women experiencing a carpal tunnel during pregnancy.
00:31:02.432 --> 00:31:06.788
Nocturnal splinting until the pregnancy is over is usually all that they need to do.
00:31:06.788 --> 00:31:28.294
In people who have moderate to severe involvement and by that on the nerve conduction studies, that means we're starting to see the motor nerves being involved or there's evidence of axon loss, and particularly if there's functional impairment with weakness, either functionally or on examination, those are the patients where we're really considering we might give them a trial of a steroid injection.
00:31:28.294 --> 00:31:41.298
Some people have a very good response to that, but those with axon loss or function impairment then really, I usually am referring them on to see a surgeon to discuss their options about a release of the carpal tunnel.
00:31:42.265 --> 00:31:50.773
One of the challenges, though, if there is evidence of axon loss, is that even with surgical intervention that doesn't necessarily result in a recovery of function.
00:31:50.773 --> 00:31:56.977
If there's been axon loss, those axons can be quite slow to grow back, and that may be incomplete.
00:31:56.977 --> 00:32:00.655
So some people, even post-surgery, do have residual symptoms.
00:32:00.655 --> 00:32:20.500
And then another thing I guess, to monitor for post-surgery we do see a small proportion of patients who, after having had surgery, down the track get a recurrence of their symptoms, and so we frequently see those in nerve conduction lab being referred back to have studies done again, and in those situations I'd definitely be recommending imaging.
00:32:20.500 --> 00:32:30.477
So ultrasound, particularly if repeat surgical intervention is being considered Scarring post-operatively can be a cause of worsening symptoms post-surgery.
00:32:31.224 --> 00:32:34.618
Yeah, it's interesting and we obviously do a lot of carpal tunnels and I audited my results for last year too, but we don't seem to get as a lot of carpal tunnels.
00:32:34.618 --> 00:32:38.814
I audited my results for last year too, but we don't seem to get as many recurrences that we expect.
00:32:38.814 --> 00:32:40.150
I don't think there's been that many.
00:32:40.150 --> 00:32:54.075
Carpal tunnels can be released in numerous ways, and when we're talking about surgery, obviously we're releasing the flexor adenaculum in the palmar aspect and that can be done through endoscopic or open approaches, and I do them under open, them under open and then the vast majority under local anesthetic alone.
00:32:54.075 --> 00:32:58.574
So the patient's wide awake and the vast majority of nerves are actually really quite big.
00:32:58.574 --> 00:33:00.874
You can see them being squashed by the flexor inaculum.
00:33:00.874 --> 00:33:03.576
It's surprising how big the nerve is in general.
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