Hopefully you will have watched the first part of this video where I provided an overview

of normative data.

If you haven’t seen this yet, please do so now, by clicking on the link via the i-card

above.

In this video, I will provide an overview as to how we piece this information together.

For any nerve, we measure the size of response, called the amplitude which reflects the size

of the underlying axons.

The speed of the response reflects the degree that the nerve is myelinated.

So when the amplitude drops, we generally attribute it to axonal loss and where the

speed of conduction drops, we generally attribute it to demyelination.

There are exceptions, which we will eventually consider.

But, for now, I just want to highlight that that because, motor nerves

are larger and more myelinated than sensory nerves, they are better at showing conduction

slowing.

Let’s start with demyelinating mononeuropathies at common compression sites.

These are by far the commonest of the conditions we encounter and include carpal tunnel, cubital

tunnel and peroneal nerve lesions at the fibula neck.

Here, single nerves are being compressed and damaged.

We test the nerves to look for focal motor conduction slowing at the entrapment site.

You can see videos on all 3 of these conditions by following the i-cards above.

Sometimes they can co-exist such as having both carpal and cubital tunnel lesions.

This is not rare and I see this in around 5% of my carpal tunnel patients.

So I keep an eye out for this and you can see me perform a typical nerve conduction

test in under 2 minutes by following the i-card above.

If we see conduction slowing across all common compression sites, especially in a young patient,

then we need to consider a condition called HNPP or hereditary liability to pressure palsies

as a potential cause.

Here a genetic mutation in a myelin component, makes the nerves susceptible to being crushed.

Keeping to the genetic neuropathy theme, when we encounter conduction slowing which is uniform,

symmetrical and outside entrapment sites, we consider the hereditary motor and sensory

neuropathies and you can see a video explaining the different types of Charcot-Marie-Tooth

disease by following the i-card above.

Inflammatory demyelinating neuropathies, by contrast, are more patchy, often more asymmetrical

and tend to demonstrate phenomenon such as conduction block and temporal dispersion where

non-uniform dysfunction leads to reduction or spread of the motor responses.

You can see a more detailed explanation of this and myelin function and nerve signalling

by clicking on the i-card above as well as some videos on the inflammatory demyelinating

neuropathies.

Any demyelinating neuropathy which is sufficiently severe will eventually lead to underlying

axonal fibre loss, recognisable as a drop in response amplitude.

So lets talk about the axonal neuropathies and these can really subdivide into a few

categories: Length dependent, Generalised, Mononeuropathies

and Mononeurtis multiplex patterns.

The commonest are the length dependent neuropathies.

These occur to the more distal and smaller caliber nerves.

Hence the sensory fibres tend to be more affected than the larger motor fibres and so feet are

affected first and tend to clinically affect the hands by the time the impairment reaches

the knees.

Of course, we can detect sub-clinical involvement earlier with NCS.

Generalised neuropathies will lead to generalised suppression of response amplitudes and will

again affect sensory fibres more than motor fibres.

Perhaps the most interesting variation are the sensory neuronopathies where there is

a complete suppression of all sensory responses and I would advocate blink reflex studies

in these situations to look for trigeminal dysfunction.

Single nerves lesions can also be detected and these are called mono-neuropathies.

These can be idiopathic or inflammatory in nature.

Where multiple single nerves are affected, this is called mono-neuritis multiplex and

tend to be associated with inflammatory or vasculitic processes.

Pure motor neuropathies are very rare.

These primarily affect the motor responses and only rarely affect the sensory responses.

Differentials can include inflammatory neuropathies such as MMNCB / MMN without CB, distal HMN

and the motor neuronopathies such as Motor Neurone Disease

Myopathies can lead to reduced motor responses, but often as they are proximal processes,

the distal motor amplitudes tend to be spared, unless it is a distal myopathy.

An interesting exception is critical care myopathy where the motor responses reduce

and become broad.

However, what we do commonly encounter are the radiculopathies.

Here myotomal motor axonal loss is demonstrable without sensory fibre loss.

Take a look at the medical student tutorials, via the link above, where I explain how we

differentiate between pre and post ganglionic lesions which is a very important concept

in neurophysiology.

So that’s the whistle stop tour and in the coming series of videos I’ll work through

specific examples.

Thanks for watching and I hope you enjoyed it.

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