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dmcfarlane
02-19-2006, 10:27 AM
SLEEPY LEG ANSWERS

1. It's a neuropraxia caused by ischaemia of the nerve.
Chris Kirtley

2. Here's a link:
http://en.wikipedia.org/wiki/Paresthesia
Tim Odell

3. The cause of the problem is vascular. The blood supply is quenched. As a result the nerve conducts less well, this gives the numb feeling and a loss of propriocepsis.
In severe cases also the nervous control of the muscles gets impaired and you cannot stand up.
A.L. Hof

4. due to direct pressure or kinking of the sciatic nerve as it winds around sciatic notch
shuen

5. Direct compression of the nerves, usually the proximal end of the sciatic after it leaves the greater sciatic notch and exits above the piriformis muscle. Vascular compression would cause a cold blue leg, while compression of the muscle would cause ischaemic 'burning' pain.
Rod Whiteley,

6. nerve. I'm 99% sure its nervous but I don't have references to research on it. As an interesting side note - NHS beds had to be changed because of an extreme of this. The design of the side bars meant that sometimes patients could have parts of their legs lying against them for hours. This cause they leg to go to sleep (complete paralysis) for approx 1 year! The interesting part is that the function does come back after this time. I don't have any knowledge of what the mechanisms might be.
Joe Wright


7. i believe it's neurovascular ... i.e., decreased blood flow supplying the nerve axons. i'm sure if you put enough pressure on a nerve though, you can get a direct effect, but that would more likely be significant force resulting in persistent injury. a vascular effect in terms of cutting off supply to the muscle & other tissue would take longer and probably manifest as pain/cramping (which does happen with prolonged sitting).

different cells can handle different degrees of ischemia. brain cells die in like seconds, whereas skeletal muscle can last something like 6 hours. in fact, in hand and other extremity surgery, the surgeon frequently applies a tourniquet to control bleeding, and leave it up for upwards of 2+ hours.

is it dangerous ... it can be extremely dangerous *if* you are immobilized or insensate ... that's what causes decubitus/pressure sores, which are a *very* common and devastating problem ...
infections of these sores can and do result in death -- case in point, christopher reeve (a.k.a. superman).

johnny t chang

8. The answer to your question can be found by researching James Cyriax, MD and his explanation of the "compression phenomenon" vs. "release phenomenon". In a nutshell, our extremities will go numb when one compresses a nerve trunk, and it's only with the release of the compression that we experience the paresthesias. The "symptoms" occur after the release of the compression. Compared to compression of a nerve root when we experience the paresthesias directly associated with the compression of the nerve root, and the symptoms go away when the compression is eliminated. This is why you may or may not feel that your foot is "asleep" when you are sitting, but as soon as you move the limb or stand up (removing the source of compression from the sciatic nerve trunk) you will experience the "rush" of paresthesia. Individuals with Thoracic Outlet Syndrome suffer from atypical compression of a nerve trunk in the brachial plexus vs. someone who experiences cervical interforaminal compression as from a disc herniation (nerve root
compression).

It is not dangerous in the lower extremities unless the compression is prolonged to the point of causing ischemia to the nerve truck, which typically does not occur in people with normal sensation. It is a major nuisance to individuals with TOS, because it can cause loss of sleep (when the release of compression occurs - lying down) as well as greater debilitation if the syndrome goes untreated.

Kevin M. Cooney, PT

9. 'Leg falling asleep' is usually a symptom 'neurapraxia' - transient loss of nerve function due to pressure on the nerve. The nerve in this case is usually the common peroneal nerve or its superficial branch as it winds around the head of the fibula. The mechanism underlying loss of nerve function has been postulated to be vascular (occlusion of blood supply to the nerve) as well as mechanical (the pressure itself). Loss of common peroneal nerve function would be expected to result in loss of dorsiflexion at the ankle and toes. Recovery in minor cases is expected to be immediate.

Neurapraxia may last longer in more severe cases: "Saturday night palsy" or neurapraxia of the radial nerve is often seen in someone who has had a little too much to drink and ends up falling asleep with pressure on the radial nerve on the back of the humerus. Neurapraxia may also be iatrogenic - peroneal nerve palsies are often reported to occur during knee joint replacement surgery. Orthopods will also keep an eye out for them during casting / bracing procedures because of its superficial location.

Neurapraxia may also have sensory symptoms: carpal tunnel syndrome is a great example. Chronic neurapraxia is often considered under the larger umbrella term of compression neuropathy - certain populations, such as folks with diabetes have shown higher incidence of compression neuropathies. Certain sites in the body, such as the carpal tunnel, tarsal tunnel, show higher incidence of compression neuropathy. If the pressure is high enough and/or chronic enough to result in loss of axons (axonotmesis) or neurotmesis (loss of the nerve cell), sensory and motor impairments will result. Wasting / atrophy of the thumb muscles have been reported in carpal tunnel syndrome.

Sorry - this is all kinda off the cuff. I've come across a some excellent resources, one is a book on Clinical Electromyography by Jun Kimura. Any textbook on neurology will usually have a section on compression neuropathies.

Smita Rao Msc, PT

That's it folks! Many thanks to one and all!

Now here's the joker in the pack; the other day I was reading a book that speculated that "software" glitches of the central nervous system can cause dysfunctional recruitment of the multifidus that causes back injuries - and mentioned in passing that this might be similar to the cause of "sleepy leg". I might be wrong (I have mislaid my notes) but I think that the author was either Jemmett or McGill. Apparently this is not generally regarded as the cause of sleepy leg - whether it is the cause of back injuries is another question.

Does anyone know if EMG is useful for diagnostic imaging of the recruitment pattern of the multifidus muscle?

Regards,

David McFarlane
Ergonomist, WorkCover Authority
New South Wales, Australia

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Reference

Rick Jemmett, (2003), "Spinal Stabilization: The New Science of Back Pain", Rev. Edition, (Novont Health Publishing, Halifax), ISBN: 0-9688715-1-8, pages 115-123


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