Have you ever hit your funny bone? In actual fact, the funny bone is not a bone at all but the ulnar nerve, which supplies about a quarter of the muscles in your arm. But what happens if it is more serious than that?
First, a quick lesson on human physiology.
A nerve is a cord like structure that is made up bundles of conductive tissue that forms the peripheral nervous system. Before they branch off from the brain and spinal cord to become nerves, they are called tracts.
Nerves are organised very much like a big fat sushi roll.
Image source: http://www.msdlatinamerica.com/ebooks/HandSurgery/sid620432.html#R6-45
At the smallest level we have axons (nerve cell tails). You can imagine this to be a single strand of fish. Now these axons then form bundles called fascicles which is surrounded by perineurium, which is like the whole fish coated in delicious Japanese mayo.
Now in most sushi rolls you find other ingredients – and that’s where you find other fascicles that are carry information about touch, pain, temperature and movement. In amongst the rice that is the internal epineurium carries tiny blood vessels that run parallel. This is all tightly packed together and finally surrounded by the seaweed wrap of nerves – the external epineurium and mesoneurium.
Now going back to the smallest strand – the axon – you will find myelin. Myelin is a fatty substance made of layers of cells called Schwann cells that organise themselves into clumps called Nodes of Ranvier. These cells allow electrical impulses to travel more quickly along a nerve because it makes the cell membranes more excitable as it allows the conduction to ‘jump’ along.
Demyelination, or the loss of myelin, can occur in nerves in a condition such as Guillain-Barre, sometimes referred to as Acute Inflammatory Demyelinating Polyneuropathy.
Schwann cells fall under a category of cells called glia. Glia is commonly known as the ‘glue’ of the nervous system and they do the following 5 things:
– protect neurons
– make myelin
– remove dead neurons
– supply nutrients
– keep neurons in place
Schwann cells also have a pro-inflammatory role and signal for other immune cells to arrive at the site of any damage, to start the process of debris removal and layering down of new material. This is slightly different to the way glia cells in the central nervous system do this (oligodendrocytes) which is why regeneration in the spinal cord is much more limited.
Peripheral nerve damage can be commonly classified into 3 types.
In neuropraxia, there are no structural changes to the nerve architecture. The nerve conduction is simply blocked temporarily, giving rise to symptoms of tingling, apparent weakness or changes in skin condition or feeling that last from hours to weeks.
As such, full recovery is expected.
A good but mild example of this is when you get pins and needles down your arm or leg from sitting for too long in one position.
Axonotmesis is the most common category of peripheral nerve injury, partly because it covers the largest range and combination of structural changes.
It occurs when the axon, endoneurium or perineurium is partly injured either in isolation or together. The key thing is that the epineurium, which I like to refer as the ‘nerve tunnels, are still intact such that the pathway for regeneration is already paved.
Within days, the distal part of the disrupted nerve begins to disintegrate – a process known as Wallerian degeneration. The proximal part gets tidied up by immune cells and new neural building blocks are laid down as it begins to regenerate. This often takes months to complete.
In historical literature, It is said that axons grow at a rate of 1mm a day. I have yet to verify the source of this statistic, whose appearance began in the 1940’s. Without knowing what conditions this was discovered in, I find it hard to take as gospel, especially in light of activity dependent neuroplasticity.
Nonetheless, recovery is not always complete. This kind of peripheral nerve injury can take up to 12 months to reach its full potential of recovery, and older age can slow this further. More research into this is definitely needed.
Many patients have conditions involving axonotmesis, such as distraction injuries (when a nerve is stretched beyond 10% of its length), blunt trauma or disc bulges that result in compression of nerve roots. This gives rise to neurological symptoms such as weakness and sensory loss.
This refers to a complete severance of the axons, endoneurium, perineurium and epineurium across the cross section of the nerve. This can occur from trauma from gunshots, knife wounds or amputation. Due to the shear forces and complete loss of nerve architecture, natural recovery is almost impossible and surgical intervention is required.
In my clinical experience, I find having a candid conversation with a neurologist who is trained in EMG studies and nerve physiology invaluable in determining someone’s capacity to improve, taking into the account the AREA and the MECHANISM of injury. It is also important to take the time to isolate which parts of the peripheral nerve is working functionally and on specific clinical testing, to help predict recovery and appropriate therapy.
Robinson, L (2000). Traumatic Injury to Peripheral Nerves. Muscle Nerve 23 p 863-873
Diagnosis and Management of Peripheral Nerve Injury and Entrapment (2014), Congress of Neurological Surgeons. Retrieved 28th July 2014, from http://w3.cns.org/education/medStudCur/curriculum2.asp?inPage=d1
Weber RA and Lee Dellon A (2004). Nerve Lacerations: Repair of Acute Injuries, Hand Surgery. Retrieved from http://www.msdlatinamerica.com/ebooks/HandSurgery/sid620432.html#R6-45
Schematic drawing of a peripheral nerve [Image]. (2004). Retrieved from http://www.msdlatinamerica.com/ebooks/HandSurgery/sid620432.html#R6-45