Expert: Dr. J. Shawn Leatherman - 11/15/2006

Question
I am a 26 year old man who was recently involved in an automobile accident.  I suffered a fracture to my femur shaft that was repaired via surgery.  I had a rod put into the middle of my femur and secured by screws.  My question is this:  Immediatly following the injury, before the surgery, I had numbness in the foot of the injured leg and an inability to move the toes.  It is now six weeks since the surgery, and still have numbness/burning/shooting pains in the toes and sole of my left foot.  Also, my ability to move my toes is extremely limited.  I am currently taking vitamin B6 to help with nerve regeneration.  Is there anything else you can suggest to help with the pain, and do you think that this condition could eventually heal up?  Thanks for your time.

Answer
Dear Dana,

Well, the extent of the injury you have described is fairly severe and will definitely affect the nerves to the foot.  When nerves are disrupted/damaged/severed, problems in muscle strength, sensation, as well as pain perception are bound to occur and can be lasting.  Nerve injuries require extensive healing, and may never fully heal.  Let me explain a bit more thoroughly, I apologize if this is very medical in nature, I will try to mainstream the terminology as much as possible.

Anatomy and Physiology of the Peripheral Nerve  
The peripheral nerve is composed of loose, soft connective tissue that protects fascicles (bundles) of nerve fibers. It has its own blood supply which feeds the inner neural capillary plexus. The vasculature is kinked to allow for stretching. The perineurium (outer covering)serves as both a mechanical barrier to external trauma and a diffusion barrier, thus protecting and preserving the internal environment of the endoneurium (inner nerve). This space, however, is not completely isolated. The pressure in the perineurium can be raised to 300-750 mmHg. The capillary walls of the endoneurium also act as a diffusion barrier--the so-called blood-nerve barrier--protecting, with the perineurium, against ions, proteins, and other macromolecules.

Effects of Pressure:  The latter is remarkably resistant to pressure, withstanding local compression of 400-600 mmHg for up to two hours. However, local crush injury, can result in abnormal permeability in this space for up to four months. This barrier can also stand a great deal of ischemia (oxygen loss due to poor blood supply) without failure--24 hours or more. During long standing ischemia, endoneurial vascular permeability is increased (as epineurial edema {swelling}occurs independently).

This long-standing disruption of the internal structures leads to fibroblastic invasion and, ultimately, to endoneurial scar formation. This may very well be the pathophysiology common to most peripheral neuropathies caused by chronic or repetitive pressure or microtrauma, the classic example being carpal tunnel syndrome, which is separate than a complete severing such as a traumatic break.

Effects of Stretch:  The human body is dynamic--constantly moving, bending, stretching, and reaching. Nerves are able to move through the tissues during this motion. Sliding of these nerves ranges from 7-15 mm under normal conditions. Peripheral nerves are remarkably resilient to a slow gradual stretch. Repeated intermittent micro- (small)or macrostretch (large stretch)may cause local edema. The sciatic nerve can withstand up to 165 kg of loading before rupturing, whereas, the median and ulnar nerves can withstand 20-65 kg. However, internal disruption occurs long before loss of continuity of the whole nerve. **Dana you may well have (internal disruption without external disruption), and during trauma, the viscoelastic properties of nerve may be overcome, allowing rupture of nerve fibers at lower strain levels. (Such as  Broken Femur)**

Microcirculation:  Some of the following facts and experimental findings concerning the microcirculation of nerves help to better understand the fundamental pathophysiology of nerves:

1)  Lundborg and Rydevik found that by elongating the sciatic-tibial nerve (leg)in rabbits, they could decrease the venous blood flow to the endoneurium. At 8% stretch, the lower limit is reached, and at 15%, complete arrest of blood flow occurs. **15% is not that much!!

2)  Increased vascular permeability occurs in two waves--one immediately following trauma and the other peaking at about two weeks after trauma. **increased swelling**

3)  A blood-nerve barrier exists in the endoneurium but no such barrier exists in the epineurium. It is, therefore, more susceptible to acute moderate trauma, shorter periods of ischemia, and/or chronic irritation. If prolonged, edema results in fibrous scar, it can permanently constricts epineurial blood vessels and reduces endoneurial supply. Ultimately, endoneurial edema results, along with increased pressure and further decreased blood flow.  **reduced blood flow=reduced function, healing, and increased pain perception.

4)  Extra protein-rich fluid in the endoneurial extracellular space will adversely affect the exchange of nutrients and waste products between capillary wall and nerve; this may also have an adverse effect on nerve function.

5)  Changes in the electrolyte content of the endoneurial fluid resulting from edema will disturb membrane function of axons (nerve tail that transmits information), thereby affecting nerve fiber function.  Oxygenation is also adversely affected.

6)  There are no lymph vessels (the bodies cleaning system for removing waste and inflammation) in the endoneurium and, therefore, drainage is greatly impaired by edema.

Pathophysiology:  The exact pathophysiology of the compression lesion is not entirely clear, but some of the following facts may clarify some of the underlying etiopathology.

1)  Spinal nerve roots lack an epineurium and are more vulnerable to compression (852).

2)  The actual makeup of the nerve (i.e., proportion of epineurium to nerve fascicle) is an important factor in terms of its ability to resist compression.

3)  Large diameter fibers are more susceptible to compression and ischemia.  **Such as the sciatic and tibial nerves in the leg

4)  Pressure over a nerve causes a temporary and reversible metabolic conduction block (hand falls asleep). Prolonged pressure results in mechanical deformation of both blood vessels and nerve fibers (long term numbness and reduced muscular function). The same occurs in tourniquet use. If prolonged, intraneurial edema results and myelin (nerve insulation) changes occur. Repair of myelin and drainage of edema may take from days to months. If axons are damaged the prognosis is worse.

5)  Experiments with prolonged exposure of nerves to a pressure of 30 mmHg demonstrated a threefold increase in endoneurial fluid pressure after eight hours. The same values were found 24 hours after release of pressure. In another study, edema was observed 28 days after decompression. They also noted demyelination (loss of nerve insulation) at only 30 mmHg. At 80 mmHg axon damage resulted.

6)  The effect of compression on axon transport has been studied extensively. Rydevik and Norborg demonstrated a complete or partial block at the site of compression with 30 mmHg applied for only two hours. That even brief ischemia can be damaging to nerves is demonstrated by the findings of Sanders et al. who examined patients who had undergone knee surgery. When tourniquet time exceeded one hour, 85% of cases had persistent abnormal EMG findings, suggesting axonotmesis. (axonotemesis, see below for definition)

The Diffuse Nature of Neural Injury:  Perhaps the single most important concept to remember is that peripheral nerves, nerve roots, the spinal cord, and the brain can be injured in such a way that damage is relatively diffuse. Overall nerve, cord, or brain function is intact; but some sensory, motor, or psychological function is impaired. Minor lesions such as these may give rise to significant impairments, yet remain below the diagnostic threshold and yield of the most sophisticated electrodiagnostic equipment.

Classification of Injury  A classification of nerve injuries was suggested by Seddon in 1943 and is still in use today. It is as follows:

1)  Neuropraxia: represents a local conduction block with axons remaining intact. Weeks or months may pass before the discontinuity of the myelin sheath is repaired.

2)  Axonotmesis: implies a more advanced compression or traction injury in which axons are disrupted.

3)  Neurotmesis: implies a complete severance of the nerve, in which a nerve lesion preserves its appearance of integrity but is, in fact, totally disorganized.

Dana, I know that was a mouthful, or an eyeful, but the complexity of your question is even more than what I have answered.  the bottom line is that science doesn't really have an answer to your question, and neurogenic pain can last for months.  Think of phantom limb pain syndrome, the patient has a leg cut off, but continues to feel lower leg and foot pain.  Their brain interprets the pain from damage to the nerves, even though the leg no longer exists.

Keep taking the B6, and I would additionally include a B vitamin complex, (dosage should be twice what the bottle recommends)  Omega III fatty acids to help reduce inflammation and nerve generated potentials, you should be taking about 6000mg per day for the next month and then reduce to 4000mg per day...  the product must be mollecularly distilled, and half of the total mg should be in the form of DHA (docosahexanoic acid)and EPA (eicosapentanoic acid).

Hope this helps Dana, stay positive.
Respectfully,
Dr. J. Shawn Leatherman