Nerve Damage & Healing
Anatomy of the Peripheral Nerve
There are two different types of somatic nerves in the body. There are central nervous system (CNS) nerves and the nerves of the peripheral nervous system (PNS). There are many more types of nerves but in this section, we will talk only of the somatic or “body” nerves that attach from the brain to the arms and legs and then back again. The central nervous system nerves are supported by “assistant cells” called oligodendrocytes and the peripheral nervous system nerves are support by” assistant cells” called Schwann cells.
There are marked differences between the two types of nerves. The CNS nerve cells do not have a protective sheath surrounding them where the PNS nerves do. This makes the PNS nerve “tougher” and less vulnerable to injury. The one exception is the PNS nerves that live in the upper portion of the spine (the cervical nerve roots) and lower portion of the spine (the lumbar nerve roots). These nerves do not obtain the protective sheath until they exit the spine which makes them more vulnerable to injury. This is unfortunately the location of compression of a nerve that may occur from a disc herniation.
Any nerve consists of a cell body and the branches that extend out of this body, the dendrites and the axons. The function of the nerve is obviously to deliver a message from one cell to another cell. The dendrites are the location of the origination of this signal and the axons carry this message to the other end of the nerve.
A term for a group of nerve cell bodies is a ganglion. Therefore, you will see some articles call the dendrites “preganglionic” and the axon “postganglionic”. This is important only for advanced understanding of nerve injury.
There is an electrical charge in the nerves which makes the general public consider the nerves as “electrical wires”. However, the axons and dendrites are really “hoses” made up of membranes. These membranes will allow molecules (or ions) to pass through at certain times. There are active pumps on these cell membranes to push the molecules or ions into or out of the interior of the cell. This difference of ion concentration between the inside and outside allows an electrical charge across the membrane of the nerve.
The nerve carries its signal by allowing some of these channels or gates to open up briefly and facilitate the quick rush of ions through the cell membrane. This inflow occurs when the electrical charge changes which will open some of these channels allowing ions to temporarily rush in and out. When the message passes this section of membrane, the gates close and the pumps on the membrane restore the original ion concentrations. Novocain or Lidocaine temporarily blocks the nerve impulse by preventing the nerve membrane from allowing ions in or out.
Some nerves have an insulating sheath present just like typical insulated wires. This sheath is called the myelin sheath and is made up of Schwann cells in the peripheral nerves and oligodendrocytes in the central nervous system nerves. This insulation can be damaged by compression just as the nerve membrane itself can be injured. Damage will delay or prevent the message or signal from travelling down the nerve.
Peripheral Nerve Injury
There are generally three types of mechanical injury that can occur to a nerve; compression such as from a disc herniation, blunt impact (this can also occur from a disc herniation) and finally, a stretch injury. Stretch injuries occur from an arm or leg stretching beyond normal limits such as an arm forcefully stretched due to fall onto an object. If a nerve is stretched, it may simply recoil to its original length when the stretching force is released or the nerve may completely snap, similar to the stretch and snap of a rubber band. In general, a nerve can stretch about 6% of its length without injury. A stretch of more than 15% of the nerve’s length will cause irreversible damage.
When the nerve cell is injured, generally the nerve membrane is damaged or the insulation (myelin sheath) is damaged. When the nerve cell membrane is damaged, the signal can be blocked which prevents the message from continuing down the nerve. The opposite effect can also occur. Injury to the membrane can cause “leaks” or ions to flow into the nerve at the wrong time, triggering an unintended impulse.
The block of a nerve membrane prevents the signal from travelling up or down the nerve. This would result in numbness of the area served by the nerve or weakness of the muscle supplied by the injured nerve. A good example is foot numbness resultant from a herniated disc causing an L5 nerve injury. Foot drop is the inability to raise up the foot due to the muscle weakness caused by blocked signal from the L5 nerve (occasionally the L4 nerve).
An unintended impulse that spontaneous occurs from the “leaky” or injured membrane (called an ectopic stimulation) will produce symptoms from that nerve just as if the far end of the nerve had been stimulated. A good example of this is foot pain due to an L4-5 herniated disc. Nobody has put a nail through the foot but nonetheless, the foot is still painful due to the injury of this nerve in the spinal canal. The brain cannot distinguish between stimulation of this nerve at the level of the foot vs. stimulation of this same nerve at the level of the lumbar disc.
A nerve injury may have the possibility of significant recovery after the initial trauma or may never recover. Recovery depends upon the type of nerve injury. Unless there has been an obvious direct injury to the nerve (a knife or a gunshot wound), it is impossible to know what type of injury has occurred to the nerve. That is; was only the nerve cell damaged, only the insulation damaged or the entire nerve and insulation both been damaged? This makes a difference in healing potential. Unfortunately, MRIs are not powerful enough to look at microscopic anatomy to determine the type of injury to the nerve.
The only way to know if the nerve will heal is to provide it the best environment to heal and then wait. Many times this means surgical decompression if a disc herniation or a large bone spur compresses the nerve. After decompression, only time will tell what injury the nerve had suffered and what recovery is possible.
Muscle weakness is caused by the lack of some muscle cells in one muscle group receiving the signal to contract. This is due to injury to portions of the nerve bundle connecting to each individual muscle cell. (A nerve is really a collection of thousands of nerve cells in one bundle- something like a telephone cable with thousands of individual wires within the cable).
Obviously, if the entire nerve was severed, the muscle would have no ability to contract and the joint would be “limp”. Weakness means that the nerve is still partially intact but not all individual nerves are functioning. Due to the loss of some neurons, only a small portion of the muscle cells will fire in that muscle group. Since many of the muscle cells are not getting the signal from the brain to contract, the ones that are still connected are too few to yield a full contraction. These working but overloaded muscle cells fatigue easily as they are overtaxed with work and cannot "keep up" with the load. This is why with continued exercise, the involved leg or arm feels even weaker.
Types of Nerve Injuries
Functional Nerve Block
This is the most common individually experienced temporary nerve injury. When any person rests his or her elbow on a counter and the arm “falls sleep”, what has actually occurred is a temporary block of conduction of the ulnar nerve (the” funny bone”) from the compression. Normally, as soon as the compression is removed, the “feeling” returns to the arm and hand.
There are some occasions that even after the compression is removed, the nerve function never fully recovers. The most common scenario for this is the so called “Saturday night palsy”. The individuals who suffer this disorder are typically alcoholics who are so inebriated that they rest their elbow on a hard surface when they are “passed out”. If the elbow remains compressed on this hard surface for a period of time, the nerve will be permanently damaged. The amount of compression and the length of time the compression is present are the two determining factors for recovery.
Immediate recovery of function can occur after a surgical decompression of the nerve in the spinal canal. The immediate return of function is from this effect.
Injury to the Myelin Sheath Only
The myelin sheath is as noted earlier, the insulation around the nerve. Not every nerve has this insulation but most important nerves do. When the myelin sheath is damaged but the nerve is still intact, the nerve may conduct its message slowly or not conduct at all (called a complete conduction block). Fortunately, the myelin sheath which is made up of Schwann cells will generally heal given time. This time period for healing can take between 8 and 14 weeks. Only time will tell if the nerve will regain conduction ability as there is no way to determine if the nerve has this type of injury.
Axonal regeneration (Regrowth of the Nerve Cell)
If the nerve cell itself is disrupted from a traction of compression injury but the insulation (myelin sheath) is still left intact, the nerve can regenerate. After the initial injury to the nerve and a delay of a day or two, the cut end of the nerve nearest the brain will develop new sprouts that will grow down the surface of the lining insulation cells (myelin sheath made up of Schwann cells). While this regrowth is going on, the cut end of the nerve that is farthest away from the brain will die back to the farthest endpoint of the nerve. This process is called Wallerian degeneration and even though the nerve dies back, the insulating tube will be left intact. The nerve ending may terminate in a muscle, a sensory organ (skin sensation) or a proprioceptive organ (coordination sensation that allows the brain to know where all its parts are in space). Again, if the insulating myelin sheath is still intact, the side of the nerve cell that is still alive (closest to the brain) can grow down this intact insulating sheath. This nerve will grow about 1mm/day or about one inch per month toward the end of the sheath.
Once the nerve grows down this tube to its end, it will reattach to the organelle it once was attached to. This means that sensation can become normal again, muscle strength will return or incoordination will be reduced.
There are three caveats to return of function. If the nerve and the insulating sheath are both damaged, the nerve will not have a pathway to regrow to the end organ. The cut end of the nerve nearest the brain will still grow new sprouts but these sprouts will have nowhere to go. These sprouts will “ball up” into a tangle of nerves called neuroma and can become quite sensitive to pressure and even touch. Individuals who have had a Morton’s neuroma in their foot will attest to the pain that can be generated.
The second caveat is that there is a time factor for regrowth. A muscle cell that has no nerve supply will atrophy and fibrose (turn into scar tissue). This occurs between 12 and 18 months. If the regrowing nerve has not reached the endpoint muscle cell in about 12 months, it will have no functioning muscle cell to work with. This means that very long nerves (L5, S1, C8, T1) have a much poorer chance of joining their target organelle and functioning normally again.
The third caveat is that injured nerve cells in the central nervous system (CNS) do not generally regrow as there are inhibitory factors within the spinal cord cells that prevent this regrowth. The oligodendrocytes (the support cells in the central nervous system that serve the same function as of the Schwann cells in the peripheral nervous system) inhibit regrowth.
Terminal Axonal Sprouting (Nerve Budding)
When the nerve is injured, some of the muscle cells lose nerve supply in a condition called “denervation”. Due to this condition, the internal workings of the muscle cell changes significantly. The denervated muscle starts to become irritable. In fact, three weeks after the nerve is disconnected from the muscle, the muscle demonstrates irritability changes that can be picked up on an EMG (electromyography), a nerve test for the muscle cell.
This irritability causes the muscle to secrete a neurochemotactic factor, essentially a chemical cry for help. Any nerve that is still functional nearby this muscle cell will form a new nerve branch in a process called budding or sprouting. These sprouts can connect to at least ten denervated muscle cells. This sprouting activity can take from 12-16 weeks after the initial injury to occur.
There have been some studies that indicate the use of electrical muscle stimulation (EMS) during this period will decrease the secretion of the neurochemotactic factors. Therefore, stimulation of muscle contraction through EMS should be avoided by therapists working with the recovery of the muscle strength.
Another possibility for motor strength recovery is muscle hypertrophy. Arnold Schwarzenegger is what many individuals imagine for an example of muscle hypertrophy and that thought is not far off. The residual functioning muscle cells can be conditioned to become stronger and last longer. Training is the key for this type of recovery and good results may take three or more months of hard work to achieve success.
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