Freyja is a two-year old female Doberman Pinscher who is brought to the Emergency Room in your teaching hospital, after being clipped by a car as she was jogging with her owner. Her hindquarters are pretty badly beaten up, with two fractures of the left femur, and, you suspect, a fractured hip. She's sedated and stabilized and you get to work setting bones and cleaning up the numerous cuts and abrasions, all the while politely explaining to the owner that this preventing this sort of "accident" is what dog leashes are for, and perhaps it was unwise to allow her dog to run alongside her in traffic, without being under direct physical control.

In the end, Freyja makes a pretty good recovery, her fractures healing well, but a year later she has a noticeable limp and an atrophied left quadriceps that will remind her owner for the rest of Freyja's life of the consequences of carelessness.


Freyja's muscle is wasted because of neurogenic atrophy. Some muscle bundles in her leg have lost the nerve supply that's required to make them contract: despite all your skill, the damage to her leg was extensive enough that some parts of it couldn't be repaired and she'll have a functional deficit because of this traumatic denervation.

Denervation is quite simply the loss of innervation to a tissue that results in the inability of that tissue to respond to nervous impulses.  Denervation to some organs results in immediate catastrophic failure of that organ (just try cutting the phrenic nerve), but denervation of muscle results in atrophy, since skeletal muscle absolutely requires neural input to maintain itself.

Denervation by trauma is a common occurrence in animals, but trauma isn't the only reason why it happens. Infectious disease that attacks nerves is another cause (e.g., distemper) as is unintended transection of nerves by well-meaning surgeons.

Atrophy is a loss of substance: it's not death of cells or tissue. In this case the muscle cells (myfibers) of the denervated bundles are quite alive, but they have no further need for lots of contractile capability, since they're never going to get the signal to contact again. The proteins in these myofibers represent an expensive metabolic investment, so the body breaks them down to recycle their amino acids in other locations. The actin and myosin are removed and the cell shrinks in size but the cells remain alive.

Denervation is not currently treatable, though active research is ongoing to find ways to deal with it by regeneration of nerves. In this case, only a few muscle groups were denervated: in the case of a spinal cord injury, entire regions of the body may be deprived of nervous stimulation. In the case of denervation of muscle, the closer to the brain such an injury occurs, the worse the paralysis that results: a neck injury at C2 will result in more or less complete paralysis (this is what happened to the late actor Christopher Reeve, whose body musculature underwent severe atrophy after the accident). The Daschund at right suffered from a spinal cord dislocation that paralyzed her caudal musculature but she pulls herself along on her front feet pretty well. In humans and animals alike, assistance devices can be used to make life more normal for patients with nerve damage.  Humans pioneered the use of wheelchairs, but they are not the only ones who can benefit from them.


Here's the story of muscle atrophy in a single image: this view shows the atrophied area at right, adjacent to normal muscle.

Notice the much smaller size of the atrophied fibers, compared to the normal ones; but otherwise their architecture is pretty much the same: multiple peripheral nuclei, endomysial connective tissue, etc. They can't work but they aren't dead.

In the image below, you can see the same comparison in a longitudinal section of a severely atrophied lesion. Notice the numerous nuclei inside the shrunken cells! The tissue still has a blood supply, it isn't going to become necrotic, and it's just "there" doing nothing useful.

Any given anatomic muscle has innumerable myofibers, and each one has its own nerve fiber to control it. The degree of loss is based on how many "motor units" are cut off from the contraction signal.

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