As I have posted several times in the past, the occipital nerves can be compressed by a number of different structures such as blood vessels (e.g. the occipital artery), fascia, scar and muscle. But someone recently asked me how these structures can cause pathologic changes in the nerve so I thought I’d put down a few thoughts. First, there are changes that can occur after injury whether surgery or a stretch injury as one would get with “whiplash” (see post: “Whiplash and occipital neuralgia: what’s the connection?”, 01/21/14). Many of the post-surgical changes are detailed in my more recent post, “WHY DO NERVES TAKE SO LONG TO RECOVER?”, 04/29/14) and will not be repeated here. So what happens to a nerve after prolonged compression?
Well, way back in 1995, some of the first peripheral nerve surgeons were able to demonstrate exactly that in a non-human primate model. They induced carpal tunnel syndrome in cynomologous monkeys and then biopsied the nerves at various time points thereafter. They then also looked to see what happens when those same nerves were decompressed. The results are seen in the attached picture. In the upper left “normal”, you see a biopsy of the median nerve in a non-compressed animal. The black rings are the thick myelin sheaths that surround the white spaces which are the nerve fascicles themselves and help the nerves conduct impulses more efficiently. After six months of compression (upper right) you can see that the myelin sheaths are already beginning to thin out and the nerves no longer conduct as quickly. Clinically that may manifest as intermittent numbness and tingling and on EMG you are likely to find prolonged conduction velocity. With prolonged compression (12 months, bottom left) you not only see further thinning of the myelin sheaths, but fewer numbers of nerves (white spaces surrounded by thin black rings). Now you may clinically have constant numbness and the EMG may find decreased amplitude since there are fewer nerve fibers actually conducting impulses. You can imagine what would happen if the nerve were left alone even longer. After decompression (bottom right) you can see that the myelin sheaths never fully return, but the number of axons (nerve fibers) increases as the nerve recovers.
So what does this have to do with ON? The answer is that it really doesn’t matter what’s compressing the nerves (muscles, discs, fascia, blood vessels) the long-term effects are the same as those noted above. Has this been proven directly for the greater occipital nerve, for example, - no, but there is no reason to suspect that the sequelae of compression of peripheral nerves in the head/neck would be different than those at the wrist. Therefore it stands to reason that if there is mechanical compression on a nerve, all the medicine in the world won’t relieve that pressure - it has to be removed. If that is done within a timely fashion, the nerve could recover, if not, it won’t. How much pressure is too much and how much time is too much? Those are questions we don’t have answers to and I’m not sure we will any time soon. However, for most people suffering from the often debilitating pain of ON, it cannot be soon enough.
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