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For a change I do not have to create a alias for this individual. This pic is all over twitter and facebook now. It was taken by Sandy Hilton, and is of her colleague Sarah Haag, who hosted a DNM class in their Chicago PT clinic this past weekend.
Sarah's issue was not pain. The woman is a very bendy woman who moves all the time, does yoga, studies burlesque dancing for fun.
Her issue was that although she could do splits on one side, she couldn't on the other.
Her issue was lack of ROM, interoceptive asymmetry, and a feeling as though there was a block in her body that wouldn't resolve no matter what she did.
Many years earlier she had been on a cycling tour. During that tour she had developed low back pain and left sciatic radiculopathy. She tells me she can vouch for Michael Shacklock's new paper, Normal multiplanar movement of the spinal cord during unilateral and bilateral straight leg raise: Quantification, mechanisms and overview - she had loss of straight leg raise with pain felt in the left side, no matter which leg she tried to raise.
She dealt with it by doing back extensions, and eventually the pain on movement resolved. She was left, however, with these residual effects. It wasn't a painful bother, but it was a bother nonetheless.
It makes sense to me that the spinal cord would hijack all input from that side to create an endless positive feedback loop of withdrawal reflex in anything it was able to commandeer.
It makes sense to me that her spinal cord got so good at maintaining its protective loop that it prevented movement with very little to no nociceptive input anymore.
It makes sense to me that all that was required was some nice sensory rehabilitation directed toward more rostral parts of her brain, i.e., somatosensory cortex (which maps skin surface) and insular cortex (which maps pleasurable input from skin, and from anywhere else too).
It makes sense to me that feeding (changing blood flow around and through) a few small cutaneous nerves, setting them up so their input would change, in a completely innocuous way, would suffice to help those brain parts mount an all-clear signal to send down through all the evolutionarily older parts of her NS, including the dorsal horn. With descending modulation. To tell the spinal cord to stop being so protective by high-jacking the ability of contractile elements to lengthen.
So, with just 15 minutes or so of attention to putative cutaneous neural tunnel syndromes of iliohypogastric and anterior inguinal nerves, and me not having to work very hard at all, her ROM improved quite dramatically and her interoception changed from a blocked experience to a yes-ciceptive one of block having been removed. A perceptual block-ectomy. All accomplished through changing of perception, via cutaneous nerve sliding, and deliberate exploitation of ruffini ending while lying relaxed in a quadruped position (legs in flexion over a bolster). Well, OK, the treatment of ilohypogastric neural structure by dragging it through neural tunnel required a bit more strategic positioning and handling and sweat. But we gotter done.
Now Sarah's ROM for splits is a lot more bilateral, with much easier trunk and hip extension available to her on the left. This was just the day before yesterday. There is another day of receptor turnover to go before Day 4 reassessment, figuring out if more treatment would even be necessary. She's doing all the motion-is-lotion business meanwhile, and maintaining her improvement.
Why makes complex things like the NS, and some holding pattern it's in, complicated by tissue-based nonsense when you can make things simple by affecting it directly, through skin?
Sarah's issue was not pain. The woman is a very bendy woman who moves all the time, does yoga, studies burlesque dancing for fun.
Her issue was that although she could do splits on one side, she couldn't on the other.
Her issue was lack of ROM, interoceptive asymmetry, and a feeling as though there was a block in her body that wouldn't resolve no matter what she did.
Many years earlier she had been on a cycling tour. During that tour she had developed low back pain and left sciatic radiculopathy. She tells me she can vouch for Michael Shacklock's new paper, Normal multiplanar movement of the spinal cord during unilateral and bilateral straight leg raise: Quantification, mechanisms and overview - she had loss of straight leg raise with pain felt in the left side, no matter which leg she tried to raise.
She dealt with it by doing back extensions, and eventually the pain on movement resolved. She was left, however, with these residual effects. It wasn't a painful bother, but it was a bother nonetheless.
It makes sense to me that the spinal cord would hijack all input from that side to create an endless positive feedback loop of withdrawal reflex in anything it was able to commandeer.
It makes sense to me that her spinal cord got so good at maintaining its protective loop that it prevented movement with very little to no nociceptive input anymore.
It makes sense to me that all that was required was some nice sensory rehabilitation directed toward more rostral parts of her brain, i.e., somatosensory cortex (which maps skin surface) and insular cortex (which maps pleasurable input from skin, and from anywhere else too).
It makes sense to me that feeding (changing blood flow around and through) a few small cutaneous nerves, setting them up so their input would change, in a completely innocuous way, would suffice to help those brain parts mount an all-clear signal to send down through all the evolutionarily older parts of her NS, including the dorsal horn. With descending modulation. To tell the spinal cord to stop being so protective by high-jacking the ability of contractile elements to lengthen.
So, with just 15 minutes or so of attention to putative cutaneous neural tunnel syndromes of iliohypogastric and anterior inguinal nerves, and me not having to work very hard at all, her ROM improved quite dramatically and her interoception changed from a blocked experience to a yes-ciceptive one of block having been removed. A perceptual block-ectomy. All accomplished through changing of perception, via cutaneous nerve sliding, and deliberate exploitation of ruffini ending while lying relaxed in a quadruped position (legs in flexion over a bolster). Well, OK, the treatment of ilohypogastric neural structure by dragging it through neural tunnel required a bit more strategic positioning and handling and sweat. But we gotter done.
Now Sarah's ROM for splits is a lot more bilateral, with much easier trunk and hip extension available to her on the left. This was just the day before yesterday. There is another day of receptor turnover to go before Day 4 reassessment, figuring out if more treatment would even be necessary. She's doing all the motion-is-lotion business meanwhile, and maintaining her improvement.
Why makes complex things like the NS, and some holding pattern it's in, complicated by tissue-based nonsense when you can make things simple by affecting it directly, through skin?
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