top of page
  • YouTube
  • Twitter
  • Facebook


Dry Needling Treatment

Dry Needling is initiated into many types of diagnosis, this is another way that Lakeway Aquatic Physical Therapy can help speed your recovery from your injury.  

I like to say we have many tools in our tool chest and we are able to use a variety of  tools to 

CALL TODAY 512 261-0620

How Does Dry Needling Work?


There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). 


DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non- opioid pain relief via serotonin and norepinephrine from the brain stem


DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines.


Recent studies demonstrate that DN combined with mechanical and/or electric stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels.


Electric DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP (Calcitonin Gene-Related Peptide) and substance-P, altering the stimulation of certain receptors to reverse hyperalgesia.


CGRP is derived mainly from the cell bodies of motor neurons when synthesized in the ventral horn of the spinal cord and may contribute to the regeneration of nervous tissue after injury. Conversely, CGRP is derived from dorsal root ganglion when synthesized in the dorsal horn of the spinal cord and may be linked to the transmission of pain


It also encourages the supra-optic nucleus to release oxytocin to quiet ASIC (acid-sensing ion channel) receptors peripherally and stimulate opioid interneurons spinally.


Moreover, EDN inhibits ERK1&2 kinase (extra-cellular signal regulated kinases, which mediates cell proliferation & programmed cell death) pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ (nociceptin/ orfan, which acts on pain sensation and fear via non-opioid pathways) to reverse C-fiber mediated central changes.


Mechano-transduction of fibroblasts and peripheral nerves via subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons.


The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling.


Mechano-transduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain.


DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

Peripheral & Spinal Mechanisms of Pain & Dry Needling (DN)- Mediated Analgesia: A Clinical Resource Guide for Healthcare Professionals.  Butts, et al. Int’l J Phys Med & Rehab. 2016.

bottom of page