Spasticity is one of the major impairments impacting motor function and pain in patients following cerebrovascular accidents (i.e., stroke survivors).1 This velocity-dependent resistance to quick stretch has a delayed onset which can occur in as little as one week to three months following vascular lesion.1,2
The mechanism of spasticity remains in question; however it has been correlated to malfunction of the reticulospinal tract and the vestibulospinal tract. These two tracts have an excitatory and inhibitory component that modify posture, locomotion, motor function, and strength.1,3,4,5 Following a vascular lesion, the inhibitory portions of the RST and VST are damaged due to their location near the injury. Ultimately this causes the excitatory portion to go unchecked by facilitating hyperexcitability of the stretch reflex causing spasticity.1
Although centrally mediated, chronic spasticity can create secondary change to peripheral tissues which may contribute to myofascial pain syndromes as a result of compensatory movement patterns.6 Furthermore, chronic spasticity leads to fibrosis of connective tissue and high concentration of collagen fibers that reduces muscle pliability.6,8
Notably, stroke-induced sarcopenia appears to contribute to a rapid decrease in muscle strength; however, the neurophysiologic mechanisms remain unknown compared with non-spastic tissue.7 The hemiparesis commonly seen in stroke survivors also perpetuates further muscle stiffness due to constant activation of the muscle spindle and 1A fibers leading to a lack of contraction release.8 Notably, adaptive changes to the Achilles tendon have been visualized on ultrasound in hemiparetic case studies linked to altered gait mechanics.9 Bone mineral density loss also has been found on the affected side with faster progression in the acute phase following a stroke.10,11
CENTRAL & PERIPHERAL MECHANISMS OF DRY NEEDLING
Dry needling can be used to treat myofascial pain syndromes and is not limited to only targeting trigger points; that is, dry needling may also target connective tissues and/or neural structures.12 The central mechanism for analgesia from dry needling likely includes the release of endogenous opioids from the pituitary gland and a decrease in epinephrine and serotonin within the brain, which drives down regulation of pain pathways.13,15
Peripherally, dry needling serves to decrease acetylcholine at the motor end plate, improve vasodilation, and increase sarcomere length.14 Mechanotransduction of the needle, including winding and electrical dry needling, have also been shown to activate fibroblasts to release adenosine triphosphate (ATP).15 Mast cells are also stimulated to release neuropeptides and histamine which contribute to increased release of ATP, local inflammation, and peripheral sensitization.15,27 This high concentration of ATP is quickly broken down into adenosine and can bind to adenosine receptors located in the central and peripheral nervous systems.15,28 Although this pathway is not fully understood, the adenosine pathway does exert an effect on CNS pain modulation.24 Furthermore, dry needling can be used to reduce fibrosis by improving the viscoelastic properties of collagen fibers (i.e., align the collagen matrix) following the mechanical stimulation of the needle along with the aforementioned chemical pathways.15
DRY NEEDLING FOR SPASTICITY
Emerging randomized controlled trials are encouraging for the use of dry needling for short-term improvement in patients with spasticity associated with chronic stroke. Dry needling has been found to reduce spasticity in the short-term (as measured by the Modified Ashworth Scale), improve resting joint position, decrease motor action potentials (via EMG), and improve gait speeds (as measured by the Timed-up-and-Go).16,17,18 In addition, several systematic reviews appear to favor the use of dry needling for management of spasticity and short-term pain relief in stroke survivors.19, 20, 21, 22 Notably, a recent clinical trial reported improvements in muscle spasticity following dry needling in post-stroke survivors.23 In addition, although lower on the evidence hierarchy, several cases studies have found dry needling useful for neurologically mediated spasticity.24,25,26
CONCLUSION
The use of dry needling in the management of spasticity for stroke survivors may include unidirectional needle rotation, bidirectional needle rotation, pistoning, and/or electrical stimulation. Dry needling may reduce the fibrotic nature of spastic tissue in hemiparesis by increasing the viscoelastic properties of muscle and collagen fibers. Moreover, dry needling may increase vasodilation to spastic tissues that are restricted in mobility and movement.
AUTHORS
Marchelle Bostic, DPT, Cert. DN
Fellow-in-Training, AAMT Fellowship in Orthopaedic Manual Physical Therapy
IRG Physical & Hand Therapy, Seattle, WA
James Dunning, PhD, DPT, MSc, FAAOMPT, Dip. Osteopractic
Director, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Montgomery Osteopractic Physical Therapy & Acupuncture, Montgomery, AL
Paul Bliton, DPT, OCS, SCS, FAAOMPT, Dip. Osteopractic
Associate Director, AAMT Fellowship in Orthopaedic Manual Physical Therapy
William S. Middleton Veterans Hospital, Madison, WI
Patrick Gorby, DPT, MPH, FAAOMPT, Dip. Osteopractic
Assistant Director, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Gorby Osteopractic Physiotherapy & Wellness, Colorado Springs, CO
James Escaloni, DPT, OCS, FAAOMPT, Dip. Osteopractic, RMSK
Senior Instructor, AAMT Fellowship in Musculoskeletal Sonography
Senior Instructor, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Wellward Regenerative Medicine, Lexington, KY
Ian Young, DSc, OCS, SCS, Dip Osteopractic, RMSK
Senior Instructor AAMT Fellowship in Musculoskeletal Sonography
Senior Instructor AAMT Fellowship in Orthopaedic Manual Physical Therapy
Tybee Osteopractic & Wellness, Tybee Island, GA
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