7 physiologic background of dry needling

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Physiologic background DR. SUBHANJAN DAS, PT [email protected] +91 8967549104 Dry Needling Instructor MPT (Musculoskeletal & Sports) Assoc. Prof., BIMLS, Burdwan

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7 physiologic background of dry needling

Transcript of 7 physiologic background of dry needling

Page 1: 7 physiologic background of dry needling

Physiologic background

DR. SUBHANJAN DAS, [email protected]

+91 8967549104Dry Needling Instructor

MPT (Musculoskeletal & Sports)Assoc. Prof., BIMLS, Burdwan

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Also in the serieshttp://www.slideshare.net/SubhanjanDas/introduction-to-dry-nee

dling

http://www.slideshare.net/SubhanjanDas/2-brief-hisory-of-needling

http://www.slideshare.net/SubhanjanDas/3-superficial-dry-needling

http://www.slideshare.net/SubhanjanDas/4-indications-of-dry-needling

http://www.slideshare.net/SubhanjanDas/6-dangers-of-dry-needling

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Physiological effectsHealing effectsEffects on trigger pointsAnalgesic effects

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Healing effectsImmediately after the needle is introduced

into the skin, there are evidences of increased capillary permeability producing rapid local vasodilatation.

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The insertion of the needle causes a minute injury to the epithelium.

Injury potentials are generated and can persist and provide electrical stimulation for days until the miniature wound heals1.

The injury potentials are known to accelerate healing by creating galvanotaxis (polarity directed cell migration) along with a host of other biochemical events.

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The needle, once inserted, can be manipulated by rotation and pistoning.

It has been found that needle manipulation produces winding and gathering of collagen around the needle.

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Within minutes of needle rotation, this pulling of collagen toward the needle induces an active cellular response in connective tissue fibroblasts up to several centimeters away from the needle2. This transduction of the mechanical signal into fibroblasts can lead to a wide variety of cellular and extracellular events leading to neuromodulation and healing3.

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Needle insertion in the skin also releases cortisol, body’s own steroid1.

Increased local cortisol levels have catabolic effect on connective tissue stimulating tissue remodelling and scar tissue breakdown.

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Effect on trigger pointTrigger points are small muscular

contractures caused by dysfunctional motor endplates4.

Activation of trigger points may be caused by acute or chronic muscle overload, activation by other trigger points, homeostatic imbalances, direct trauma to the vicinity,  radiculopathy, infections etc.

Needling is a widely accepted treatment choice for deactivation of trigger points.

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When the needle is inserted directly to the trigger point (Deep Dry Needling: DDN), a small muscle contraction is obtained, which is called Local Twitch Response (LTR).

LTRs normalize the chemical environment of active MTrPs and diminish endplate noise associated with trigger point instantaneously5.

On the other hand in superficial dry needling (SDN) only the skin overlying the trigger point is pierced. This releases the trigger point by reflex inhibition.

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Analgesic effectNeedling produces stimulation of superficial

A delta fibers in the skin6. This effect may persist for hours after

needling due to the injury potential7. Stimulation of the sensory afferent A δ

activates enkephalinergic, serotonergic, and noradrenergic inhibitory systems. Together they work as opioid mediated analgesia system (OMAS).

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This analgesic system involves segmental as well as suprasegmental pathways8 working through Substantia Gelatinosa of Rolando (SGR) in the spinal cord.

The following description of needling related pain modulation is based on Bowsher’s work9.

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Pain pathway

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The segmental modulation

A delta primary afferent receptors project to marginal cells (M) which carries pinprick sensations in the lateral spinothalamic tract.

The A delta primary afferent receptors also project to enkephalinergic stalked cells (ST) in the spinal cord, which inhibits the SGR cells and blocks the transmission of C pain.

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The serotonergic system

The fast pain carrying fibers of lateral spinothalamic tract give collaterals to peri aqueductal gray matter (PAG) of mid brain.

PAG in turn activates Nucleus Raphe Magnus (NRM) of medulla which stimulates ST cells and inhibit SGR.

The prefrontal cortex can influence the PAG activation via hypothalamus and activate this descending pain suppression system.

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The noradrenergic system

The nucleus paragigantocellularis (PGC) of medulla influences locus coeruleus (LC) of pons or similar noradrenergic brainstem structures which controls firing of SGR and modulates pain.

This too can be influenced by Pre frontal cortex- hypothalamus axis.

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Direct input of A delta generated information to Reticularis Dorsalis (R) in medulla inhibits pain by its influence on spinal segment.

Diffused noxious inhibitory control

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references1. Gunn C. Chan, Acupuncture and the Peripheral Nervous System A

Radiculopathy Model2. Helene M et al, Connective Tissue Fibroblast Response to Acupuncture: Dose

Dependent Effect of Bidirectional Needle Rotation, J Altern Complement Med. 2007 April ; 13(3): 355–360.

3. Langevin HM et al. Subcutaneous tissue fibroblast cytoskeletal remodeling induced by acupuncture: Evidence for a mechanotransduction-based mechanism. J Cell Physiol 2006;207:767-774

4. Simons DG, Hong CZ, Simons LS. Endplate potentials are common to midfiber myofacial trigger points. Am J Phys Med Rehabil 2002;81(3):212-22.

5. Shah JP, Phillips TM, Danoff JV, Gerber LH. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol 2005;99:1980-1987.

6. Bowsher D, Physiology and pathophysiology of pain, , aim.bmj.com September 19, 2012

7. Baldry PE, Superficial Versus Deep Dry Needling, ACUPUNCTURE IN MEDICINE 2002;20(2-3):78-81.

8. Baldry PE. Acupuncture, Trigger Points and Musculoskeletal Pain. Edinburgh, UK: Churchill Livingstone, 2005.

9. Bowsher D. Mechanisms of acupuncture. In: Filshie J White A, editors. Medical Acupuncture - A Western Scientific Approach. Edinburgh: Churchill Livingstone; 1998. p. 69-82