Needling Sensation

Needling is a process of nociceptive stimulation with both mechanical and biochemical effects. Mechanical effects include physical pressure on and disturbance of the nociceptors of the sensory nerve endings. The biochemical effects are needle-induced neurogenic inflammation and the secretion of neuropeptides from nociceptive nerve endings and tissues, substance P, bradykinin, prostaglandins, serotonin, somatosta-tin, and calcitonin gene-related peptide (CGRP).

Sterile, disposable stainless-steel needles with plastic guide tubes are currently available, which technically facilitates needling. Once the needle touches or penetrates the superficial skin, the responses from the nociceptors of cutaneous sensory nerves are very diverse. The sensation could be nerve shock spreading proximally and distantly, sharp pain, tingling, and sometimes a stinging or burning sensation. Once the needle reaches deeper tissues, such as the fascia, muscles, blood vessels, and periosteum, the affected nerves are mostly muscular nerves and sensory nerves such as unmyelinated nerve endings (group IV, or C fibers) that innervate blood vessels and other soft tissues. Sharp pain is felt when blood vessels are penetrated, but otherwise the sensations may include dull ache, pressure, heaviness, distention, compression, soreness, tingling, numbness, and nerve shock. The sensation depends on the type of nerve fibers that the needle encounters and on the condition of the surrounding tissue, such as the presence of tissue perfusion and inflammatory mediators.4

Anything that has produced tissue damage or that threatens to do so in the immediate future can be defined as noxious, and the type of axon that responds selectively to the noxious quality of a stimulus is therefore, by definition, a nociceptor. Such axons are not pain receptors because nociception is not pain.

One important neurophysiologic occurrence during nociceptive needling is the antidromic activity of peripheral nerves. Needling as a nociceptive excitation stimulates the release of substance P from the unmyelinated nerve endings, which triggers a cascade of events that result in neurogenic inflammation, a sterile inflammation that is caused by antidromic neuronal activity in sensory nerve fibers through the release of endogenous substances with vascular and cellular actions. When nocicep-tive stimulation occurs, the action potential of sensory neurons travels in the periphery (not centrally) and releases those endogenous substances from the receptive endings. This indicates that a nociceptor not only is a passive sensor of noxious stimuli but also is capable of changing the chemical composition of its environment as part of its reaction to a tissue-threatening stimulus5,6 (Fig. 6-4).

Stimulation of nociceptors activates the release of substances stored in the varicosities of the nerve ending.

Needling points on limbs may produce a brief sensation of electric shock, running up or down along the whole length of the limb. When the torso is needled, the sensation can be experienced as a local response. A few patients experience the unusual sensation of energy circulating from the needling site up to the head and down to the toes. This might happen because of the combination of cutaneous and muscular nerve conduction.

Arteriole

Arteriole

Mast cell

Unmyelinated (group IV)

fiber

Axon

Noxious

reflex

Figure 6-4 Antidromic neuronal activity during tissue-threatening stimulus. When noxious stimulation occurs, the sensory nociceptor senses the tissue injury and releases endogenous substances that change the chemical environment as part of the reaction. The action potentials propagate distantly (against afferent direction), a sensation often felt during needling therapy. The free nerve endings terminate on the wall of an arteriole. In the varicosities of the nerve ending, neuropeptides such as substance P (SP), somatostatin (SOM), and calcitonin gene-related peptides (CGRP) are stored. The mechanical stimulus also acts indirectly on the ending by releasing endogenous algesic substances from the blood such as bradykinin (BK), prostaglandins (PGs), or serotonin (5-HT). Substance P causes vasodilation, an increase in vascular permeability, and degranulation of mast cells, which release histamine as a vasodilator. (Adapted from Mense S, Simons DG: Muscle pain, Philadelphia, 2001, Lippincott Williams & Wilkins, Fig. 2.7.)

The diversity of the sensations can be explained by the types of nerve fibers stimulated by the needling (Table 6-1). Patients should be warned that some needling sensations such as aching or soreness may last for 1 or 2 days.

A needling-induced lesion stimulates the epidermis, dermis, and underlying connective tissues (elastic fibers, collagen, basal lamina, deeper fascia), muscular tissues (skeletal muscles and smooth muscles of blood vessels) and nervous tissues (nerve fibers of sensory neurons and postganglionic

TABLE 6-1 Needling Sensation and the Related Nerve Fibers in the Muscles

Types of Afferent Nerve Fibers Velocity (Milliseconds-1) Types of Sensation

TABLE 6-1 Needling Sensation and the Related Nerve Fibers in the Muscles

Types of Afferent Nerve Fibers Velocity (Milliseconds-1) Types of Sensation

Type I (Aa) (Muscle spindles

72-

120

None or numbness

and tendon spindles)

Type II (AP)

42-

72

Numbness, pressure

Type III (AS)

12-

-36

Heaviness, distention, pressure, compression, aching

Type IV (unmyelinated, C)

0.5

-1.2

Soreness, tingling, and burning pain

neurons). The cells injured by the needling will be replaced with fresh cells of the same type without scar formation.

The needling mechanisms are both local and systemic:

1. Local skin reaction and cutaneous microcurrent mechanism

2. Local interaction between needle shaft and connective tissues

3. Local relaxation of current muscle shortening and contracture, which improves local blood circulation through the autonomic reflex

4. Neural mechanism: nociceptive and motor neuronal activation, CNS-mediated neuroendocrine activity, segmental and nonsegmental pathways

5. Blood coagulation and lymphatic circulation

6. Local immune responses

7. DNA synthesis to replace the injured tissues and repair the lesions

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