Fibromyalgia Meets the Gun Dry Needlers

By John Quintner (Physician in Pain Medicine and Rheumatology)

John Quintner - 12.3.12

John Quintner

In Aussie slang, the term “gun” was originally applied to the champions of the sheep shearing industry. But its origins have been traced back to Old English, when the girls’ name Gunhilda became slang for “war machine”. It seems an appropriate term to use for therapists that skilfully wield long needles in the course of their occupation.

Intramuscular stimulation (IMS) is one technique of “dry needling” that is being recommended by some authorities as a scientifically credible form of treatment for those with fibromyalgia (chronic widespread pain):

This article is written to assist those with fibromyalgia who might be considering IMS. The source of the information discussed in this article is easily accessible on the “Gunn IMS” website:

What is intramuscular stimulation?

During the latter decades of the 20th century, Dr Chit Chan Gunn, a distinguished Canadian physician, developed his technique of dry needling muscles, which became very popular in Vancouver, British Columbia. It is here where he founded the “Institute for the Study and Treatment of Pain”. IMS is now being offered by specially trained physical therapists around the world.

The rationale for using acupuncture needles to penetrate deeply within muscle tissue is the belief that such muscles have become “contracted and shortened from distress.”

According to Dr Gunn, “Penetration of a normal muscle is painless; however, a shortened, supersensitive muscle will ‘grasp’ the needle in what can be described as a cramping sensation.”

IMS is said to “release” muscle shortening, which in turn relieves “mechanical pain from muscle pull”. At face value, IMS therefore appears to be a panacea for the treatment of a variety of musculoskeletal conditions:

“When competently performed, IMS has a remarkable success rate, as proven by the amelioration of symptoms and signs, even for chronic back pain with root signs.”

What is the theory behind IMS?

Dr Gunn’s theory derives from what is known as “Cannon and Rosenblueth’s Law of Denervation.” This Law holds that “the normal physiology and integrity of all innervated structures are dependent on the arrival of nerve impulses via the intact nerve to provide a regulatory or trophic effect.”

When the flow of nerve impulses is blocked, the innervated structures become “highly irritable” and develop abnormal sensitivity or “supersensitivity.”

According to Cannon and Rosenblueth’s Law: “All denervated structures develop supersensitivity (including skeletal muscle, smooth muscle, spinal neurons, sympathetic ganglia, adrenal glands, sweat glands, and brain cells).”

When muscles lose their nerve supply, “These structures overreact to many forms of input, not only chemical, but physical inputs as well, including stretch and pressure. Supersensitive muscle cells can generate spontaneous electrical impulses that trigger false pain signals or provoke involuntary muscle activity.”

But Dr Gunn has gone further by declaring that complete physical interruption of the nerve supply to an organ (e.g. a muscle) is not necessary for the development of supersensitivity. Partial denervation is said to result in the same effect. However, whether this phenomenon has ever been demonstrated is doubtful, either in humans or experimental animals.

Quite a lot is now known about the effects of denervation on muscles. According to Massey [2006]:

when there is axonal or anterior horn cell injury, muscle fibers are denervated and no longer able to contract, producing weakness. With partial denervation, the muscle is proportionally weak … When denervation within a muscle is incomplete, soon there are attempts to reestablish innervation. If there are nearby surviving axons, they produce collateral sprouts directed toward the denervated or orphaned muscle fibers. These sprouts are capable of reestablishing a neuromuscular junction with the denervated muscle fiber.”

How does partial denervation occur?

Gunn claims that partial denervation of muscles can be the result of nerve damage from any number of disease processes:

“Of the innumerable causes of nerve damage, such as trauma, metabolic, degenerative, toxic, and other conditions, chronic attrition from spondylosis (the structural disintegration and morphologic alterations that occur in the intervertebral disk, with pathoanatomic changes in surrounding structures) is by far the most common. The spinal nerve root, because of its vulnerable position, is notably prone to injury from pressure, stretch, angulation, and friction.”

In other words, age-related changes present in intervertebral discs (“spondylosis”), which are almost universal in adults, renders adjacent nerve roots more vulnerable to injury:

“Ordinarily, spondylosis follows a gradual, relapsing, and remitting course that is silent, unless and until, symptoms are precipitated by an incident often so minor that it passes unnoticed by the patient. All gradations of Spondylosis can exist, but early or incipient spondylotic changes, even when unsuspected, can nevertheless irritate and upset function in the segmental nerve.”

The remarkable claim

Without scientific evidence, Dr Gunn then speculates: “Many diverse pain syndromes of apparently unknown causation may be attributed to the development of hypersensitive receptor organs and supersensitivity in pain sensory pathways.”

How are these changes of denervation detected?

According to Dr Gunn, there are no objective means (e.g. by electromyography, laboratory tests, or radiology) of detecting the presence of (partial) denervation supersensitivity in muscles.

On the contrary, changes of muscle denervation have been observed on muscle biopsy [Bernat & Ochoa 1978] and are detectable by the use of electromyography [Mills 2005].

In any case, the physical signs of “denervation supersensitivity” are said to be quite subtle and detectable only by a properly trained clinician.

These signs may include: muscle tenderness and shortening, palpable muscle knots and restricted joint range. Other local signs, which are autonomic in origin, might include increased sweating over the area of pain, “goose bumps”, hair loss, coldness, and swelling.

Location of needle insertion

A warning is issued to the clinician undertaking intramuscular stimulation: “Treatment, when limited to painful peripheral muscles, can fail if the pain is perpetuated by shortening in paraspinal muscles (at the same segment levels) that compresses the nerve root.”

It is claimed, again without evidence, that shortening in paraspinal muscles can be detected by palpation; needle exploration is said to be confirmatory when “resistance to needle penetration is substantially increased at the involved level compared to the levels above and below.”

But the clinician may encounter considerable difficulties with “needle diagnosis”:

“Occasionally, the needle encounters a shortened muscle that seems bony-hard and cannot be penetrated to the depth reached at other levels. Penetration then is only possible by applying some considerable force, and after repeated “pecking”. When the needle finally enters the dense contracture, the patient experiences the intense cramp described above. This gradually diminishes as the needle-grasp is liberated.”

What are the so-called effects of IMS?

In Dr Gunn’s opinion, the needle firstly stimulates a “stretch receptor” (i.e. a muscle spindle) and this produces a reflex relaxation (i.e. lengthening) of the muscle. Secondly, because the needle also causes a small injury with bleeding, the natural healing process is initiated. The third claim is that the treatment “creates an electrical potential in the muscle to make the nerve function normally again.”

None of these effects are supported by scientific evidence.

How is this information relevant to the treatment of fibromyalgia?

Based on many of its clinical features, Dr Gunn suggests that fibromyalgia could well be the clinical expression of functional and/or structural changes that have occurred in the peripheral nervous system.

He believes that in patients with fibromyalgia, “shortened muscles are diffusely present in axial as well as limb musculature; although they can produce muscle ache and pain by compressing intramuscular nociceptors, they can also produce pain by pulling upon tendons and ligaments. However, most significantly, shortening of paraspinal muscles can compress the intervertebral disc and irritate the nerve root to create a vicious circle that can perpetuate the problem.

If this were true, it would seem quite logical to attempt to lengthen the involved muscles by following Dr Gunn’s protocol of IMS.

But are there major flaws in Gunn’s formulation?

There is little if any scientific evidence to support the practice of IMS. Yet a search on Google quickly shows that this treatment is being offered in many parts of the world. It is therefore appropriate to point out the obvious flaws in the construct of IMS:

  1. The concept of partial denervation of muscles causing them to become “supersensitive” is not supported by the neurophysiological literature.
  2. There is no evidence that inserting needles into muscles can result in their lengthening (if indeed they were ever in a shortened condition).
  3. It is unclear how the healing process of a needle-inflicted muscle injury is able to desensitise that muscle (if indeed it has been sensitised).
  4. The ability to reliably detect the subtle clinical signs of muscle shortening and supersensitivity said to typify partially denervated muscles has not been independently confirmed.
  5. The belief that an acupuncture needle can be a specific diagnostic tool for any musculoskeletal condition defies logic.
  6. Very few randomised controlled studies have been conducted to assess the outcome of IMS treatment. In their systematic review Kim et al. [2012] found insufficient evidence to support the efficacy of IMS for several localised musculoskeletal conditions (low back pain, tension type headache and shoulder pain attributed to “myofascial trigger points”). No trials of IMS included patients with a diagnosis of fibromyalgia.
  7. There is no mention of the possibility that temporary pain relief following IMS (a painful procedure) is an example of counter-irritation analgesia, which has a long history. Link:
  8. There is no discussion of contextual factors that may be important in determining the outcome of treatment. They include: the context in which the treatment is administered (“the clinician’s language and manner”); the expectation bias of the clinician and the patient (“this treatment always works”); confirmation bias (“you have improved as a result of my treatment”); regression to the mean (“I have good days and bad days. You treated me on a bad day”) and a natural tendency for the patient to recover, irrespective of the administered treatment.
  9. In contemporary neuroscience, the use of the terms as “pain sensory pathways” and “pain signals” are outdated. There are no such things!


From the available evidence, IMS (along with other forms of “dry needling”), even when performed by “gun” needlers, cannot be recommended as rational scientific treatment for patients with fibromyalgia.


Bernat JL, Ochoa JL. Muscle hypertrophy after partial denervation: a human case. J Neurol Neurosurg Psychiatr 1978; 41(8): 719-725.

Kim T-H, Lee C-R, Lee MS. Intramuscular stimulation therapy for healthcare: a systematic review of randomised controlled trials. Acupunct Med 2012; 30: 286-290. doi: 10.1136/acupmed-2012-010182

Massey JM. In: Kimura J, ed. Peripheral Nerve Diseases, Handbook of Clinical Neurophysiology, vol 7. Elsevier Health Sciences, 2006: 467-486.

Mills KR. The basics of electromyography. J Neurol Neurosurg Psychiatry 2005; 76 (Suppl ii): ii32-ii35