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IN-DEPTH:
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
Acupuncture and Pain Management
James D. Kenney, DVM
There is a large and expanding body of scientific evidence supporting the use of acupuncture in pain
management. In the last decade, our understanding of how the brain processes acupuncture analgesia has undergone considerable development. Profound studies on neural mechanisms underlying
acupuncture analgesia have evolved rapidly and predominately focus on cellular and molecular
substrate and functional brain imaging. The currently understood mechanisms of acupuncture
analgesia are complex and involve direct and indirect neurohumoral effects that block pain perception, reduce the pain response, relieve muscle spasms, and reduce inflammation. The analgesic
mechanisms of acupuncture involve the spinal cord grey matter, hypothalamic-pituitary axis, midbrain periaqueductal grey matter, medulla oblongata, limbic system, cerebral cortex, and autonomic
nervous system. Electroacupuncture (EA) stimulation of these sites results in activation of descending pathways that inhibit pain through endogenous opioid, noradrenergic, and serotonergic systems. There are growing numbers of human trials supporting the use of acupuncture as an evidencebased practice for pain management in human medicine. There are many studies that support the
efficacy of acupuncture for low back pain, neck pain, chronic idiopathic and migraine headaches, knee
pain, shoulder pain, fibromyalgia, temporomandibular joint pain, and postoperative pain. Although
the number of well-designed, controlled clinical research studies in veterinary medicine is lagging
behind the number of studies in human medicine, much of the basic science research has been done
in animals with neurophysiology that is more similar to veterinary patients than humans. Although
there is research to support EA as an evidence-based practice for the control of back pain in horses,
additional studies are needed in other clinical situations in veterinary medicine where pain management is required. Author’s address: PO Box 717, Clarksburg, NJ 08510-0717; e-mail: jdkenneydvm@
msn.com. © 2011 AAEP.
1.
Introduction
According to the World Health Organization (WHO),
the effectiveness of acupuncture analgesia has been
established in controlled clinical trials, and the use
of acupuncture to control chronic pain is comparable
with morphine without the risk of drug dependence
and other adverse side effects.1 Acupuncture is an
effective treatment for many types of pain, is welltolerated by patients, and has a minimal likelihood
of serious adverse effects.1–3 Modern and traditional acupuncture techniques have been shown to
provide relief from low back pain, neck pain, chronic
idiopathic or tension headaches, migraine headaches, knee pain, shoulder pain, fibromyalgia, temperomandibular joint pain, and postoperative pain.2
Acupuncture was more effective for chronic pain
than placebos (sham acupuncture) based on the results of systematic reviews of pooled data from highquality randomized controlled trials.1,3 For shortterm outcomes (less than 6 mo), acupuncture was
significantly superior to sham treatments for back
pain, knee pain, and headache. For longer-term
NOTES
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Table 1.
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
Definitions of Terms
Term
Neuropathic pain
Nociceptive pain
Nociceptors
Nociception
Noxious
Analgesia
Anti-nociception
Internuncial neuron
Inhibitory neurotransmitters
Excitatory
neurotransmitters
PAG
Hyperalgesia
Allodynia
Primary hyperalgesia
Secondary hyperalgesia
Synaptic plasticity
Endorphins
Lower motor neurons
Definition
Pain from damage to the nervous system
Pain from stimulation of nociceptors
Peripheral nerve endings in the skin, muscles, ligaments, joints, viscera, and
other structures that initially respond to a painful stimulus
Pain sense
Mechanical, thermal, or chemical stimulus that alters nociceptors and causes
pain
Reduced sensitivity to painful stimuli
Analgesia
Neuron interposed between and connecting two other neurons
Inhibit receptors on neurons; examples are serotonin, GABA,
norepinephrine, and epinephrine
Activate receptors on neurons; examples are glutamate and aspartate
Periaqueductal grey matter that surrounds the cerebral aqueduct in the
midbrain
Increased sensitivity to pain
Non-noxious stimuli perceived as painful
Hypersensitivity of the peripheral nociceptors
Central sensitization and hypersensitivity of CNS neurons associated with
synaptic plasticity
Ability of the connection or synapse between two neurons to change in
strength and responsiveness
Endogenous opioid polypeptide neurotransmitters that inhibit pain stimuli
similar to morphine; includes ␤-endorphins, enkephalins, dynorphins,
endomorphin-1, and endomorphin-2
Neurons with cell bodies in the spinal cord whose axons form peripheral
motor nerves and terminate in skeletal, cardiac, and smooth muscles
outcomes (6 –12 mo), acupuncture was significantly
more effective for knee pain and tension-type headache but inconsistent for back pain (one meta-analysis was positive and one meta-analysis was
inconclusive).
Acupuncture can effectively treat chronic pain of
the locomotor system with restricted movements of
the joints, because it not only alleviates pain but
also reduces the muscle spasm that causes reduced
mobility.4,5 Muscle spasm can result in abnormal
loads placed on joints, often causing clinical signs of
pain before changes are demonstrable on radiographs. In controlled studies of joint pain of unknown etiology, acupuncture was superior to
conventional therapy, delayed-treatment controls,
and several other sham acupuncture techniques.
According to the WHO analysis of controlled studies,
acupuncture can effectively reduce pain from cervical spondylitis and other causes of neck pain, periarthritis of the shoulder, fibromyalgia, fasciitis,
epicondylitis, low back conditions, sciatica, osteoarthritis, and radicular and pseudoradicular pain syndromes.1 In some cases, acupuncture integrated
with conventional treatments was more effective
than conventional treatments alone.
Although acupuncture may not reduce pain to the
degree that some conventional treatments reduce
pain, it is associated with a low incidence of serious
adverse side effects.1 For example, acupuncture
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2011 Ⲑ Vol. 57 Ⲑ AAEP PROCEEDINGS
may not be as effective as corticosteroids for pain
relief in some patients with rheumatoid arthritis,
but chronic corticosteroid use may result in gastrointestinal ulceration, osteopenia, muscle loss, and
other adverse effects. Acupuncture not only reduces pain and inflammation but has positive effects
on the immune system, which directly benefits patients with rheumatoid arthritis, and less conventional medication may be needed.1
2.
Pain Pathways and Modulation
Pain may be classified as acute or chronic, adaptive
or maladaptive, and neuropathic or nociceptive, and
these types of pain have different underlying mechanisms.2 Neuropathic pain occurs from damage to
the peripheral or central nervous system (PNS or
CNS, respectively). Pain associated with activation of sensory (afferent) receptors (nociceptors) by
mechanical, thermal, or chemical stimuli is considered nociceptive pain and will primarily be reviewed
here. The pathways involved in nociceptive pain
are also involved with the modulation of pain by
acupuncture. Understanding PNS and CNS pain
pathways is essential to understanding acupuncture
analgesia.6 Terms associated with pain and pain
modulation are defined in Table 1.
Nociception (the sensation of pain) is extremely
complex and involves more than simple transmission of pain signals from nociceptors of the PNS to
IN-DEPTH:
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
Fig. 1. The basic three neuron pathways of pain (blue, first-order neurons; red, second-order neurons; green, third-order neurons) of
the neo-spinothalmic system and the multisynaptic pathways of the paleo-spinoreticulo-diencephalic system and the bilateral
spinothalamic system common in non-primate animals (black broken lines).
regions of the CNS for conscious perception. Pain
signals are modified by substances released from
cells at the site of pain, within the spinal cord grey
matter, and by the concomitant stimulation of CNS
inhibitory descending pathways from higher brain
centers. The main neuroanatomic structures involved in the complex process of pain perception
include the peripheral sensory receptors (nociceptors), afferent peripheral nerve fibers, dorsal horns
of the spinal cord (body) or sensory nucleus of the
trigeminal nerve (head), ascending pathways to the
reticular formation in the medulla oblongata and
midbrain, thalamus, hypothalamus, limbic system,
and cerebral cortex as well as descending CNS pathways from all these sites.6,7
Ascending Pathways
From a simplified functional neuroanatomic standpoint, the most direct pain pathways, like other sensory systems, can be basically viewed as a three
neuron system: first-order, second-order, and
third-order neurons (Fig. 1).7 Noxious (painful)
mechanical, thermal, or chemical stimuli are detected by nociceptors (primarily free nerve endings)
of somatic and visceral first-order afferent nerves.
When a specific threshold of excitation is reached,
electrical action potentials transmit along their peripheral processes to cell bodies in the dorsal root
ganglia and then into the spinal cord, where they
synapse on second-order neurons in the dorsal horn
grey matter. Stimulated second-order neurons
propagate electrical signals along their axons, forming ascending tracts in the spinal cord and brainstem that synapse on third-order neurons in the
thalamus and other brain stem structures. The activated third-order neurons propagate electrical signals along their axons that terminate in the
somatosensory cortex of the cerebrum as well as
other regions of the brain, where conscious perception and evaluation of pain occur (Fig. 1). Conscious perception of pain may occur at both thalamic
and cortical levels in animals.7
For nociception from the head, electrical impulses
of first-order neurons ascend in the trigeminal nerve
(cranial nerve V) to cell bodies in the trigeminal
ganglia and continue on to enter the brainstem and
synapse with second-order neurons in the trigemiAAEP PROCEEDINGS Ⲑ Vol. 57 Ⲑ 2011
123
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Paleo-spino-reticulothalamci
SC Laminae I, II,
and V
SC Laminae I and
II
Medulla, medulla oblongata.
*Unmyelinated; all other types have some myelin.
0.5–2.0
C*
IV*
0.2–1.5
1–5
A␦ (␦)
III
3–30
Free nerve endings
Touch, pain, and
temperature
Pain and temperature
Gracilus and cuneatus
(dorsal columns)
Neo-spino-thalamic
Proprioception and touch
Muscle spindles and all
cutaneous mechanoreceptors
Free nerve endings
6–12
A␤ (␤)
II
35–75
13–20
A␣ (␣)
Ib
80–120
Golgi tendon organ
Proprioception
Spino-cerebellar
Medulla SC Lamina
VII (T1-L1)
Medulla SC Lamina
VII (T1-L1)
Medulla
Spino-cerebellar
Proprioception
Muscle spindles
12–20
A␣ (␣)
Ia
80–120
Ascending
tract system
Sensation
Receptors
Conduction
velocity (m/s)
Diameter
(␮m)
Erlanger-Gasser
system
Fiber
type
nal sensory nuclei in the medulla oblongata, pons,
and midbrain (Fig. 1).6,7 The second-order neurons, from the trigeminal sensory nuclei, ascend the
brainstem to synapse with third-order neurons in
the thalamus and other brainstem regions similar to
second-order neurons from the body and viscera.
The first-order neurons that transmit pain and
other sensations are classified according to their
diameter, speed of conduction, function, and degree
of myelination (Table 2).6 There are two classifications for these fibers, numerical and alphabetical,
which can be confusing when reading the literature.
The alphabetical Erlinger-Gasser classification will
be used throughout this review. The A␦ and C fibers primarily conduct signals from nociceptive
stimuli. A␦ fibers are myelinated, are rapidly conducting, and mainly sense pain from the skin, and C
fibers are unmyelinated, are slowly conducting, and
sense pain from skin, bone, viscera, and other structures (Table 2). If A␦ and C fibers are stimulated
simultaneously, the pain experienced will come in
two phases. The first phase will be sharp and localized and may be of short duration, because it is
mediated by the faster-conducting A␦ fibers. The
later phase is from the smaller and slower-conducting C fibers, and it will be dull and non-localized but
last longer.
The second-order neuron cell bodies are located in
one or more physiologically distinct layers (laminae)
of the spinal cord dorsal horn grey matter (Table
2).6,7 There are six laminae in the dorsal horn (IVI), three in the ventral horn (VII-IX), and an additional column of cells clustered around the central
canal as Lamina X. The C fibers terminate mainly in
Laminae I and II, where their axons secrete Substance P or Vasoactive Intestinal Polypeptide depending on whether they arise from somatic or
visceral structures, respectively. The A␦ afferents
terminate primarily in Laminae I, II, and V.
Axons of the second-order neurons of the spinal
cord grey matter form two main ascending pathway
systems that carry nociception: the neo-spinothalamic pathway system and the paleo-spino-reticulodiencephalic pathway system (Fig. 1 and Table
3).4,6 – 8 In Laminae I and V, where the majority of
A␦ nerves terminate, second-order neurons immediately cross to the opposite side and form the neospinothalamic tract system in the anterolateral
portion of the spinal cord. These neurons terminate on third-order neuron cell bodies in the ventral
posterior lateral (VPL) nucleus of the thalamus and
project to the somatosensory cortex (Fig. 1 and Table
3). The neo-spinothalamic system is direct, fast,
and localizing and is the basic three-neuron system
of discriminative pain.
The paleo-spino-reticulo-diencephalic pathways
primarily originate from neurons in Laminae VII
and VIII in the ventral horn of the spinal cord grey
matter, with some input from Lamina V, and they
connect to C fibers that terminate in Laminae I and
II through internuncial neurons (Fig. 1 and Table
Termination
site
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
Table 2. Sensory Peripheral Nerve Types and Their Function
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Table 3.
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
Comparison of the Two Main Central Pain Pathway Systems
Neo-Spinothalamic System
Paleo-Spino-Reticulo-Diencephalic System
Origination
Laminae I, IV, and V (stimulated by A␦
neurons)
Transmission
speed
Subcortical targets
Direct fast
Thalamic nuclei
Cerebral cortex
Pain type
Ventral posterior lateral
Parietal lobe (primary somatosensory cortex)
Sharp pain, discriminative pain, and pin-prick
pain
Laminae I, IV, and V (stimulated by C neurons)
connect through internuncial neurons to Laminae
VII and VIII
Indirect slow
None
2).4,6 – 8 Most axons from neurons in Laminae VII
and VIII cross to the opposite side in primates and
form their pathways in the anterolateral portion of
the spinal cord adjacent to the neo-spinothalamic
pathways. They pass medially into the reticular
formation (central core) of the brain stem and the
medial intralaminar nuclei of the thalamus, and
then, they project to the cingulate gyrus and frontal
cortex (Table 2).8
In non-primates, some second-order neurons cross
and others remain on the same side to form crossed
and uncrossed spinothalamic pathways.6,7 The
spinothalamic pathways in animals are interrupted
by axons exiting and reentering after synapsing
with other spinal cord neurons, forming diffuse,
bilaterally represented multisynaptic pathways.
Some second-order nociceptive neurons may also ascend to the thalamus and other brainstem regions
through the dorsal column medial-lemniscal system,
which mainly transmits proprioceptive information
as well through multifunctional spinoreticular
tracts and the fasciculus proprius.7
The reticular formation (central core of the medulla oblongata, pons, and midbrain) contains bifurcating axons that project up through the paleospino-reticular-diencephalic pathways to the
diencephalon (thalamus and hypothalamus) and
down through reticulospinal tracts to the spinal cord
to influence muscle tone. Axons from the reticular
formation that terminate in the hypothalamus also
synapse with autonomic neurons, which descend to
the medulla oblongata and spinal cord to affect autonomic lower motor neurons and alter vascular
tone, heart rate, gastrointestinal function, and other
visceral functions.4,6 – 8 Consequently, pain may
cause autonomic signs of increased heart and respiratory rates, vasoconstriction, nausea, and
vomiting.
Part of what makes the pain experience so complex and varied between individuals is the interpretation of pain by higher brain centers. The limbic
system, which includes the hypothalamus, hippocampus, amygdala, and cingulate gyrus, is
thought to control the motivational, behavioral, and
emotional responses to pain.4,6 – 8 The pain stimu-
Reticular formation, hypothalamus, and limbic
system
Intralaminar nuclei and other midline nuclei
Cingulate gyrus, prefrontal cortex, and frontal lobe
Dull pain, affective arousal components of pain, and
tissue-damage pain
lus projected to the frontal cortex is interpreted
along with past experiences, mood, and current circumstances, and this combination influences the
pain experience.
Pain Modulation
The normal neurophysiology of pain modulation is
also important to review to better understand potential sites of acupuncture pain control.6 When a
noxious stimulus is experienced, endogenous networks are activated that modulate pain at the peripheral nociceptors within tissues, in the dorsal
horn grey matter of the spinal cord, in the network
of relay stations between the dorsal horn and the
cerebral cortex, and within the cerebral cortex (Fig.
2).4,6 – 8
The first-order afferent fibers not only connect to
second-order neurons for the ascending pain pathways but also send off branches that synapse with
inhibitory internuncial neurons in the spinal cord
grey matter.4,6 – 8 Considerable modulation of pain
occurs at the dorsal horn grey matter, where inhibitory internuncial neurons secrete ␥-aminobutyric
acid (GABA) and other neurotransmitters that inhibit C fibers and reduce activation of second-order
spinal cord nociceptive neurons. Larger-diameter
afferent nerves, like A␤ and A␦ fibers, terminate on
inhibitory internuncial neurons in the dorsal horn
grey matter, which in turn, inhibit the nociceptive C
fibers and reduce the amount of Substance P released (Fig. 2).4,6,8
The ascending pathways of second-order nociceptive neurons give off branches that synapse with
neurons at several sites in the brainstem that form
descending pathways that inhibit pain. Neurons in
the midbrain periaqueductal grey matter (PAG)
send descending projections to the rostral ventromedial medulla and spinal cord dorsal horn, which
form the primary neuroanatomical pathways mediating opioid-based analgesia (Fig. 2).4,6,8 –10 Endorphins (␤-endorphin, enkephalin, and dynorphin) are
neurotransmitters released by neurons in response
to painful stimuli and used internally to reduce
pain. ␤-Endorphin is found primarily in the pituitary gland, but enkephalin and dynorphin are proAAEP PROCEEDINGS Ⲑ Vol. 57 Ⲑ 2011
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Fig. 2. Three main regions for normal pain modulation and sites of EA pain suppression. (1) Spinal cord dorsal horn. Some of the
painful stimuli from C fibers (blue) are blocked (black bar) by impulses from the A␤ and A␦ fibers (purple) stimulated by EA and pain,
which arrive first and compete for sites on the second-order neurons in the spinal cord dorsal horn grey matter. In addition, branches
of the A␦ fibers stimulate spinal cord internuncial neurons that release enkephalin, dynorphin, GABA, and other inhibitory
substances. (2) Descending endogenous opioid pathways. Neurons in the diencephalon, midbrain PAG, and medulla oblongata
(stimulated by ascending pain pathways and EA) release endorphins through descending pathways to the spinal cord grey matter to
block ascending pain impulses (red line represents the primary pathways mediating opioid-based analgesia) as well as into the blood
through the pituitary. (3) Descending seratonergic and noradrenergic inhibitory pathways. Neurons in the cerebrum, diencephalon,
midbrain, pons, and medulla (stimulated by ascending pain pathways and EA) release serotonin, norepineprine, and other inhibitory
neurotransmitters through descending pathways to the spinal cord grey matter to block ascending pain impulses (green line
represents the primary seratonergic pathways).
duced throughout the nervous system, including the
dorsal grey matter of the brainstem and spinal cord.
Enkephalinergic internuncial neurons are located
on the border of Laminae I and II of the spinal cord
grey matter and alter the responses of second-order
nociceptive neurons located there. Endorphins interact with opioid receptors on neurons to reduce the
intensity of pain. Opioid receptors are found in
many areas of the brain, but they are especially
concentrated in the PAG and dorsal horns of the
spinal cord.
Serotoninergic descending inhibitory pathways
are also suggested to be an important mechanism of
analgesia (antinociception). Serotonin (5-hydroxy
tryptophan [5HT]) is a neurotransmitter, which in126
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hibits pain transmission, leading to a decrease in
perceived pain. Descending pathways from the
midbrain PAG and locus coeruleus and raphe nuclei
of the medulla oblongata are inhibitory to dorsal
grey column nerves of the spinal cord, and some of
the inhibition is mediated by serotonin (Fig.
2).6,7,9,10 The pain suppressing effect of antidepressants is probably because of their ability to enhance
transmission down these pathways by blocking the
uptake of 5HT.
Pathological Pain States
The peripheral terminals of C fibers become sensitized during tissue damage and subsequent inflammation by the release of bradykinin, serotonin,
IN-DEPTH:
INTEGRATIVE MEDICINE (COMPLEMENTARY & ALTERNATIVE MEDICINE)
potassium, adenosine 5⬘-triphosphate (ATP), prostaglandins, and leukotrienes from damaged tissue and
inflammatory cells. These sensitized C fibers secrete Substance P (a neuropeptide) and calcitonin
gene-related peptide, which have a vasodilatory effect on local blood vessels and stimulate additional
release of inflammatory mediators, further sensitizing the peripheral nociceptors.4,8 Sensitization
lowers the threshold for activation, increases the
magnitude and duration of activation, and results in
peripheral (primary) hyperalgesia and allodynia
(non-noxious stimuli being perceived as painful).
If there is massive or prolonged stimulation of C
fibers, there is activation of N-methyl-D-aspartate
(NMDA) receptors, which reduces the receptor
threshold for activation of the dorsal horn neurons
and spontaneous depolarization. This activation
results in increased pain impulses ascending to
higher levels in the brain.4,6 Chronic pain stimulation not only causes local and spinal cord hypersensitivity to pain but also increases sensitivity
through its effects on higher synaptic sites in the
brainstem and cerebrum. These changes are a type
of synaptic plasticity and central (secondary) hyperalgesia and allodynia result.4,11
Chronic pain, as distinct from acute pain, distinguishes itself by its persistence in the absence of
inflammation or other obvious ongoing tissue-damaging processes, delay in onset after the precipitating injury, and abnormal or unpleasant sensations
such as burning, searing, or deep, aching pain unresponsive to conventional anti-inflammatory
drugs.11 Persistent pain and sensitization can often lead to additional loss of function from reduced
range of motion in joints and the mechanical effects
of muscle shortening. Prolonged limitations of
movement can result in disuse atrophy of muscles,
which also limits mobility.
Pain not only originates from cutaneous structures but also arises from nociceptive receptors in
muscles, tendons, and joints.4,5 Focal acute pain
may be associated with muscle spasm and lactic acid
accumulation and may result in muscle shortening.11 A major consequence of muscle shortening is
the continuous, unremitting pull on the structures
to which the muscle attaches. Muscle contraction
that spans a joint can create pressure within the
joint, abnormal patterns of motion, arthralgia (joint
pain), injury, and finally, degenerative joint disease.
The presence of muscle shortening also has deleterious effects on the tendons and ligaments. Unrelenting muscle tension on these structures may be
the precipitating factor in bicipital bursitis, epicondylitis, hock and stifle degeneration, upper suspensory pain, chondromalacia of the stifle joint, and
other pathologic conditions that are frequently seen
in veterinary practice. Continuous pressure on
vertebral joint surfaces from muscle contractions
causes vertebral facet degeneration, which may be a
key factor in interspinal osteoarthrosis (spondylosis)
or kissing spine conditions in the equine and other
species.
Neuropathic pain is also common in humans and
animals. Inflammation and primary damage to
nerves alter their normal response to stimulation
and modulation and can cause muscle spasm and
shortening,
which
also
amplify
the
pain.4,5,11 Nerve root inflammation from spondylosis, intervertebral disk protrusion and other degenerative vertebral column changes causes spasm and
shortening of paravertebral muscles that compress
intervertebral discs and create a self-perpetuating
cycle of contraction, inflammation, radiculopathy,
and pain.11
3.
Mechanisms of Acupuncture Pain Control
Acupuncture is the stimulation of specific pre-determined points (acupoints) near the surface of the
body, which produces a therapeutic effect by evoking
homeostatic mechanisms within the nervous, immune, endocrine, cardiovascular, and other body
systems to promote self-healing.6,8 –12 Acupuncture stimulates small nerve endings and other structures around the acupoints, which result, in both
local and distant changes within the body. Ancient
traditional Chinese medical theories have explained
the effects of acupuncture based on empirical observations and descriptions of naturally occurring phenomena, and the underlying complex neurochemical
mechanisms behind their observations have been
explored in scientific studies for the past 50 yr.13
Our understanding of how the brain processes
acupuncture analgesia has undergone considerable
development.14 Acupuncture analgesia is manifested only when the intricate feeling (soreness,
numbness, heaviness, and distension) of acupuncture in patients occurs after acupuncture manipulation. Manual acupuncture (MA) is the insertion of
an acupuncture needle into an acupoint followed by
the twisting of the needle up and down by hand.
In MA, all types of afferent fibers (A␤, A␦, and C) are
activated. In electrical acupuncture (EA), a stimulating current through the inserted needle is delivered to acupoints. Electrical current intense
enough to excite A␤ and part of A␦ fibers can induce
an analgesic effect. Acupuncture signals ascend
mainly through the spinal ventrolateral funiculus to
the brain. Many brain nuclei composing a complicated network are involved in processing acupuncture analgesia, including the nucleus raphe magnus
(NRM), PAG, locus coeruleus, arcuate nucleus (Arc),
pre-optic area, nucleus submedius, habenular nucleus, accumbens nucleus, caudate nucleus, septal
area, amygdale, etc. Acupuncture analgesia is essentially a manifestation of integrative processes at
different levels in the CNS between afferent impulses from pain regions and impulses from acupoints. In the last decade, profound studies on
neural mechanisms underlying acupuncture analgesia predominately focus on cellular and molecular
substrate and functional brain imaging and have
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developed rapidly. Diverse signal molecules contribute to mediating acupuncture analgesia, such as
opioid peptides (␮-, ␦-, and ␬-receptors), glutamate
(NMDA and AMPA/KA receptors), 5HT, and cholecystokinin octapeptide (CCK-8). Among these molecules, the opioid peptides and their receptors in the
Arc-PAG-NRM-spinal dorsal horn pathway play a
pivotal role in mediating acupuncture analgesia.
The release of opioid peptides evoked by electroacupuncture is frequency-dependent. EA at 2 and 100
Hz produces, respectively, releases of enkephalin
and dynorphin in the spinal cord. CCK-8 antagonizes acupuncture analgesia. The individual differences of acupuncture analgesia are associated
with inherited genetic factors and the density of
CCK receptors. The brain regions associated with
acupuncture analgesia identified in animal experiments were confirmed and further explored in the
human brain by means of functional imaging. There are still many unanswered questions
concerning the mechanisms of acupuncture analgesia, but there is no doubt that acupuncture produces
effects at many different sites that result in
analgesia.9,10,12,13
The analgesic effects of EA on brain function can
be visualized using functional magnetic resonance
imaging (fMRI) and positron emission tomography
(PET) scans.9 With a painful stimulus, the fMRI
shows activation of areas in the cingulate cortex,
thalamus, and other regions of the brain, but there
is a significant decrease of activation in these areas
after acupuncture. This finding suggests that acupuncture desensitizes or blocks pain at these levels.9
This finding may be associated with acupuncture
modulation of pain at the dorsal horn grey matter
and a reduction of ascending impulses along the
spinothalamic pathway systems, or it may be associated with neurochemical alterations higher in the
brainstem.
The currently understood mechanisms of acupuncture pain control are complex and involve direct
and indirect neurochemical effects that block pain
perception, reduce the pain response, relieve muscle
spasm, and reduce inflammation. The acupuncture technique used affects the degree of pain control. In studies comparing EA with dry-needle
acupuncture, EA produced greater brain changes on
fMRI than dry needles and also elicited a better
analgesic effect.15,16 In other studies, bilateral EA
stimulation was superior to unilateral stimulation
for analgesia, and unilateral stimulation had the
most powerful analgesic effects on the contralateral
side.17,18 EA is recommended over non-manipulated, dry-needle acupuncture for pain management
and is used in most studies of acupuncture analgesia.13,19 fMRI data suggest that acupuncture needle stimulation at two different depths of needling,
superficial and deep, does not elicit significantly
different blood oxygen level-dependent (BOLD)
responses.20
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Analgesic effects of EA have been shown to occur
in the spinal cord grey matter, hypothalamic-pituitary axis, midbrain PAG, pons, medulla oblongata,
limbic system, cerebral cortex, and autonomic nervous system (Fig. 2). Changes in EA stimulation
frequency can alter the site of antinociceptive activities, and the antinociceptive effects of EA in normal
and hypersensitized painful humans and animals
can be quite different.6,13 A striking feature of acupuncture-induced analgesia is its long-lasting effect,
which has a delayed onset and gradually reaches a
peak even after acupuncture needling is terminated.
A non-repeated, event-related (NRER) fMRI paradigm and control theory-based approach was adopted to capture the detailed temporal profile of
neural responses induced by acupuncture.21 Neural activities at the different stages of acupuncture
presented distinct temporal patterns in which consistently positive neural responses were found during the period of acupuncture needling, whereas
much more complex and dynamic activities were
found during a post-acupuncture period. The
amygdala and perigenual anterior cingulate cortex
(pACC), exhibited increased activities during the
needling phase, which decreased gradually to reach
a peak below the baseline. The PAG and hypothalamus presented saliently intermittent activations
across the whole fMRI session. The overall findings indicate that acupuncture may engage differential temporal neural responses as a function of time
in a wide range of brain networks.
A relatively new analysis method, functional connectivity fMRI (fcMRI), has great potential for
studying continuous treatment modalities such as
EA. Compared with sham acupuncture, EA can
significantly reduce PAG activity when subsequently evoked by experimental pain. Findings indicate the intrinsic functional connectivity changes
among key brain regions in the pain matrix and
default mode network during genuine EA compared
with sham EA.22
One of the earliest proposed mechanisms of EA
pain control used the Melzack-Wall Gate Control
Theory in which modulation of pain occurred
through normal antinociceptive neuronal circuits in
the spinal cord.6 Based on this theory, it was proposed that EA stimulates A␤ and A␦ nerve fibers
(Table 1), which would transmit impulses to the
spinal cord faster than C nerve fibers and engage
synaptic sites on dorsal horn neurons. The later
arriving pain signals from C fibers would have fewer
sites on which to synapse, because the gates would
be closed (synaptic sites are already occupied) (Fig.
2). Using this theory, EA was thought to induce a
segmental spinal inhibition of nociceptive inputs
and result in an immediate, short-term, non– opioidmediated analgesia because of reduced release of
Substance P from C fibers.6,9,23
The analgesic effects of EA are more complex than
can be described using the Gate Control theory
alone, because branches of A␦ and C fibers also
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synapse with inhibitory internuncial neurons in the
spinal cord grey matter, resulting in the release of
inhibitory neurotransmitters that block incoming
and outgoing pain impulses.13,19,23 EA of the A␦
fibers results in the stimulation of inhibitory enkephalinergic internuncial neurons in the outer part
of Lamina II of the spinal cord that block C fiber
pain impulses. Low-frequency EA at ST-36 significantly inhibited cold allodynia in a rat tail model of
neuropathic pain through stimulation of GABA inhibitory interneuron systems in the spinal cord,
whereas sham EA at a non-acupoint and dry-needle
acupuncture at ST-36 were ineffective.16 The analgesic effects of EA have also been shown to be related to inhibition of the release of excitatory
neurotransmitters (glutamate and aspartic acid),
which normally transmit pain signals from the spinal cord to higher brain levels.24
Activation of the NMDA subtype of glutamate receptors and subsequent nitric oxide (NO) production
are important factors in central sensitization and
the development of hyperalgesia.4,6,25,26 In a study
of the role of NO in a carrageen-induced inflammation model, it was suggested that EA was a biochemical modulator in the spinal cord and prevented the
activation of the NMDA receptors and central sensitization.25 The combination of EA with ketamine, an NMDA receptor antagonist, also
enhanced the antihyperalgesic effect. In another
rat neuropathic pain model study, EA stimulation
decreased NO synthase expression in the L4 –5 spinal cord and decreased mechanical allodynia secondary to nerve injury.26
Other studies have shown the profound effect of
EA on the hypothalamic-pituitary axis.6,13,19,27
The hypothalamic-pituitary axis not only produces
the well-known neuroendocrine effects, but it is part
of the central descending pain-inhibitory pathways
involving endogenous opioids and most likely also
plays a role in cholinergic anti-inflammatory mechanisms through the vagus nerve.28 EA has been
shown to increase circulating ␤-endorphin in the
blood, which is most likely associated with ascending afferent stimulation of the hypothalamus and
release
of
these
substances
from
the
pituitary.6,13,19,23,27
EA also activates neurons in the midbrain PAG
region that stimulate the descending endogenous
opioid inhibitory pathways to reduce pain (Fig.
2).4,6,13,18,23 Low-frequency EA (10 –20 Hz) stimulates the release of ␤-endorphin, enkephalin, and
endomorphin, which activates the ␮- and ␦-opioid
receptors, and higher-frequency (100 –200 Hz) EA
stimulates dynorphin, which activates the ␬-opioid
receptors to produce analgesia.13 A mixture of frequencies (low-frequency stimulation for a period followed by high-frequency stimulation) is suggested to
be most effective, because it stimulates all opioid
receptors.23 In a carrageenan-induced arthritis
pain model in rats, low-frequency EA pre-treatment
had an antinociceptive effect against inflammatory
pain through the ␮-opioid receptor.18 EA of 10 Hz
at ST-36 significantly improved the weight-bearing
force, and this positive effect was abolished when a
selective antagonist of the ␮-opioid receptor was
administered.
Central sensitization (secondary hyperalgesia)
can be associated with tissue inflammation or peripheral nerve injury and is an important cause of
persistent pain. Animal models of capsaicin-induced pain have well-defined peripheral and central
sensitization components, and therefore, they are
useful for studying the peripheral and central analgesic effects of acupuncture. In a recent study of
the analgesic effects of EA on capsaicin-induced central sensitization, EA produced a stimulation pointspecific analgesic effect that was mediated by
activating endogenous ␮- and ␦-opioid receptors in
the spinal cord.29 In a mouse cancer pain model,
EA decreased the overexpression of Substance P in
the dorsal horn, increased ␤-endorphin, and reduced
the pain response to mechanical stimulation, showing the effectiveness of EA to control pain, even in
the presence of central sensitization.30
High-frequency EA (100 –200 Hz) not only induces
dynorphin release in the spinal cord but also increases the release of serotonin, epinephrine, and
norepinephrine (inhibitory neurotransmitters),
which inhibit pain signals.6,13,19,31 In another rat
neuropathic pain model, studying pain modulation
in the PAG region, EA completely abolished histamine and dopamine release, which is normally increased after a painful stimulus, and increased the
release of norepinephrine in the PAG regions.32
EA is thought to also enhance the effects of descending serotoninergic pain inhibition.13 EA has been
shown to activate neurons containing serotonin, epinephrine, and norepinephrine in the nucleus raphe
magnus and locus coeruleus of the medulla oblongata, which suppress pain and hyperalgesia through
descending pathways to the spinal cord.33
In a study of neuropathic pain in rats, changes of
spinal synaptic plasticity were affected by EA.34
EA at a low frequency of 2 Hz at acupoints ST-36
and SP-6 reduced neuropathic pain and induced
long-term depression of the C fiber-evoked potentials in a spinal nerve ligation model in rats.
Muscle contracture (non-voluntary muscle contraction) creates an energy crisis and pain in shortened muscles but can be relaxed by inserting
needles into the corresponding acupoints to restore
normal muscle physiology.4,11,35 Acupuncture can
alleviate the pain, and it can allow the muscles to
relax and the associated structures to return to normal patterns of motion. Intramuscular stimulation
(IMS) is a modified version of acupuncture and is
based on neuroanatomic principles.11 A basic tenet
of IMS is that acupuncture points are usually situated close to motor points within muscles or at musculotendinous junctions. Points that are effective
for treatment are at the same segmental level as the
presenting clinical signs or the injury. These
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points usually coincide with palpable muscle bands
that are tender to manual pressure. Tender points
are distributed in a segmental fashion in muscles
supplied by both dorsal and ventral nerve roots,
indicating radiculopathy. Muscles with tender
points are shortened from spasm and contracture.
Symptoms and signs typically disappear when the
tender and tight muscle bands are stimulated with
acupuncture.11 Surface electromyography (EMG)
can measure gross muscle fiber strength and show
the fatigue and asymmetrical recruitment associated with myofascial pain syndromes. The typical
myofascial pain patient has surface EMG evidence
of one or more inhibited muscles. Evidence of fatigue shown by asymmetrical scalene muscle contractions and the increased activity of the muscles
recorded on the EMG when an acupuncture needle
is inserted can be shown.11 Another clinical example of the use of IMS is acupuncture of Ashi points
for the treatment of piriformis muscle pain (piriformis syndrome). In a recent study of 80 cases of
piriformis syndrome, one-half of the cases were randomly assigned to a group that received an inhibitory-needling acupuncture method on Ashi points,
and the other one-half of the cases received a routine-needling acupuncture method at GB-30, BL-54,
and GB-34. Both groups responded positively (92%
in Ashi points inhibitory-needling group and 82.5%
in transpositional acupoint routine-needling group),
but stimulating Ashi points produced a significantly
better response than routine stimulation of transpositional acupoints (p ⬍ 0.05).36
The midbrain PAG region not only inhibits pain
through the release of endogenous opioids but also
causes changes in the heart and respiration rates
and blood pressure associated with pain through the
hypothalamus and autonomic nervous system.
EA alters the effects of pain on viscera and blood
vessels by its effects on the PAG and hypothalamic
regions and descending pathways from these regions to the vagus nerves and parasympathetic and
sympathetic spinal cord lower motor neurons. EA
also induces local spinal cord segmental reflexes
that affect vascular tone and other autonomic functions.6,13 EA affects the inflammatory reflex
through the autonomic nervous system, regulates
the immune system, and reduces inflammation-induced hyperalgesia.13 At 10 Hz, EA significantly
reduced complete Freund’s adjuvant-induced hind
paw edema and increased plasma levels of corticosterone, but it produced no noticeable signs of stress.
At 10 Hz but not 100 Hz, EA suppresses inflammation by activating the hypothalamus-pituitary-adrenal axis (HPA) and the nervous system.37 Besides
the mediation by different central structures, acupuncture may have direct effects on regulating peripherally the release of some inflammatory and
pain mediators.38 It has been shown that EA significantly suppresses behavioral hyperalgesia in a
rat model of persistent inflammatory pain by suppressing the spinal neurokinin-1 (NK-1) receptors
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and that NK-1/Substance P receptors play important roles in nociception and hyperalgesia at the
spinal cord level.39 Electroacupuncture can effectively decrease the pro-inflammatory cytokine of interleukin-1 (IL-1) and IL-6, increase the inhibition
cytokine of IL-4 and IL-10, and improve the internal
environment of occurrence and progression of rheumatoid arthritis.40
Chronic pain syndromes often involve the autonomic nervous system, and persistent increased
sympathetic tone causes regionalized hypothermia
from vasoconstriction.41 Because these pain syndromes are not related to inflammation, they are
unresponsive to anti-inflammatory medication.
The types of pain experienced include hyperesthesia, burning, aching, throbbing, and allodynia.
Thermal imaging provides objective, measurable evidence of the ability of acupuncture to restore normal blood flow through effects on autonomic
regulation of vasomotor tone.41 Increased sciatic
nerve blood flow measured in rats by laser Doppler
flowmetry was observed with nerve root stimulation
(100%) compared with lumbar muscle acupuncture
(56.9%), suggesting that, in addition to its influence
on the pain inhibitory system, acupuncture triggers
a transient change in blood circulation.42
EA may also affect the motivational, behavioral,
and emotional responses to pain through effects on
the hypothalamic, limbic, and higher cortical regions.6,19 The effects of acupuncture to calm Shen
and reduce anxiety are well-known, and anxiety and
depression are factors in chronic pain. In a study of
changes in cortical metabolites using fMRI in depressed and normal human patients, EA was shown
to have a significant effect on brain neurochemistry
compared with controls and EA positively affected
depressed patients.44
Known variations in the response of individuals to
acupuncture treatment complicates the evaluation
of acupuncture for pain control.9 According to the
work by Cho et al.,9 about 28% of humans are excellent responders, 64% are good and average responders, and 8% are weak or non-responders.9 In a pilot
study of psychophysical pain responses in humans
after dry-needle, EA, and sham treatments, all subjects receiving one of the acupuncture techniques
had improved pain tolerance, but some responded
better to EA, and others responded better to dry
needles.44 The results of this study indicate the
existence of both individual subject and acupuncture
mode variability in the analgesic effects of acupuncture. This finding suggests that switching the acupuncture mode may be a treatment option for
unresponsive patients.
4. Clinical Research on Acupuncture for Pain Control
in Humans
A review of all the clinical research for pain control
in humans is beyond the scope of this paper, but a
few current studies that are applicable to veterinary
medicine will be discussed here. Although clini-
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cians have continued their respect and reverence for
tradition in their training, they have also recognized
the need for evidence-based medicine in their practice of acupuncture. The evidence base for acupuncture treatment in humans has changed. For
example, in 2000, an article in Cochrane Database
System Review45 stated that the evidence summarized in the systematic review did not indicate that
acupuncture was effective for the treatment of back
pain.45 In 2005, an updated systematic review of
chronic low back pain research, within the framework of the Cochrane Database System Review collaboration, indicated that acupuncture was more
effective for pain relief and functional improvement
than no treatment or sham treatment.46 Immediate and sustained pain relief was observed in people
with low back pain from lumbar spinal canal stenosis and herniated intervertebral discs who received
EA at the nerve root compared with manual acupuncture.42 Acupoint electrical stimulation at the
true acupoints, compared with placebo and sham
groups, effectively reduced postoperative pain and
analgesic usage in patients with spinal surgery receiving patient-controlled analgesia.47
A randomized, controlled trial was conducted in
255 human practices in Germany to assess quality of
life, costs, and cost-effectiveness of acupuncture
treatment plus routine care versus routine care
alone in osteoarthritis patients.48 Four hundred
eighty-nine patients with chronic pain caused by
osteoarthritis of the knee or hip were evaluated for
quality of life and costs at baseline and after 3 mo
using health insurance funds data and standardized
questionnaires. Patients receiving acupuncture
had an improved quality of life but had significantly
higher costs over the 3-mo treatment period compared with routine care alone. This increase in
costs was primarily because of the cost of acupuncture. The study concluded, however, that acupuncture was an effective treatment strategy in patients
with chronic osteoarthritis pain but might cost more
than some conventional drugs.48
Moxibustion at San-yin-jiao (SP 6) can relieve
uterine contraction pain and has no side effect to
mother and infant; it is safe, effective, and a simple
non-drug analgesia method.49 One hundred seventy-four cases of singleton pregnancy and cephalic
presentation primipara were single-blinded and
randomly divided into three groups: observation
group (59 cases), placebo-treated group (57 cases),
and control group (58 cases). The observation
group was treated with moxibustion at San-yin-jiao
(SP 6) for 30 min when the uterus cervix opening
was 3 cm, the placebo-treated group was treated
with moxibustion at no acupoint for 30 min, and the
control group was treated with routine labor nursing; the uterine contraction pain and safety of the
mother and infant were compared among the three
groups. (1) The uterine contraction pain was tested
by the Visual Analogue Scale (VAS): the scores of
VAS in the observation group were obviously de-
creased after 15 and 30 min moxibustion (both p ⬍
0.05), there were no obvious changes of the VAS
scores in the placebo-treated and control groups, and
the scores of VAS in the observation group decreased
much more obviously than the scores in the other
two groups (all p ⬍ 0.05). (2) The midwife rated the
uterine contraction pain: after 30 min moxibustion, the effective rate of labor analgesia was 69.5%
(41/59) in the observation group, which was higher
than the rates of 45.6% (26/57) in the placebotreated group and 43.1% (25/58) in the control
group, with significant differences between them
(both p ⬍ 0.05). (3) The post-partum hemorrhage
amount of the observation group was obviously
lower than the amounts of the placebo-treated and
control groups (both p ⬍ 0.05). (4) The Apgar score
of newborn was higher in the observation and placebo-treated groups than the control group (both p ⬍
0.05).
Cancer pain can destroy the quality of life of humans and animals. Treatment with opioid analgesics has significant adverse effects, including
inhibition of respiratory function, constipation, addiction, and tolerance that further decrease quality
of life. EA may be used to reduce cancer pain.
In a study of neuropathic cancer pain, sarcoma cells
were inoculated around the sciatic nerves of mice.30
The presence of embedded cancer cells that induced
mechanical allodynia was confirmed by MRI. EA
treatment significantly prolonged paw withdrawal
latency as well as shortened cumulative lifting duration compared with tumor control, suggesting reduced pain after EA.
In a review of five studies of 1,334 patients with
chronic knee pain, acupuncture was found to be
superior to sham acupuncture for pain reduction
and improved function.50 The differences were still
significant when patients were followed long term.
Their conclusions were that adequate acupuncture
treatment is superior to sham acupuncture and no
treatment for improving pain and function in patients with chronic knee pain.
A systematic review and meta-analysis of randomized controlled trials of acupuncture for neck
pain found that acupuncture was more effective
than controls in the treatment of neck pain.51 A
randomized controlled multicenter trial in Germany
was performed in 14,161 patients with chronic neck
pain (duration ⬎ 6 mo).52 Treatment with acupuncture added to routine care in patients with
chronic neck pain was associated with improvements in pain and reduced disability compared with
treatment with routine care alone.
Pain is a prevalent consequence of spinal cord
injury that can persist for years after the injury
and can have a significant impact on physical and
emotional function and quality of life. In a review of several studies, acupuncture was as effective to treat neuropathic pain from spinal cord
injury as anticonvulsant agents and tricyclic
antidepressants.53
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The etiology of peripheral neuropathy (PN) often
remains elusive, resulting in a lack of objective therapeutic strategies. Data suggest that there is a
positive effect of acupuncture on PN of undefined
etiology, which was measured by objective parameters.54 In a pilot study to evaluate the therapeutic
effect of acupuncture on PN as measured by changes
in nerve conduction and assessment of subjective
symptoms, 192 consecutive patients with PN as diagnosed by nerve conduction studies (NCS) were
evaluated over a period of 1 yr. Of the 47 patients
who met the criteria for PN of undefined etiology, 21
patients received acupuncture therapy according to
classical Chinese medicine, whereas 26 patients received the best medical care but no specific treatment for PN. Sixteen patients (76%) in the
acupuncture group improved symptomatically and
objectively as measured by NCS, whereas only four
patients in the control group (15%) did. Three patients in the acupuncture group (14%) showed no
change, and two patients showed aggravation (10%),
whereas in the control group, seven patients showed
no change (27%); additionally, in the control group,
15 patients showed aggravation (58%). Importantly, subjective improvement was fully correlated
with improvement in NCS in both groups.
Acupuncture combined with rehabilitation therapy may improve motion recovery of impaired joints.
Compared with rehabilitation therapy alone, EA
combined with rehabilitation therapy can achieve a
significant effect on the motion function recovery of
the elbow joint after fracture repair.55 EA and exercise have a greater therapeutic effect (p ⬍ 0.001)
compared with exercise on movement disorders of
shoulder joint after surgical repair of fracture of the
neck of the humerus.56 Acupuncture combined
with rehabilitation was superior to rehabilitation
alone in pain score, passive range of motion of shoulder joint, muscle strength of the middle group of
the deltoid, and upper limb motion post-stroke.57
Treatment of acute soft-tissue injury of the shoulder
joint with EA and exercise was more effective than
oral administration of ibuprofen slow-release capsules.58 Specific, one-time acupoint stimulation
significantly improved gait performance statistically
during geriatric ward rehabilitation.59 In a multiple-blinded, randomized, controlled intervention
trial, gait performance was objectively measured by
an electronic walkway before and after needling.
All gait parameters showed statistically significant
improvement in velocity, cadence, stride length, cycle time, step time, single support, and double support after verum acupuncture compared with control
treatment.
Acupuncture may be much safer than conventional treatments. Previous surveys indicated that
there was a significant but low risk of serious side
effects with acupuncture in humans ranging from
1:10,000 to 1:100,000.60 A comprehensive review of
the complementary and alternative therapies database, Medline database (1966 –1993), with extensive
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cross-referencing concluded that there were 216 reported instances of serious complications worldwide
over a 20-yr period.61
In a report of the adverse effects of 32,000 acupuncture treatments, minor adverse events, defined
as “any ill effect, no matter how small, that is unintended and non-therapeutic, even if not unexpected,” resulted from 6.71% of treatments. Most
common minor events were needle site bleeding
(3.1%), needle site pain (1.1%), and aggravation of
symptoms (0.96%), but 70% of symptoms subsequently improved.62 In a second report, 574 acupuncturists reported adverse effects of 34,000
acupuncture treatments.63 Minor adverse events
occurred in 15% of cases; the most common events
were aggravation of symptoms (2.8%), bruising
(1.7%), needle pain (1.2%), and needle site bleeding
(0.4%). Most (86%) aggravated symptoms improved, possibly indicating a healing crisis, which is
a therapeutic process involving temporary exacerbation of existing symptoms that precedes improvement. These two studies reported no lifethreatening events associated with acupuncture.
The extent of actual risk of acupuncture treatment
is difficult to quantify; however, there is a low but
significant incidence of adverse effects, usually minor, which includes needle pain, bruising, nausea or
syncope (mild and transient), and aggravation of
symptoms.64 A few case reports describe serious
side effects such as pneumothorax, spinal cord injury, hepatitis, cellulitis, and trauma from broken or
embedded needles. The serious adverse affects of
acupuncture treatment reported in the literature
may easily be prevented by straightforward precautions.60 Conditions that increase the risk of complications in acupuncture treatment in humans
include hemophilia, advanced liver disease, anticoagulation therapy, diabetes, human immunodeficiency virus (HIV) infection, and other forms of
immunosuppression, such as high-dose corticosteroid administration.65
5. Clinical Research on Acupuncture for Pain Control
in Animals
Currently, much of the practice of acupuncture in
animals is based on the results of pilot research
studies, case reports, and clinical experiences. Compared with human acupuncture, the
clinical application of veterinary acupuncture is in
the early stages of development as a science. On
the basis of the findings of a systematic review performed in 2006, there is no compelling evidence to
recommend or reject acupuncture for any condition
in domestic animals. Some encouraging data do
exist that warrant additional investigation in independent rigorous trials.66 There is a mixture of
results in clinical trials of acupuncture for pain control in animals, but there are only a few high-quality
research studies in animals that evaluate EA for
pain control.
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Analgesic effects from acupuncture have been observed in horses and other species.31,67–74 Acupuncture has been used clinically to treat lameness
and chronic back pain, including fibromyalgia syndrome.23,75– 84 There are several studies that measured the release of ␤-endorphin and cortisol during
equine acupuncture.23,85,86 In one study, dry-needle acupuncture and EA provided cutaneous analgesia in horses without adverse cardiovascular and
respiratory effects, and EA was more effective than
dry-needle acupuncture for activating spinal cord
release of ␤-endorphin into the CSF of horses.86
Controlled clinical trials have shown significant
improvement of thoracolumbar pain in horses using
objective methods of pain evaluation.83,84 In a
study of 15 horses with thoracolumbar pain, EA was
compared with phenylbutazone and saline using
thoracolumbar pain scores before and after treatment. Thoracolumbar pain scores were based on
behaviors recorded on videotape and were evaluated
and scored by a blinded, independent investigator.
EA significantly lowered pain scores of horses with
chronic thoracolumbar pain compared with phenylbutazone or saline.83 In a randomized, doubleblind, controlled trial of 23 sport horses with back
pain, objective measurements of pain threshold levels were obtained with a pressure algometer.84
Painful points (trigger points) were identified on
each horse, and baseline pain threshold measurements were taken. EA was performed at GV-20
and GV-6 and bilaterally at BL-26, BL-54, BL-21,
and BL-17 at a frequency of 20 Hz for 15 min and
80 –120 Hz for 15 min. After five treatments, pressure-induced pain was significantly reduced at trigger points in the treatment group compared with the
control group.
In another blinded, controlled study using an experimental model of lameness in the horse, the effects of EA were studied for pain control of the hoof
sole.23 Lameness scores were assigned based on an
established lameness scale with two independent
evaluators; one evaluator assessed lameness by
watching video only and was blinded to treatment.
Lameness was evaluated before tightening the
screw, after tightening the screw, after treatment
with either EA, a 0.5% bupivacaine nerve block (positive control), or a saline nerve block (negative control), immediately after loosening the screw, and 95
min later. The EA caused a significant reduction in
the lameness score compared with the saline nerve
block (negative control) as well as a significant increase in plasma ␤-endorphin.
Equine myofascial trigger points can be identified
and have similar objective signs and electrophysiological properties as those signs documented in human and rabbit skeletal muscle tissue.87 Four
horses with chronic pain signs and impaired performance showed signs compatible with the diagnosis
of myofascial trigger points in their brachiocephalic
muscle (i.e., localized tender spots in a taut band of
skeletal muscle that produced a local twitch re-
sponse on palpation). Needle EMG activity and
twitch responses were recorded at 25 positions at
the trigger point and at a nearby control point during the course of each horse’s acupuncture treatment. All subjects showed objective signs of
spontaneous electrical activity, spike activity, and
local twitch responses at the myofascial trigger
point sites within taut bands. The frequency of
these signs was significantly greater at myofascial
trigger points than control sites (p ⬍ 0.05).
EA can reduce visceral pain, regulate gastrointestinal motility, and improve regional blood flow in
animal models.23,88,89 However, EA was not as effective as butorphanol in one rectal distention
model, and bilateral EA at Guan-yuan-shu was ineffective in reducing the acute signs of discomfort
induced by small intestinal distention in a clinical
model.90,91 These results indicate the need for additional research in acupuncture for domestic animal visceral pain. EA at Nei-guan (PC-6)
significantly inhibits the frequency of transient
lower esophageal sphincter relaxations (TLESR)
and the rate of common cavity during TLESR in
cats. This effect seems to act on the brain stem and
may be mediated through NO, CCK-A receptor, and
␮-opioid receptors.92 Electroacupuncture with a
high frequency at ST-36 enhances lower esophageal
sphincter pressure (LESP) as well as esophageal
motility, whereas EA with a low frequency decreases
LESP. The effect of EA is acupoint-specific, and
this effect seems to be mediated through gastrin,
motilin, and vasoactive intestinal peptide.93
Cardiac MRI (CMRI), an important tool in monitoring cardiovascular diseases, provides a reliable
method to monitor the effects of electroacupuncture
on the cardiovascular system. Ketamine/xylazine
cocktail anesthesia caused a transient hypertension
in the cats; EA inhibited this anesthetic-induced
hypertension and shortened the post-anesthesia recovery time, countering the negative effects of anesthetics on cardiac physiology.94
In a recent study of the use of EA for postoperative
pain in intervertebral disk disease in dogs, the total
dose of fentanyl administered during the first 12 h
after surgery was significantly lower in the EA
group than in the control group, but dosages of analgesics administered from 12 to 72 h after surgery
did not differ between groups. Pain scores were
significantly lower in the treatment group than in
the control group 36 h after surgery but did not
differ significantly between groups at any other
time.95 The clinical efficacy of EA and acupuncture
combined with medication for the treatment of thoracolumbar intervertebral disc herniation in dogs
was compared with dogs treated with conventional
medicines alone in paraplegic dogs with intact deep
pain perception.96 Treatment efficacy was evaluated by postoperative neurologic function, ambulation, relapse, complication, and urinary function.
The results suggest that a combination of electro-AP
and AP with conventional medicine is more effective
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than conventional medicine alone in recovering ambulation, relieving back pain, and decreasing relapse. EA was more effective than decompressive
surgery for recovery of ambulation and improvement in neurologic deficits in dogs with long-standing severe deficits attributable to thoracolumbar
IVDD.97 The clinical success for dogs that underwent decompressive surgery and EA was
intermediate.
In controlled, double-blind clinical trial of chronic
hip pain from hip dysplasia in 78 dogs, the effect of
gold bead implants in acupoints was compared with
a sham treatment 2 wk, 3 mo, and 6 mo after treatment.98 The dogs with gold bead implants in acupoints had reduced pain and greater mobility
compared with control dogs receiving the sham
treatment.
EA may be combined with conventional anesthetic
agents to reduce dose requirements for maintenance
of anesthesia and improve cardiopulmonary function.90,99 In a study of goats, EA plus low-dose xylazine provided analgesia that was significantly
better than EA or xylazine alone.99 Furthermore,
EA plus xylazine administration at 0.1 mg/kg provided better analgesia than xylazine alone at 0.4
mg/kg.
As is the case for humans, few adverse side effects
have been associated with acupuncture in animals.
In a review of 1,292 acupuncture treatments that
were performed on 221 animals (cats, cattle, dogs,
and horses), adverse reactions to acupuncture needles totaled 4 of 12,274 needles or approximately 1
per 3,000 needles.100 Two of these reactions consisted of transient superficial edema of the skin, and
because they did not require treatment, did not appear painful, and did not show other more serious
signs, they were considered to be clinically trivial.
There was one abscess, which resolved with antibiotic treatment, and one seizure event in a 7-yr-old
spayed female Beagle that resolved without treatment and did not reoccur within a 7-mo follow-up
period. Neither complication required hospitalization nor was life-threatening. There were 377
treatments of 74 horses using a total of 2,865 needles. A 10-yr-old Hanoverian gelding being treated
for back pain and palmar heel pain of the left forelimb experienced a mild local swelling on the axial
surfaces of heel bulbs on the treated foot for 1 wk
after its treatment. Treatment was resumed, and
13-mm needles were placed in the extranavicular
points; no additional adverse events were noted.
Although safe in most conditions, acupuncture
should be used with caution in animals with debilitation, frailty, or febrile illness. Needles should not
be inserted directly into skin infections, ulcers, tumors, or scar tissue. There is a traditional contraindication to acupuncture in the first trimester of
pregnancy, and ST-12, ST-25, SP-6, BL-60, CV-1,
CV-3 through CV-7, LI-4, and BL 67 are the transpositional acupoints typically avoided during
pregnancy.101
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Other than pain relief, acupuncture does not directly address any specific clinical sign but normalizes physiological homeostasis and promotes selfhealing through normal endogenous pathways.
Thus, acupuncture, in terms of its therapeutic mechanisms, is non-specific.9 As a physiological therapy, the efficacy of acupuncture depends on the
pathology involved and the healing potential intrinsic to each patient. Therefore, acupuncture effectiveness varies from person to person and animal to
animal.
In conclusion, there is a well-researched scientific
basis for the mechanisms of acupuncture analgesia,
the extent and depth of which continues to expand.
As well, there are growing numbers of human trials
supporting the use of acupuncture as an evidencebased practice for pain management in human medicine. Although the number of well-designed
clinical studies in veterinary medicine is lagging
behind human medicine, the basic science research
has been done in species with neurophysiology more
similar to non-primate animals than humans, and
therefore, the scientific basis for the use of acupuncture in domestic animals is clear. Although there
is research to support EA as an evidence-based
practice for the management of back pain in horses,
additional studies are needed in other clinical situations where analgesia is required. As contemporary conventional biomedical and laboratory
research merges with the practical clinical experience of traditional Chinese medicine, it is reasonable
to believe that the neurophysiologic mechanisms of
actions of acupuncture will be further understood,
and it will be shown to be an effective means of
managing many different types of acute and chronic
pain as well as other disorders.
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