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CASE STUDY
A Case Study Looking at the Effectiveness
of Deep Dry Needling for the Management of Hypertonia
Pablo Herrero Gallego
Orlando Mayoral del Moral
ABSTRACT.
Backgrounds: The patient is a four-year-old child with spastic tetraparesia.
Findings: A decrease in spasticity was observed in all the muscles being treated with deep dry
needling, measured with the Modified Ashworth Scale [MAS]. There was also a gain in passive
range of movement in the thumb.
Conclusions: Treatment with deep dry needling decreased resistance to passive movement. It is
difficult to determine whether decreased resistance to passive movement measured with the MAS
is due to changes in viscoelastic properties or to decreased spasticity. Since we treat trigger points,
it is possible that improvement in MAS scores could be more due to changes in the viscoelastic
properties than in spasticity.
doi:10.1300/J094v15n02_09 [Article copies available for a fee from The
Haworth Document Delivery Service: 1-800-HAWORTH. E-mail address: <docdelivery@haworthpress.com>
Website: <http://www.HaworthPress.com> © 2007 by The Haworth Press, Inc. All rights reserved.]
KEYWORDS. Muscle spasticity, muscle hypertonia, myofascial pain syndromes, trigger point,
dry needling, Modified Ashworth Scale
INTRODUCTION
The resistance felt when moving a limb pas
-
sively, or the resistance to passive movement
[RTPM], is called hypertonia. Hypertonia in
patients with upper motor neurone [UMN] le
-
sions results from a combination of spasticity,
thixotropy, and changes in the viscoelastic
properties of muscle, which may ultimately
lead to the development of fixed muscle con
-
tractures.
Pablo Herrero Gallego, PT, C.E.E Alborada [Gobierno de Aragón].
Orlando Mayoral del Moral, PT [Escuela Universitaria de Enfermería y Fisioterapia, Universidad de Castilla La
Mancha].
Address correspondence to: Pablo Herrero Gallego, Avda Gómez Laguna 17 3ºD, C.P 50009. Zaragoza, Spain
[E-mail: pablofisio@hotmail.com].
The authors would like to thank Diana Love, PT, MCSP, SRP, for translation review.
Submitted: November 30, 2005.
Revision accepted: April 25, 2006.
Journal of Musculoskeletal Pain, Vol. 15(2) 2007
Available online at http://jmp.haworthpress.com
© 2007 by The Haworth Press, Inc. All rights reserved.
doi:10.1300/J094v15n02_09 55
Spasticity is defined as “a velocity depend
-
ent increase in the tonic stretch reflex with ex
-
aggerated tendon reflexes, resulting from the
hyperexcitability of the stretch reflex, as one
component of the upper motor neurone syn
-
drome” (1). It is now accepted that the exagger
-
ated stretch reflex in a muscle is only partly re
-
sponsible for hypertonia and that other positive
features of the UMN syndrome and biomech
-
anical changes contribute significantly to
RTPM.
Pediatric physiotherapists who work with
profoundly impaired children often realize that
one of the most important difficulties for par
-
ents managing their children [dressing, bath
-
ing, etc.] is the increase of RTPM.
The current methods of treatment for muscle
spasticity include systemic antispascity drugs
such as baclofen, dantrolene, tizanidine, diaze-
pam, chlorazepate dipotassium, clonazepam,
or clonidine, which are nonselective in their ac-
tion and may cause functional loss. Paradoxi-
cally, in some patients, some of these drugs re-
duce force in the normal muscles without
having an effect on muscle spasticity. Further-
more, the value of the oral antispasticity drugs
diminishes with prolonged use. Tolerance
develops after a few months of treatment, and
incremental increases in dosage are often re-
quired to mantain the initial clinical response.
The high doses required often increase the in-
cidence and severity of these drugs’ adverse
effects. An alternative strategy in the man-
agement of muscle spasticity is chemical neur-
olysis with alcohol such as phenol. However,
nerve blocks and motor point injections in the
upper limbs often cause skin sensory loss and
may cause dysesthesic painor causalgia, which
can be persistent. Additionally, their effect of
-
ten diminishes with repeated treatment. In re
-
centyears botulinumtoxin type A [BTX-A] has
been shown to be an effective antispasticity
agent. However it can also have minor adverse
effects such as skin rashes, flu-like symptoms,
and weakness of the injected muscles.
Focal injection of BTX-A has been demon
-
strated to be the elective treatment for spasticity
although the review of the current evidence
suggests the lack of general consensus amongst
clinicians about the dose, site of injection, in
-
jection technique, etc. The BTX-A inhibits the
release of acetylcholine into the synaptic cleft.
It also seems to have a remote effect, which
could be explained by indirect central effect.
For about 30 years, dry needling has been
used as a pain-relieving procedure. It has also
proved its efficacy in the treatment of the
hemipareticshoulder pain syndrome (2). In this
study, the effectiveness and efficiency of deep
dry needling [DDN] of trigger points [TrPs]
was investigated based on the widely reported
success of DDN on neuropathic pain. Apart
from pain, TrPs have been associated with a
wide variety of signs and symptoms, such as
tingling, weakness, resistance to passive stret
-
ching, muscle shortening, and autonomic dys
-
function (3).
When comparing BTX-A treatment with
DDN, we couldstate that the effect ofBTX-A is
produced in the same place as DDN, the motor
endplatezone.However, the way theyact is dif-
ferent; while BTX-A acts in a chemical way,
DDN acts in a mechanical way.
ThehypotheticactionmechanismofDDNin
TrP treatment is the mechanical disruption of
dysfunctional motor endplates in which, ac-
cording to the integrated hypothesis described
by David Simons about etiopathogeny of TrPs
(3,4), there are contraction knots [active loci]
which lead to palpable findings of TrPs and taut
bands.
TheBTX-Ahasalsoproventobeeffectivein
the treatment of TrPs, which has been used to
support the integrated hypothesis. According
to this hypothesis, TrPs are located in dysfunc
-
tional motor endplates in which excessive
acetylcoline release occurs [neurotransmision
inhibition provoked by BTX-A would solve
part of the problem of TrPs as it acts on its initial
cause]. From this point of view, DDN and
BTX-A would act inthe same anatomical struc
-
ture, although by different mechanism means.
Recent pioneering research (5) has proven how
twitch obtaining DDN produces a lavage of
sensitizing substances whose presence could
promote the persistence of motor endplate
dysfunction (6).
In the case report that we are presenting, it is
examined whether DDN can also have an effect
on resistance to passive muscle stretch in a pa
-
tient with hypertonia.
56 JOURNAL OF MUSCULOSKELETAL PAIN
CASE DESCRIPTION
The patient is a four-year-old child. He was
born in the 38th week of pregnancy by caesar
-
ean section.
Medical diagnosis was severe hypoxic-
ischemic encephalopathy caused by perinatal
fetal distress which appears clinically as a spas
-
tic tetraparesia with axial hypotonia, with se
-
vere impairment of the right upper limb.
The child has central hypovision and severe
ocular motricity impairment. He depends on a
caregiver for all his activities of daily living.
His only means of communicationisbysmiling
or crying to express happiness or pain.
ASSESSMENT
Passive Range of Movement
Passive range of movement[PROM] was as-
sessed in the elbow, wrist, and fingers joints.
Although the upper limb is fixed in a position of
30º shoulder abduction, fully flexed elbow, and
70º of wrist flexion with a fisted hand, it is pos-
sible to attain the full PROM for all joints ex-
cept the thumb, if the stretch is performed
slowly. For this reason, PROM was only as-
sessed in the thumb. With the hand in the pa-
tient’s resting position the following positions
were used: the thumb fully flexed and opposed,
one-quarter open, one-half open, three-quar-
ters open, and fully extended with passive mus
-
cle stretch. On initial assessment, the patient’s
thumb could only be passively stretched to
one-half open.
The hand is closed in the resting position and
it can be moved to one-half open with passive
muscle stretch.
Spasticity and Resistance to Passive
Movement
Spasticity was assessed with the Modified
Ashworth Scale [MAS] (7) before and after the
treatment. The patient was in the supine posi
-
tion, with head in middle line to prevent the
tonic-asimetric reflex possibly causing in
-
creased spasticity.
Spasticity assessment shows a grade 3 in el
-
bow, wrist, and finger flexors muscles, and in
thenar muscles.
INTERVENTION
Objectives of the intervention set by both
parents and the physiotherapist were to dimin
-
ish spasticity or RTPM in order to improve the
parents’ management of the child.
Muscles treated were the thenar muscles
[opponens pollicis], the wrist flexors [flexor
carpis radialis, flexores digitorum superfi
-
cialis, and profundus], and the elbow flexors
[biceps brachii and brachialis].
Intervention consisted of nine sessions for
the thenar muscles. From the fifth to the ninth
session, elbow and wrist flexor muscles were
also treated. Intervention was performed twice
a week for the first four sessions [thenar mus-
cles] and once a week for the remaining five
sessions [all muscles].
For diagnosis of the TrPs the following crite-
ria were used:
Essential Criteria
1. Restriction to passive stretching (3)
2. Taut band palpable (3) in affected mus-
cles
3. Palpable nodule in a taut band
Confirmatory Criteria
1. Visual or tactile identification of local
twitch response [LTR]. This finding is
probably the most specific single clinical
test of a TrP (8).
2. Global increase of a spastic response
[GIS] in the axial muscles. This criteria
has not been published, but it has been es
-
tablished through clinical experience.
The presence of GIS response may or
may not be associated with LTR. This re
-
sponse did not correspond with any sign
of pain or discomfort in the patient, and
the GIS was immediately followed by a
substantial decrease in muscle resistance
of muscles treated for a few seconds.
Case Study 57
Muscles were positioned in a sub-maximal
stretch position, where a significant increase of
resistance is felt. As the treatment works, the
therapist applies a muscle stretch until a new in
-
crease of resistance is felt.
Once the needle has been introduced in the
TrP, two DDN techniques have been used:
1. Hong’s [fast-in, fast-out] technique until
a LTR or GIS can be felt.
2. Other manipulation of the needle [twist
-
ing].
OUTCOMES
The primary outcome measure was the de-
gree of RTPM of the target muscle group which
was assessed using the MAS of spasticity.
Video recording was used to allow observa-
tional analysis of both parameters.
A clinically significant improvement in
spasticity for all muscles treated was reported.
See Tables 1, 2, and 3.
An improvement in the hand opening in the
restingpositionandwithpassivemusclestretch
was reported. When treatment started, the hand
was fisted and the thumb could be passively
moved to a half opened position. After nine
treatments, the hand was in a one-quarter open
position and it could be fully opened with pas
-
sive muscle stretch.
Although it is a very subjetive measurement,
parents reported that they experienced fewer
difficulties in handling the child and that they
have also observed a decrease in RTPM in the
contralateral limb. Nevertheless, this last point
cannot be supported by the MAS measure
-
ments, which showed no changes in left upper
limb RTPM. In this case report, the last treat-
ment was just before the Christmas holidays; a
new assessment was performed after this vaca-
tion period. This showed that results had been
mantained.AftertheChristmasholidays wedid
not continue with the treatment because the
child started a new medical regime with diaze
-
pam that could interfere with the outcome mea
-
sures.
DISCUSSION
As stated in the introduction, RTPM is a
complex measure that will be influenced by
many factors, only one of which could be
spasticity. The MAS has important limitations
and does not reliably distinguish between the
different components of hypertonia. Another
limitation of the MAS is that the test conditions
havenotbeen standardized. For example, while
some clinicians assess the muscle tone from the
resting state without previous muscle stretch,
58 JOURNAL OF MUSCULOSKELETAL PAIN
Opponens Pollicis
Modified Ashworth
Scale
Number of Treatment
4
3
2
1+
1
0
1234
5
6
7
89
Before needling
After needling
TABLE 1. Improvements in Spasticity for Oppo
-
nens Pollicis
Wrist and Finger Flexors
Modified Ashworth
Scale
Number of Treatment
4
3
2
1+
1
0
1234
5
6
7
89
Before needling
After needling
TABLE 2. Improvement in Spasticity for Wrist and
Finger Flexor Muscles
Elbow Flexors
Modified Ashworth
Scale
Number of Treatments
4
3
2
1+
1
0
1234
5
6
7
89
Before needling
After needling
TABLE 3. Improvement in Spasticity for Elbow
Flexor Muscles
others (9) have recommended flexion and ex
-
tension of the limb a few times immediately be
-
fore the actual measurement is taken. This lack
of standardization may introducemeasurement
error because the stretch reflex excitability in
the resting state may be different from that of
the activated muscle (10). Nevertheless the
MAS is probably the most widely used test for
the measurement of muscle spasticity in re
-
search and clinical practice, and it has been
demonstrated to be moderately reliable for
classifyingtheRTPM at the elbow andthewrist
flexors (11).
Some authors state that the MAS measures
resistance to passive muscle stretch [hyper
-
tonia] rather than spasticity (12-14).
There are factors that can confound the
MAS. Evidence from the literature suggests
that the increase in RTPM could have resulted
from decreased soft tissue compliance associ-
ated with reduced use (13). The RTPM is influ-
enced by the immediate past history of move-
ment. This would suggest that the increase in
RTPM observed in the impaired arm might
have been predominantly associated with
changesin the viscoelastic properties of thesoft
tissues and not spasticity (13,14).
It was also observed that prior to treatment,
there was a high velocity-dependent RTPM
that diminished after the treatment. This can
also be attributed to viscoelastic properties of
muscles, which are velocity dependent, but
these changes can also be due to changes in
spasticity. We have found, as a limitation of the
study, the possibility that the improvement
could also be achieved performing DDN in
zones other than the endplate zone, even in
other parts of the body.
Although treatment in neurologic patients
mustbe assessed on the basis of motor and func
-
tional improvent, for this severly impaired pa
-
tient, reducing muscle tone, as assessed by
MAS and PROM, is the real goal.
Deep dry needling has been tested in differ
-
ent children treated in the school [non-pub
-
lished data] and in adult patients with incom
-
plete spinal cord injury (16). In these clinical
cases, despite not having scientific evidence, it
was observed that DDN had more lasting ef
-
fects in upper limbs than in lower limbs, possi
-
bly caused by the weight bearing factor that
could be a perpetuating factor of spasticity. In
the treatment of children, results were better
with severe spasticity and restriction of PROM
than with mild impairments. Apart from these
factors, some difficulty was experienced in the
treatment of children capable of recognizing
the “threatening presence” of a needle. Accord
-
ing to all these data obtained from the clinical
practice, it was decided that the most suitable
patienthad to be a child with severe spasticityor
restricted PROM, and that he/she should have a
cognitive impairment and/or a visual loss that
would prevent him/her from realizing that he
was going to be treated with needles.
Although this kind of treatment seems to
have very restricted effects [mainly for upper
limb severe spasticity], it can help many pa
-
tients with the characteristics previously de
-
scribed.
There is a lack of published knowledge in
this field. The effect of TrP injection (17), acu-
puncture needling (18), and electroacupunc-
ture and moxibustion (19) for treating spas-
ticity have been reported, but not the use of
DDN in TrP for decreasing spasticity/resis-
tance to passive muscle stretching. The only
clinical evidence of effectiveness of DDN for
spasticity treatment was shown in patients with
incomplete spinal cord injury (16).
Although the efficacy of DDN has yet to be
demonstrated for the treatment of spasticity, an
advantageof this technique is thatit does not in-
volve medication.
In reference to esential diagnostic criteria:
The criteria “restriction to passive stretching”
has been obtained in comparison with the crite
-
ria“painfullimit to full stretch range of motion”
because PROM restriction may be caused by
TrPs, perpetuated by spasticity.
The criteria “taut band palpable” can only be
used for superficial muscles, which is, in fact, a
limitation.
In reference to confirmatory diagnostic cri
-
teria: The first criterion [LTR] is explored only
with the needle because snapping palpation
may increase spasticity which obscures the ob
-
servation of LTR.
The second criterion [GIS] has not been doc
-
umented in the literature, but can be used as a
guide for the treatment of spasticity. According
to the authors’ clinical experience, there is a re
-
laxation period after GIS during which more
muscle stretch is allowed. Some may interpret
Case Study 59
GIS as the patient expressing pain or discom
-
fort, but in the authors’ experience, this is un
-
likely since the patient’s facial expression does
not change. The patient has been observed to
cryto express paininresponseto other stimuli.
CONCLUSIONS
The treatment with DDN decreased RTPM
in the treatment session and throughout the ses
-
sions in spastic muscles located in our patient’s
upper limb. It is difficult to determine whether
decreased RTPM measured with the MAS is
due to changes in viscoelastic properties or to
decreased spasticity. Since we treat TrPs, it is
possible that improvement in MAS scores
couldbe more due to changesin the viscoelastic
properties than in spasticity.
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doi:10.1300/J094v15n02_09
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