Special Section-Spasticity

Chemodenervation and Nerve Blocks in the

Diagnosis and Management of Spasticity and
Muscle Overactivity
Elie P. Elovic, MD, Alberto Esquenazi, MD, Katharine E. Alter, MD, John L. Lin, MD,
Abraham Alfaro, PhD, DO, Darryl L. Kaelin, MD

This article will discuss many of the key concepts regarding chemodenervation and
neurolysis in the management of spasticity. Topics that will be discussed include techniques
for localization, strengths and limitations of various agents (botulinum toxin, phenol, and
alcohol), the value of combination therapies, and the role of nerve blocks (diagnostic and
therapeutic). With advancing technology have come newer methods to improve accuracy of
localization for the performance of chemodenervation and neurolysis such as electro-
myographic guidance, electrical stimulation, and ultrasound guidance. During the last 2
decades, the addition of botulinum toxin chemodenervation as an adjunct to traditional
neurolysis, medication, and therapy modalities has expanded the field of treatment of
intramuscular hyperactivity in upper motor neuron syndrome. The technique of diagnostic
blocks as predictors of response and the therapeutic value of nerve blocks will be discussed.

INTRODUCTION
Numerous factors must be taken into account when deciding on the treatment approach for
an individual with spasticity. Etiology, chronicity, prognosis, distribution, location, sever-
ity, and medical comorbidities are all important factors. In addition, clinicians must take
into account the patient’s and caregiver’s goals to effectively plan a course of action that is
realistic, meaningful, and maximizes the potential for success. The classic model of deliv-
ering spasticity treatment using a linear, hierarchal approach has been supplanted by a more
modern approach of choosing singular or multiple interventions that are based on the
factors previously listed.
Spasticity and the upper motor neuron syndrome (UMNS) differ greatly in their presen- E.P.E. Division of Physical Medicine and Re-
habilitation, University of Utah, 30 North 900
tations and response. A critical factor in the treatment algorithm is the distribution of the East, Salt Lake City, UT 84132. Address
spasticity. It can be focal, affecting a single joint or functional group of joints such as the correspondence to: E.P.E.; e-mail: Elie.Elovic@
hand; more widespread, affecting most of a limb; or multisegmental as in spastic hemipa- hsc.utah.edu
Disclosure: 2A, Allergan, Ipsen, and Merz; 7B,
resis when it affects many areas simultaneously. Because chemodenervation affects a limited Allergan
area, it is important to have realistic outcome expectations. Examples of appropriate goals
A.E. Moss Rehab Hospital, Elkins Park, PA
include improved range of motion, reduction of co-contraction, and improved local Disclosure: 7B, Allergan; 9
function. As the severity of spasticity increases, there is greater emphasis on aggressive K.E.A. Mt. Washington Pediatric Hospital,
management so as to lessen suffering and prevent secondary complications such as contrac- Cheverly, MD
ture and skin breakdown. Diagnostic nerve blocks are minimal risk procedures that may be Disclosure: nothing to disclose
helpful in determining the presence of contractures and the risk of excessive weakness, as J.L.L. Shepherd Center, Atlanta, GA
well as estimating potential functional gains after chemodenervation. Often these individ- Disclosure: nothing to disclose

uals have other medical conditions that affect decision making, such as altered cognition, A.A. Bacharach Institute for Rehab, Pomona,
diabetes, venous thrombosis, and anticoagulation. When dealing with spasticity in complex NJ
Disclosure: 2A/3A, Allergan
neurologic patients, physicians should be holistic in their approach.
D.L.K. Shepherd Center, Atlanta, GA
Disclosure: 3, Allergan, Cephalon, Medtronic;
7, Allergan, Medtronic, Pfizer; 8, NIDDR
TECHNIQUES FOR LOCALIZATION
Disclosure Key can be found on the Table of
Once a method of chemodenervation has been selected for treatment of problematic Contents and at www.pmrjournal.org
hypertonia, the next steps are to correctly identify the involved muscle(s) and select Submitted for publication August 6, 2009;
injection sites. Several localization techniques are used for chemodenervation, ranging from accepted August 6.

PM&R © 2009 by the American Academy of Physical Medicine and Rehabilitation

1934-1482/09/$36.00 Vol. 1, 842-851, September 2009
842
Printed in U.S.A. DOI: 10.1016/j.pmrj.2009.08.001
PM&R
simple palpation to sophisticated imaging technology. The
goals of all localization techniques are to accurately and
quickly identify target muscle(s) and to avoid injection of
untargeted structures such as vessels, nerves, or organs.
All muscle identification techniques begin with anatomic
localization. Many physicians use one or more supplemen-
tary methods, ostensibly to enhance the accuracy of needle
placement. Available adjunctive technologies include elec-
tromyography (EMG), EMG auditory signal amplifiers
(EMG-SA), electrical stimulation, and ultrasound (US) [1].
Computed tomography or fluoroscopy is used in special
circumstances for botulinum toxin (BoNT) injections, but
have limited use owing to the risk of ionizing radiation
exposure with repeated treatment [2]. The following is a
more detailed discussion of the most frequently used local-
ization techniques for chemodenervation.
Anatomic Localization
All physicians who perform EMG regularly use their knowl-
edge of surface anatomy to place needle electrodes in mus-
cles. These techniques include observation, identification of
bony landmarks, palpation, and muscle activation and relax-
ation. Many experienced clinicians rely solely on anatomic
localization techniques for neurotoxin injections with good
results. This requires meticulous technique and an extensive
knowledge of surface and three-dimensional anatomy, mus-
cle functional anatomy, and the complex relationship be-
tween muscle groups [3].
Some superficial muscles are easily identified using an ana-
tomic approach (eg, biceps, triceps, gastrocnemius, or ham-
strings). Even when easily palpated, needle placement in the
target superficial muscle is not guaranteed [4,5]. And identifica-
tion is more challenging with deep muscles (eg, in the calf and
hip girdle or in the forearm flexor compartment) [6]. Spasticity
may lead to secondary changes in muscles (hypertrophy, con-
tracture, resistance to range of motion [ROM]), which may
actually assist in the identification of target muscles. Unfortu-
nately, secondary changes such as atrophy may also obscure
muscle identification. Hypertrophy and contractures occur less
frequently in patients with focal dystonias, making it more
difficult to identify a muscle with palpation alone. Therefore,
anatomic localization alone may be insufficient in patients with
severe spasticity or dystonia.
The advantages of anatomic localization include its uni-
versal availability, physician experience, portability, lack of
equipment, and low cost. Injections may be less painful as
smaller needles can be used [3]. Disadvantages with this
method include errors in needle placement as a result of
anatomic variations or muscle rearrangement (eg, contrac-
tures or surgery) and inadvertent targeting of unintended
structures. Patient factors that reduce accuracy include im-
paired motor control and poor patient cooperation. Ana-
tomic localization cannot be used for phenol or alcohol
injection, which requires electrical stimulation to assist with
motor point localization.
Vol. 1, Iss. 9, 2009 843
EMG and EMG-SA
Historically, EMG has been the most frequently used adjunctive
technique for muscle localization for BoNT injections. Equip-
ment requirements include either an EMG machine or EMG
auditory amplifier, injection needle electrodes (concentric or
monopolar), a ground electrode, and a reference electrode for
monopolar injection needles. The needle is placed in a target
muscle, and activity at rest and with voluntary recruitment is
observed. The examiner listens for the auditory frequency and
intensity of the motor unit action potential (MUAP) signal to
identify correct placement. The needle is repositioned, as
needed, guided by the EMG signal. Other techniques may be
required if a patient does not have voluntary control of a given
muscle. The clinician can passively move the muscle, with the
EMG electrode in the target muscle, and look for needle move-
ment with passive ROM (PROM) or listen for sounds of depo-
larization or sound amplification. Abnormally high EMG activ-
ity on insertion or at rest is often used to identify sites of
increased muscle activity associated with spasticity or dystonia.
In addition, increased activity during volitional muscle activa-
tion can identify residual function, whereas increased activation
during rapid stretch may further delineate the presence of spas-
ticity. Using EMG localization has the potential to identify which
muscle is most spastic when choosing how to divide dosing.
Some physicians specifically target the most active area for
injection as it is speculated that toxin uptake may be higher in
more active muscles [7]. In some studies, EMG-guided injec-
tions have been associated with improved clinical results [8].
Advantages of EMG and EMG-SA include their wide avail-
ability and clinician experience. Most physiatrists require no
additional training to use this technology. Although EMG-SA
may increase the accuracy of needle placement for injection
therapy, it has limitations. Many patients have impaired
motor control and can minimally recruit or activate a muscle
on command. This limits muscle identification. Co-contrac-
tion of adjacent muscles may obscure localization of an
individual muscle. For example, activity in the flexor digito-
rum profundus or sublimis (FDP, FDS) may be falsely attrib-
uted to activity in the flexor carpi radialis. EMG needle
electrodes may also be more painful to insert.
Electrical Stimulation
Electrical stimulation guidance is divided into two primary
techniques: electrical muscle activation and electrical motor
point stimulation (EMPS). Electrical muscle activation typically
requires higher current for activation and has the disadvantage
of activation of multiple regional muscles and simultaneous
afferent fiber stimulation, leading to discomfort and pain. As
such, the primary mode of electrical stimulation-guided BoNT
injection is through EMPS. EMPS-guided BoNT injection has
been a successful adjunctive tool in addition to anatomic local-
ization and EMG-SA [1,9]. Its utility in guiding BoNT injection
has become more prominent as studies have shown lack of
comparable accuracy and efficacy from relying solely on ana-
tomic guidance [8,10,11] (without using the multisite injection
844 Elovic et al
technique [12]). Accuracy and efficacy have been reported to be
comparable to EMG-SA guidance [13]. This technique has the
further advantage of allowing the clinician to definitively isolate
different fascicles of muscles such as the FDS.
EMPS requires passing of a relatively low current of 5 to 10
mA (but as low as 0.5 mA) through the injecting needle to the
target muscle, causing it to contract and allowing visual
confirmation. Advantages of EMPS technique includes in-
creased accuracy of BoNT injections [10,14-16], especially
when the target muscles are located among a group of other
muscles that have similar function, eg, hip adductors [10].
Disadvantages include training required for mastering the
technique, cost of time and equipment for the neural stimu-
lator, and inability to independently assess the degree of
muscle hyperactivity before injecting. Contraindications may
include regional hardware (eg, electrical wire, catheters, or
metallic implants).
US
Advances in US and transducer technology have led to in-
creased use of this noninvasive technique for diagnostic
musculoskeletal imaging and procedural guidance. Experi-
enced clinicians routinely use US for joint, tendon, and
muscle injections. US provides direct visualization of target
muscles and other structures. In addition US does not require
patient cooperation or active movement; therefore US is
perfectly suited to assist in BoNT muscle injection and nerve
localization for phenol or alcohol neurolysis.
As a large number of major peripheral nerves travel with
major vessels, the risk of neurologic or vascular injury using
anatomic guidance for nerve blocks has been shown [17].
Real-time visualization of the neurovascular bundle in the
experienced ultrasonographer can minimize vascular in-
volvement [18,19]. Ironically, peripheral needle-nerve con-
tact does not always produce sensory alterations or electrical
stimulation responses [20]. The efficacy of US guidance,
either alone or in combination with electrical stimulation
confirmation, is comparable to electrical nerve stimulation
guidance alone [21-24]. US-guided regional blocks have
been described for various nerves, including axillary [21],
femoral [25], sciatic [23], and obturator [26].
US may increase the accuracy of needle placement in
BoNT injections, especially in patients who lack motor con-
trol, have contractures or deformity, or cannot cooperate
with instructions. It has particular utility in localizing deep
muscles that are difficult to palpate, such as the piriformis,
iliopsoas, and tibialis posterior [27-29]. US imaging allows
the physician to guide needle insertion and to avoid vessels,
nerves, and other structures during the procedure. In high-
risk muscle locations such as the scalenes or intercostal
muscles, US is particularly useful for avoiding the underlying
lung tissue. In the facial region, US can be used to isolate the
parotid or submandibular salivary glands that cannot be
localized by other techniques [30]. In patients with focal
dystonia, US is extremely useful for identifying individual
muscle fascicles. For example, in a pianist, treatment may
CHEMODENERVATION AND NERVE BLOCKS IN SPASTICITY
require isolation of FDS and FDP to digit 3, but not FDS to
digits 2 or 4. This can be easily and quickly achieved using
US. Disadvantages of US include the availability and prohib-
itive cost of the equipment. Clinicians require additional
training in US technology as well as musculoskeletal imaging
and pattern recognition of individual muscles and other
structures.
Depending on their experience and training, equipment
availability, and patient-specific clinical issues, physicians
may select one or all of the above localization techniques for
BoNT, phenol, or alcohol injection [31]. No technology will
assist a clinician who has little experience or knowledge of
functional anatomy and muscle action. Injection therapy
must be performed by highly trained physicians who under-
stand the potential risks and benefits of injection therapy.
BoNT AND OTHER CHEMODENERVATING
THERAPEUTIC AGENTS: STRENGTHS AND
LIMITATIONS
Chemodenervation is a process used by clinicians to manage
focal muscle overactivity through the use of an established
agent such as phenol or alcohol or one of the newer BoNTs
that have become available more recently [32]. The utility of
phenol has been reported by numerous authors for more
than 4 decades [33-35], whereas the utility of alcohol has also
been demonstrated more recently [36-38]. BoNTs have been
used most recently, and there are numerous publications that
have demonstrated their efficacy in the management of spas-
ticity and cervical dystonia [39-50]. The question that arises
from reviewing the literature is what agent should be used
and what clinical criteria should be used when making this
choice? The decision should be based on a patient’s clinical
condition and the relative strengths and weaknesses of the
different agents.
Phenol and Alcohol
Phenol in concentrations between 5% and 7% and alcohol in
concentrations between 45% and 100% mediate their effect
through neurolysis. Phenol and alcohol have the advantages
of lower cost, rapid onset of action, and potency. Disadvan-
tages of these agents include the risk of dysesthesia, soft tissue
fibrosis, and the requirement for significant clinician skill to
administer. A more complete list of the pros and cons of
phenol and alcohol are outlined in Table 1.
BoNTs
In the United States there are currently 3 different toxins
available on the market; Botox, Myobloc, and the recently
approved Dysport. Botox and Dysport are BoNT type A
products, whereas Myobloc is a BoNT type B. There are
numerous publications that have documented the utility of
Botox [39-43] and Dysport [44-47] in the management of
spasticity; however, the same cannot be said for Myobloc as
limited efficacy has been demonstrated for this indication
PM&R
Table 1. Advantages and disadvantages of phenol and alcohol as chemical denervating agents
Pros
Less costly than botulinum toxin
Rapid onset of action
Facilitation of serial casting
Potency
Its effect on sensory fibers can further decrease spasticity reflex arc
Potency for large muscle groups (hip adductors)
Less injection sites
More spastic regions can be treated at one time than botulinum toxin
Less storage requirements
Can reinject or booster in less than 3 months
[48,49]. There is abundant literature and FDA approval
supporting the use of all three agents in the treatment of
cervical dystonia; however, Comella et al [50] suggest that
the side effect profile may be in favor of the type A toxins
(Botox versus Myobloc). Ease of administration, better pa-
tient tolerance, and easy titration are clearly a benefit for the
BoNTs when compared with phenol and alcohol, although
the cost, dose ceilings, and longer onset of action are limita-
tions. For a complete list of pros and cons see Table 2.
The Final Choice of an Agent
The physician needs to look at the entire clinical picture and
decide whether the use of a combination of agents (eg, phenol
and toxins) or individual agents alone is the best way to address
a patient’s problem. The risk of side effects, condition being
treated, time since onset, and prognosis are just some of the
issues that clinicians must consider when making their selec-
tion. Table 3 summarizes the differences between phenol and
the BoNTs. A clinician’s experience and skill set is critical.
Without significant experience, one must be leery of using
phenol or alcohol. As a result, the use of them by an injector who
is not doing it on a regular basis may be inadvisable.
ADJUNCTIVE TREATMENTS AND NEW
DEVELOPMENTS IN INTRAMUSCULAR
INJECTION OF BoNT-A FOR MUSCLE
OVERACTIVITY
Many impairments of body structure or function are associated
with focal spasticity and dystonic overactivity of the lower limb
Table 2. Advantages and disadvantages of the botulinum toxins
Pros
Supported by double-blinded, placebo-controlled trials
Muscle effect is reversible
Easier to titrate dosing
Better patient acceptance
Easier to perform procedure
When using EMG can identify the most pathologic firing units
Numerous clinical trials demonstrating effect with dystonia
Effective in areas with dense sensory innervation
Has the potential to reduce pain
EMG ⫽ electromyography; FDA ⫽ U.S. Food and Drug Administration.
Vol. 1, Iss. 9, 2009 845
Cons
Risk of dysesthesias
Muscle fibrosis
Need for patient sedation
Scarring
Risk of granuloma formation
Reduce contraction during voluntary movement
Edema can develop after injection
Greater patient discomfort during procedure
Procedure requires more time to perform
Procedure requires more skill to perform than toxin
resulting from neurologic disorders in adults. Gracies [51]
points out that patients with spasticity represent a uniquely
recognizable population from a clinical and physiologic per-
spective and that they are affected by 3 main features: (a) paresis,
ie, reduced recruitment of skeletal motor units; (b) soft tissue
contracture, eg, muscle shortening and joint retraction; and (c)
muscle overactivity, ie, reduced ability to relax muscle and
co-contraction. These changes give rise to the commonly ob-
served UMNS with a clinical picture of shortened overactive
muscles, velocity-dependent stiffness, loss of fine motor control,
weakness, muscle spasms, changes in limb posture, and fatigue
[52]. Injection of BoNT is indicated to reduce focal muscle
overactivity [51] and provide a window of opportunity to ad-
dress related problems such as soft tissue shortening or fixed
joint contracture, and to promote strengthening and selective
movement control. BoNT is a microbial protein that exists in
seven serotypes, designated A through G. All BoNTs contain an
enzyme that acts in the cytosol of nerve endings to cleave three
polypeptides that govern exocytosis. Only serotypes A and B
have clinical utility at this time. The ability of BoNT to block
acetylcholine release at neuromuscular junctions accounts for its
therapeutic action to relieve dystonia, spasticity, and related
muscle overactivity disorders. Undesirable effects associated
with administration of BoNT fall into three broad categories:
diffusion of the toxin from the intended sites of action, sustained
blockade of transmission that can produce muscle atrophy, and
potential development of immunoresistance to BoNT [53].
However, neutralizing antibodies to BoNT are now deemed to
be of minimal clinical relevance after the reformulation of
BoNT-A Botox in 1997 [54].
Cons
Greater cost
Maximal effect can take up to 4 weeks
Without negotiated carve out in inpatient rehabilitation cost
can be prohibitive
Ceiling dose may limit efficacy in severely spastic muscles or
Injections should be at least 3 months apart
Risk of distal effects with FDA black box warning
Can develop resistance
Some patients report headache and fatigue
Relative contraindication with neuromuscular disease
846 Elovic et al
Table 3. Comparison of phenol with botulinum toxin (BoNT)
Characteristic
Titratable to symptom severity Yes
Adjustable dilution to maximize diffusion Yes
Toxic to tissue No
Pain during injection Needle only
Motor point injection technique required No
Reversible side effects Yes
Duration of benefit 3 to 4 months
Repeated use long-term safety record Yes
Cost Expensive
Preparation Storage in refrigerator, easy reconstitution
Risk of dysesthesias No
Easier to administer with noncooperative patient Yes
Rapid onset of action No
Adjunctive Treatment Techniques
There is evidence for the impact of adjunctive treatment
when used in combination with BoNT injection. Widespread
clinical opinion supports physical and occupational therapy
treatment after BoNT-A injection for focal spasticity. Not
only does it improve the delivery of the therapy, but it also
appears to improve the outcomes. Radensky et al [55] per-
formed a cost comparison of three treatment strategies
for poststroke spasticity: physiotherapy only, Botox plus
physiotherapy, and oral baclofen plus physiotherapy. The
authors found that BoNT-A combined with physiotherapy
was more cost-effective than oral baclofen combined with
physiotherapy.
There is strong evidence to support the beneficial effect on
spasticity (muscle overactivity) from soft tissue stretching after
BoNT-A injection [56-58]. Giovannelli et al [56] in a single-
blind, randomized controlled trial on 38 subjects with multiple
sclerosis compared BoNT-A injection of 100 to 300 units
(Botox) to the gastrocsoleus or tibialis posterior with BoNT plus
daily stretch therapy for 15 days after injection, aimed at increas-
ing muscle length. A problem with this study is that the authors
poorly defined what they meant by the term physical therapy.
The combined treatment group had statistically significantly
greater reduction in tone measured objectively using the Modi-
fied Ashworth Scale and subjectively using a self report of
satisfaction with reduction of spasticity using a 10-point visual
analog scale at weeks 4 and 12 after injection. A dynamic
orthosis is an alternative stretching technique that has a benefi-
cial effect on joint ROM and muscle length resulting from the
use of spring-loaded splinting after BoNT injection to reduce
ankle plantarflexion and knee flexion contractures. Several case
reports of patients with Parkinson disease or traumatic brain
injury presenting with knee flexion contracture after total knee
joint arthroplasty that improved using injection of 200 to 300
units of BoNT-A (Botox) to the hamstrings plus a dynamic knee
orthosis suggests that this combination of treatment can pro-
duce functionally meaningful improvement in knee ROM [59].
There is extensive literature regarding the combination of
BoNT-A injection and serial casting to correct contracture
(mostly ankle equinovarus deformity) in children with cere-
CHEMODENERVATION AND NERVE BLOCKS IN SPASTICITY
BoNT Phenol
Yes
No
Yes
Yes
Yes
No
Up to 6 months
No literature
Relatively affordable
Requires hood for preparation
Yes
No
Yes
bral palsy and adults with UMNS [60-62]. Verplancke et al
[63] published a prospective double-blind, randomized pla-
cebo-controlled trial of BoNT-A with or without casting to
lengthen the plantar flexor (PF) muscles in 35 patients hos-
pitalized with moderate to severe traumatic brain injury.
Subjects were randomly allocated to one of three groups
(controls, saline plus casting, 200 units of Botox to the
gastrocsoleus complex plus casting). All subjects gained
ROM, but there was no difference between BoNT-A plus
casting and placebo injection plus casting. The quality of the
study was marred by significant subject dropouts and cross-
overs to the active drug group (rescue treatment) [63]. Evi-
dence exists to support targeted strengthening programs,
including progressive-resistance exercise (PRE) and graded
functional activity, to augment outcomes of BoNT injection
and the efficacy of PRE to improve muscle strength and
reduce activity limitation in adults with neurologic disorders.
The concern about increased spasticity associated with PRE
programs is unsupported by the literature [64-67].
It is reasonable, although not yet demonstrated experi-
mentally, to assume that combining the known effects of
BoNT to improve gait deficits associated with equinovarus
deformity of the ankle and principles underpinning the effect
of task-specific training of gait and mobility function is likely
to improve outcomes of BoNT-A treatment [68]. Advantages
of body weight support treadmill training (BWSTT) include
the potential to provide a sufficient “dose” of practice to
improve endurance and quality of gait and to likely facilitate
neuroplastic adaptation, while reducing effort of gait and risk
of falls. BoNT-A injection to muscles of the leg and foot can
augment functional outcomes when combined with task-
specific targeted practice, such as that achieved by BWSTT,
reportedly improving gait quality, speed, and endurance, and
reduce activity limitation in adults with neurologic disorders
[69,70]. Robertson et al [71] recently described a technique
to enhance swing phase knee flexion during locomotion in
stroke patients using BoNT injections. Constraint-induced
movement therapy (CIMT) has been shown to improve the
amount of arm use and quality of movement [72]. At this
time there is limited evidence to support the improvement of
PM&R
upper limb outcomes after stroke when a combination of
BoNT-A and CIMT treatment is implemented [73,74].
A single-blind, randomized controlled trial (n ⫽ 18
chronic stroke patients) compared injection alone of a mod-
erate dose of Botox (190 to 300 units) to the gastrocsoleus
complex with or without the tibialis posterior versus a low
dose of Botox (100 units) to the tibialis posterior only plus
taping of the ankle in eversion. Beneficial effects were dem-
onstrated in both groups; however, the duration of benefit
was shorter in the single-muscle, lower dose group [75].
Sixty-five adult subjects affected by spasticity of the wrist
and finger flexors were treated with BoNT-A [76]. Using a
case-control design, two postinjection treatment groups were
created. One was treated with stretching through the use of
adhesive taping for 6 days and the other with electrical
stimulation and splinting for 6 days. Patients treated with
adhesive taping and BoNT-A achieved a greater reduction in
muscle overactivity as measured with Modified Ashworth
Scale, with less staff time dedicated for the treatment [76].
Neuromuscular electrical stimulation (NMES) has been
applied to muscles injected with BoNT to potentially aug-
ment the beneficial effect of the toxin. A case-control series
with blinded assessment (n ⫽ 10 chronic stroke survivors)
were injected with 2000 units of BoNT-A (Dysport) to the
gastrocsoleus complex and tibialis posterior. Five subjects
subsequently received alternating NMES to the plantar flex-
ors and tibialis anterior for 30 minutes 6 times per day for 3
days. The combined treatment produced greater improve-
ment in gait quality and quantitative measures such as Mod-
ified Ashworth Scale for ankle PF, clonus, and toe clawing
than the injection-only group [77]. In an open-label case
series of 11 patients with longstanding diagnosis of blepha-
rospasm or idiopathic facial hemispasm, subjects were in-
jected with 3 units of Botox into the extensor digitorum
brevis muscle in both feet. Shorts bursts of NMES were
applied continuously for a period of 2 days to only one of
these muscles. Compound muscle action potential, mea-
sured during a 30-day period, consistently showed the in-
jected plus stimulated muscle to be weaker than the injected-
only muscle [78].
A randomized case series of 11 patients with chronic
stroke comparing injection of 400 units of Botox with 100
units of Botox combined with EMS using the same method-
ology previously described by Hesse et al [77] demonstrated
no significant difference between groups in any of the mea-
sured variables. The authors concluded that NMES could be
used to achieve therapeutic outcomes with lower doses of
BoNT [79].
Esquenazi and Mayer [80] described the beneficial use of
NMES to prolong the duration of BoNT-A (Botox) effect on
elbow flexor and ankle PF muscle overactivity on 30 subjects
with the diagnosis of subacute acquired brain injury.
A nonblinded, randomized controlled trial [81] with 18
subacute stroke patients, randomized to physiotherapy alone
or BoNT-A (Dysport 800 units) to the gastrocnemius and
tibialis posterior plus physiotherapy and the additional use of
Vol. 1, Iss. 9, 2009 847
functional electrical stimulation (FES) for most of the day
during a 12-week period, showed improvements in gait
speed in both groups; however, only the FES-treated group
showed an increase in functional mobility using the River-
mead Motor Assessment and reduced effort of walking using
the physiologic cost index. These authors concluded that
treatment with BoNT-A and FES combined effectively im-
proved walking and function. This study unfortunately did
not compare outcomes with a BoNT-A only group, so it is
difficult to conclude which part of the intervention had the
most effect on the measured outcomes.
Another intervention that can impact the care of patients
treated with BoNT is the dilution for injection and the injection
technique used for targeting the muscle. A randomized, con-
trolled parallel-group trial, with blinded outcome assessment,
was recently reported by Mayer at el [12] using 31 patients with
acquired brain injury who had an Ashworth Scale score of 3.
They were injected with low doses of BoNT-A 60 units (Botox)
in 2.4 mL of normal saline solution with multisite EMG-guided
injection technique or 30 units (Botox) in 1.2 mL with electrical
stimulation– guided motor point technique after obtaining two
baseline evaluations of the main outcome measures. Postinter-
vention testing at 3 weeks showed no significant differences
between the groups (P range, .31–.82 across three outcome
measures). However, within each group, significant treatment
effects were observed on all outcome measures (P ⬍ .01).
Findings suggest that low-dose, high-volume strategies may
have a potential role in reducing drug utilization per muscle and
helping clinicians stay within accepted limits for total body dose
in patients with UMNS requiring multiple muscle injections
[12]. A different approach using end-plate localization com-
pared with a multisite distribution injection technique showing
similar results was recently published by Gracies et al [82].
Changes in functional outcomes of a distant limb after
injection is also a possible adjuvant technique. A prospective,
open-label, multicenter, interventional evaluation study of
15 patients with residual hemiparesis attributable to chronic
acquired brain injury evaluated Modified Ashworth Scores
and gait velocity before and after treatment with 120 to 200
units of BoNT-A (Botox) to the biceps, brachialis, or brachi-
oradialis [41]. The treated group demonstrated a statistically
significant reduction in elbow Ashworth score after treat-
ment (P ⬍ .003), and a significant increase in walking veloc-
ity (P ⬍ .037) was evident. The study concluded that treat-
ment of upper-limb spasticity may be an important adjuvant
treatment for patients with gait disturbance related to the
UMNS [41].
A group of clinicians from across Europe experienced in
the use of BoNT-A for the treatment of spasticity after ac-
quired brain injury recently published a consensus statement
on best practice in managing adults with spasticity [83]. They
concluded that BoNT-A provides a valuable tool in the mul-
timodal treatment of adult spasticity and that further research
in adjuvant techniques including different injection tech-
niques, therapy interventions, and the use of orthosis is
necessary.
848 Elovic et al
NERVE BLOCKS FOR SPASTICITY AND
DYSTONIA
Diagnostic Nerve Blocks
Diagnostic nerve blocks (DNB) have an important role in the
management of patients who have intramuscular hyperactiv-
ity (MH) regardless of its origin. It will allow the clinician to
determine the potential benefits of performing longer lasting
interventions such as chemodenervation or surgery. Al-
though not perfectly mimicking the longer lasting effects of
other interventions, it allows the patient to experience the
potential benefit of reduced muscular hyperactivity (MH)
and have a better understanding of what to expect from more
definitive procedures. DNB can also assist the clinician in
diagnosing contractures (that will not respond to chemode-
nervation or neurolysis) [84], identifying potentially unde-
sirable outcomes (eg, excessive muscle weakness), and ap-
preciating the beneficial effects of pain reduction and
improved limb posture on function and hygiene.
Protocol for Performance of DNBs
There are several criteria required for the proper performance
of DNB. First is a thorough understanding of the relevant
anatomic landmarks, neurovascular structures, and kinesiol-
ogy and function of the regions where IMH is prevalent. The
next is a working hypothesis of what may be altered (both
positive and negative effects) as a result of the DNB. Finally,
availability of the appropriate equipment needed for the
performance of the block is essential.
The equipment needed for a DNB includes an electrical
stimulator, a Teflon-coated hypodermic needle of sufficient
length that allows access to the nerve but with the smallest
bore that is practical to minimize pain, and a syringe contain-
ing the anesthetic agent with the lowest dose and concentra-
tion possible to limit side effects. Palpation and ultrasonog-
raphy may help with the identification and avoidance of
neurovascular structures. Electrical stimulation is critical in
the localization of the perineural area. Ideally, it is identified
when a current of ⬍1 mA results in a strong muscle contrac-
tion. Surface stimulation may facilitate the initial localization
of superficial nerves, but is often of limited value and may
cause unnecessary discomfort for deep nerves. Using low
doses of the anesthetic agent limits diffusion and minimizes
prolonged weakness and anesthesia. However, when assess-
ing for contractures, higher volumes and concentration of the
selected anesthetic agent may be required.
Upper Extremity DNBs
Common spasticity patterns are seen in the upper extremi-
ties. Nerves that are commonly blocked in the upper extrem-
ity include the musculocutaneous nerve (MCN) [85,86],
anterior interosseus nerve (AIN) [87], median and ulnar
nerves [87], recurrent motor branch of the median nerve
[88], thoracodorsal nerve [85,86], and pectoral nerve [86].
CHEMODENERVATION AND NERVE BLOCKS IN SPASTICITY
Clenched Fist, Thumb in Palm, and Adducted
Finger Deformities. For patients who present with a
clenched fist, thumb in palm deformity, or increased finger
adduction, DNB can help differentiate whether the MH orig-
inates from the extrinsic or intrinsic finger flexors. It can also
differentiate between FDP MH, which flexes the distal inter-
phalangeal (DIP) joints, or the FDS, which flexes the proxi-
mal interphalangeal (PIP) joints. DNB of the AIN evaluates
the contribution of MH of the FDP for digits 2 and 3 and of
the flexor pollicis longus (FPL) to the clinical presentation.
This will enable the selection of the most involved muscles
for chemodenervation while preserving as much residual
function as possible. Properly planned intervention has the
potential to improve overall hand function [74,89].
In the assessment of the thumb in palm, DNB of the AIN
and median and ulnar nerves can be considered. If DNB of
the AIN corrects the thumb in palm, then chemodenervation
to the FPL can be implemented; whereas, if a DNB of the
recurrent motor branch of the median nerve resolves the
problem, this suggests that chemodenervation of the oppo-
nens pollicis and flexor pollicis brevis (FPB), superficial head,
should be performed. If DNB of the ulnar nerve is required,
consider treating the deep head of the FPB. DNB of the ulnar
nerve can also address adduction of digits 2 through 4 as well
as adduction or flexion at the MCP joints.
Flexed Elbow and Wrist, and Pronated Forearm.
Performance of a DNB of the MCN can significantly reduce
elbow flexor MH arising from the brachialis and biceps brachii.
A motor point block of the brachioradialis muscle can assess its
contribution to this abnormal posture. Evaluation of volitional
elbow flexion and extension before and after a diagnostic block
can assess the effect of MH and weakness. When performing
DNB of the MCN, insert the needle at the medial arm and volar
to the median nerve and brachial artery; as the needle is ad-
vanced laterally, electrical stimulation will produce a contrac-
tion of muscles innervated by the median nerve and then the
MCN. DNB of the median nerve in that region will assess MH of
forearm pronators, flexor carpi radialis, palmaris longus, the
FDS, and muscles innervated by the AIN.
DNB of the median nerve performed at the proximal
forearm will evaluate the effect of IMH for wrist and finger
flexors (which can contribute to wrist flexor spasticity).
Shoulder Adduction, Internal Rotation, and Sub-
luxation. The most common patterns seen as a result of MH
at the shoulder is adduction and internal rotation. Muscles that
are involved in these abnormal patterns include the pectoralis
major and minor, subscapularis, teres major, and latissimus
dorsi. DNB can be useful in the identification of contractures as
well as assessing the functional significance and limitations that
result from MH of these muscles. A DNB of the thoracodorsal
nerve will reduce the activity of the latissimus dorsi, whereas
block of the pectoral nerves will help elucidate muscles produc-
ing shoulder internal rotation and adduction. Other muscles
such as the subscapularis [90] and teres major can be blocked
using a motor point technique.
PM&R
Lower Extremity DNBs
The most common gait abnormalities seen with MH of the
lower extremities are scissoring, stiff knee, and equinovarus
deformities. DNB can be performed to the obturator nerve for
scissoring [85,91], to the femoral nerve motor branches for
stiff knee [92], and to the tibial nerve to the gastrocnemius
[93], soleus [94], and tibialis posterior [94] muscles for
equinovarus deformity.
Scissoring gait with a resulting narrow base of support can
result from hip adductor MH or hip abductor muscle weak-
ness. Some patients with hip external rotation during swing
phase may be using their adductor muscles to assist with limb
advancement in the swing phase of ambulation. A DNB of the
obturator nerve can help evaluate these issues. If the DNB
reduces scissoring and improves balance and gait without
loss of hip flexion, then a longer lasting procedure can be
contemplated [95].
Limited hip flexion during swing phase of the gait cycle
can be caused by weakness of the hip flexor muscles or MH of
the hip extensors (hamstring muscles and gluteus maximus).
If there is no significant hip flexor weakness with straight
leg-raising, then assess MH of the hamstring muscles with
physical examination. If there is MH of the rectus femoris
(RF), and the patient has a stiff knee gait, then a DNB of the
femoral nerve motor branch to the RF can be considered. In
addition a DNB of the sciatic nerve can be considered to
reduce the hamstring MH.
A stiff knee gait can be caused by MH or weakness of the
knee extensor muscles or ankle plantar flexor muscles. A
DNB of the RF muscle without blocking the vasti may im-
prove hip and knee flexion without weakening knee extensor
muscles when MH is caused by the RF [96,97]. If improve-
ment is not noted then consideration for further blockade of
the other quadriceps can be considered.
Numerous gait abnormalities can result from MH of the
plantar flexors or the ankle invertors. These include difficulty
with foot clearance during the swing phase of gait. Distur-
bances in the base of support may also contribute to a stiff
knee gait. The latter is especially true for patients with a
plantar flexion contracture with a ground reaction force that
is anterior to the knee during stance phase. If there is an
equinovarus deformity, a DNB of the tibialis posterior muscle
is indicated. Secondary to their contribution to the defor-
mity, a blockade of the flexor digitorum longus, flexor hallu-
cis longus, and the motor branches to the gastrocnemius and
soleus muscle could be considered.
Therapeutic Nerve Blocks
In addition to neurotoxin injections, nerve blocks—selective
motor or sensory blocks or regional anesthesia— have dis-
tinct roles in the management of MH. Neurolysis can achieve
a longer denervation against overactive muscles, compared
with BoNT. Unfortunately, the involvement of sensory anes-
thesia and dysesthesia makes this a highly selective proce-
dure. Possible beneficiaries include patients with complete
Vol. 1, Iss. 9, 2009 849
spinal cord injury or hypoesthetic hemiplegia from stroke or
brain injury. The risk of this side effect does depend on the
skill of the injector and the nerve being treated. Nerves with
relatively limited sensory involvement (eg, musculocutane-
ous and obturator) can also be blocked by a skilled injector
with a very favorable risk– benefit ratio. In addition, transient
nerve blocks are used before serial casting in the treatment of
muscle overactivity and the consequent joint contracture, to
temporarily block the activity of the overactive muscle and to
alleviate possible pain during forced PROM required for
serial casting. In addition, the use of regional anesthesia
through peripheral nerve blocks can minimize the morbidity
of undergoing contracted joint manipulations under general
anesthesia [98].
REFERENCES
1. Schroeder AS, Berweck S, Lee SH, Heinen F. Botulinum toxin treatment
of children with cerebral palsy—a short review of different injection
techniques. Neurotox Res 2006;9:189-196.
2. Fanucci E, Masala S, Squillaci E, et al. Pyriformis muscle syndrome:
CT/MR findings in the percutaneous therapy with botulinic toxin.
Radiol Med 2003;105:69-75.
3. Jankovic J. Review. Treatment of cervical dystonia with botulinum
toxin. Mov Disord 2004;19(Suppl 8):S109-S115.
4. Dogu O, Apaydin D, Sevim S, Talas DU, Aral M. Ultrasound-guided
versus ‘blind’ injection of botulinum toxin-A for treatment of sialor-
rhoea in patients with Parkinson’s disease. Clin Neurol Neurosurg
2004;106:93-96.
5. Yang EJ, Rha D, Yoo JK, Park ES. Accuracy of manual needle placement
for gastrocnemius muscle in children with cerebral palsy checked
against ultrasonography. Arch Phys Med Rehabil 2009;90:741-744.
6. Westoff B, Seller K, Wild A, Jaeger M, Krauspe R. Ultrasound guided
botulinum toxin injection technique for the iliopsoas. Dev Med Child
Neurol 2003;45:829-832.
7. Lee LH, Chang WN, Chang CS. The finding and evaluation of EMG-
guided BOTOX injection in cervical dystonia. Acta Neurol Taiwan
2004;13:71-76.
8. Cordivari C, Misra VP, Vincent A, Catania S, Bhatia KP, Lees AJ.
Secondary nonresponsiveness to botulinum toxin A in cervical dysto-
nia: The role of electromyogram-guided injections, botulinum toxin A
antibody assay, and the extensor digitorum brevis test. Mov Disord
2006;21:1737-1741.
9. Lim EC, Quek AM, Seet RC. Botulinum toxin-A injections via electrical
motor point stimulation to treat writer’s cramp: Pilot study. Neurol
Neurophysiol Neurosci 2006 Jun 30:4.
10. Chin TY, Nattrass GR, Selber P, Graham HK. Accuracy of intramuscular
injection of botulinum toxin A in juvenile cerebral palsy: A comparison
between manual needle placement and placement guided by electrical
stimulation. J Pediatr Orthop 2005;25:286-291.
11. Molloy FM, Shill HA, Kaelin-Lang A, Karp BI. Accuracy of muscle
localization without EMG: Implications for treatment of limb dystonia.
Neurology 2002;58:805-807.
12. Mayer NH, Whyte J, Wannstedt G, Ellis CA. Comparative impact of 2
botulinum toxin injection techniques for elbow flexor hypertonia. Arch
Phys Med Rehabil 2008;89:982-987.
13. Geenen C, Consky E, Ashby P. Localizing muscles for botulinum toxin
treatment of focal hand dystonia. Can J Neurol Sci 1996;23:194-197.
14. Childers MK. The importance of electromyographic guidance and
electrical stimulation for injection of botulinum toxin. Phys Med Reha-
bil Clin N Am 2003;14:781-792.
15. Lim EC, Ong BK, Seet RC. Botulinum toxin-A injections for spastic toe
clawing. Parkins Rel Disord 2006;12:43-47.
850 Elovic et al
16. O’Brien CF. Injection techniques for botulinum toxin using electro-
myography and electrical stimulation. Muscle Nerve Suppl 1997;6:
S176-S180.
17. Hogan Q. Finding nerves is not simple. Reg Anesth Pain Med 2003;28:
367-371.
18. Chin KJ, Chan V. Ultrasound-guided peripheral nerve blockade. Curr
Opin Anaesthesiol 2008;21:624-631.
19. Brull R, Perla A, Cheng PH, et al. Minimizing the risk of intravascular
injection during ultrasound-guided peripheral nerve blockade. Anes-
thesiology 2008;109:1142-1143.
20. Perlas A, Niazi A, McCartney C, et al. The sensitivity of motor response
to nerve stimulation and paresthesia for nerve localization as evaluated
by ultrasound. Reg Anesth Pain Med 2006;31:445-450.
21. Casati A, Danelli G, Baciarello M, et al. A prospective, randomized
comparison between ultrasound and nerve stimulation guidance for
multiple injection axillary brachial plexus block. Anesthesiology 2007;
106:992-996.
22. Dhir S, Ganapathy S. Comparative evaluation of ultrasound-guided
continuous infraclavicular brachial plexus block with stimulating cath-
eter and traditional technique: A prospective-randomized trial. Acta
Anaesthesiol Scand 2008;52:1158-1166.
23. Dufour E, Quennesson P, Van Robais AL, et al. Combined ultrasound
and neurostimulation guidance for popliteal sciatic nerve block: A
prospective, randomized comparison with neurostimulation alone.
Anesth Analg 2008;106:1553-1558.
24. Geffen GJ, Broek EV, Braak GJJ, et al. A prospective randomized
controlled trial of ultrasound guided versus nerve stimulation guided
distal sciatic nerve block at the popliteal fossa. Anaesth Intensive Care
2009;37:32-37.
25. Reid N, Stella J, Ryan M, Ragg M. Use of ultrasound to facilitate accurate
femoral nerve block in the emergency department. Emerg Med Aus-
tralas 2009;21:124-130.
26. Akkaya T, Ozturk E, Comert A, et al. Ultrasound-guided obturator
nerve block: A sonoanatomic study of a new methodologic approach.
Anesth Analg 2009;108:1037-1041.
27. Berweck S, Heinen, F. Use of botulinum toxin in pediatric spasticity
(cerebral palsy). Mov Disord 2004;19(Suppl 8):S162-S167.
28. Berweck S, Feldkamp A, Francke A, Hehles J, Schwerin A, Heinen F.
Sonography guided injection of botulinum toxin A in children with
cerebral palsy. Neuropediatrics 2002;33:221-223.
29. Willenborg MJ, Shilt JS, Smith BP, Estrada RL, Castle JA, Koman LA.
Technique for iliopsoas ultrasound-guided active electromyography-
directed botulinum a toxin injection in cerebral palsy. J Pediatr Orthop
2002;22:165-168.
30. Pena A, Gahill AM, Gozalez L, Baskin K, Kim H, Towbin R. Botulinum
toxin A injection of salivary glands in children with drooling and
chronic aspiration. J Vasc Interv Radiol 2009;20:368-373.
31. Jordan S, Ahan S, Gelabert H. Combining ultrasound and EMG for
botulinum toxin chemodenervation treatment of thoracic outlet syn-
drome: Comparison with fluoroscopy and EMG guidance. Pain Physi-
cian 2007;10:541-546.
32. Elovic EP, Eiseberg ME, Jasey NN. Spasticity and muscle overactivity as
components of the upper motor neuron syndrome. In: Frontera W, ed.
Physical Medicine and Rehabilitation: Principles and Practice. 5th ed.
New York: Demos Medical Publishing [in press].
33. DeLateur BJ. A new technique of intramuscular phenol neurolysis.
Arch Phys Med Rehabil 1972;53:179-181.
34. Halpern D, Meelhuysen FE. Phenol motor point block in the manage-
ment of muscular hypertonia. Arch Phys Med Rehabil 1966;47:659-
664.
35. Khalili AA, Harmel MH, Forster S, Benton JG. Management of spasticity
by selective peripheral nerve block with dilute phenol solutions in
clinical rehabilitation. Arch Phys Med Rehabil 1964;45:513-519.
36. Chua KS, Kong KH. Alcohol neurolysis of the sciatic nerve in the
treatment of hemiplegic knee flexor spasticity: Clinical outcomes. Arch
Phys Med Rehabil 2000;81:1432-1435.
CHEMODENERVATION AND NERVE BLOCKS IN SPASTICITY
37. Chua KS, Kong KH. Clinical and functional outcome after alcohol
neurolysis of the tibial nerve for ankle-foot spasticity. Brain Inj 2001;
15:733-739.
38. Kong KH, Chua KS. Outcome of obturator nerve block with alcohol for
the treatment of hip adductor spasticity. Int J Rehabil Res 1999;22:327-
329.
39. Brashear A, Gordon MF, Elovic E, et al. Intramuscular injection of
botulinum toxin for the treatment of wrist and finger spasticity after a
stroke. N Engl J Med 2002;347:395-400.
40. Elovic EP, Brashear A, Kaelin D, et al. Repeated treatments with
botulinum toxin type a produce sustained decreases in the limitations
associated with focal upper-limb poststroke spasticity for caregivers
and patients. Arch Phys Med Rehabil 2008;89:799-806.
41. Esquenazi A, Mayer N, Garreta R. Influence of botulinum toxin type A
treatment of elbow flexor spasticity on hemiparetic gait. Am J Phys Med
Rehabil 2008;87:305-310.
42. Gordon MF, Brashear A, Elovic E, et al. Repeated dosing of botulinum
toxin type A for upper limb spasticity following stroke. Neurology
2004;63:1971-1973.
43. Simpson DM, Gracies JM, Yablon SA, Barbano R, Brashear A; BoNT/
TZD Study Team. Botulinum neurotoxin versus tizanidine in upper
limb spasticity: A placebo-controlled study. J Neurol Neurosurg Psy-
chiatry 2009;80:380-385.
44. Bakheit AM, Thilmann AF, Ward AB, et al. A randomized, double-
blind, placebo-controlled, dose-ranging study to compare the efficacy
and safety of three doses of botulinum toxin type A (Dysport) with
placebo in upper limb spasticity after stroke. Stroke 2000;31:2402-
2406.
45. Bakheit AM, Pittock S, Moore AP, et al. A randomized, double-blind,
placebo-controlled study of the efficacy and safety of botulinum toxin
type A in upper limb spasticity in patients with stroke. Eur J Neurol
2001;8:559-565.
46. Bakheit AM, Sawyer J. The effects of botulinum toxin treatment on
associated reactions of the upper limb on hemiplegic gait—a pilot
study. Disabil Rehabil 2002;24:519-522.
47. Hyman N, Barnes M, Bhakta B, et al. Botulinum toxin (Dysport)
treatment of hip adductor spasticity in multiple sclerosis: A prospec-
tive, randomised, double blind, placebo controlled, dose ranging
study. J Neurol Neurosurg Psychiatry 2000;68:707-712.
48. Brashear A, McAfee AL, Kuhn ER, Fyffe J. Botulinum toxin type B in
upper-limb poststroke spasticity: A double-blind, placebo-controlled
trial. Arch Phys Med Rehabil 2004;85:705-709.
49. Ozcakir S, Sivrioglu K. Botulinum toxin in poststroke spasticity. Clin
Med Res 2007;5:132-138.
50. Comella CL, Jankovic J, Shannon KM, et al. Comparison of botulinum
toxin serotypes A and B for the treatment of cervical dystonia. Neurol-
ogy 2005;65:1423-1429.
51. Gracies J-M. Pathophysiology of spastic paresis. I: Paresis and soft
tissue changes and II: Emergence of muscle overactivity. Muscle Nerve
2005;31:535-571.
52. Simpson J-M, Gracies HK, Graham JM, et al. Assessment: Botulinum
neurotoxin for the treatment of spasticity (an evidence-based review):
Report of the Therapeutics and Technology Assessment Subcommittee
of the American Academy of Neurology. Neurology 2008;70;1691-
1698.
53. Brin MF. Botulinum toxin: Chemistry, pharmacology, toxicity, and
immunology. Muscle Nerve 1997;20(Suppl 6):S146-S168.
54. Yablon SA, Brashear A, Gordon MF, et al. Formulation of neutralizing
antibodies in patients receiving botulinum toxin type A for treatment of
poststroke spasticity: Pooled-data analysis of three clinical trials. Clin
Ther 2007;29:683-690.
55. Radensky PW, Archer JW, Dournaux SF, O’Brien CF. The estimated
cost of managing focal spasticity: A physician practice patterns survey.
Neurorehabil Neural Repair 2001;15:57-68.
56. Giovannelli M, Borriello G, Castri P, Prosperini L, Pozzilli C. Early
physiotherapy after injection of botulinum toxin increases the benefi-
cial effects on spasticity in patients with multiple sclerosis. Clin Rehabil
2007;21:331-337.
PM&R
57. Albany K. Physical and occupational therapy considerations in adult
patients receiving botulinum toxin injections for spasticity. Muscle
Nerve Suppl 1997;6:S221-S312.
58. Royal College of Physicians. National Clinical Guidelines for Stroke,
prepared by the Intercollegiate Stroke Working Party. 2nd ed. London:
Royal College of Physicians; 2004.
59. Kulkarni J. Efficacy of botulinum toxin for spasticity management in
neurorehabilitation. Int J Ther Rehabil 2004;11:211-212.
60. Robertson A, Ashford S, Heward, et al. The role of physiotherapists in
the management of spasticity with botulinum toxin in adults and
pediatric patients: A guideline. Berkhamsted, UK: Medendium Publish-
ing Group Ltd; 2006.
61. Shah SN, Hornyak J, Urquhart AG. Flexion contracture after total knee
arthroplasty in a patient with Parkinson’s disease: Successful treatment
with botulinum toxin type A. J Arthroplasty 2005;20:1078-1080.
62. Kay RM, Rethlefsen SA, Fern-Buneo A, Wren TA, Skaggs DL. Botuli-
num toxin as an adjunct to serial casting treatment in children with
cerebral palsy. J Bone Joint Surg Am 2004;86:2377-2384.
63. Verplancke D, Snape S, Salisbury CF, Jones PW, Ward AB. A random-
ized controlled trial of botulinum toxin on lower limb spasticity follow-
ing acute acquired severe brain injury. Clin Rehabil 2005;19:117-125.
64. Taylor NF, Dodd KJ, Prasad D, Denisenko S. Progressive resistance
exercise for people with multiple sclerosis. Disabil Rehabil 2006;28:
1119-1126.
65. Dibble LE, Hale TF, Marcus RL, Droge J, Gerber JP, LaStayo PC.
High-intensity resistance training amplifies muscle hypertrophy and
functional gains in persons with Parkinson’s disease. Mov Disord
2006;21:1444-1452.
66. Ada L, Dorsch S, Canning CG. Strengthening interventions increase
strength and improve activity after stroke: A systematic review. Aust J
Physiother 2006;52:241-248.
67. Scholtes VA, Dallmeijer AJ, Knol DL, et al. The combined effect of
lower-limb multilevel botulinum toxin type a and comprehensive
rehabilitation on mobility in children with cerebral palsy: A random-
ized clinical trial. Arch Phys Med Rehabil 2006;87:1551-1558.
68. Gracies JM, Singer BJ, Dunne JW. The role of botulinum toxin injec-
tions in the management of muscle overactivity of the lower limb.
Disabil Rehabil 2007;29:1789-1805.
69. Dobkin BH. Training and exercise to drive poststroke recovery. Nat
Clin Pract Neurol 2008;4:76-85.
70. Hesse S. Treadmill training with partial body weight support after
stroke: A review. NeuroRehabilitation 2008;23:55-65.
71. Robertson JV, Pradon D, Bensmail D, Fermanian C, Bussel B, Roche N.
Relevance of botulinum toxin injection and nerve block of rectus
femoris to kinematic and functional parameters of stiff knee gait in
hemiplegic adults. Gait Posture 2009;29:108-112.
72. Bonaiuti D, Rebasti L, Sioli P. The constraint induced movement
therapy: A systematic review of randomized controlled trials on the
adult stroke patients. Eura Medicophys 2007;43:139-146.
73. Levy CE, Giuffrida C, Richards L, Wu S, Davis S, Nadeau SE. Botulinum
toxin A, evidence-based exercise therapy, and constraint-induced
movement therapy for upper-limb hemiparesis attributable to stroke: A
preliminary study. Am J Phys Med Rehabil 2007;86:696-706.
74. Sun SF, Hsu CW, Hwang CW, Hsu PT, Wang JL, Yang CL. Application
of combined botulinum toxin type A and modified constraint-induced
movement therapy for an individual with chronic upper-extremity
spasticity after stroke. Phys Ther 2006;86:1387-1397.
75. Reiter F, Danni M, Lagalla G, Ceravolo G, Provinciali L. Low-dose
botulinum toxin with ankle taping for the treatment of spastic equino-
varus foot after stroke. Arch Phys Med Rehabil 1998;79:532-535.
76. Carda S, Molteni F. Taping versus electrical stimulation after botuli-
num toxin type A injection for wrist and finger spasticity. A case-
control study. Clin Rehabil 2005;19:621-626.
77. Hesse S, Jahnke MT, Luecke D, Mauritz KH. Short-term electrical
stimulation enhances the effectiveness of botulinum toxin in the treat-
ment of lower limb spasticity in hemiparetic patients. Neurosci Lett
1995;201:37-40.
Vol. 1, Iss. 9, 2009 851
78. Eleopra R, Tugnoli V, De Grandis D. The variability in the clinical effect
induced by botulinum toxin type A: The role of muscle activity in
humans. Mov Disord 1997;12:89-94.
79. Bayram S, Sivrioglu K, Karli N, Ozcan O. Low-dose botulinum toxin
with short-term electrical stimulation in poststroke spastic drop foot: A
preliminary study. Am J Phys Med Rehabil 2006;85:75-81.
80. Esquenazi A, Mayer N. Abstract. Electric stimulation to prolong the
duration of botulinum toxin type A effect on spasticity: A double-blind,
placebo-controlled study. Arch Phys Med Rehabil 2007;88E105.
81. Johnson CA, Burridge JH, Strike PW, Wood DE, Swain ID. The effect of
combined use of botulinum toxin type A and functional electric stim-
ulation in the treatment of spastic drop foot after stroke: A preliminary
investigation. Arch Phys Med Rehabil 2004;85:902-909.
82. Gracies JM, Legacy M, Weiss DJ, Echo M, Flanagan S, Simpson DM.
Botulinum toxin dilution and endplate targeting in spasticity: A dou-
ble-blind controlled study. Arch Phys Med Rehabil 2009;90:9-16.e2.
83. Wessel J, Ward AB, Retard P, et al. European consensus table on the use
of botulinum toxin type A in adult spasticity. J Rehabil Med 2009;41:
13-25.
84. Buffenoir K, Decq P, Lefaucheur JP. Interest of peripheral anesthetic
blocks as a diagnosis and prognosis tool in patients with spastic
equinus foot: A clinical and electrophysiological study of the effects of
block of nerve branches to the triceps surae muscle. Clin Neurophysiol
2005;116:1596-1600.
85. Kishner S. Chemical neurolysis with phenol. An AAEM workshop,
October 1998.
86. Shin DY, Lennard TA. Proximal upper extremity, trunk, and head
blocks. In: Lennard TA, ed. Physiatric Procedures in Clinical Practice.
Philadelphia: Hanley & Belfus, Inc; 1995:130-138.
87. Mauldin CC, Brooks DW. Arm, forearm, and hand blocks. In: Lennard
TA, ed. Physiatric Procedures in Clinical Practice. Philadelphia: Hanley
& Belfus, Inc; 1995:139-149.
88. Keenan MAE, Botte MJ. Technique of percutaneous phenol block of the
recurrent motor branch of the median nerve. J Hand Surg Am 1987;
12:806-8007.
89. Lukban MB, Rosales RL, Dressler D. Effectiveness of botulinum toxin A
for upper and lower limb spasticity in children with cerebral palsy: A
summary of evidence. J Neural Transm 2009;116:319-331.
90. Harrison TP, Sadnicka A, Eastwood DM. Motor points for the neuro-
muscular blockade of the subscapularis muscle. Arch Phys Med Rehabil
2007;88:295-297.
91. Shin DY, Lennard TA. Proximal lower extremity blocks. In: Lennard
TA, ed. Physiatric Procedures in Clinical Practice. Philadelphia: Hanley
& Belfus, Inc; 1995:150-156.
92. Albert T, Yelnik A, Colle F, Bonan I, Lassau JP. Anatomic motor point
localization for partial quadriceps block in spasticity. Arch Phys Med
Rehabil 2000:81:285-287.
93. Jang SH, Ahn SH, Park SM, Kim SH, Lee KH, Lee ZI. Alcohol neurolysis
of tibial nerve motor branches to the gastrocnemius muscle to treat
ankle spasticity in patients with hemiplegic stroke. Arch Phys Med
Rehabil 2004;85:506-508.
94. Deltombe T, De Wispelaere J-F, Gustin T, Jamart J, Hanson P. Selective
blocks of the motor nerve branches to the soleus and tibialis posterior
muscles in relation to anatomic surface landmarks for selective motor
nerve blocks in the management of the spastic equinovarus foot. Arch
Phys Med Rehabil 2004;85:54-58.
95. Wassef MR. Interadductor approach to obturator nerve blockade for
spastic conditions of adductor thigh muscles. Reg Anesth 1993;18:13-
17.
96. Sung DH, Bang HJ. Motor branch block of the rectus femoris: Its
effectiveness in stiff-legged gait in spastic paresis. Arch Phys Med
Rehabil 2000;81:910-915.
97. Chantraine F, Detrembleur C, Lejeune TM. Effect of the rectus femoris
motor branch block on post-stroke stiff-legged gait. Acta Neurol Belg
2005;105:171-177.
98. Farmer SE, James M. Contractures in orthopaedic and neurological
conditions: A review of causes and treatment. Disabil Rehabil 2001;23:
549-558.