Eur Radiol (2008) 18: 1506–1512

DOI 10.1007/s00330-008-0909-x MUSCULO SKELETAL

Jongmin Lee
Yang Soo Lee
Percutaneous chemical nerve block
with ultrasound-guided intraneural injection

Received: 19 September 2007 Y. S. Lee musculocutaneous nerves. After iden-

Revised: 6 December 2007
Accepted: 5 January 2008
Published online: 21 March 2008
# European Society of Radiology 2008
J. Lee (*)
Department of Diagnostic Radiology,
Kyungpook National University
Hospital,
50, Sam-deok 2 Ga,
Jung Gu, Daegu 700–721, South Korea
e-mail: jonglee@knu.ac.kr
Tel.: +82-53-4205472
Fax: +82-53-4222677
Departement of Physical Medicine and
Rehabilitation, Kyungpook National
University Hospital,
50, Sam-deok 2 Ga,
Jung Gu, Daegu 700–721, South Korea
e-mail: leeysu@knu.ac.kr
Abstract Ultrasound-guided, intra-
neural chemical nerve block was
performed to control intractable limb
spasticity and its feasibility was eval-
uated. Twenty-nine patients showing
spastic limb were controlled by 53
intraneural injections of chemical
agents, either lidocaine or phenol. The
main targets were the sciatic, tibial and
tification of the spastic muscle and
target nerve, an ultrasound-guided,
intraneural injection was administered
through a 25–G needle. The average
effective duration was 9.1±19.6 days
in the lidocaine injection group and
was 164.5±169.4 days in the perma-
nent blocking group with phenol
injection. The ultrasound-guided in-
traneural injection technique was
convincing. Intraneural injection of
phenol achieved long-lasting im-
provement of spasticity.
Keywords Nerve block . Muscle
spasticity . Ultrasonic imaging

Introduction flaccid paralysis and atrophy. Although selective, posterior

Muscular spasticity has been defined as “a condition in
which there is a velocity-dependent increase in resistance
of the muscle group to passive stretch with a ’clasp-knife’
type component associated with hyperactive tendon
reflexes” [1]. On the basis of Sherrington’s studies, a
neurophysiological knowledge of muscle tone and patho-
genesis of spasticity was developed [2].
To relieve a spasm of the appendicular skeletal muscle
caused by neurological disorder, various surgical proce-
dures have been tried [3]. To interrupt either afferent or
efferent components of the spinal nerve root, posterior or
anterior rhizotomies were performed [2, 3]. Anterior
rhizotomy resulted in a flaccid extremity instead of
muscular spasm [3, 4]. Posterior rhizotomy succeeded,
but at the expense of sensory loss. However, these
procedures are no longer applied because of the resulting
rhizotomy has evolved as the predominant neurosurgical
procedure for the reduction of spasticity in children with
spastic cerebral palsy, peripheral neurectomy has become
popular to overcome postoperative flaccid paralysis. In
addition, other ablative and non-ablative procedures have
been used for the successful reduction of spasticity in
certain patients [3]. Munro et al. [4] tried sciatic and sacral
nerve block by intraneural injection of procaine after
surgical dissection of target nerves. Other injections into
the muscle belly were performed using an electrode needle
after identification of the motor point with a surface
electrode [3].
On the other hand, ultrasound-guided, perineural blocks
have recently become popular in the anesthetic literature
for temporary local anesthesia. Ultrasonography has come
to be regarded as a useful aid, whether to locate arteries, to
mark the skin for unguided blocks or to act as a real-time

guide of needle or catheter position relative to the nerve or
related blood vessels. Ultrasonography can also be used to
define the spread of local anesthetics [5]. Recently, Gruber
et al. [6] reported the successful results of ultrasound-
guided phenol injection into painful stump neuromas.
In this study, the ultrasound guidance technique and
intraneural chemical nerve block technique were inte-
grated. The purpose of this study was to evaluate the
feasibility of ultrasound guidance during intraneural injec-
tion and the effect of intraneural chemical block of normal-
featured nerves to control intractable limb spasticity
originating from central neurological abnormality. The
feasibility evaluation of the nerve block technique was
performed retrospectively after 3-year clinical application.
Materials and methods
Twenty-nine patients, 23 male and 6 female, showing
muscular contracture of their extremities were controlled
by 53 intraneural injections of chemical agents. Patient age
ranged from 2 to 75 years old, with a mean age of 34. All
patients showed spasticity during forced passive motion or
intentional voluntary motion of their extremities, but none
complained of spasm. The causes of neurological deficit
were cerebral palsy (n=11), cerebral stroke (n=5), traumatic
brain (n=10) and spinal cord (n=3) injuries (Table 1). The
inclusion criterion for the sciatic and tibial nerve block was
patients with a spastic tip toe or crouched gait that was
refractory to conventional rehabilitation for more than
6 months. The exclusion criteria were patients who could
not walk without support and were not treated with an
adequate rehabilitation technique. For the musculocutane-
ous nerve block, the inclusion criteria were marked
spasticity of the elbow flexor muscles, spasticity for more
than 1 year after onset and severe finger flexor spasticity
resulting in a non-functional hand. The exclusion criteria
were patients who had spasticity in the elbow for less than
Table 1 Patient data of lidocaine and phenol injection groups
Lidocaine injection Phenol injection
group group
Age (years) 23.0±20.2 51.8±16.5
Male ofemale ratio 16: 3 7: 3
Cerebral palsy (persons) 7 4
Traumatic brain injury 6 4
(persons)
Cerebral stroke (persons) 4 1
Spinal cord injury 2 1
(persons)
Subject number (persons) 19 10
Duration of illness 67.9±46.1 44.6±32.6
(months)
1507
1 year and who could extend their fingers. Our institutional
review board approved all aspects of this retrospective
study. Informed consent was obtained from all patients or
their parents in the case of children prior to the procedure.
A board-certified physiatrist with 9–year experience
evaluated all the patients’ spasticity according to the
Ashworth scale before and after the intraneural injections.
For Ashworth scaling, patients laid down in supine position
and relaxed all muscles. Resistance of extremity during its
passive movement was stratified as follows: 0= no increase
in tone, 1= slight increase in tone giving a ‘catch’, 2= more
marked increase in tone, but limb easily flexed, 3=
considerable increase in tone-passive movement difficult
and 4= limb rigid in flexion or extension [7].
Injected agents were 2~5 ml of a solution containing 2%
lidocaine or 7% phenol. The 7% phenol solution was made
by dissolving pure phenol in distilled water. Lidocaine was
used for temporary nerve block and phenol for permanent
block. Ultrasonography (HDI-5000, Philips, Eindhoven,
The Netherlands) equipped with 7–15 MHz linear
transducers was used. The lidocaine injection group
comprised 19 patients and 41 intraneural injections. The
target nerves were sciatic nerve (n=25), tibial nerve (n=11),
musculocutaneous nerve (n=2), anterior interosseous nerve
(n=1), median nerve (n=1) and ulnar nerve (n=1), whereas
the phenol injection group comprised 10 patients and 12
injections. In this group, the target nerves were the
musculocutaneous nerve (n=10), anterior interosseous
nerve (n=1) and tibial nerve (n=1).
As an initial step of the nerve-blocking procedure, the
physiatrist re-confirmed a spasticity of extremity based on
the patient’s complaint and defective movement. Subse-
quently, a major causative muscle for the spasticity was
identified through a physical examination, and the nerve
innervating the muscle was targeted. The blocking agent
was decided according to the literature-based knowledge
about the proportion of motor and sensory neural
components. If the muscle was a mixed motor and sensory
nerve, lidocaine was chosen as blocking agent since the
risk of dysesthesia was high, whereas the nerves with low
risk of dysesthesia, such as musculocutaneous and obtu-
rator nerves, were blocked using phenol [7, 8]. A
permanent blocking agent could be applied for the pure
motor nerve, such as the musculocutaneous and anterior
interosseous nerves. However, a local anesthetic drug was
the first choice for preliminary and temporary nerve block
for a nerve containing both sensory and motor components,
such as the sciatic, tibial, radial and ulnar nerves.
Subsequently, a permanent nerve block was performed
only when the spasticity-free effect overwhelmed the
sensory deficit. A temporary block was preceded in cases
where the effect and the safety of the permanent block were
not definite. In this study, four patients received temporary
nerve block prior to permanent block. These cases
comprised two musculocutaneous, anterior interosseous
and tibial nerves as target nerves. The other six patients
1508
received permanent block of their musculocutaneous
nerves without preliminary testingof the temporary block.
The rationale for temporary nerve block by intraneural
injection of local anesthetic drugs is firstly, checking the
possibility of blocking mixed sensory and motor nerves
permanently and secondly, temporary but hopefully longer
relief of spasticity than a blinded injection of local
anesthetic drug around a target nerve. The intraneural
injection procedures were performed by a board-certified
radiologist with 12-year experience of ultrasound-guided
targeting of the internal structures, such as the joints,
masses, blood vessels and nerves in a 1,000-bed general
hospital.
After ultrasonographic identification of the target nerve,
a 25-gauge needle with beveled tip was inserted into the
nerve with real-time guidance. The general technique used
to locate the nerves precisely involved with an ultrasono-
graphic scan from the point where the target nerve could be
depicted easily. For example, the radial nerve was readily
identified at the wrist around the radial artery, and the radial
nerve was then traced proximally up to the point of the
block. The ulnar nerve was traced from the cubital tunnel.
The musculocutaneous nerve was identified beneath the
biceps brachii muscle and lateral to the brachial artery in
the supine position. After identifying the musculocutane-
ous nerve, the needle was inserted into the antero-lateral
aspect of the proximal arm until it reached the target
through the biceps brachii muscle. The tracing of the tibial
nerve and sciatic nerve began from the popliteal fossa
distally and proximally. The blocking level of the sciatic
nerve was at the level of the gluteal fold, and the entry point
was the posterior or posterolateral aspect of the proximal
thigh at the prone position. The median nerve tracing
started from either the axilla or anterior midline of proximal
arm. On the way down to the wrist, the anterior interos-
seous nerve could be identified. The anterior interosseous
nerve was the branch of the median nerve at the proximal
level of the distal arm, which reached the anterior aspect of
the interosseous membrane. The blocking of the anterior
interosseous nerve was performed at the mid-level of the
distal arm.
A small amount of nerve blocking agent was initially
injected when the needle tip was within the target nerve.
Due to real-time ultrasonographic guidance, the intraneural
injection could be retried until the expanding nerve was
visualized during the initial small injection. The full dose of
phenol was injected after reconfirmation by the initial test
injection. For even distribution of the agents, multiple,
small-amount injections were done moving the tip of the
needle along the whole area of the nerve. The pre-loaded
volume of the sclerosing agent was determined according
to the size of the target nerve. For the sciatic nerve block,
the musculocutaneous and tibial nerve block, radial and
ulnar nerve block, and anterior interosseous nerve block,
5-ml, 4-ml, 3-ml and 2-ml of the agents were loaded,
respectively. However, the injection was stopped when the
cross-sectional area of the target nerve doubled even before
the full pre-loaded dose had been injected. The intraneural
injection was determined to be successful when the
injected nerve expanded and immediate improvement of
the muscular contracture was noted. Usually, the assistants
holding the distal limb could feel the sudden effacement of
rigidity when the intraneural injection of the blocking agent
started. Since either the phenol or lidocaine and either
intraneural or perineural injections might show immediate
improvement of the spasticity right after the procedure, in
this study, the immediate post-procedure effect was not
regarded as an index for the feasibility. Instead, an
evaluation of the effective duration after the intraneural
nerve block was the main focus of this study. The degree of
improvement in spasticity varied according to the blocking
level of the target nerve and the presence of co-working
nerves or muscles. The whole process of the intraneural
block took approximately 15 min even though the time
needed to depict the target nerve varied.
The patients were educated to revisit to our outpatient
clinic immediately when spasticity was felt to have
recurred. In the outpatient clinic, the post-procedure
follow-up evaluation was performed by a physiatrist who
evaluated the patients initially. The spasticity-free ‘effec-
tive duration’ was defined as the time between the moment
of nerve block and that when the patients felt recurring
spasticity in their extremities. In cases when the spasticity-
free interval lasted until the last follow-up time, the
effective duration was defined as the interval between the
date of nerve block and the finishing date of data collection
for this study after reconfirming via telephone. The
influence of blocking agents and target nerves on the
effective duration was evaluated.
Results
In all 53 injections, the nerve expanded, and the spasticity
was immediately released, indicating a technical success
rate of 100%. At the initial moment of intraneural injection,
in all cases, pricking pain occurred shortly and subse-
quently disappeared during the other period of injection.
No intraneural injection was stopped due to patient’s
intolerance to the pain in both the lidocain- and phenol-
injection groups. The diameter expansion ratio of the target
nerve ranged from 1.2 to 3.8 with a mean of 2.1 (Figs. 1, 2).
In the lidocaine injection group (n=19), the mean pre-
injection Ashworth scale was 2.6±0.8. If the three patients
who were lost to follow-up were excluded, the average pre-
injection Ashworth scale of the remaining 16 patients was
2.5±0.7. Although the spasticity disappeared immediately
in all cases given the lidocaine injection, the spasticity
recurred at the first follow-up in all cases except for one.
All patients except for two (n=14) were evaluated within
4 weeks. The follow-up evaluation period ranged from 3 to
120 days with mean and standard deviation of 12.6±

Fig. 1 Phenol sclerotherapy of the musculocutaneous nerve
performed for a 59-year-old female patient complaining of spastic
elbow after cerebral stroke. In the initial transverse (a) and
longitudinal (b) ultrasonography using 5–12 MHz linear transducer,
the musculocutaneous nerve (+) was identified beneath the biceps
brachii muscle (*). A 25-guage needle (arrows) was inserted into the
musculocutaneous nerve and subsequently 5-ml phenol was slowly
injected by moving the tip in the whole area of the nerve (c).
Postprocedure transverse (d) and longitudinal (e) ultrasonography
revealed a swollen musculocutaneous nerve (+), suggesting
21.8 days. The effective duration could not be measured
numerically since spasticity-recurrence time was declared
based on patient’s memory during the first follow-up, and
no physical exam was performed during the spasticity-free
interval. The post-injection Ashworth scale of the 16
patients was 2.4±0.8. In this study protocol, there was no
significant improvement in the Ashworth scale after the
lidocaine injection.
The phenol injection group (n=10) showed an average
pre-injection Ashworth scale of 3.1±0.3. If the two patients
Fig. 2 A 32-year-old male suffering from spastic pronation of the
forearm after brain injury by motor vehicle accident became a
candidate for phenol sclerotherapy of the anterior interosseous
nerve. Preprocedure transverse (a) and longitudinal (b) ultrasonog-
raphy using a 5–12-MHz transducer revealed an anterior interosseous
1509
successful intraneural injection. The echogenecity of the swollen
nerve (+) is slightly decreased due to injected phenol. Six months
after the procedure, follow-up ultrasonography (f) revealed an
atrophic musculocutaneous nerve (arrow) and biceps brachii muscle
(*), implying the effect of neurectomy. Despite non-functioning
biceps muscle, the patient was able to flex her elbow intentionally
by relying on the function of the brachialis muscle, which is
innervated by the radial nerve. In addition, the patient did not
complain of any spasticity of her elbow
who were lost to follow-up were excluded, the average pre-
injection Ashworth scale was 3.1±0.4. In contrast to the
lidocaine injection group, the phenol injection group
showed statistically significant improvement in the average
post-injection Ashworth scale of 2.1±0.8 during the follow-
up evaluation (p<0.05 in Wilcoxon signed rank test). The
first follow-up interval ranged from 3 to 420 days with
mean and standard deviation of 97.0±144.1 days (p<0.01).
The follow-up evaluation was performed within 4 weeks in
four patients. The other four patients were evaluated after
nerve (+) beneath the flexor pollicis longus muscle (*) at the level of
the distal forearm. During intraneural injection of phenol (c), the
needle (arrows) and swelling anterior interosseous nerve (+) can be
identified
1510

4 weeks. In the phenol injection group, the average
effective duration ranged from 3 to 420 days with mean and
standard deviation of 164.5±169.4 days. Two patients
showed recurring original spasticity at the first follow-up
evaluation on the 5th and 12th days. The other patients did
not show any aggravation of the improved spasticity during
the follow-up evaluation up to the 420th day (Table 2).
Although temporary and tolerable, causalgia with a
duration of several days developed in seven cases given the
tibial nerve block using lidocaine. No other significant
complication occurred. During the follow-up, one patient
whose musculocutaneous nerve had been blocked using
phenol revisited the interventional suite due to slightly
increasing arm spasticity. The dynamic ultrasonography
during the voluntary motion revealed atrophic and non-
functioning biceps brachii muscle, suggesting a successful
musculocutaneous block. The non-functioning muscle was
documented by ultrasonography when the axial thickening
and decrease in echogenecity did not occur during the
voluntary contraction of the muscle. The recurrent spas-
ticity was concluded to be due to a hypertrophied brachialis
muscle, and no further neurolysis was performed (Fig. 1).
The other patients (n=7) were followed up clinically, and
no ultrasonographic evaluation of the target nerve and
muscle atrophy was performed.
Discussion
In the literature, various peripheral neurectomies have been
applied to control intractable appendicular spasticity with
favorable results, despite undesirable side effects, such as
weakness, atrophy and sensory loss. The target nerves were
the obturator nerve, musculocutaneous nerve, tibial nerve,
sciatic nerve and brachial plexus collaterals [3]. Triggered
by successful, non-destructive, sciatic and sacral nerve
block by intraneural or perineural injection of procaine, the
intraneural chemical blocking technique was recruited as
an alternative method to control the spasticity [4]. Common
target nerves of intraneural injection were the median and
ulnar nerves for wrist and finger spasticity, the musculo-
cutaneous nerve for elbow spasticity, the obturator nerve
for scissoring and the tibial nerve for equinus deformity [3].
The most common agent injected was 2–5% phenol acting
by protein denaturation, followed by alcohol, anesthetics
such as lidocaine and procaine, botulinum toxin inhibiting
release of acetylcholine from the presynaptic terminals and
blocking neuromuscular transmission [4, 9]. Since blind
nerve blocking techniques had a failure rate of up to 20%,
surgical dissection of nerve or electrophysiological guid-
ance was required for successful intraneural or perineural
injection of blocking agents [10].
Botulinum type-A toxin injections have been widely
used to control spasticity in a variety of disorders,
including cerebral palsy. The advantages of botulinum
type-A toxin are the easy administration. However, several
drawbacks of botulinum type-A toxin have been reported.
The toxin is expensive [11]. Since botulinum toxin attacks
the neuromuscular junction, the injection should be
performed at the motor point of the muscle [12]. In
addition, since the blockade is reversible after several
weeks, repeated injections every 3–6 months are essential
for a sustained effect [13]. In addition, resistance to the
botulnium toxin by autoantibiodies has been reported [14].
In this study, botulinum toxin was not used because it was
not feasible for both intraneural injections and achieving a
permanent blockade.
A perineural infiltration of phenol solution has been used
for many decades to treat spasticity [15]. The phenol
neurolytic block was performed under electrophysiological

Table 2 Clinical results during follow-up evaluation after intraneural phenol injection
Injection Target Pre-injection The 1st follow-up date The 1st follow-up The 2nd follow-up date The 2nd follow-up
number nerves AS (day) AS (day) AS

1 Rt MCN 3 12 3
2 Rt MCN 3
3 Lt AION 3 5 3
4 Lt MCN 3 420 2
5 Lt MCN 3
6 Rt MCN 3
7 Rt MCN 3 3 1
8 Rt MCN 3 90 1 180 1
9 Lt MCN 3
10 Rt MCN 3 60 2
11 Lt MCN 3 180 2 180 2
12 Rt TN 4 6 3 180 3
AS, Ashworth scale; Rt, right; Lt, left; MCN, musculocutaneous nerve; AION, anterior interosseous nerve; TN, tibial nerve

guidance, such as nerve stimulation technique [16, 11, 17].
A Teflon-coated needle connected to the nerve stimulator,
was slowly advanced until the maximum muscle contrac-
tion had occurred at a pre-set electric current. Subse-
quently, the phenol solution was injected until the muscle
contraction ceased [17]. The advantages of phenol neuro-
lysis are the low cost and long-lasting effect [17]. However,
dysesthesia, numbness and hematoma were the reported
side effects of phenol neurolysis [18]. In the literature, it
has been reported that phenol blocks were temporary and
generally lasted 3–12 months [19]. In this study, phenol
was injected exactly into target nerves due to real-time
ultrasound guidance. In contrast to the perineural infiltra-
tion techniques, the intraneural injection technique
achieved a longer effective duration (Table 2). In contrast
to phenol, lidocaine block lasted variously by subjects and
target nerves. Although it was not used in this study,
multilevel intraneural injections of a lidocaine solution at a
single nerve might extend the effective period.
In recent decades, the ultrasonographic examination of
peripheral nerves has become popular due to development
of ultrasonographic equipment and further understanding
of ultrasonographic feature of nerves [20, 21]. Ultrasound
has become a useful aid for locating nerves and a real-time
guide of needle during an injection of local anesthetics [5].
Ultrasonographic guidance has been applied in the intra-
lesional injection of alcohol to ablate Morton’s neuroma
and stump neuroma [1, 22], whereas, to our knowledge,
there has been no report about the application of ultrasound
guidance during intraneural nerve block for spasticity
control. For more specific block of the motor component, a
chemical block in the motor point of the muscle belly was
also tried, with an effect lasting up to 6 months [19]. Since
the motor point cannot be delineated by ultrasonography,
blind block at the presumed motor point area should be
performed. However, even in such a case, ultrasonography
can still facilitate reaching the motor point by showing
adjacent anatomical structures.
In the phenol injection group, the effective duration was
satisfactory to either patient or physician in 75% (six out of
eight). During the follow-up of a musculocutaneous nerve
block case, ultrasonography revealed that the recurring arm
spasticity was due to partially hypertrophied brachialis
muscle innervated by the radial nerve. In this case, the
biceps brachii muscle that had been innervated by muscu-
locutaneous nerve was atrophied. Therefore, it was
assumed that the recurring spasticity was due to the
strengthened adjuvant muscles, which perform alternative
tasks, and not by the resumed function of the ablated nerve
itself. Furthermore, these phenomena should be more likely
1511
for the distal muscles supplied by small nerves, such as
interosseous or obturator nerves. For example, in one case
of a phenol block, two intraneural injections were
performed at the musculocutaneous and anterior interos-
seous nerves to simultaneously release both the elbow
flexion and forearm pronation. The spastic elbow flexion
disappeared completely, whereas the spastic pronation of
the forearm recurred in 5 days. The smallest nerve in the
phenol group, the anterior interosseous nerve, achieved the
shortest effective duration. However, due to an insufficient
number of small nerves in the phenol group, the relation-
ship between the nerve size, dose of the blocking agent and
the effective duration could not be clarified.
Causalgia and dysesthesia, cardiac arrhythmias and
permanent neurological deficits are complications com-
monly reported during perineural block. Since the periph-
eral nerve usually consists of both motor and sensory
components, an intraneural chemical block may destroy the
sensory fibers resulting in dysesthesia or causalgia [23]. In
this study, no complication was encountered in the phenol
group, while mild temporary causalgia occurred in seven
cases of the lidocaine group. The causalgia occurred as a
complication because the lidocaine group included nerves
containing sensory fibers, such as sciatic, tibial and ulnar
nerves. The estimated reasons for the causalgia were nerve
fiber damage caused by a needle-related intraneural
physical injury and lidocaine-induced chemical injury
(unpublished experimental data), as well as causalgia-
mimicking pain by an altered ergonomic mechanism of the
extremity. In our consideration, the slow infusion of agent
at multiple points within a nerve reduced physical injury
and subsequent complications. In addition, to prevent
possible, severe sensory deficit, partial ablation might be a
solution. Based on the detailed anatomical information
using high-resolution ultrasonography, a partial area can
intentionally be saved from needle penetration during the
procedure. In cases of a sciatic nerve block, high-resolution
ultrasonography could differentiate the peroneal and tibial
nerve components, and a focused intraneural injection of
lidocaine into the tibial nerve component could be
performed.
In this study, we concluded that ultrasonography was a
perfect guiding tool for intraneural injection. In addition,
ultrasound-guided nerve block was suitable for controlling
spasticity of the extremities, either temporarily or perma-
nently. Intraneural injection of phenol achieved long-
lasting improvement of spasticity. One caveat is that
achieving an acceptable balance between reduction of
spasticity and possible sensory change should precede the
intraneural injection of the permanent-blocking agent.
1512
References
1. Lance JW (1980) Symposium synopsis.
In: Feldman RG, Young RR, Koella
WP (eds) Spasticity-disordered motor
control. Mosby-Year Book, St. Louis,
pp 45–45
2. Sherrington CS (1898) Decerebrate
rigidity and reflex coordination of
movements. J Physiol (Lond) 22:319–
337
3. Smyth MD (2000) Peacock WJ. The
surgical treatment of spasticity. Muscle
Nerve 23:153–163
4. Munro D, Spatz EL (1959) A pre-
liminary clinical report on a nondes-
tructive method for the relief of
so-called “Mass-Reflex” spasm. New
Eng J Med 260:1–6
5. Peterson MK, Millar FA, Sheppard DG
(2002) Ultrasound-guided nerve
blocks. Br J Anaesth 88(5):621–624
6. Gruber H, Kovacs P, Peer S, Frischhut
B, Bodner G (2004) Sonographically
guided phenol injection in painful
stump neuroma. AJR 182:952–954
7. Elovic E, Bogey R (2005) Spasticity
and movement disorder. In: Delisa JA,
Gans BM, Walsh NE (eds) Rehabilita-
tion medicine & rehabilitation-
principles and practice. 4th edn.
Lippincott Williams & Willkins,
Philadephia, pp 1427–1446
8. Netter FH (1987) The CIBA collection
of medical illustrations. volume 8,
musculoskeletal system. part 1, anato-
my, physiology, and metabolic disor-
ders. In: Netter FH (ed) Anatomy.
CIBA-Geicy corporation, Summit,
pp 38–82
9. Carpenter EB (1983) Role of nerve
blocks in the foot and ankle in cerebral
palsy. Foot Ankle 4:164–166
10. Thierney E, Lewis G, Hurtig JB,
Johnson D (1987) Femoral nerve block
with bupivacaine 0.25 per cent for
postoperative analgesia after open knee
surgery. Can J Anaesth
34:455–458
11. Kirazli Y, On AY, Kismali B, Aksit R
(1988) Comparison of phenol block
and botulinus toxin type A in the
treatment of spastic foot after stroke.
Am J Phys Med Rehabil
77:510–515
12. Petersen MC, Palmer FB (2001) Ad-
vances in prevention and treatment of
cerebral palsy. MRDD Research Re-
views 7:30–37
13. Brin M (1997) Botulinum toxin:
chemistry, pharmacology, toxicity, and
immunology. Muscle Nerve Suppl 6:
S146–S168
14. Greene PFS, Diamond B (1994) De-
velopment of resistance to botulinum
toxin type A in patients with torticollis.
Movement Disorders 9:213–217
15. Easton J, Ozel T, Halpern D (1984)
Intramuscular neurolysis for spasticity
in children. Arch Phys Med Rehabil
60:156–158
16. Botte MJ, Abrams RA, Bodine-Fowler
SC (1995) Treatment of acquired mus-
cle spasticity using phenol peripheral
nerve blocks. Orthopics 18:151–159
17. Wong AMK, Chen CL, Chen CPC,
Chou SW, Chung CY, Chen MJL
(2004) Clinical effects of botulinum
toxin A and phenol block on gait in
children with cerebral palsy. Am J Phys
Med Rehab 83:284–291
18. Gormley ME, Krach LE, Murr S (2004)
No-operative treatment. In: Gage JR
(ed) The treatment of gait problems in
cerebral palsy. 2nd edn. Mac Keith
Press, London, pp 245–272
19. Spira R (1971) Management of spas-
ticity in cerebral palsied children by
peripheral nerve block with phenol.
Dev Med Child Neurol 13:164–173
20. Fornage BD (1988) Peripheral nerves
of the extremities: imaging with ultra-
sound. Radiology 167:179–182
21. Martinoli C, Bianchi S, Derchi LE
(1999) Tendon and nerve sonography.
Radiol Clin North Am 37:691–711
22. Fanucci E, Masala S, Fabiano S, Perugia
D, Squillaci E, Varrucciu V, Simonetti G
(2004) Treatment of intermetatarsal
Morton’s neuroma with alcohol injection
under US guide: 10-month follow-up.
Eur Radiol 14:514–518
23. Garland DE, Lucie RS, Waters RL (1982)
Current uses of open phenol nerve block
for adult acquired spasticity. Clin Orthop
Rel Res 165:217–222