Anda di halaman 1dari 15

BOTULINUM TOXIN TYPE A AND SERIAL LIDOCAINE INJECTIONS

FOR POST STROKE UPPER LIMB SPASTICITY: COMPARTIVE STUDY


Eman A. Alkady*, Naema M. Mostafa*, Nehal Fathi*, Walid A Abdel Ghany **, Fatma H.
Alnoby*

Rheumatology & Rehabilitation Department, Assiut University, Assiut* and Neurosurgery


Department, Ain Shams University, Cairo**, Egypt
Key words: upper limb; spasticity; stroke; rehabilitation; Botulinum toxin type-A; Lidocaine

ABSTRACT
Background: The management of spasticity remains a major challenge in rehabilitation
medicine. Many studies have demonstrated the efficacy of local injections of botulinum toxin A
(BTX-A) into the upper limb for reducing spasticity. Lidocaine has been used as a nerve block
for the treatment of spasticity of the upper limb.
Objectives: to evaluate the outcome and to compare the efficacy of rehabilitation program
after botulinum toxin type-A injection versus serial lidocaine injections.
Patients and methods: 50 patients suffering from spasticity of the upper limb after stroke
attending the Rehabilitation Clinic were enrolled in the study. Assessment of spasticity, upper
limb function, self care ability and pain were done by using the Modified Ashworth Scale
(MAS), Medical research council scale (MRCS), the Barthel-Index and Visual Analogue Scale
(VAS) respectively. Electrophysiological assessment was done by conventional nerve
conduction studies; H-Reflex and Hmax/Mmax ratio and F-wave and F/M ratio. The patients
were divided into two equal groups. The first group submitted to botulinum toxin type-A
intramuscular injection and the second group submitted to 10 serial lidocaine intramuscular
motor point block. Both groups were subjected to the same rehabilitation program after injection
and had been worn the suitable orthotic. Evaluation of all patients had been done before
treatment and at one and four month after treatment.
Results: the spasticity in both studied groups was alleviated and the patients experienced
relief of pain, increase muscle power and decrease disability. These acquired benefits continued
through the fellow up period. No much difference found between efficacies of the two treatment
modalities used in this study.
Conclusion: Lidocaine might be considered as an effective and costless in the
symptomatic treatment of the post stroke upper limb spasticity. The study suggests that this
effect can be maintained with repeated serial and booster dose injections and intensive regular
rehabilitation program.

INTRODUCTION
Severe disabling spasticity of the upper limb muscles is a complication in patients of
upper motor neuron lesion (UMNL) that complicates the rehabilitation of many stroke patients.
Lundstrm et al (2008) stated that upper limb spasticity was present in 17% of patients at one
year post-stroke. Spasticity in the hands and wrist is especially disruptive because it can interfere
with dressing, washing, and other activities of daily living and that treatment of spasticity will
improve these movements (Bakheit et al., 2004, Decq et al., 2005). In some patients spasticity
also causes persistent pain or discomfort.
The clinical evaluation of spasticity remains a complex problem. Observation of clonus
or tendon hyperreflexia is easy, but it is not always easy to distinguish between resistance to
stretching related to tonic spasticity and resistance related to increased intrinsic stiffness of the
muscle. This difficulty could explain the absence of the efficacy of antispastic treatments in
some clinical situations. Local anesthetics (lidocaine, bupivacaine), which transiently block
afferent and efferent impulses in muscle or nerve, may recede casting or intramuscular injection
of other agents, or be used as a trial when there is consideration for long-term block (Gracies et
al., 1997).
Lidocaine, etidocaine and bupivacaine are currently the preferred local anesthetics for
relaxation of over active muscle (Saulino and Jacobs, 2006). Local anesthetics block nerve
conduction when they are applied locally and at a sufficient concentration in nervous tissue.
Their effect is reversible, creating no tissue injury. Lidocaine produces more prompt, intense,
long-lasting and extensive anesthesia than does an equal amount of procaine. Unlike procaine,
which is an ester, lidocaine is an aminoethylamide and, therefore, is less likely to provoke
hypersensitivity reactions (Kalichman et al 1992).
Over the last decade, studies have suggested that chemodenervation using botulinum
toxin-A (BTX-A) can be helpful, safe and effective treatment for over activity of focal or
segmental muscles. Its ability to improve function in spastic limbs is less well documented
(Anwar & Barnes 2005; Pathak et al., 2006). The clinical effects of BTX-A is mostly but not
fully due to the peripheral mechanism. Various investigators have postulated an indirect
influence of BTX-A on spinal cord circuits. Prolonged motor-evoked potential latencies, central
conduction times, normalized reciprocal inhibition and intracortical inhibition have been
reported (Pauri et al., 2000; Bakheit, 2001). The only real disadvantages are the need for
repeated injections and the overall cost of the treatment (Anwar & Barnes 2005).
Repeated injections are reported to be safe and effectively reduced spasticity and
sustained improvement in disability and function (Gordon et al., 2004). No serious adverse
effects and neutralizing BTX-A antibodies were not detected upon repeated dosing (Bakheit et
al., 2004). The peak effect may be enhanced by instituting physical therapy after treatment. The
role of electric stimulation for both, the injected muscles and the antagonist, has been shown to
enhance the peak and duration of action of the costly toxin. Sprouting can be delayed and toxin
uptake increases by electric stimulation (Bakheit 2001; Hesse et al., 2001).
For patients with UMNL, rehabilitation has to become a way of life. It is vital to teach
them to stretch their limbs and perform specific manoeuvres, and help them come to terms with
the fact that these will be life-long requirements, since the underlying pathology is irreversible
(Ward 2002). With the above in mind, we conducted this study of a cohort of patients attending a
rehabilitation clinic with the following Objectives: To evaluate the outcome and to compare the
efficacy of rehabilitation program after botulinum toxin type-A injection versus serial lidocaine
injections. To evaluate the current modalities involved in the rehabilitation of post stroke
spasticity.
SUBJECTS AND METHODS:
Fifty adult patients suffering from severe or moderately severe spasticity of the upper
limbs at least 6 months duration after stroke were recruited from the outpatient clinic of Physical
Medicine, Rheumatology and Rehabilitation department, Assiut University Hospital, Assiut,
Egypt. They were included in this study if they had a muscle tone score of two or more on the
Modified Ashworth Scale (MAS) in moving at least two joints of the elbow, wrist and fingers
and a score of 1+ in the remaining area. Also, they had limited range of elbow, wrist or /and
fingers motion and absence of muscle contractures as evidenced by nerve block test. All
neurological disorders causing spasticity or rigidity other than stroke, patients with recurrent
stroke and bilateral upper limb weakness have been excluded from the study. All patients were
assessed neurologically with standard clinical examination.
The study was approved by the Ethical Committee of Faculty of Medicine, Assiut
University. All the patients had been informed about the details of treatment steps and written
informed consent was obtained from each participant before the start of the study. Video tapping
as a modality for follow up assessment had been used. Assessment of patients had been done on
study entry, at the end of 1st month and 4th month after treatment.

Patients groups:
The patients were randomly classified into two equal groups using closed envelopes.
First group: 25 patients had been submitted for BTX-A intramuscular injection according to
standard technique in Bakheit (2001), Boyd and Graham (1997) followed by rehabilitation
program. Injection in all patients was guided with EMG recording and stimulation. Average dose
at injection was 300U.
Second group: 25 patients had been submitted for serial lidocaine intramuscular motor point
block (according to Casey and Sekula 2004) followed by rehabilitation program. The injection
was three times weekly totally ten injections; lidocaine (0.5%) was injected into the target
muscle using a hollow EMG needle and a standard EMG machine for guidance.

Outcomes measures:
Efficacy of treatment was measured with the following assessment scales:
Medical research council scale (MRCS) (1976) has been used to assess muscle power from 0 5
grading for each muscle group and the mean was taken for the whole limb. Detection of
improvement or deterioration was done by calculating the difference between baseline and
follow up means.
The modified Ashworth scale (MAS), from 0- 4, was used for muscle tone assessment
and physical evaluation of spasticity. For statistical analysis purpose, the grade 1+ in the scale
was numbered as 2, and one was added to the remaining grades, so grades will be from 0 to 5
(Francis et al., 2004). Tone was graded for each muscle group and the mean was taken for the
whole limb. Detection of improvement or deterioration was done by calculating the difference
between baseline and follow up means.
Manual goniometer was used to measure joint range of motion (ROM). For statistical
analysis purpose, the patient joint range of motion was calculated as a percentage (%) of the
reference range for this joint. The sum of all joints percentages were divided by number of tested
joints to find the mean value. Detection of improvement or deterioration was done by detection
of difference between baseline and follow up means.
Assessment of disability was done by using the Barthel-Index, A five grades (from 0-IV) scale
was used for evaluation of overall disability in adults. Visual analogue scale (VAS), a scale from
0 mm (no pain) to 100 mm (worst pain) was used for assessment of painful spasticity.
Electrophysiological Assessment:
Nerve conduction studies:
a) Conventional nerve conduction studies: were done to detect or to exclude associated lower
motor neuron lesions.
b) H-Reflex and Hmax/Mmax ratio: H-reflex is measured according to methods described in
Daniel (1995) for upper limb (flexor carpi radialis muscle).
c) F-wave and F/M ratio: F-wave is measured according the technique described by Daniel
(1995) for assessment of spinal neuronal excitability.

Rehabilitation program applied to all patients:


1- Passive stretch: A daily stretching regimen continues to be an integral part of any management
program for spastic hypertonia.
2- Vibration: Applied at 100-200 Hz over tendons or muscles, especially the antagonist muscles
in a spastic limb.
3- Topical cold: Applied to spastic muscle.
4- Electrical stimulation: Applied on the antagonist muscles in an attempt to decrease muscle
tone and transcutaneous electrical nerve stimulation (TENS) to treat muscle spasticity.
5- Muscle strengthening.
6- Splinting: to compensate for the paresis of a segment of a limb, may prevent deformities
secondary to contracture, and may reduce limb pain.
The two groups of patients have been received the same program of physical therapy and
rehabilitation after injection and have been worn the suitable orthotics.

Statistical analysis:
Data were collected and analyzed using the statistical package for the social science
program (SPSS) version 16, Chicago, USA. The data were summarized using descriptive
statistics: mean standard deviation (SD) for quantitative data or frequencies (n) and
percentages (%) for qualitative data. Within the patients' cohort, differences were tested by One-
way analysis of variance (ANOVA) in fellow up of the patients and post hoc test to assess the
correlation between the two studied groups. In all cases p< 0.05 was considered statistically
significant.

RESULTS:
In this study, the wrist and fingers were most affected (96%) of the cases and the shoulder was
the least (4%). All patients were attending follow up schedule after one month and four months.
No complications were encountered apart from local transient discomfort. The patients
demographic data of both groups are given in table 1.
Table (1): Demographic characteristics of the patients in both groups

BTX-A Group Lidocaine Group


p-value
N = 25 % N = 25 %

F 11 44.0% 11 44.0%
Gender 0.99
M 14 56.0% 14 56.0%

Age 46.6813.94 47.5610.473 0.802

Duration of spasticity in
15.0013.01 10.923.64 0.137
months

Patients outcomes:
Tables 2-7 represent the outcomes measures and efficacy of the BTX-A and lidocaine in the
treatment of spasticity. BTX-A and lidocaine injections reduced muscle tone in spastic upper
limb, increased joint ROM, improved disability and decrease pain. Although their efficacy was
decreased by the end of 4th month but these improvements were continued and still below
baseline values. Regarding muscle power, both groups showed decrease in motor power, after
one month and significantly increased after four months post injection. Their efficacy manifested
also in electrophysiological outcomes. Hmax/Mmax and F/M ratio was significantly decreased
after one month post injection assessment in both studied groups then slightly increased after 4
months post-injection but still less than baseline values.
Table (2): Physical outcome in BTX-A group, baseline, after one month and 4 months post
injection.

Baseline After one month After 4 months

Mean SD p value Mean SD p value Mean SD p value

MRCS 2.960.79 0.03* 2.280.74 0.04** 3.120.73 NS

MAS 4.00.76 0.001* 1.680.85 0.03** 2.440.87 0.02***

AROM Elbow 58.1224.16 0.002* 74.5226.17 0.01** 66.8526.36 NS


Wrist 11.027.21 NS 14.336.55 NS 14.184.91 NS

Elbow 95.5918.19 NS 95.0218.62 NS 95.0019.36 NS


PROM
wrist 100 0.0 NS 100 0.0 NS 100 0.0 NS

*significance difference between baseline and after 1 month; **significance difference between
after 1 month and after 4 months; ***significance difference between baseline and after 4
months; MRCS: Medical research council scale; MAS: modified Ashworth scale; AROM: active
range of motion; PROM: passive range of motion; NS: non significant.
Table (3): Physical outcome in lidocaine group, baseline, after one month and 4 months post
injection.
Baseline After one month After 4 months

Mean SD p value Mean SD p Mean SD p value


value

MRCS 2.280.61 0.04* 1.840.69 0.02** 2.400.71 NS

MAS 4.200.5 0.001* 1.960.79 NS 2.241.17 0.02***

AROM Elbow 40.1019.65 0.003* 61.6422.42 NS 53.1516.65 0.01***

Wrist 7.343.48 0.001* 17.065.71 0.01** 10.423.30 0.03***

PROM Elbow 95.1216.16 NS 97.0015 NS 99.174.08 NS

Wrist 97.646.138 NS 100.00 NS 99.88.61 NS


*significance difference between baseline and after 1 month; **significance difference between
after 1 month and after 4 months; ***significance difference between baseline and after 4
months; MRCS: Medical research council scale; MAS: modified Ashworth scale; AROM: active
range of motion; PROM: passive range of motion; NS: non significant.

Table (4): Functional outcome in BTX-A group, baseline, after one month and
4 months post injection.
Baseline After one month After 4 months

Mean S.D p value Mean S.D p value Mean S.D p value

Barthel Points 78.4013.52 0.04* 85.409.57 NS 86.609.65 0.03***

VAS 48.4023.57 0.001* 8.008.16 NS 14.8017.34 0.001***


*significance difference between Baseline and after 1 month; **significance difference between
after 1 month and after 4 months;***significance difference between Baseline and after 4
months; VAS: visual analogue scale; NS: non significant.

Table (5): Functional outcome in lidocaine group, baseline, after one month
and 4 months post injection.
Baseline After one month After 4 months

Mean S.D P value Mean S.D p value Mean S. D P value

Barthel Points 75.0010.80 0.04* 81.809.45 NS 82.208.43 0.03***

VAS 53.6022.15 0.001* 4.407.68 NS 6.258.7 0.001***

*significance difference between Baseline and after 1 month; **significance difference between
after 1 month and after 4 months;***significance difference between Baseline and after 4
months; VAS: visual analogue scale; NS: non significant.

Table (6): Electrophysiological outcome in BTX-A group, base line, after one month
and 4 months post injection.
Base line After one month After 4 months

Mean S.D p value Mean S.D p value Mean S. D p value


H/M ratio 0.420.33 0.005* 0.7 0.15 0.04** 0.270.23 NS
F/M ratio 0.200.05 0.03* 0.090.06 NS 0.110.012 0.03***

*significance difference between Baseline and after 1 month; **significance difference between
after 1 month and after 4 months;***significance difference between Baseline and after 4
months; NS: non significant.
Table (7): Electrophysiological outcome in lidocaine group, base line,
after one month and 4 months post injection.
Base line After 1 month After 4 months
Mean S.D p value Mean S.D p value Mean S. D p value
H/M ratio 0.330.18 0.03* 0.130.12 NS 0.190.12 0.01***
F/M ratio 0.270.12 0.007* 0.100.08 NS 0.130.6 0.02***
*significance difference between Baseline and after 1 month; **significance difference between
after 1 month and after 4 months;***significance difference between Baseline and after 4
months; NS: non significant.
Tables 8, 9, 10 represented the correlation between outcomes of treatment modalities in two
patients groups at 4 months follow-up period. Regarding physical outcome, there was significant
difference between two groups in the active ROM of Lt elbow, motor power (MRCS) and
muscle tone (MAS) in favour to BTX-A Group, p = 0.001, 0.001 and 0.05 respectively (figure 1
A). In functional assessment, there was significant difference in pain recording in VAS between
two groups in favour to lidocaine group due to repeated injections (figure 1 B).
Table (8): Difference between the two treatment groups in term of
physical assessment (at 4 month follow up):
BTX-A Group Lidocaine Group
Physical Assessment p-value
Mean S. D Mean S. D
Elbow 40.2821.25 52.1514.18 0.42
Active ROM
Wrist 17.3812.44 10.343.24 0.33
Elbow 90.6226.52 98.894.71 0.20
Passive ROM
Wrist 100.000.00 99.820.73 0.41
MRCS 3.120.73 2.400.71 0.001
MAS 2.440.87 1.960.79 0.05

Table (9): Difference between the two treatment groups in term of functional
assessment (at 4 month follow up):
BTX-A Group Lidocaine Group
p-value
Functional Assessment
N =
N = 25 % %
25

Independent 3 12.0% 2 8.0%

Barthel-Index Severity Mild 20 80.0% 22 88.0% 0.7

Moderate 2 8.0% 1 4.0%

Points (Mean S. D) 86.609.65 82.208.43 0.09

VAS (Mean S. D) 14.8017.34 6.258.7 0.04

Table (10): Difference between the two treatment groups in


electrophysiological assessment (at 4 month follow up):
BTX-A Group Lidocaine Group
p-value
Mean S.D Mean S. D
H/M ratio 0.290.13 0.180.13 0.2

F/M ratio 0.130.03 0.140.05 0.41

90
80
70
60
B TX-A G roup 50
L idoc aine G roup 40
30
20
10
0
VAS B arthel-Index points

Figure 1: In functional assessment, there was significant difference in Barthel index between the
two groups in favour to BTX-A group and pain recording in VAS in favour to lidocaine group.

Discussion:
The present study has demonstrated that the treatment with BTX-A reduces post stroke
upper limb spasticity and its sequelae and support the findings of previous randomised controlled
trials (Simpson et al., 1996; Bakheit et al., 2000; Bhakta et al., 2000; Brashear et al., 2002;
Hyman et al., 2000; Fedorova et al., 2004). In addition, it is one of the few studies comparing
effect of BTX-A injection and lidocaine serial injections in a group of patients suffering from
post stroke upper limb spasticity.
Spasticity is the only symptom in the UMNL that has responded to treatment, the
intensity of which sometimes needs to be reduced when it interferes with the patients remaining
or restored function. There is no evidence in the literature for any one follow-up strategy
producing better results than any others (Ward 2002).
In our study, the minimum duration of spasticity was six months after the onset of the
disease. Hiersemenzel et al. (2000) tested the adaptation changes in the excitability of spinal
neuronal circuits following UMNL by serial measurements of Hmax/Mmax ratio. They found
that ratio to be maximum and remained stable in average of six months after the onset of the
disease therefore it is important to evaluate the patients after this period.
Fifty patients were selected to be treated with BTX-A injection and lidocaine serial
injections in two equal groups, all of them had a moderate but progressive form of focal
spasticity with still full passive joint ROM.
No doubt that majority of patients in our study experienced variable degrees of transient
weakness one month post injection. The explanation of this weakness, it may become unmasked
when the tone is reduced. Throughout follow-up period, power was improving and by the 4th
month, power showed steady increase as the mean values of MRCS exceed those of baseline in
both BTX-A and lidocaine groups. In concordance to our results, Hesse et al (1995) and Pandyan
et al (2002) reported that weakness occurred in 50% of their patients group.
Reduction in the tone was significant one month after injection in both groups. Four
months later, when efficacy of BTX- A started to decrease, we noticed significant increase in
tone in all patients but remained statistically significant. This could be explained as all studied
patients received an intensive regular rehabilitation program after injection. But in lidocaine
group, MAS continued to decrease throughout the fellow up period compared to the baseline
values. This could be due to repeated serial injections of lidocaine and 2-3 injections as booster
doses at the end of the 2nd month during the study. This is consistent with the results of Kaji et al
(1999). Although the joints ROM were decreased at 4th month compared to the 1st month post
injection but still above baseline values in both studied groups. This is in agreement to the BTX-
A studies of Simpson et al. (1996), Bakheit et al. (2000), Richardson et al. (2000), Smith et al.
(2000); Walid Abdel Ghany (2007) and lidocaine studies of Mezaki et al (1999) and Yukimasa et
al (2005)
In evaluation of the patients disability in this study, there was highly significant change
in Barthel index occurred through the fellow up period in both BTX-A and lidocaine groups.
This contradictory to the results of previous BTX-A studies (Simpson et al., 1996; Bakheit et al.,
2000; Richardson et al., 2000; Smith et al., 2000) where the injected dose of BTX-A was not
more than 150 U, they stated that, there was no significant change in barthel index. While our
results are in accordance to more recent studies of Gordon et al. (2004) of 110 patients received
mean dose 220 U and evaluated at ten months after injection, Francis et al. (2004) series of 137
patients evaluated at four months after injection, mean dose 300 U and Walid Abdel Ghany
(2007) with 27 patients received 335 U and evaluated at 6th month after injection.
Improvement of Barthel-Index parameters were detected and found to be significant in all
studies but had delayed onset. The obvious functional improvement after BTX-A injection in our
study may be related to the injected dose and intensive rehabilitation program after injection.
Regarding the delayed onset in other studies, Walid Abdel Ghany (2007), explained that when
tone is reduced and patients undergo an intensive rehabilitation and motor learning programs,
this give the chance for spinal interneurons (central pattern generators) to recognize the acquired
motor skills in the injected limb. These process which is known as neuroplasticity takes time to
recognize and to generate the acquired motor pattern.
In this study, pain score was very highly significant reduced in all studied patients
groups at 1st month post injection and slightly increased at four months but with a lower intensity
compared with pre-injection scores. In agreement to our results, Pierson et al. (1996) and Walid
Abdel Ghany (2007) demonstrated that pain is significantly reduced in their patients series at 1st
month post injection and recurrence of pain again during fellow up period at 6th month in Walid
Abdel Ghanys group of patients.
Regarding electrophysiological changes, in our study, Hmax/Mmax showed significant
decrease one month after injection in BTX-A and lidocaine groups. Then gradual increase
occurred in fellow up. This increase reflects clearly the recurrence of reflex activity but did not
reach baseline values. Our results are consistent with the results of Walid Abdel Ghany (2007)
and Pauri et al (2000) who found the significant decrease was observed only in 1st month post
BTX-A injection. Also, they are consistent with results of Deltombe et al (2008) who reported
the decrease of the Hmax/Mmax ratio after peripheral nerve block. To our knowledge almost all
published related articles mentioned the use of this ratio to evaluate the effect of BTX-A
injection on stretch reflex activity.
Changes in F/M ratio was found to be significant almost all through the follow-up
measurements which may reflect a change in spinal neuronal circuitry excitability and/or
organization more than the Hmax/Mmax ratio. This was similar to the published data of Joodaki
et al. (2001) who proved that F-wave changes are more sensitive indicator for spasticity than H-
reflex.
Regarding the correlation between outcomes of treatment modalities in our study, the
significant differences between two groups in the active ROM, motor power and muscle tone
were in favour to BTX-A Group. But the significant difference in pain between two groups was
in favour to lidocaine group. This colud be due to repeated serial and booster injections of
lidocaine.
In comparison between the two types of treatments, the expression of BTX-A has been
reported as not earlier than 2-3 days after injection (Bhakta et al., 1996) and the peak were
reported to be between 2-6 weeks post injection (Sampatio et al., 1997; Reiter et al., 1996). The
first effect of peripheral nerve block is earlier than that of BTX-A. Mezaki et al (1999) showed
that the prompt effect muscle afferent block (MAB) is due to its action on the injected muscle via
a sodium channel blockade of gamma motor fibers, and the longer lasting effect is through alpha
motor denervation after repeated treatments.
The reported duration of the effect of treatment with BTX-A has varied between 10
weeks to 4 months (Lagalla et al., 2000; Sampatio et al., 1997; Simpson et al., 1996; Rodriques
et al., 2000) and that of the lidocaine was approximately within 2 months (Yukimasa et al., 2005)
then its effect decreased gradually. In our study, there were 2-3 lidocaine injections at the end of
the 2nd month as booster dose which prolonged the duration of the effectiveness of lidocaine
approximately within 4 months. In other studies, they used a mixture of lidocaine and pure
ethanol in a ratio of 10:1 to increase the duration of efficacy. The mixture is expected to work as
a short - latency, long anesthetic because ethanol in a 5 to 10 % concentration is a long acting
sodium channel blocker; this has been used successfully for treating spasticity of upper limb
(Kaji et al., 1999; Mezaki et al., 1999; Yukimasa et al., 2005). Also, among problems in using
BTX- A the possibility of antibody development and its high cost.
In conclusion, lidocaine is a simple technique and considered economically acceptable
especially in developing countries. We could probably consider this study as a new stone in the
building of future guidelines in the care of spastic patients. So, we recommend that additional
investigations should be conducted into the management of upper limb spasticity using
peripheral nerve block through large prospective, double-blinded and placebo-controlled studies.

REFERENCES:
1. Anwar K & Barnes MP (2005): Botulinum Toxin Injections for Spasticity. Oper Tech
Neurosurg Elsevier Inc; 7:128-135.
2. Bakheit A M O, Fedorova N V, Skoromets A A, Timerbaeva S L, Bhakta B B, Coxon L
(2004): The beneficial antispasticity effect of botulinum toxin type A is maintained after
repeated treatment cycles. J Neurol Neurosurg Psychiatry; 75: 15581561. doi:
10.1136/jnnp.2003.035139.
3. Bakheit AMO, Pittock S, Moore AP, Wurker M, Otto S, Erbguth F, Coxon LA (2001):
randomized, double-blind, placebo-controlled study of the efficacy and safety of
botulinum toxin type A in upper limb spasticity in patients with stroke. Euro J Neurol; 8
(6): 559565.
4. Bakheit AMO, Thilmann AF, Ward AB, Poewe W, Wissel J, Muller J, Benecke R, Collin
C, Muller F, Ward CD, Neumann C (2000): 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; 31: 2402-2406.
5. Bhakta BB, Cozens JA, Bamford JM, Chamberlain MA (1996): Use of botulinum toxin
in stroke patients with severe upper limb spasticity. J Neurol Neurosurg Psychiatry; 61-
30-35.
6. Bhakta BB, Cozens JA, Chamberlain MA, et al (2000): impact of botulinum toxin type A
on disability and carer burden due to arm spasticity after stroke: a randomized double
blind placebo controlled trial. J Neurol Neurosurg Psychiat; 69: 217-221.
7. Boyd R, Graham HK (1997): Botulinum toxin A in the management of children with
cerebral palsy: indications and outcome. Euro J Neurol; 4(2): S15-S22.
8. Brashear A, Gordon MF, Elovic E, et al (2002): Intramuscular injection of botulinum
toxin for the treatment of wrist and finger spasticity after stroke. N Engl J Med; 347: 395-
400.
9. Casey KF, Sekula R (2004): Ablative surgery for spasticity. In H. Richard Winn (ed.)
Youmans Neurological Surgery, Elsevier inc. 5th ed., Part V, ch.176: 2863-2872.
10. Daniel D (1995): Special nerve conduction techniques. In Daniel D (ed.):
Electrodiagnostic medicine. Hanley & Belfus, INC. /Philadelphia.
11. Decq P, Filipetti P, Lefaucheur JP (2005): Evaluation of spasticity in adults. Oper Tech
Neurosurg 7:100-108.
12. Deltombe T, Jamart J, Hanson P, Gustin T. Soleus H reflex and motor unit number
estimation after tibial nerve block and neurotomy in patients with spastic equines foot.
Clinical Neurophysiology. 2008; Neucli 22181-7. doi: 10. 1016/j.neucli.2008.03.003.
13. Fedorova NV, Skoromets AA, Timerbaeva SL, Bhakta BB, Coxon L Bakheit AMO
(2004): Neurol Neurosurg Psychiatry; 75: 15581561. doi: 10.1136/jnnp.2003.035139.
14. Francis HP, Wade DT, Turner-Stokes L, Kingswell RS, Dott CS & Coxon EA (2004):
Does reducing spasticity translate into functional benefit? An exploratory meta-analysis.
J Neurol Neurosurg Psychiat; 75: 15471551.
15. Gordon MF, Brashear A, Elovic E, Kassicieh D, Marciniak C, Liu J, Turkel C (2004):
Repeated dosing of botulinum toxin type A for upper limb spasticity following stroke.
Neurology; 63 (10): 1971-1973.
16. Gracies JM, Simpson D (1997): Neuromuscular blockers. Lock. Reg Anesth; 20 (4): 352-
355
17. Hesse S, Brandl-Hesse B, Bardeleben A, Werner C, Funk M (2001): Botulinum toxin A
treatment of adult upper and lower limb spasticity. Drugs Aging; 18(4): 255-262.
18. Hesse S, Jahnke MT, Luecke D, Mauritz KH (1995): Short-term electrical stimulation
enhances the effectiveness of botulinum toxin in the treatment of lower limb spasticity in
hemiparetic patients. Neurosci Lett; 201: 37-40.
19. Hiersemenzel LP, Curt A, Dietz V (2000): From spinal shock to spasticity. Neuronal
adaptations to spinal cord injury. Neurol; 54:1574-1582.
20. Hyman N, Barnes M, Bhakta B, et al (2000): Botulinum toxin (Dysport) treatment of hip
adductor spasticity in multiple sclerosis: a prospective, randomized, double blind,
placebo controlled, dose ranging study. J Neurol Neurosurg Psychiat; 68: 707-712.
21. Joodaki MR, Olyaei GR, Bagheri H (2001): The effects of electrical stimulation of the
lower extremity on H-reflex and F-wave parameters. Electromyogr Clin Neurophysiol;
41: 21-28.
22. Kaji R, Mezaki T, Hirota N (1999): Treatment of Spasticity with Muscle Afferent Block.
Neurology; 53: 1156-1157.
23. Kalichman MW, Calcutt NA (1992): Local anesthetic-induced conduction block and
nerve fiber injury in streptozotocin diabetic rats. Anesthesiology; 77(5): 941-947.
24. Lagalla G, Danni M, Rieter F, Ceravolo MG, Provinciali L (2000): Post stroke spasticity
management with repeated botulinum toxin injections in the upper limb. Am J Phys Med
Rehabil; 79(4): 377-384.
25. Lundstrm E, Ternt A, Borg J (2008): Prevelance of disabling spasticity 1 year after
first-ever stroke. Eur J Neurol; 15: 533-539.
26. Medical Research Council (1976): Aids to examination of the peripheral nervous system.
Memorandum; 45. London: Her Majestys Stationary Office.
27. Mezaki T, Kaji R, Hirota N, Kohara N, Kim ura J (1999): Treatment of spasticity with
muscle afferent block. Neurology; 53: 1156- 1157.
28. Pandyan AD, Vuadens P, Van Wijck FMJ, Stark S, Johnson GR, Michael P Barnes MP
(2002): Are we underestimating the clinical efficacy of botulinum toxin (type A)?
Quantifying changes in spasticity, strength, and upper limb function after injection of
botox to the elbow flexors in a unilateral stroke population. Clinical Rehabilitation; 16 (6);
65-60.
29. Pathak MS, Nguyen HT, Graham HK, Moore AP (2006): Management of spasticity in
adults: practical application of botulinum toxin. Euro J Neurol; 13 (Suppl.1): 4250.
30. Pauri F, Boffa L, Cassetta E, Pasqualetti P, Rossini PM (2000): Botulinum toxin type-A
treatment in spastic paraparesis: a neurophysiological study. J Neurol Scinc; 181:89-97.
31. Pierson SH, Katz DI, Trasy D (1996): Botulinum toxin A in the treatment of spasticity:
Functional implications and treatment selection. Arch Phys Med Rehabil; 77: 717-719.
32. Reiter F, Danni M, Ceravolo MG, Provinciali L (1996): Disability change after treatment
of upper limb spasticity with botulinum toxin. Neurol Rehab; 10: 47-52.
33. Richardson D, Sheean G, Werring D (2000): Evaluating the role of botulinum toxin in the
management of focal hypertonia in adults. J Neurol Neurosurg Psychiat; 69:499-505.
34. Rodriquez AA, McGinn M, Chappell R (2000): Botulinum toxin injection of spastic
finger flexors in hemiplegic patients. Am J Phys Med Rehabil. Jan-Feb;79(1):44-7.
35. Sampatio C, Ferreira JJ, Pinto AA, Crespo M, Ferro JM, Castrocaldas A (1997):
Botulinum toxin type A for the treatment of arm and hand spasticity in stroke patients.
Clin Rehabil; 11: 3-7.
36. Saulino M, Jacobs BW (2006): The Pharmacological Management of Spasticity. J
Neurosci Nurs; 38(6): 456-459.
37. Simpson DM, Alexander DN, OBrien CF, Tagliati M, Aswad AS, Leon JM, Gibson J,
Mordaunt J M, Monaghan EP (1996): Botulinum toxin type A in the treatment of upper
extremity spasticity: a randomized, double blind, placebo controlled trial. Neurology; 46:
1306-1310.
38. Smith SJ, Ellis E, White S, Moore AP (2000): A double blind placebo controlled study of
botulinum toxin in upper limb spasticity after stroke or head injury. Clin Rehabil; 14: 5-
13.
39. Walid Abdel Ghany (2007): Evaluation of outcome of different modalities in treatment of
intractable spasticity. Thesis submitted for partial fulfillment of M.D degree in
neurosurgery, Faculty of medicine, Ein Shams University library,N 2007.
40. Ward AB (2002): A summary of spasticity management-a treatment algorithm. Euro J
Neurol 9 (suppl.1): 48-52.
41. Yukimasa I, Taro O, Katsunori I (2005): Muscle Afferent Block for the Treatment of
Upper Limb Spasticity: A Report of Two Cases. Jpn J Rehabil Med; 42: 869-874.

"
: .


.

. , .

.

.
.
.

.

.
.
.

Anda mungkin juga menyukai