Archives of Physical Medicine and Rehabilitation
Volume 89, Issue 5 , Pages 982-987, May 2008

Comparative Impact of 2 Botulinum Toxin Injection Techniques for Elbow Flexor Hypertonia

  • Nathaniel H. Mayer, MD

      Affiliations

    • Department of Physical Medicine and Rehabilitation, Temple University School of Medicine, Philadelphia, PA
    • Moss Rehabilitation Research Institute, Albert Einstein Healthcare Network, Philadelphia, PA
    • Motor Control Analysis Laboratory, MossRehab, Elkins Park, PA.
    • Corresponding Author InformationCorrespondence to Nathaniel H. Mayer, MD, MossRehab, 60 E Township Line Rd, Elkins Park, PA 19027
    • ,
  • John Whyte, MD, PhD

      Affiliations

    • Moss Rehabilitation Research Institute, Albert Einstein Healthcare Network, Philadelphia, PA
    • Department of Rehabilitation Medicine, Thomas Jefferson University, Philadelphia, PA
    • ,
  • Gunilla Wannstedt, MS, PT

      Affiliations

    • Motor Control Analysis Laboratory, MossRehab, Elkins Park, PA.
    • ,
  • Colin A. Ellis, ScB

      Affiliations

    • Moss Rehabilitation Research Institute, Albert Einstein Healthcare Network, Philadelphia, PA

Article Outline

Abstract 

Mayer NH, Whyte J, Wannstedt G, Ellis CA. Comparative impact of 2 botulinum toxin injection techniques for elbow flexor hypertonia.

Objective

To compare 2 techniques of botulinum toxin injection for elbow flexor hypertonia.

Design

Parallel-group, randomized, controlled trial with blinded outcome assessment.

Setting

Laboratory, tertiary rehabilitation hospital.

Participants

Adults (N=31) with acquired brain injury (21 with traumatic brain injury, 8 with stroke, 2 with hypoxic encephalopathy) provided 36 sets of elbow flexors with Ashworth Scale scores equal to 3.

Intervention

Botulinum toxin type A (BTX-A) was injected with a motor point or a multisite injection technique after obtaining 2 baseline evaluations of the main outcome measures. Motor point technique involved decremental electric stimulation with delivery of 60U of BTX-A (Botox) in 2.4mL or 30U BTX-A in 1.2mL of preservative-free saline at single biceps and brachioradialis motor points, respectively. Distributed injection was performed using electromyographic feedback. Fifteen units in 0.6mL were delivered to each of 4 biceps sites and 2 brachioradialis sites. Total dose (90U) and total injection volume (3.6mL) were identical across groups. Only sites and injection techniques varied. The brachialis was not injected in either group.

Main Outcome Measures

Ashworth Scale, Tardieu catch angle, and root mean square surface electromyographic activity of the biceps, brachialis, and brachioradialis.

Results

Postintervention testing at 3 weeks showed no significant differences between groups (P range, .31–.82 across 3 outcome measures). However, within each group, significant treatment effects were observed on all outcome measures (all P<.01). For the uninjected brachialis muscle, electromyographic reduction was greater for the distributed group.

Conclusions

In 31 adults with acquired brain injury, single motor point and multisite distributed injections of low-dose, high-volume BTX-A had similar impact. Findings suggest that low-dose, high-volume strategies may have a potential role in reducing drug cost and helping clinicians stay within accepted limits for total body dose in patients with upper motoneuron syndrome requiring many injections.

Key Words: Botulinum toxins, Brain injuries, Injections, Muscle hypertonia, Rehabilitation

 

IN RECENT YEARS, botulinum toxin type A (BTX-A) has gained in usage as a treatment for the consequences of muscle overactivity in patients with an upper motoneuron syndrome (UMNS).1, 2, 3, 4, 5 Because upper and lower limbs are frequently involved, patients with UMNS often have many target muscles to treat. One practical problem of treating many muscles is keeping the total dose of BTX-A within current guidelines for maximum body dose of toxin a visit.6 Therefore, using elbow flexor hypertonia as our clinical model, our goal in this study was to find a more efficient way to treat UMNS patients with BTX-A. Ways of tackling this problem have included winnowing muscle selection through better history and physical examination, using gait laboratory and motion analysis to aid muscle selection, injecting smaller amounts of toxin in larger volumes, and finding better ways to inject. For example, Childers et al,7 concerned with finding a better way to inject large muscles, compared 2 different delivery techniques of BTX-A in the large gastrocnemius muscle of spastic hemiplegics. In this study, we also looked at large upper-limb muscles using 2 different methods of injection: a motor point technique and a distributed quadrants technique. Clinical benefits of BTX-A injections depend primarily on preventing release of acetylcholine at the neuromuscular junction, also called the endplate.8 Dosing for UMNS hypertonia was initially determined empirically and through shared clinical experiences. Because differently sized muscles were involved, clinicians soon emphasized injecting many sites for larger muscles and fewer sites for smaller ones.9 For the biceps, 4 distributed sites have been recommended, using a dose range of 50 to 200U (Botox). Some injectors divided the biceps into 4 quadrants for injection, and others injected the estimated middle of the muscle or its greatest palpable bulk. For the brachioradialis, 2 injections distributed along the long axis of the muscle were recommended, using a dose range of 25 to 75U. Because BTX-A diffuses after injection, perhaps as much as 5cm, even crossing anatomic barriers such as fascia,10, 11 the utility of multisite injections depends on diffusion to cover as much territory as possible for toxin to find its way to endplates.

The distributed method inefficiently encourages larger doses of toxin because it does not target endplates. Endplate targeting has been reported to potentiate effects of BTX-A in a canine model.12 Animal models and clinical studies have indicated that distance to endplates influences efficiency of treatment with BTX-A. Shaari and Sanders13 observed that injections 5mm from the endplate resulted in a 50% decrease (compared with endplate injections) in glycogen staining as a marker of paralysis for rabbit longissimus dorsi. In humans, Gracies et al14 injected a small volume of BTX-A close to endplates of the biceps brachii using an endplate-targeting technique. The result was more effective than injecting the same volume at a greater distance from the endplate region. Injecting the same dose in a larger volume at a greater distance from the endplate was as effective as the smaller volume closer to the endplate.

What do we know about the location of endplates for the biceps? Coërs and Woolf15, 16 found that the innervation band (zone of endplates) of human biceps underlies its motor point, found on the skin by electric stimulation. Warfel's map17 for the motor point of the biceps diagrams it as half-way between the proximal and distal tendons of the biceps. Aquilonius et al18 described biceps brachii endplates as a 5- to 10-mm–wide band in a 4- to 6-cm–long region half-way between the proximal and distal tendons of the biceps. Deshpande et al19 recently described the endplates of the biceps as an inverted V-shaped band just below the midpoint of the humerus.

Much less is known about the motor point of the brachioradialis. Unlike the biceps, whose motor point overlies its end plates, Coërs15 noted that the motor endplates of the brachioradialis were deeply situated. The fasciculi of the brachioradialis arise from a superficial layer of the fascia, running toward a deeply situated musculotendinous junction. As a consequence, nerve endings of the endplate, in relation to the surface site of the motor point, lie at an uncertain distance. We reasoned that careful electric stimulation with iteratively decreasing current intensity might help guide the needle tip closer to the vicinity of the endplates, if indeed the endplates are located close to the motor point of the brachioradialis. We also reasoned that greater dilutions might also promote toxin diffusion onto endplates of the brachioradialis.

Given the relationship between the anatomic location of endplates and physiologically determined motor points described by Coërs and others in the literature cited earlier, we reasoned that toxin instilled with a motor point technique, especially in larger fluid volumes, might disperse more efficiently into the vicinity of the endplates of the biceps and brachioradialis. Accordingly, we arrived at the following hypothesis: given an injection of a constant dose of BTX-A delivered in a constant volume per muscle to patients with spastic hypertonia, a single-site motor point injection technique will be superior in reducing hypertonia compared with the more standard distributed technique of injecting the biceps in 4 sites and the brachioradialis in 2 sites, remote from their motor points.9

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Methods 

Participants 

Participants were 31 adult patients with acquired brain injury who were referred to the Motor Control Analysis Laboratory for evaluation and treatment of severe elbow flexor hypertonia. Five patients were bilaterally involved; therefore, 36 elbows were studied. All limbs had an Ashworth Scale score of 3. There were no contraindications to treatment with BTX-A such as concurrent use of aminoglycosides, myasthenia gravis, or treatment with BTX-A within 3 months. Patients were excluded if they had hypertonia elsewhere in the upper limb that required additional medical intervention. An initial exclusion criterion was flexion contracture greater than 60°; this was later relaxed to 70°. Patients or their surrogates gave written informed consent, and the project was approved by our institutional review board. Characteristics of the participants can be seen in table 1. Of the 10 patients with nontraumatic brain injury, 8 patients had stroke and 2 patients had hypoxic encephalopathy.

Table 1. Balance of Experimental Groups at Baseline
CharacteristicsDistributed Quadrants (n=18)Motor Point (n=18)Effect Sizet34P
Age (y)34.7±21.937.9±19.9.160.470.64
Time postinjury (d)481.9±890.1256.7±418.7.320.970.34
Maximum passive elbow extension (deg)31.5±25.223.9±26.5.300.890.38
Sex (n) 1.800.18⁎
Male1713
Female15
Etiology (n) 0.500.73⁎
TBI1113
Non-TBI75
Chronicity (n) 0.121.00⁎
Subacute (<6mo)1211
Chronic (>6mo)67
Outcome Variables Mann-Whitney U
TCA (deg)105.1±9.6102.9±11.9.21178.50.60
RMS EMG values (mV)
Biceps0.158±0.1360.119±0.106.321950.30
Brachialis0.091±0.0680.070±0.054.341960.28
Brachioradialis0.197±0.1660.132±0.077.501850.47
3-muscle average0.149±0.1190.107±0.067.43190.50.37

NOTE. Values are mean ± standard deviation (SD) or n or as indicated.

Abbreviations: EMG, electromyographic activity; TCA, Tardieu catch angle.

⁎Fisher exact test.

Outcome Measures and Instrumentation 

Three clinicophysiologic variables were studied: the Tardieu catch angle (part of the Modified Tardieu Scale20, 21), the Ashworth Scale,22 and the root mean square (RMS) quantification of surface electromyographic activity recorded during the Ashworth maneuver.

Tardieu catch angle 

The available range of motion (ROM) at the elbow was measured with a handheld goniometer.a Maximum passive elbow extension was performed at a very slow rate so as not to trigger a spastic reaction that could influence the degree of extension. To determine the Tardieu catch angle, the examiner extended the elbow as rapidly as possible and reported the angle at which a sudden palpable increase in resistance (the catch) was perceived.20, 21 Five consecutive trials were performed by an experienced physical therapist and averaged to create the session's value.

Ashworth Scale 

The 5-point ordinal Ashworth Scale22 was used to measure passive resistance. Passive stretch of elbow flexors was initiated at a velocity that would cover the available ROM in 1 second23 if resistance to stretch was not encountered by the examiner. This was assessed with a strain gauge electrogoniometer.b Trials in which the measured velocity was more than 30% different from the target velocity were discarded. The median value of 5 acceptable trials was used for data analysis.

Electromyography 

Surface electromyographic activity was recorded from the biceps brachii, brachialis, and brachioradialis during Ashworth maneuvers. Ag/AgCl electrodesc were centered over the midbelly mound of the biceps. Brachioradialis electrodes were placed 4cm distal to the elbow crease, and brachialis electrodes were placed just medial to the biceps tendon and proximal to the crease to minimize biceps crosstalk. A ground electrode was placed on the back of the shoulder.

Electromyographic signals, sampled at 1kHz, were fed through a MyoPac differential amplifier,d bandwidth filtered (20–495Hz) and processed by DataPac 2K2 software.d RMS values were calculated for each muscle on the interval between 20% and 80% of the amplitude of stretch, the most rapidly changing portion of stretch. Five trials were averaged for each session. One subject's electromyographic value for the brachioradialis during the third testing session was an extreme outlier and was removed.

Protocol 

Each patient was tested 3 times. Two baseline sessions took place on separate days (mean ± standard deviation [SD], 4.2±3d). At the end of the second session, each elbow was randomized to an injection technique (described below) and injections of BTX-A (Botox) were performed by the principal investigator. A posttreatment session was conducted approximately 3 weeks later (mean, 23.5±4.4d). The examiner was blind to injection technique assignments. Adverse events and medication changes were monitored throughout the study.

Injection techniques: motor point injection technique 

Anatomically, a motor point is the most distal electrosensitive site of a motor nerve that corresponds to its entry site into the muscle or to an area where motor endplates cluster and where minimal stimulating current generates a perceptible twitch of muscle fibers.24, 25 Single biceps and brachioradialis motor points were first approximated by stimulating skin sites17 with short-duration electric pulses at 1Hz (EZ Stim Model ES200e) to optimize needle insertion site. After skin preparation with iodine, alcohol, and a local anesthetic, a Teflon-coated 27-gauge hypodermic needle, 38mm long, serving to stimulate the motor point electrically as well as to inject it, was advanced toward the motor point. Muscle twitches were monitored visually and by palpation. As the needle tip advanced closer to the motor point, current intensity was turned down because less was needed to generate a twitch. Injection was generally performed when current intensity reached 0.3 to 0.2mA.

Injection techniques: distributed quadrants technique 

Two sites, the biceps tendon at the elbow crease and the distal end of the anterior deltoid, were estimated by palpation. A longitudinal line traversing the mound of the biceps muscle was generated between these 2 sites. A midpoint perpendicular to the longitudinal line was approximated, resulting in 4 sectors or quadrants. A 27-gauge Teflon-coated hypodermic needle was inserted toward the outer diagonal edge of each of the 4 quadrants, using auditory electromyography guidance to verify that the needle tip was in muscle. The 4 needle sites, rectangularly configured, were separated from each other by at least 5cm. The distributed quadrants technique for the brachioradialis was performed with the forearm held in neutral. Injection was performed at 2 sites along the long axis of the muscle, 2.5 and 5cm below the elbow crease, typically into the visible bulk of the muscle using auditory electromyography guidance.

Dosing 

Motor point injections occurred at 1 site in the biceps (60U, 2.4mL) and 1 site in the brachioradialis (30U, 1.2mL). Distributed injections occurred at 4 sites in the biceps and 2 sites in the brachioradialis (15U, 0.6mL per site). Thus, total dose (90U) and volume (3.6mL) were constant for both groups; only the injection sites and localization techniques varied between groups.

Data Analysis 

Baseline balance of the experimental groups was assessed with the following tests: Student t test for age, days postinjury, and maximum passive range of elbow extension; Pearson chi-square and Fisher exact tests for sex, etiology, and chronicity; and Mann-Whitney U test for Tardieu catch angle and electromyographic outcome measures. Where appropriate, effect sizes (Cohen d) were also calculated as the difference of means divided by the pooled SDs. For both Tardieu catch angle and electromyography data, the 2 baseline sessions had high test-retest reliability and were averaged to create a single baseline value for each elbow. Baseline Ashworth scores were 3 for all elbows studied.

Comparisons between injection techniques took baseline values into account for each outcome measure. This was not necessary for Ashworth scores, with all scores being 3 at baseline. Thus, posttreatment Ashworth scores for the 2 groups were compared by a Mann-Whitney U test. However, the distribution of Tardieu catch angle and electromyography scores violated statistical assumptions underlying statistical adjustment by means of regression or analysis of covariance. Therefore, log-transformed electromyography data were fit to a general linear model using baseline electromyographic activity and treatment group as predictors and session 3 electromyographic activity as the dependent variable. Tardieu catch angle values required nonparametric stratification into 4 bins, and a stratified Wilcoxon test was used to take baseline strata into account when comparing the 2 treatment groups.

To assess the within-group effect of chemodenervation, paired t tests were used for Tardieu catch angle, and electromyographic measures and effect sizes were also computed. A Wilcoxon signed-rank test was used for the ordinal Ashworth score. Finally, to assess the possible contribution of spontaneous recovery to treatment effects within groups, the entire cohort of subjects was divided based on a median split of time postinjury (median, 84d), regardless of injection technique. Treatment effect sizes were calculated for these 2 groups (defined as acute and chronic).

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Results 

Baseline Characteristics of the Experimental Groups 

Table 1 shows the characteristics of the motor point and distributed quadrants groups at baseline. There were no significant differences between the groups in terms of demographic features or baseline measures of hypertonia. Although 22 of 36 elbows had some level of flexion contracture, these contractures were well balanced between groups; furthermore, contracture angle did not correlate with Tardieu catch angle at baseline (r34=.03, P=.86) and so was unlikely to confound the results. Ashworth scores are not shown in table 1 because all 36 elbows had scores of 3 at baseline.

Between-Group Treatment Effects 

There were no significant differences between the 2 groups for any of the outcome measures assessed. Median Ashworth scores after treatment decreased by 1 point compared with baseline for both groups (Mann-Whitney U test, P=.53). The Tardieu catch angle posttreatment did not differ significantly either when analyzed in a simple 2-sample Wilcoxon test (P=.46) or when stratified by baseline Tardieu catch angle (P=.31). Comparison of the log-transformed composite electromyography signal from the 3 elbow flexors did show a significant effect of baseline electromyographic activity (P=.003), with a slope of .465 (95% confidence interval [CI], .192–.737), indicating larger-magnitude electromyographic signals posttreatment for subjects with larger baseline electromyographic measures. However, the group difference was small in magnitude (.046) (95% CI, .350–.441) and nonsignificant, corresponding to 4.5% lower electromyographic magnitude in the distributed quadrants group than the motor point group after adjustment for baseline electromyographic activity. Results were similar for electromyography data of individual muscles as well.

Within-Group Treatment Effects 

To make sure that a lack of difference between groups was not due to ineffective treatment in both groups (ie, floor effects related to the choice of a low treatment dose), we checked for treatment effects within each group. For the motor point group, a clinicophysiologic effect of toxin injection was observed at the 3-week postintervention session (table 2). A significant intervention effect was found for each outcome variable, with the exception of electromyographic activity of the uninjected brachialis muscle.

Table 2. Effects of the Motor Point Injection (n=18)
Outcome MeasureBaselinePosttreatmentEffect Sizet17P
TCA (deg)102.9±11.976.8±21.11.524.99<.001
RMS EMG (mV)
Biceps0.119±0.1060.050±0.0430.853.08.007
Brachialis0.070±0.0540.053±0.0740.261.53.146
Brachioradialis0.132±0.0770.048±0.0281.454.46<.001
Ashworth score3(3)2(0–2) 3.82⁎<.001

NOTE. Values are mean ± SD or median (range).

⁎Wilcoxon z.

For the distributed quadrants group, a clinicophysiologic effect of toxin injection was also observed at the 3-week postintervention session (table 3). A significant intervention effect was found for each outcome variable, including electromyographic activity of the uninjected brachialis muscle.

Table 3. Effects of the Distributed Injection (n=18)
Outcome MeasureBaselinePosttreatmentEffect Sizet17P
TCA (deg)105.1±9.674.4±28.71.444.49<.001
RMS EMG (mV)
Biceps0.158±0.1360.051±0.0411.073.38.004
Brachialis0.091±0.0680.056±0.0580.562.52.02
Brachioradialis0.197±0.1660.059±0.0481.133.59.002
Ashworth score3(3)2(0–3) 3.63⁎<.001

NOTE. Values are mean ± SD or median (range).

⁎Wilcoxon z.

Effect of Spontaneous Recovery During the Study Period 

To assess the possible contribution of spontaneous recovery to treatment effects within groups, the entire cohort of subjects was divided, based on a median split of time postinjury (84d), regardless of injection technique. In chronic patients (n=18), electromyography data showed a small effect size in the untreated brachialis (.09) but large effect sizes in toxin-treated muscles (.86–.95), suggesting that the medication had a large impact unrelated to spontaneous recovery. In acute patients (<84d, n=18), the corresponding effect sizes were increased (brachialis, .65; treated muscles, 1.11–1.3). However, for Tardieu catch angle, which measures hypertonia across the joint as a whole, there was virtually no difference in effect size between acute (1.54) and chronic (1.57) patients.

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Discussion 

In this study of 31 adults with acquired brain injury and elbow flexor hypertonia, we found that localizing motor points before injection was not superior to distributed electromyography-guided injections when using low doses and high volumes of BTX-A as specified. The lack of a significant group difference does not appear to be related to low statistical power, because effect sizes reflecting group differences for the 3 outcome measures were small. Although there was no difference between groups, there was a robust treatment effect within each group, as discussed later.

Our study, like others, found significant reductions in Ashworth scores.1, 5, 26, 27, 28 However, the ordinal Ashworth Scale lacks sensitivity, and it measures nonneural as well as neural components of resistance. More sensitive, continuous measures may be able to distinguish between treatment techniques where the Ashworth Scale cannot.29, 30, 31, 32 We therefore included the Tardieu catch angle in our study, a measure of the angle at which a catch or sudden palpable resistance occurs during very rapid passive stretch. Critically, this catch reflects neurally mediated hypertonia33, 34, 35, 36 and is considered a truer score of spasticity than Ashworth scoring. In this study, the Tardieu catch angle value was also significantly reduced for each technique, so we can conclude with greater confidence than we had with Ashworth reduction that the toxin intervention truly had an effect on the neural component of hypertonia.

The study also included a quantitative electromyography measure to provide muscle-specific information, something Ashworth and Tardieu catch angle measures cannot do. Our findings indicate that each injection technique reduced the biceps and brachioradialis activity significantly. The relation between biceps endplates and its motor point is known from Coërs's work,15 but less is known regarding the brachioradialis. Our finding of reduced brachioradialis electromyographic activity suggests that the motor point technique may well be creating access for toxin to the brachioradialis endplates. Of additional interest is the finding of a moderate effect size (Cohen d=.56) for the uninjected brachialis in the distributed group. The distributed technique used 4 biceps needle insertions compared with one for the motor point method. With multiple sticks, depth of needle insertion has a greater chance for variability, suggesting that leakage of toxin onto the brachialis, which lies beneath the biceps, has a greater chance of occurring. Alternatively, the distributed technique, covering more areas of muscle, might favor toxin effect on broadly distributed muscle spindles,37, 38 which could account for more widespread C5-6 segmental reduction of hypertonia, of which the brachialis, a C5-6 muscle, could partake.

With respect to volume or dilution considerations, recent investigations looked at the issue of high and low volumes at constant dosing. Francisco et al39 compared 2 different volumes for wrist and finger flexor spasticity, using the same dose of BTX-A. Modified Ashworth Scale scores decreased significantly for both high- and low-volume groups with a nonsignificant trend in favor of the high-volume preparation. Gracies et al40 injected the biceps of chronic hemiplegics with high and low volumes containing constant doses of BTX-A (160U). A greater reduction in Tardieu angle was found in the high-volume group. Gracies et al14 elsewhere reported that injecting a small volume of BTX-A close to the neuromuscular junction was more effective than injecting a similar volume at a distance from the junction. However, injecting a large volume more distant from the junction was as effective as a small volume close to the neuromuscular junction. In our study, we used large volumes with a dose three eighths that of the Gracies study and achieved competitive reductions of our outcome measures. These findings suggest that a low-dose, high-volume strategy may be a consideration when treating UMNS patients with many muscles to treat, especially when trying to stay within total body dose guidelines. Finally, although the consensus standard for volume has been “up to 1 cc per injection site,”6(p157) we note that the maximum injection volume of Gracies40 of 2mL (40U) and our volume of 2.4mL (60U) resulted in no serious adverse events.

Study Limitations 

Certain study limitations must be considered. We cannot be certain about the relationship between distributed quadrants sites and motor point sites because we did not identify motor point sites of the distributed quadrants group. Moreover, spread of toxin and mechanisms of diffusion are unknown variables. Given the specified high volumes of this study, we may not have come close to a floor effect with the low doses used—for example, a low-dose, low-volume injection at the motor point compared with similar dosing with a distributed technique might have produced group differences.

The use of surface electromyography as a measure of muscle specificity raises a number of concerns. Measurement of surface electromyographic activity is subject to tissue impedance variability across subjects, electrode placement variability across test sessions, and cross-talk (electrode pickup of activity from nearby nontarget muscles). Cross-talk is difficult to quantify. Nevertheless, the finding of significant reduction of electromyographic activity of injected muscles within each group indicates that the amount of cross-talk was not sufficient to obscure an experimental effect. The much larger treatment effect for the biceps and brachioradialis compared with the uninjected brachialis also provides some evidence that surface electromyography yields muscle-specific information.

Although oral antispasticity drugs were kept unchanged, other medications taken by the patients might have affected hypertonia. We examined a subset of 20 subjects (10 in each group) who had no changes of medication in the postintervention period. Descriptive statistics for all outcome measures in this subset were found to be similar to those of the full cohort of subjects. Treatment effect sizes both between and within groups were also similar. It seems unlikely that medication changes could have confounded our results.

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Conclusions 

The impacts of 2 different injection techniques on elbow flexor hypertonia were compared, using low-dose (60U in the biceps, 30U in the brachioradialis), high-volume (2.4mL in the biceps, 1.2mL in the brachioradialis) injections of BTX-A. Single motor point and multisite distributed injections were found to have similar impact at these doses and volumes. Findings suggest that low-dose, high-volume strategies may have a potential role in reducing drug cost and helping clinicians stay within accepted limits for total body dose in patients with UMNS requiring many injections.

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Acknowledgments 

We gratefully acknowledge Caron Morita, BA, for project supervision, Shane Eynon, PhD, for assistance with data collection and management, and Inna Chervoneva, PhD, for statistical consultation.

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  • a Lafayette Instrument Co, PO Box 5729, Lafayette, IN 47903.
  • b Biometrics Ltd, PO Box 340, Ladysmith, VA 22501.
  • c Ambu Inc, 6740 Baymeadow Dr, Glen Burnie, MD 21060.
  • d Run Technologies, 22702 Via Santa Maria, Mission Viejo, CA 92691.
  • e Life-Tech Inc, 4235 Greenbriar Dr, Stafford, TX 77477.

 Supported in part by the National Institute on Disability and Rehabilitation Research (grant no. H133A020505) and an educational grant from Allergan Inc.No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated.Reprints are not available from the authors.

PII: S0003-9993(08)00071-3

doi:10.1016/j.apmr.2007.10.022

Archives of Physical Medicine and Rehabilitation
Volume 89, Issue 5 , Pages 982-987, May 2008

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