Objective: To know if changes in compound muscle action potential (CMAP) of human extensor digitorum brevis (EDB) muscle can be enhanced by increase in dilution volume of botulinum toxin type A.

Method: In 11 healthy volunteers, 2.5 U of botulinum toxin (Botox^Ⱂ, Allergen Inc.) in a volume of 0.1 ml normal saline was injected in EDB muscle and the same dose with the dilution volume of 0.5 ml was injected in the opposite side. We measured the pre- and post-injection M-wave amplitude and area of EDB muscle.

Results: The mean post/pre injection amplitude ratio of CMAP were 0.49⁑0.21 with the 0.1 ml of dilution volume and 0.40⁑0.12 with the 0.5 ml of dilution volume. The mean post/pre injection area ratio of CMAP were 0.51⁑0.18 with the 0.1 ml of dilution volume and 0.44⁑0.15 with the 0.5 ml of dilution volume. There was no significant difference between the two dilution volumes.

Conclusion: Five fold increase in dilution volume did not enhance the paralyzing effect of botulinum toxin type A in human EDB muscles.

Objective: Botulinum toxin works at the neuromuscular junction by inhibiting the release of acetylcholine from the presynaptic membrane. It has been indicated for limb spasticity in patients with upper motor neuron lesions. The paralytic effect of this toxin usually lasts for 3 to 4 months, and repeated injections are needed to maintain the effect. This study was performed to investigate whether electrical stimulation can prolong the paralytic effect induced by botulinum toxin type A.

Method: Ninety male Sprague-Dawley rats, 30 for control and 60 for experimental, were studied. Botulinum toxin type A (Dysport^Ⱂ) was injected into the gastrocnemius muscle in the experimental groups (10 units for group 1 and 5 units for group 2), and normal saline 0.05 ml was injected into the same muscle in the control group. Thirty minutes of electrical stimulation was applied to the injected muscle with surface-stimulating electrodes. The stimulation was given once a day for 3 times in subgroup E1 and once every other day for 6 times in subgroup E2. No electrical stimulation was applied to subgroup N. Amplitudes of action potentials were measured serially on the injected muscles. At the third week, hematoxylin-eosin stained sections and synaptophysin immunohistochemical stained sections were examined.

Results: 1) At the second week after the toxin injection, amplitudes of action potentials maximally declined to 2.1∼3.7% in group 1 and to 4.0∼5.3% in group 2, compared to the initial amplitude. The amplitudes were beginning to recover from the third week. 2) Electrically stimulated groups demonstrated significantly more depressed amplitudes than non-stimulated group N. These effects lasted till week 2∼4. 3) Hematoxylin-eosin staining for muscle sections showed degenerative changes of muscle fibers. Synaptophysin immunoreactivity in the muscle demonstrated multiple synaptophysin-positive areas in a muscle fiber of the toxin injected muscle.

Conclusion: Transient electrical stimulation to the botulinum toxin injected muscles seems to enhance the paralytic effects of the toxin.

Objective: The purpose of this study was to investigate the dose-dependent responses to botulinum toxin A (BTX-A) injection on compound muscle action potential (CMAP) amplitude and needle electromyography (EMG) in local and distant muscles.

Method: The BTX-A (Botox^®, Allergan Co.) was injected to the left tibialis anterior (TA): 2, 4, 6, 8 U for each 4 Sprague-Dawley rats; 5, 10, 15, 20 U for each 2 rats. The sciatic nerve conduction and needle EMG were performed in the right and left TA immediately before BTX-A injection, on 2 days after injection, weekly for 1 to 10 weeks, and then monthly for 4 months.

Results: The range of dose-dependent maximal paralysis of the injected muscle was from 94% to 99.2% on 7 days after injection. With the lapse of time, the amplitudes in the left sciatic nerve conduction recovered, the abnormal spontaneous activities disappeared, and the power in spectral analysis of motor unit action potential increased. The range of dose-dependent reductions of the CMAP amplitude of the right TA was from 41.8% to 69.9% in the distant muscle, but there was no abnormal spontaneous activity in needle EMG study. As higher doses of BTX-A were injected, the degree of amplitude reduction became larger and the duration of amplitude reduction became longer in both local and distant TA muscles.

Conclusion: We observed the dose-dependent muscle paralysis with injection of BTX-A. The systemic effects by local injection were induced and the durations of local and systemic effects were proportional to the BTX-A dosage.

Objective: To investigate waveform changes of compound muscle action potentials (CMAPs) related to voluntary muscle contraction and alteration of muscle length and to evaluate the effect of peripheral neuropathy on temporal and spatial summations of CMAPs.

Method: The influence of voluntary muscle contraction and alteration of muscle length on CMAP was studied in 37 median nerves of 21 patients with median neuropathy.

Results: In patients with no apparent axonopathy, temporal summation was partially disturbed without significant change of spatial summation. Shortening of muscle length or voluntary contraction produced a physiologic improvement of spatial and temporal summations. There was a decrease in temporal and spatial summations, more prominent in temporal summation, with lengthening of the muscle. In axonopathy, spatial summation was markedly deteriorated with partial reduction of temporal summation. Spatial summation was not affected by the change of muscle length or voluntary contraction. Temporal summation was improved by muscle shortening or voluntary contraction and was decreased by muscle lengthening.

Conclusion: Peripheral neuropathy has an effects on physiological spatial and temporal summations of CMAPs. Temporal summation is preferentially decreased in cases without axonopathy. When axonopathy is apparent, spatial summation is profoundly disturbed with partial reduction of temporal summation.

Objective: To quantify the effect of botulinum toxin A injection, by the compound muscle action potential (CMAP) measure from the gastrocnemius muscles (GCM) and to compare them with the clinical data.

Methods: Seventeen legs of 10 cerebral palsy (CP) children were studied with botulinum toxin A injection on the motor points of their GCM. Each GCM was injected up to 6 units of the botulium toxin A per kilogram of the body weight. The CMAP were measured at the motor points of GCM with the surface electrodes on the post-injection day 1, day 3, day 7, 2 weeks and at 1 month then monthly thereafter for 6 months. Physician rating scale (PRS) and the angle of passive ankle dorsiflexion were evaluated at the same time.

Results: The amplitude and the area of the CMAP decreased from post-injection day 1 to 3 months. The most pronounced decrement was seen at 2 weeks post-injection (p＜0.05). The most pronounced increase of the dorsiflexion angle and PRS were seen at 1 and 2 months post-injection, respectively (p＜0.05).

Conclusion: The compound muscle action potential measure can be used for the neurophysiological quantification of the effect of botulinum toxin A, especially for the superficial muscles of extremities.

The influence of voluntary muscle contraction and alteration of muscle length on compound muscle action potential (CMAP) was studied in 20 healthy volunteers. The CMAPs were evoked by a supramaximal stimulation and recorded by a surface electrode array. Onset latencies were not significantly changed regardless of the muscle length and contraction. On shortening of the muscle there was a decrease in an area and duration of CMAP with no significant changes in an amplitude. During muscle contractions, there was an increase in amplitude and a decrease in area and duration. On a lengthening of the muscle with relaxation, the amplitude of CMAP decreased with an increased area and duration. During a voluntary contraction, there was a decrease in amplitude, area, and duration. The results are considered due to a peripheral factor such as an alteration of temporal or spatial summation rather than a central mechanism. We conclude that in nerve conduction studies, it is important to monitor the finger position and muscle relaxation to differentiate the waveform changes from the muscle length or contraction and those from the nerve lesions.

Chemical neurolysis can be an extremely effective intervention for reducing spasticity. Phenol nerve block as a method of chemical neurolysis has been used over 40 years, nevertheless, many clinicians remain reluctant to perform this procedure. This is largely due to the fear of its side effects and complications such as excessive muscle weakness or increased spasticity of antagonistic muscles.

The purpose of this study was to titrate the nerve block effects of phenol with different concentrations and different volumes of the phenol solution. Left tibial nerves of forty eight adult rabbits were injected with phenol solution of different concentrations(5%, 4%, 3%) and volumes(0.3 ml, 0.2 ml, 0.1 ml) into the epineural sheath. Nerve conduction study of the gastrocnemius muscle was performed before and after the nerve blocks(1day, 1week, 2weeks, 4weeks, 8weeks). The proportion of compound muscle action potential(CMAP) amplitudes and areas before and after the nerve blocks was used for the evaluation of nerve block effect.

There was a statistically significant difference in the proportion among three volumes of phenol solution(p＜0.05). However there was no statistical difference in the proportion among three concentrations of phenol solution(p＞0.05) although the higher concentration of phenol solution showed the tendency for smaller proportion. The area of histological degeneration appeared at 2 weeks following nerve block alongside the perineurium. The depth of degeneration area of nerve fascicle varied according to the distance from injection point.

These data suggest that the nerve block effect of phenol can be titrated more easily with the volume of phenol solution rather than the concentration until 8 weeks after the nerve block. The variation of the extent of degeneration with different volumes of phenol solution seems to be the mechanism for the titration.

Botulinum toxin develops muscular paralysis through the inhibition of acetylcholine release from presynaptic membrane in neuromuscular junction. It has been used clinically to treat strabismus, blepharospasm and spasmodic dysphonia. Recently it was introduced for the treatment of limb spasticity as well. Serial compound muscle action potential(CMAP) amplitudes were measured and repetitive nerve stimulation test(RNST) was performed with 2Hz and 30Hz on the rat gastrocnemius muscle to observe the effect of muscle paralysis. Also, Periodic acid Schiff (PAS) staining sections of the muscle for glycogen was studied to quantify the degree of muscular paralysis.

Thirty Sprague-Dawley rats, 10 for control and 20 for experimental group were studied for 12 weeks. Normal saline 0.025 ml and 0.125 ml was injected into gastrocnemius muscle in cotrol group 1 and 2, respectively. Botulinum toxin type A(Botox) was injected 5.0U/0.025 ml in experimental group 1, 2.5U/0.025 ml in group 2, 2.5U/0.125 ml in group 3, and 0.5U/0.025 ml in group 4. The amplitudes of CMAP declined markedly by 81.1% to 96.5% of basal amplitudes on the first week after Botox injection, but slightly recovered on 12th week by 20.8% to 42.2% with greater recovery in lower dose group. RNST with 2Hz produced no remarkable 1 : 5 amplitude change in experimental group. RNST with 30Hz produced marked increment in 1 : 5 amplitude up to 24.4%. PAS staining for muscle sections showed residual glycogen after tetanic stimulation due to neuromuscular block by Botox.