Botulinum toxin injection of the subscapularis muscle

Patients with hemiplegia frequently suffer from pain and have a limited range of motion (ROM) of the shoulder. The common pattern of shoulder movement in a patient with spastic hemiplegia is primarily adduction and internal rotation. Spasticity of the subscapularis muscle limits the abduction, external rotation and flexion of the shoulder. Injection of botulinum toxin or application of phenol can reduce the spasticity of the subscapularis muscle and various techniques to inject this muscle have been reported. We injected five patients with hemiplegia with botulinum toxin using our previously reported inferior approach, which is easy, safe and effective. We observed a reduction in pain and spasticity and improvement in the ROM of the shoulder for all patients.     

Botulinum toxin: description of injection techniques and examination of controversies surrounding toxin diffusion

The benefits derived from botulinum toxin (BTX) injections may be negated by unintentional weakness of adjacent uninjected muscles. Such weakness may be the result of inaccurate targeting, or diffusion of BTX to surrounding muscles. Several techniques, using electromyographic, endoscopic or imaging guidance are purported to increase the accuracy of targeting. Diffusion of BTX is thought to be influenced by factors such as dose, concentration, injectate volume, number of injections, site and rate of injection, needle gauge, muscle size, muscular fascia, distance of needle tip from the neuromuscular junction, and protein content of the BTX formulation. This article describes techniques that aim to increase the accuracy of BTX injections and examines the controversies surrounding diffusion of BTX following injection.     

Botulinum toxin injection in patients with hereditary spastic paraparesis

In an open label study, we analyzed the efficacy of botulinum toxin injection at the lower limbs of patients with hereditary spastic paraparesis (HSP). Fifteen patients who showed disabling spasticity with no or poor effect of oral treatment were recruited consecutively. Botulinum toxin was injected (400 U; Botox^®) into the spastic muscles identified by clinical examination (equinus, varus, and pathological hip adduction). Patients were regularly assessed from the first day to the fifth month: spasticity (Ashworth), motor strength, range of movements, Functional Ambulation Categories (FAC), gait parameter, Rivermead Motor Assessment, self-analysis of benefit and satisfaction. We observed a moderate and significant ( P  < 0.05) reduction of ankle plantar flexor and hip adductor spasticity, with a partial increase in the range of the active and passive motion at the ankle and in gait velocity. At an individual level, six of 15 patients showed an increase in gait velocity. The FAC and RMA did not change. Patients often reported partial improvement in foot position and lower limb propulsion, and fair satisfaction. In conclusion, botulinum toxin injection can be effective in HSP patients with relatively ancient spasticity. This technique can be introduced into the therapeutic panel, which also includes physiotherapy, oral treatment and baclofen pump.     

Botulinum toxin injection for post‐stroke spasticity

Introduction: The aim of this study was to evaluate test feasibility, validity, and reproducibility of the rate of force development scaling factor (RFD‐SF) for the hip muscles. Methods: Feasibility was assessed as the testing compliance, validity as the ability to compute the RFD‐SF from a linear regression, and reproducibility with a test–retest design in 20 healthy subjects. Reliability and agreement (reproducibility) were evaluated using intraclass correlation coefficient (ICC_3,1) and percent standard error of measurement (SEM), respectively. Results: The RFD‐SF testing protocol was completed successfully by all subjects, although the analysis had to be modified for hip rotators. Reliability was high (ICC_3,1 > 0.70) for all muscles except hip abductors (ICC_3,1 = 0.69) and internal rotators (ICC_3,1 = 0.58). Agreement was high for all muscles (SEM < 10%). Conclusions: Hip adductor, flexor, and external rotator RFD‐SF can be evaluated with confidence, provided the analysis is modified for external rotators, whereas hip abductor and internal rotator RFD‐SF assessment is not recommended. Muscle Nerve 50: 932–938, 2014     

Botulinum toxin type A treatment of hip and thigh spasticity: a technique for injection of psoas major muscle

Spasticity of the hip and thigh can result from spinal cord injury, multiple sclerosis, cerebral palsy and numerous other neurological conditions. Chronic hip spasticity causes the patient extreme difficulty in walking and maintaining a comfortable posture. First-line treatment usually consists of oral anti-spastic agents, although these are often associated with a high side-effect burden. intramuscular injections of botulinum toxin type A (BTX-A), particularly into the psoas major muscle, have proved to be of functional benefit to the patient. A highly reliable and reproducible method for injecting the psoas major muscle through a para-spinal route has been developed to reduce the power of the muscle and hip flexion deformity. Injection occurs through the middle of the erector spinae muscle at L2, L3 and L4, delivering a total of 150 U BTX-A to the psoas major muscle. Follow-up with a substantial rehabilitation programme reliably ensures a decrease in Modified Ashworth Scores and improvements in the outcome assessment scores measured.     

Botulinum toxin A injection for spasticity in diplegic-type cerebral palsy

Botulinum toxin type A can be both safe and effective in relieving spasticity in pediatric patients with cerebral palsy. In our prospective study, we evaluated the functional effect of botulinum toxin A in spastic diplegic-type cerebral palsy. Patients were examined on enrollment and at 1, 3, and 6 months after injection. Passive dorsiflexion of the ankle joint was measured using a goniometer as an angle of possible maximal dorsiflexion with the knee extended and flexed. Spasticity was graded using the Modified Ashworth Scale. Selective motor control at the ankle was assessed, and observational gait analysis was done. The functional status of the patients was determined by using the gross motor classification system. Botulinum toxin A was injected into the gastrocnemius muscle in all patients, and in four patients with concomitant jump knee gait, a hamstring muscle injection was added. Fourteen patients were included in the study. The mean age was 58.81 +/- 15.34 months. Following injection, spasticity was clinically decreased and statistically significant improvement was noticed in all clinical parameters after 1, 3, and 6 months of injection. The improvement in the clinical parameters decreased after 6 months but not to the baseline. One patient was Level II, four patients were Level III, and six patients were Level IV according to the Gross Motor Function Classification System at baseline. Improvement in the gross motor classification system is continued after 6 months in 12 children. The main goal of spasticity treatment in cerebral palsy is functional improvement. In our study, most of our patients had functional improvement according to the gross motor function classification system and did not change at 6 months.     

Botulinum toxin A injection in the treatment of hemifacial spasm

Introduction – There are conflicting reports concerning the variation in duration of symptoms relief for patients with hemifacial spasm who have undergone several injections of botulinum A toxin (BOTX-A). We present our experience of BOTX-A injections in Taiwanese patients to analyze this issues, and to inspect whether the efficacy of treatment depends on the pre-injection severity. Material and method — From July 1992 to December 1994, 137 patients received injections of BOTX-A. We used objective and subjective score system to evaluate the efficacy and side effects of BOTX-A injection. Results — The overall successful rate of substantial relief of spasm was 88%. The mean duration of response was 20 weeks. Patents with more severe spasm tended to have shorter duration of improvement. The effects of consecutive injections remained fairly constant over the first 4 injections. Conclusion — The BOTX-A injection is an effective and safe treatment for patients with hemifacial spasm and the effect could be sustained over the consecutive injections.     

Botulinum toxin: clinical use

Since its development for the use of blepharospasm and strabismus more than 2.5 decades ago, botulinum neurotoxin (BoNT) has become a versatile drug in various fields of medicine. It is the standard of care in different disorders such as cervical dystonia, hemifacial spasm, focal spasticity, hyperhidrosis, ophthalmological and otolaryngeal disorders. It has also found widespread use in cosmetic applications. Many other indications are currently under investigation, including gastroenterologic and urologic indications, analgesic management and migraine. This paper is an extensive review of the spectrum of BoNT clinical applications.     

Botulinum toxin treatment of muscle cramps: A clinical and neurophysiological study

Botulinum toxin is now widely used in the treatment of severla hyperkinetic movement disorders. To evaluate its efficacy in treating muscle cramping syndromes, we studied clinical and neurophysiological variables before and after botulinum toxin injections into calf muscles and small flexor muscles of the foot in patients with an inherited benign crampfasciculation syndrome. At each assessment the clinical severity of cramp was scored and the cramp threshold frequency was measured with repetitive electrical peripheral nerve stimulation. Botulinum toxin injection signifcantly lowered our patients' clinical cramp severity scores (mean ± SD: before, 3.80 ± 0.44; after, 1.40 ± 0.54), left muscle strength unchanged and significanlty increased their cramp threshold frequencies (before, 4.22 ± 2.26 Hz; after, 10.0 ± 3.74 Hz). The clinical beefit induced by botulinum toxin lasted about 3 months. Boutlinum toxin injections also significantly reduced fasciculation potentials in relaxed muscles (before, 0.86 ± 0.19 fasciculations/sec; after, 0.45 ± 0.11 fasciculations/sec). These findings show that local intramuscular injection of botulinum toxin provide effective, safe, and long-lasting relief of cramps possibly by reducing presynaptic cholinergic stimulation of motor nerve terminals and by impairing the input/output function of intrafusal and extrafusal motor end plates.     

Botulinum toxin therapy

Botulinum toxin therapy has emerged as a treatment modality for a variety of spastic- or contracture-related muscle diseases. Its safety has been proven for long-term use in the treatment of benign essential blepharospasm, hemifacial spasm, and certain types of strabismus. Recent approval from the Federal Drug Administration should make botulinum toxin available for use in a greater number of patients.     

Botulinum toxin drugs: future developments

Summary Botulinum toxin (BoNT) drugs have been used with remarkable success for more than 20 years generating an industry with annual sales in excess of 1 billion US dollars. However, BoNT drugs are not at the end of their development cycle. Product development will focus on an improved antigenicity by increasing the specific biological activity, by separation of complexing proteins, by introduction of high affinity BoNT or by shielding of antigenic BoNT epitopes. Other development will include transdermal application, drug labeling for imaging guided applications, ready made solutions, and drug stability. New BoNT drugs are already offering some of these improved features. BoNT drugs are safe and effective, but need continuous development. Correspondence: Dirk Dressler, Department of Neurology, Rostock University, Gehlsheimer Str. 20, 18147 Rostock, Germany     

Botulinum toxin: mechanisms of action

Botulinum toxin (BT) has been perceived as a lethal threat for many centuries. In the early 1980s, this perception completely changed when BT's therapeutic potential suddenly became apparent. We wish to give an overview over BT's mechanisms of action relevant for understanding its therapeutic use. BT's molecular mode of action includes extracellular binding to glycoprotein structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated by blockade of substance P, glutamate and calcitonin gene-related peptide.     

Botulinum toxin: mechanisms of action

This review describes therapeutically relevant mechanisms of action of botulinum toxin (BT). BT's molecular mode of action includes extracellular binding to glycoproteine structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. BT affects the spinal stretch reflex by blockade of intrafusal muscle fibres with consecutive reduction of Ia/II afferent signals and muscle tone without affecting muscle strength (reflex inhibition). This mechanism allows for antidystonic effects not only caused by target muscle paresis. BT also blocks efferent autonomic fibres to smooth muscles and to exocrine glands. Direct central nervous system effects are not observed, since BT does not cross the blood-brain-barrier and since it is inactivated during its retrograde axonal transport. Indirect central nervous system effects include reflex inhibition, normalisation of reciprocal inhibition, intracortical inhibition and somatosensory evoked potentials. Reduction of formalin-induced pain suggests direct analgesic BT effects possibly mediated through blockade of substance P, glutamate and calcitonin gene related peptide.     

Botulinum toxin a improves muscle spasms and rigidity in stiff-person syndrome

We studied the effect of botulinum toxin A (BTA) on painful muscular spasms and rigidity in two bedridden patients with clinical, electrophysiologic, and immunologic evidence of stiff-person syndrome. We injected BTA of saline solution into several limb muscles with both the rater and patient blinded to the order of the injections. A physician, unaware of the treatment order, used an objective rating scale for rigidity and spasm frequency scale and independently assessed the treatment results. BTA administration significantly reduced rigidity and stopped the spasms in all limbs. Following BTA injection on one side, the spasm frequency decreased bilaterally possibly because of the spread of hematogenous toxin.