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Localized and distant actions of BTX‐A injections

One of the reasons we ask the parents of our children to sign a consent form prior to botulinum toxin A (BTX-A) injections in our institution is to make them aware of the possibility of systemic weakness leading, especially, to respiratory, facial, or bladder muscle weakness respectively as a consequence of systemic spread of the toxin. However, another aspect of the discussion usually acknowledges that some parents observe a reduction in unpleasant drooling or, perhaps more surprisingly, improved speech or hand function1 after lower limb BTX-A injections. Indeed, improved upper limb function was recently reported at this autumn’s meeting of the American Academy for Cerebral Palsy & Developmental Medicine in Vancouver. There are now two important animal studies describing techniques which potentiate the effects of BTX-A in the injected muscle,2 and the latest of these gives further clear evidence that systemic spread can be minimized, the latter of which must be good news for a risk-minimizing practice. The first paper by Kim and colleagues appeared in DMCN in 2003,2 demonstrating that first, doubling the dilution of BTX-A and second, mechanical stretching after BTX-A injections potentiated the effects of the toxin. This resulted in an immediate change in my practice which has included vigorous post-injection passive stretching of the injected muscles and advice to parents to encourage as much use as possible of the injected limb. A secondary benefit of this alteration in injection practice has been the financial saving to our institution. What we don’t of course know is whether trebling the dilution of BTX-A (i.e. trebling the instilled volume of injections) potentiates the effects of injections still further. In this issue, Minamoto et al. carried out a similar study in mice rather than rabbits. They used similar total doses of BTX-A per kilogram. They also examined the effects of BTX-A alone, BTX-A with electrical stimulation of the muscles, or BTX-A with passive stretch of the muscles. They found that injected muscles which received short bursts of electrical stimulation or passive stretching, 10 periods over only 20 minutes, were significantly weaker, but contralateral muscles were relatively protected from distant effects of BTX-A. Both groups confirmed the effects of toxin histologically and with neurophysiological techniques. In addition, Minamoto et al. measured the tetanic torque post-injections according to the three injection methods, both in the injected and non-injected limbs. In contrast to the Kim study, short periods of passive stretching concentrated the effect of the toxin in the injected limbs. An issue meriting further attention is a comparison between the relative weakness and wasting following other conventional surgical procedures such as muscle slides, fascial releases, and tenotomies in similar models to these BTX-A studies, as well as longer-term studies of the effects of BTX-A injections. Minamoto and colleagues very rightly quote one of my favourite papers by Pattullo and colleagues,3 but don’t actually talk of surgical releases as such or the histological effects of these procedures. This is important when thinking of the tissue-level effects of different therapeutic modalities. An intriguing area for debate remains: ‘systemic effects of targeted BTX-A injections, bane or bonus?’ Reduced drooling and improved hand use following leg muscle injections could be seen as a ‘three for the price of one’ effect. Surely a cue for more clinical studies.