Demystifying Spasticity: Reply to Dietz

Abstract

REPLY: I was glad to read Dr. Volker Dietz's recent letter to the editor (Dietz 2007) comparing his work on spasticity in humans to my studies of spasticity in the sacral spinal rat (Bennett et al. 2004). His comments highlight many of the confusions that have shrouded the study of spasticity and give me a chance to clear the air on this topic.The first confusion relates to the complexity of spasticity and the lack of consensus on which aspects of spasticity are most relevant. The spastic syndrome in humans (or what Dietz calls the "spastic movement disorder") is a complex collection of clinical conditions, including excess muscle tone (hypertonus), changes in muscle properties (like contractures), excess reflex activity (hyperreflexia), muscle oscillations (clonus), and massive uncontrolled motoneuron firing and contractions (spasms; Bennett et al. 2004; Dietz and Sinkjaer 2007;Kuhn and Macht 1948). In my laboratory, we mostly study spasms triggered by brief cutaneous stimulation and we have shown these to result from excess motoneuron excitability (Bennett et al. 2004;Li et al. 2004a). Dietz has spent a lot of time studying muscle properties (Dietz et al. 1986) and emphasizes their importance in his letter to the editor (Dietz 2007). From this perspective, he criticizes research that does not focus on muscle properties, suggesting that it is not relevant to the study of spasticity. This seems a bit odd because upward of 80% of spinal cord injured humans suffer from spasms caused by excess motoneuron activity (Maynard et al. 1990), and thus understanding spasms is important.The second confusion has arisen because spasticity research has for decades focused exclusively on correlating spastic behavior with short-lasting reflexes (mono-and polysynaptic) that can be conveniently measured in the laboratory in humans, as though these reflexes were the only forms of neuronal activity possible from the spinal cord. I think that research should instead focus on measuring neuronal activity during actual spastic episodes, such as during spasms, even though this means studying complex long-lasting reflexes, rather than simple short-lasting reflexes (Bennett et al. 2004). Dietz rightly points out that after years of studying short-latency monosynaptic reflexes and other short-lasting polysynaptic reflexes, it is clear that they do not "contribute greatly to the spastic movement disorder" (Dietz 2007; Dietz and Sinkjaer 2007). However, he then seems to fall into the classic trap of assuming that these reflexes are the only forms of neuronal activity possible from the spinal cord, and thus makes the overgeneralization that human spasticity is not "primarily caused by an increased neuronal activity" (Dietz 2007). Because muscle properties change somewhat in spastic patients (Dietz and Sinkjaer 2007), Dietz then concludes, without any further evidence, that properties of muscles must instead be primarily responsible for spasticity (Dietz 2007; Dietz and Sinkjaer 2007). Importantly, Dietz has not considered longer-lasting refle...

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