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One expects that convincing research results would have an impact on clinical practice. However, whether or not a new concept becomes transferred to an application in clinical practice is dependent on the medical field and on the therapeutic consequences. The issue discussed here concerns spasticity, a common motor disorder in, for example, patients who have had a stroke or a spinal cord injury.
The traditional concept
Over many years it was widely accepted that spasticity consists of muscle hypertonia (that is, “a velocity dependent resistance of a muscle to stretch”1) caused by exaggerated reflexes, leading to the spastic movement disorder.2 This concept was based on animal experiments (for example, in the decerebrate cat3) and on the physical signs evident on clinical examination at the bedside. Consequently, the aim of any treatment was to reduce reflex activity by antispastic drugs. Possible differences in pathophysiology between the clinical signs of spasticity and the spastic movement disorder which hampers the patient were not considered.
The new concept
Early clinical observations4 and studies in the 1980s on spastic movement disorders5 clearly failed to support the traditional concept. In the subsequent 20 years an increasing number of studies using different technological approaches with electromyographic (EMG) and biomechanical recordings focused on the relation between muscle EMG and reflex activity and muscle tone during various functional6–8 and clinical9–12 conditions. All these studies fused into a new concept of spasticity (reviewed in several articles13–15). This concept has never been questioned in its basic aspects.
The new concept was based on the following observations. First, in the active muscle (that is, during movement) the presence of exaggerated tendon tap reflexes is associated with a loss of the functionally essential polysynaptic or longer latency reflexes, with the consequence that overall muscle activity is reduced during functional movements. Second, as a response to the primary lesion, changes in non-neuronal factors (muscle and connective tissue) compensate for the loss of supraspinal drive and essentially contribute to spastic hypertonia in both passive9,12 and active8 muscles.
The scientific consequence of this is that the physical signs obtained during the clinical bedside examination are an epiphenomenon rather than the cause of the functional condition (which impairs the patient). During movement, essential reflex mechanisms are involved which cannot usually be assessed by clinical testing. Consequently, the clinical examination required for diagnostic purposes has to be separated from functional testing, which should determine the therapeutic approach. For example, motor function can be assessed by a walking index, such as WISCI.16
The therapeutic consequence of these observations is that antispastic drugs should be used only with caution in the mobile spastic patient, as a decrease in muscle tone achieved by these drugs could be associated with an accentuation of paresis, impairing the performance of functional movements.17,18 Consequently, spastic muscle tone is required so that a patient can walk again after a stroke.
Facts and consequences
Although this new concept has become well established scientifically in journals with a mainly scientific orientation during the past 20 years, there has been little transfer to clinical practice. This is reflected in recent review articles in journals with a practical orientation19–21 read predominantly by clinical neurologists.
The following factors may contribute to the persistence of some old fashioned concepts in clinical neurology:
The old concept was simple to understand and had a clear therapeutic consequence: the prescription of antispastic drugs. It is seemingly logical that exaggerated reflexes cause muscle hypertonia. The new concept is more complex and its implications—that antispastic drugs should not generally be used—make the doctor somewhat resourceless.
It is not rewarding for a neurologist to take care of patients after a stroke and to have to explain that there are limited therapeutic options (that is, that it will be impossible to restore normal function, and that physical exercises will be more helpful than drug treatment).
It is, of course of no interest for companies producing antispastic drugs to support graduate medical education in this new concept, with its limited opportunities for drug treatment.
The consequences of this experience should be as follows. First, scientific research results should be translated into an understandable and pragmatic format, to convince doctors and patients of the superiority of the new concept. Second, such a novel concept should initiate the development of new forms of treatment (for example, in the field of active physiotherapy); at very least it should be associated with a well structured physical treatment programme which allows the doctor to become involved. Third, the concept should emphasise that immobilised patients may benefit from the use of antispastic drugs (for example, in the management of spasms and for easier nursing); this would make the concept more acceptable to the drug companies. Finally, the concept should include perspectives and limitations of any possible achievements.
Competing interests: none declared