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ARTICLES: P. Schwenkreis, F. Janssen, O. Rommel, B. Pleger, B. Völker, I. Hosbach, R. Dertwinkel, C. Maier, and M. Tegenthoff Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand Neurology 2003; 61: 515-519 [Abstract] [Full text] [PDF]

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Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand

Phillip Krause, S. Foerderreuther, A. Straube   (19 November 2003)

Reply to Krause et al

Peter Schwenkreis, Martin Tegenthoff   (19 November 2003)

Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand 19 November 2003
Phillip Krause, Munich, Germany Marchioninistrasse 15, 81377 Munich, S. Foerderreuther, A. Straube Send Correspondence to journal: Re: Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand pkrause{at}nefo.med.uni-muenchen.de Phillip Krause, et al.	Recently Schwenkreis et al [1] reported motor cortical disinhibitions in CRPS I patients. We also conducted our own investigation and report some similarities and differences from their findings. In 11 CRPS I patients, motor evoked potentials (MEP) and resting motor threshold (RMT) were recorded and compared to 10 healthy subjects. Stimulations were done with a circular coil connected to a Magstim 200 positioned on both hemispheres at optimal spots. The RMT was determined as that stimulation intensity which led in 5 out of 10 responses to an amplitude >50 µV in the EMG. Electrodes of the surface-EMG were affixed at long extensor muscles on both sides, due to the possibility of changed skin resistance of edemic hand muscles. We did find a general reduced MEP amplitude on both sides in CRPS patients, significantly smaller compared to that of healthy subjects (right/left side: 0.15/0.14 mV in patients vs. 0.36/0.43 mV in healthy subjects). MEP amplitudes did not differ between both hemispheres in patients. Furthermore, the mean RMT was higher, but not significantly so, in the patients than in healthy subjects (44 % vs. 40 % of maximal stimulator output). We propose that this data indicate a general disturbed inhibitory-excitatory balance with a slightly increased inhibition of pyramidal cells as shown by the reduced MEP amplitude and increased RMT. Our findings differ from Schwenkreis including the significantly smaller MEP amplitudes and the higher RMT in our patient group. Schwenkreis found no difference in amplitudes between their groups and also no differences in RMT, apart from some patients suffering from allodynia with a reduced motor threshold in the affected side. Aside from the coil location (vertex vs. motor hot spot) and surface-EMG electrodes (first dorsal interosseus) the stimulation parameters were very similar, so that these and the differences in the clinical state may provide explanations of these different findings. These conflicting findings underline the heterogenic and multifactorial dependency of motor cortical mechansims, but also the need to further clarify the central mechanisms involving the motor cortex in CRPS I. References 1). Schwenkreis P, Janssen F, Rommel O, Pleger B, Volker B, Hosbach I et al. Bilateral motor cortex disinhibition in complex regional pain syndrome (CRPS) type I of the hand. Neurology 2003; 61:515-519.
Reply to Krause et al 19 November 2003
Peter Schwenkreis, Department of Neurology BG-Kliniken Bergmannsheil, Buerkle-de-la-Camp-Platz 1, D - 44789 Bochum, Martin Tegenthoff Send Correspondence to journal: Re: Reply to Krause et al peter.schwenkreis{at}ruhr-uni-bochum.de Peter Schwenkreis, et al.	Krause et al's findings in CRPS patients are interesting. They also report bilateral alterations of motor cortex excitability in CRPS patients, which corresponds to our results. [1] However, their results point towards decreased motor cortex excitability, whereas our results suggest bilateral motor cortex disinhibition. Krause's study sample was small and further stimluation details are needed including: stimulus intensities used; exclusion of spinal / peripheral influences; and clinical features of their patients. It is difficult to assess their results properly without these answers. Nevertheless, there might be several explanations for these different findings: 1. We agree that the differences in RMT might be explained by clinical differences between patients. This view is supported by the differences in RMT between clinical subgroups as observed in our study (patients with allodynia vs. patients without allodynia). 2. The MEP amplitudes reported in our study are amplitudes after single control stimuli, i.e., the stimulus intensity was adjusted to evoke an MEP of approximately 1mV. Therefore they cannot differ between patients and controls, and do not provide any information about motor cortex excitability. We assume that Krause used stimulus intensities adjusted to RMT to determine MEP amplitudes as a measure of motor excitability, a parameter that was not assessed in our study. 3. MEP amplitudes and intracortical inhibition/facilitation (ICI/ICF) as assessed by paired-pulse TMS represent different physiological mechanisms, and are independent of each other. MEP amplitudes depend on postsynaptic and synaptic function, ICI/ICF reflects the activity of intracortical inhibitory and facilitatory interneurones, and is transsynaptically mediated. [2] For example, a dissociation of these parameters was found in healthy subjects after administration of sertraline, a selective serotonine reuptake inhibitor (SSRI), with increased amplitudes and a decreased ICF. [3] In conclusion, Krause's results can be considered complementary rather than contradictory, and most of the apparent differences can be resolved. Taken together, there is evidence for a disturbance and dissociation of different inhibitory and excitatory mechanisms in the motor cortex, which might account for the motor abnormalities in CRPS patients. References 2). Hallett M, Chen R, Ziemann U, Cohen LG. Reorganization in motor cortex in amputees and in normal volunteers after ischemic limb deafferentation. Electroencephalogr Clin Neurophysiol Suppl 1999;51:183- 187. 3). Ilic TV, Korchounov A, Ziemann U. Complex modulation of human motor cortex excitability by the specific serotonin re-uptake inhibitor sertraline. Neurosci Lett 2002;319:116-120.