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Cortical activation by phasic cold stimuli in patients with central post-stroke pain – A magnetoencephalographic study
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Society Proceedings / Clinical Neurophysiology 118 (2007) e9–e116
Cortical activation by phasic cold stimuli in patients with central post-stroke pain – A magnetoencephalographic study—E. Lang, C. Maiho¨fner, M. Kaltenha¨user (University of Erlangen-Nuremberg, Department of Neurology, Erlangen, Germany) Aims: Central post-stroke pain (CPSP) is hypothesized to result from disinhibition of pain by cold (Craig et al., Pain Forum, 1998). In a previous study in healthy subjects, we demonstrated by magnetoencephalography that innocuous cold stimulation of one hand activates exclusively the contra- and ipsilateral insular cortex whereas noxious cold activates additionally the contra- and ipsilateral SII cortex and variably the cingulate cortex (Maiho¨fner et al., Pain, 2002). Aims: To test if in patients with CPSP due to thalamic stroke the insular cortex on the lesion side is deafferentiated from innocuous cold input and if there are abnormal activation patterns. Methods: We examined three patients with CPSP following stroke in the posterolateral thalamus. Two patients complained about continuous pain, one patient about pain only during movements of the symptomatic side. All patients reported cold allodynia. One hundred innocuous cold stimuli (5 ± 2 °C in 50 ms) were applied separately to each hand. Cortical responses were recorded with a dual 37-channel neuromagnetometer. Equivalent current dipoles were calculated from averaged signals and corresponding head coordinates were superimposed on magnetic resonance images of the brains. Results: Cold sensation on the symptomatic hand was markedly reduced. In the two patients with continuous pain, magnetic source localisation did not reveal activation of the insular cortex on the side of thalamic lesion following cold stimulation at any of both hands. In the patient without continuous pain, stimulation of the symptomatic hand activated the posterior insular cortex in both hemispheres. In all three patients, posterior insular cortex on the side contralateral to thalamic lesion was normally activated by cold stimulation of both hands. Conclusions: Absent activation of the posterior insular cortex in patients with continuous pain in CPSP supports the hypothesis of disinhibition of central pain pathways by cold afferents. Absence of cold allodynia to short cold stimuli indicates that cold allodynia in CPSP needs longer temporal summation of cold. doi:10.1016/j.clinph.2006.11.155
Stimulus intensity, coil characteristics and peripheral reafferent activation contribute to the suppressive effects of 1 Hz rTMS on cortical excitability—N. Lang 1, J. Harms 1, T. Weyh 2, J.C. Rothwell 3, W. Paulus 1, R.N. Lemon 3, H.R. Siebner 4 (1 Department of Clinical Neurophysiology, Georg-August-University, Goettingen, Germany, 2 Heinz Nixdorf-Lehrstuhl fuer Medizinische Elektronik, TU Muenchen, Germany, 3 Sobell Department of Motorneuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, UK, 4 Department of Neurology, Christian-Albrechts University, Kiel, Germany) Objective: Low-frequency (1 Hz) repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex (M1) can suppress corticospinal excitability. Here we examined whether
these inhibitory after effects depend on the stimulus intensity, the type of TMS coil and peripheral reafferent activation. Methods: In 15 healthy volunteers, 900 biphasic pulses of 1 Hz rTMS were given to the left M1 at an intensity of 90% or 115% of the individual resting motor threshold (subthreshold vs. suprathreshold intensity) using two commercially available ‘figure-ofeight’ shaped TMS coils (Magstim or Dantec coil) attached to the same magnetic stimulator. Before and twice after intervention we recorded motor evoked potentials (MEPs) evoked with the same set-up used for rTMS (MEPrTMS). Using a Magstim coil connected to two Magstim 200 stimulators, we also gave monophasic single and paired pulses to the M1 and assessed unconditioned MEPs (MEPtest), paired-pulse excitability and cortical silent period (cSP). In a control experiment, the same measurements were performed after 15 min of 1 Hz repetitive electrical nerve stimulation (rENS) of the right ulnar nerve at the wrist using a suprathreshold intensity. Results: We found that the suppressive effect on MEPrTMS depended on the intensity and the type of coil used for rTMS conditioning. The suppression of corticospinal excitability was more pronounced and lasted longer when a suprathreshold intensity and a Dantec coil was used. The intensity but not the type of coil also had an effect on time-dependent changes in intracortical facilitation and cSP. Suprathreshold 1 Hz rENS also induced a short lasting inhibition of MEPrTMS. Conclusions: Both, the stimulation intensity and the type of TMS coil have an impact on the suppressive after effects of 1 Hz rTMS. The stronger suppression of suprathreshold 1 Hz rTMS can at least in part be attributed to repetitive peripheral stimulation caused by reafferent feedback. Significance: These data should be taken into account when rTMS is used for therapeutic means. doi:10.1016/j.clinph.2006.11.156
Somatosensory evoked potentials (SSEP) in Hashimoto encephalopathy – A case report—M. Lanz 1,2, S. Bunten 1, O. Grothues 2, K. Wittig 2, H.U. Voelter 2, S. Happe 1 (1 Department of Clinical Neurophysiology, Klinikum Bremen Ost, Bremen, Germany, 2 Department of Neurology, University of Go¨ttingen, Germany) We report a case of Hashimoto encephalopathy with a significant reduction in amplitude of the parietal cortical component of the early somatosensory evoked potentials of the median nerve. This reduction was significant when using a frontal reference as compared to the palmar reference and showed a complete recovery after sufficient treatment. A 43 old female patient with a change of personality including aggressive behaviour and a progressive choreatiform movement disorder was admitted to hospital with the suspected diagnosis of Huntington’s disease (HD). Further investigations excluded HD and revealed a thyroiditis encephalopathy (Hashimoto) with complete clinical remission after treatment with corticosteroids. The phenomenon of a reduced amplitude when using a frontal reference in SSEP is usually attributed to Huntington’s disease and progresses with the severity of the disease. The finding is even less often described in other degenerative disorders of the basal ganglia.
Society Proceedings / Clinical Neurophysiology 118 (2007) e9–e116
Cortical activation by phasic cold stimuli in patients with central post-stroke pain – A magnetoencephalographic study—E. Lang, C. Maiho¨fner, M. Kaltenha¨user (University of Erlangen-Nuremberg, Department of Neurology, Erlangen, Germany) Aims: Central post-stroke pain (CPSP) is hypothesized to result from disinhibition of pain by cold (Craig et al., Pain Forum, 1998). In a previous study in healthy subjects, we demonstrated by magnetoencephalography that innocuous cold stimulation of one hand activates exclusively the contra- and ipsilateral insular cortex whereas noxious cold activates additionally the contra- and ipsilateral SII cortex and variably the cingulate cortex (Maiho¨fner et al., Pain, 2002). Aims: To test if in patients with CPSP due to thalamic stroke the insular cortex on the lesion side is deafferentiated from innocuous cold input and if there are abnormal activation patterns. Methods: We examined three patients with CPSP following stroke in the posterolateral thalamus. Two patients complained about continuous pain, one patient about pain only during movements of the symptomatic side. All patients reported cold allodynia. One hundred innocuous cold stimuli (5 ± 2 °C in 50 ms) were applied separately to each hand. Cortical responses were recorded with a dual 37-channel neuromagnetometer. Equivalent current dipoles were calculated from averaged signals and corresponding head coordinates were superimposed on magnetic resonance images of the brains. Results: Cold sensation on the symptomatic hand was markedly reduced. In the two patients with continuous pain, magnetic source localisation did not reveal activation of the insular cortex on the side of thalamic lesion following cold stimulation at any of both hands. In the patient without continuous pain, stimulation of the symptomatic hand activated the posterior insular cortex in both hemispheres. In all three patients, posterior insular cortex on the side contralateral to thalamic lesion was normally activated by cold stimulation of both hands. Conclusions: Absent activation of the posterior insular cortex in patients with continuous pain in CPSP supports the hypothesis of disinhibition of central pain pathways by cold afferents. Absence of cold allodynia to short cold stimuli indicates that cold allodynia in CPSP needs longer temporal summation of cold. doi:10.1016/j.clinph.2006.11.155
Stimulus intensity, coil characteristics and peripheral reafferent activation contribute to the suppressive effects of 1 Hz rTMS on cortical excitability—N. Lang 1, J. Harms 1, T. Weyh 2, J.C. Rothwell 3, W. Paulus 1, R.N. Lemon 3, H.R. Siebner 4 (1 Department of Clinical Neurophysiology, Georg-August-University, Goettingen, Germany, 2 Heinz Nixdorf-Lehrstuhl fuer Medizinische Elektronik, TU Muenchen, Germany, 3 Sobell Department of Motorneuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, UK, 4 Department of Neurology, Christian-Albrechts University, Kiel, Germany) Objective: Low-frequency (1 Hz) repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex (M1) can suppress corticospinal excitability. Here we examined whether
these inhibitory after effects depend on the stimulus intensity, the type of TMS coil and peripheral reafferent activation. Methods: In 15 healthy volunteers, 900 biphasic pulses of 1 Hz rTMS were given to the left M1 at an intensity of 90% or 115% of the individual resting motor threshold (subthreshold vs. suprathreshold intensity) using two commercially available ‘figure-ofeight’ shaped TMS coils (Magstim or Dantec coil) attached to the same magnetic stimulator. Before and twice after intervention we recorded motor evoked potentials (MEPs) evoked with the same set-up used for rTMS (MEPrTMS). Using a Magstim coil connected to two Magstim 200 stimulators, we also gave monophasic single and paired pulses to the M1 and assessed unconditioned MEPs (MEPtest), paired-pulse excitability and cortical silent period (cSP). In a control experiment, the same measurements were performed after 15 min of 1 Hz repetitive electrical nerve stimulation (rENS) of the right ulnar nerve at the wrist using a suprathreshold intensity. Results: We found that the suppressive effect on MEPrTMS depended on the intensity and the type of coil used for rTMS conditioning. The suppression of corticospinal excitability was more pronounced and lasted longer when a suprathreshold intensity and a Dantec coil was used. The intensity but not the type of coil also had an effect on time-dependent changes in intracortical facilitation and cSP. Suprathreshold 1 Hz rENS also induced a short lasting inhibition of MEPrTMS. Conclusions: Both, the stimulation intensity and the type of TMS coil have an impact on the suppressive after effects of 1 Hz rTMS. The stronger suppression of suprathreshold 1 Hz rTMS can at least in part be attributed to repetitive peripheral stimulation caused by reafferent feedback. Significance: These data should be taken into account when rTMS is used for therapeutic means. doi:10.1016/j.clinph.2006.11.156
Somatosensory evoked potentials (SSEP) in Hashimoto encephalopathy – A case report—M. Lanz 1,2, S. Bunten 1, O. Grothues 2, K. Wittig 2, H.U. Voelter 2, S. Happe 1 (1 Department of Clinical Neurophysiology, Klinikum Bremen Ost, Bremen, Germany, 2 Department of Neurology, University of Go¨ttingen, Germany) We report a case of Hashimoto encephalopathy with a significant reduction in amplitude of the parietal cortical component of the early somatosensory evoked potentials of the median nerve. This reduction was significant when using a frontal reference as compared to the palmar reference and showed a complete recovery after sufficient treatment. A 43 old female patient with a change of personality including aggressive behaviour and a progressive choreatiform movement disorder was admitted to hospital with the suspected diagnosis of Huntington’s disease (HD). Further investigations excluded HD and revealed a thyroiditis encephalopathy (Hashimoto) with complete clinical remission after treatment with corticosteroids. The phenomenon of a reduced amplitude when using a frontal reference in SSEP is usually attributed to Huntington’s disease and progresses with the severity of the disease. The finding is even less often described in other degenerative disorders of the basal ganglia.