Combining functional neuroimaging with TMS

Combining functional neuroimaging with TMS

Clinical Neurophysiology 119 (2008) e67–e74 Society Proceedings Symposium of Clinical Neurophysiology Society of Serb...

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Clinical Neurophysiology 119 (2008) e67–e74

Society Proceedings

Symposium of Clinical Neurophysiology Society of Serbia and Montenegro with International Participation Belgrade, Serbia, October 26, 2007 Zˇarko Martinovic´


Department of Epilepsy and Clinical Neurophysiology, Institute of Mental Health, President of the Society, Palmoticeva 37, 11000 Belgrade, Serbia and Montenegro

Combining functional neuroimaging with TMS—Hartwig Siebner (Department of Neurology, Christian-AlbrechtsUniversity, Kiel, Germany, NeuroImage-Nord, HamburgKiel-Lu¨beck, Germany) The combined use of functional neuroimaging and focal TMS was established about 10 years ago. This talk will provide an overview of how TMS and functional neuroimaging can be combined to investigate human brain function. First, we address methodological issues concerning the combination of TMS with positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and EEG. Second, we discuss possible applications of the combined TMS–neuroimaging approach for studying human brain function. We outline how this approach can be used to: (i) examine the regional responsiveness of the cortex to TMS as well as inter-regional coupling in the intact human brain; (ii) explore inter-regional patterns of acute reorganization at the systems level; (iii) further our understanding of potential therapeutic effects of TMS conditioning; and (iv) trace dynamic aspects of the pathophysiology in neuropsychiatric disorders. Finally, we address future perspectives of the combined TMS–neuroimaging approach. doi:10.1016/j.clinph.2007.11.016

Purpose: To analyze electroneuromyography (ENMG) findings in patients with asymptomatic hyper-CK. Methods: We retrospectively reviewed ENMG documents of all patients examined at Clinic for Child Neurology and Psychiatry from 2001 to 2007 separating patients who met criteria for subclinical hyper-CK. Results: There were 17 patients (sporadic: 8; familiar: 9) from 11 families, aged from 1 to 42 years. CK was chronically elevated, range 500–218 000 UI/L, followed sometimes with myoglobinuria. Etiology was defined in 2 sporadic cases: McArdle disease 1; dystrophic process according to muscle biopsy 1 and all family cases: Hyper-K periodic paralysis (PP) 3; dystrophinopathy 3; dystrophic process according to biopsy 3. ENG was normal in all cases. Spontaneous activity (myotonic) only in family with hyper-K PP. Myopathic EMG in single muscle was found in 3 patients, whose biopsy finding confirmed dystrophic process. Other myopathic signs were not detected. Conclusion: Etiology was not defined in the most sporadic hyper-CK cases. Diagnostic value of ENMG was confirmed in our patients with channelopathy, but it was very small in others, including patients with subclinical dystrophic process. doi:10.1016/j.clinph.2007.11.017

Electroneuromyography study in subclinical hyper-CKemia—V. Milic-Rasic (Clinic for Child Neurology and Psychiatry, Belgrade, Serbia)

Neuromuscular dysfunction in critically ill patients (critical care illness)—S. Pavlovic´, D. Pavlovic´ (Clinical Center ‘‘Bezˇanijska Kosa’’, Belgrade, Serbia)

Elevated serum creatine kinase (CK) level commonly reflects a neuromuscular disorder. Occasionally, chronic hyper-CK-emia is isolated sign in apparently healthy persons.

Critical illness or systemic inflammatory response syndrome (SIRS) is present in 20–50% of patients treated with mechanical ventilation in intensive care units (ICU) for longer than a week. The most frequent cause of SIRS is infection (sepsis). Activated mediators of inflammation lead to disturbances of microcirculation and local tissue hypoxia resulting in multiorgan failure. Pathogenetic mechanisms od neuromuscular dysfunction in SIRS


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