This study estimated the whole-scalp topography and possible generators of thecortical potential associated with volitional self-paced inspirations (sniffs). In 17 healthy subjects we recorded a 32-channel electroencephalogram(EEG) during sniffing, for comparison during finger flexions. We averaged the EEG with respect to movement onset, and performed current source density and principal component analysis on the grand averaged data. We identified an early negative sniffing-related cortical potential starting Ž1.5s before movement at the vertex, which, in its time-course and dipole orientation, closely resembled Bereitshaftspotential preceding finger flexions. Around the movement onset, its topography became unique with three negative current sources: one at the vertex, and two bilaterally over the fronto-temporal derivations. We conclude that sequential cortical activation in preparation for sniffing is similar to other volitional movements. The current sources at sniff onset at the vertex likely reflect somatotopic motor representation of the diaphragm, neck and intercostal muscles, whereas currentsources over fronto-temporal derivations likely reflect the somatotopicrepresentation of the orofacial muscles.
COBISS.SI-ID: 9459284
Our aim was to investigate changes in movement-related cortical potentials (MRCPs) in ALS patients with different degrees of upper motor neuron (UMN) involvement. Since respiratory failure is the main cause of death in ALS, changes in inspiratory-related (sniffing) potentials were studied in addition to finger-flexion-related potentials. Subjects (21 ALS, 19 controls) performed two self-paced motor tasks while their EEGs were recorded. The first task required flexions of the right index finger and the second, brisk nasal inspirations. The early (BP1), late (BP2) and motor potential (MP) components of MRCPs were evaluated. Results showed that patients generated higher MRCPs than controls. However, this effect was most significant in the subgroup of patients with low UMN burden (LUB). The high UMN burden (HUB) subgroup did not differ from controls, but had significantly lower MP amplitudes than the LUB subgroup. Progressive UMN deterioration was associated with an initial increase, followed by a later decrease, in MP amplitudes in ALS. In conclusion, the increased MRCPs in LUB compared to HUB patients indicate different processes of ALS pathophysiology that force opposing changes in MRCP amplitudes.
COBISS.SI-ID: 1001132
Introduction: The most common etiology of hypercapnic respiratory failure is chronic obstructive pulmonary disease (COPD). However, the differential diagnosis also includes neuromuscular disorders. We studied the specificity ofreduced amplitude phrenic nerve compound motor action potential (CMAP) to diagnose neuromuscular disorders. Methods: A group of patients with advanced COPD were recruited prospectively and compared with controls. Phrenic nerve CMAPs were measured bilaterally using supraclavicular surface stimulation and bipolar recording (G1: 5 cm above the xiphoid; G2: 16 cm from G1). Results: A group of 20 patients (15 men) and a group of 29 controls (15 men) were included. Phrenic nerve CMAPs of patients with COPD had significantly longer latency and higher amplitude. Conclusion: Our study demonstrates that patientswith hypercapnic respiratory failure and reduced phrenic nerve CMAP amplitude most probably have a neuromuscular disorder affecting the diaphragm and not COPD or another lung disorder.
COBISS.SI-ID: 715948