The mechanism of action of laser radiation on the development of ischemic arrhythmias after stimulation of the sensorimotor cortex

1996 ◽  
Vol 122 (4) ◽  
pp. 976-978
Author(s):  
S. D. Mikhailova ◽  
G. I. Storozhakov ◽  
A. V. Kudinova ◽  
T. M. Semushkina
1989 ◽  
Vol 62 (3) ◽  
pp. 711-722 ◽  
Author(s):  
T. Allison ◽  
G. McCarthy ◽  
C. C. Wood ◽  
P. D. Williamson ◽  
D. D. Spencer

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.


NeuroImage ◽  
2017 ◽  
Vol 162 ◽  
pp. 289-296 ◽  
Author(s):  
Martin Tik ◽  
André Hoffmann ◽  
Ronald Sladky ◽  
Livia Tomova ◽  
Allan Hummer ◽  
...  

2002 ◽  
Vol 282 (2) ◽  
pp. G332-G337 ◽  
Author(s):  
Shaheen Hamdy ◽  
John C. Rothwell ◽  
Chris Fraser ◽  
Maxine Power ◽  
David Gow ◽  
...  

To better understand the relationship between cortical plasticity and visceral pain, we developed a pain-induced model of altered esophageal corticobulbar excitability. In eight healthy volunteers, corticoesophageal electromyographic responses were recorded via an intraluminal catheter, following magnetic stimulation of the right sensorimotor cortex using perithreshold intensities. Corticothenar responses were used as control. Responses were assessed both before and for up to 1 h after either painful or nonpainful balloon distension of the esophagus (frequency = 1 Hz, dwell time = 200 ms, duration = 10 min), each being delivered to each subject in random order. Painful esophageal distension (mean volume = 11 ± 3 ml) induced a profound increase in esophageal responses compared with baseline levels (at 30 min: 141 ± 12 vs. 101 ± 9 μV, P < 0.01), whereas nonpainful esophageal distension (mean volume = 4 ± 2 ml) showed a decrease (at 30 min: 72 ± 8 vs. 88 ± 12 μV, P < 0.03). Thenar responses were unaffected. The results show that painful and nonpainful stimuli induce different patterns of esophageal corticobulbar excitability, suggesting a physiological link between cortical plasticity and visceral pain.


2006 ◽  
Vol 186 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Neveen S. Geweely ◽  
Salama A. Ouf ◽  
Mohamed A. Eldesoky ◽  
Amera A. Eladly

1978 ◽  
Vol 235 (6) ◽  
pp. E586 ◽  
Author(s):  
Z Naor ◽  
C P Fawcett ◽  
S M McCann

Anterior pituitary content of cyclic AMP (cAMP) and cyclic GMP (cGMP) has been measured during stimulation of gonadotropin release by luteinizing-hormone-releasing hormone (LHRH) in vitro to gain more information concerning the relationship between the mechanism of action of LHRH and cyclic nucleotides. During the increased gonadotropin release obtained by incubation by hemipituitaries with LHRH (0.25--25 X 10(-9) M) for 180 min, the glands taken from both male and female rats exhibited increased cGMP content, whereas cAMP content rose only in those taken from male rats. The increase in cGMP content was observed after only 2 min in the presence of LHRH (5 X 10(-9) M) and prior to augmented gonadotropin release. The increase in cAMP content in the male glands was detectable only after 60 min of incubation. These results suggest that cGMP might be involved in the mechanism of action of LHRH.


2007 ◽  
Vol 98 (2) ◽  
pp. 878-887 ◽  
Author(s):  
Xiang Yang Chen ◽  
Shreejith Pillai ◽  
Yi Chen ◽  
Yu Wang ◽  
Lu Chen ◽  
...  

Sensorimotor cortex (SMC) modifies spinal cord reflex function throughout life and is essential for operant conditioning of the H-reflex. To further explore this long-term SMC influence over spinal cord function and its possible clinical uses, we assessed the effect of long-term SMC stimulation on the soleus H-reflex. In freely moving rats, the soleus H-reflex was measured 24 h/day for 12 wk. The soleus background EMG and M response associated with H-reflex elicitation were kept stable throughout. SMC stimulation was delivered in a 20-day-on/20-day-off/20-day-on protocol in which a train of biphasic 1-ms pulses at 25 Hz for 1 s was delivered every 10 s for the on-days. The SMC stimulus was automatically adjusted to maintain a constant descending volley. H-reflex size gradually increased during the 20 on-days, stayed high during the 20 off-days, and rose further during the next 20 on-days. In addition, the SMC stimulus needed to maintain a stable descending volley rose steadily over days. It fell during the 20 off-days and rose again when stimulation resumed. These results suggest that SMC stimulation, like H-reflex operant conditioning, induces activity-dependent plasticity in both the brain and the spinal cord and that the plasticity responsible for the H-reflex increase persists longer after the end of SMC stimulation than that underlying the change in the SMC response to stimulation.


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