Somasosensory evoked potentials and neuraxial blood flow in central nervous system decompression sickness

1984 ◽  
Vol 311 (2) ◽  
pp. 307-315 ◽  
Author(s):  
D.R. Leitch ◽  
J.M. Hallenbeck
1968 ◽  
Vol 29 (1) ◽  
pp. 20-37 ◽  
Author(s):  
Raoul DiPerri ◽  
Anant Dravid ◽  
Arlene Schweigerdt ◽  
Harold E. Himwich

1986 ◽  
Vol 251 (6) ◽  
pp. E644-E647 ◽  
Author(s):  
L. Jansson ◽  
C. Hellerstrom

Earlier experiments with the microsphere technique suggested that a heightened serum glucose concentration consistently leads to an increase in islet blood flow (IBF). Several lines of evidence suggest that this glucose-sensitive control mechanism is located at an extrapancreatic site. The purpose of this study was to define the possible role of the central nervous system in such a mechanism. D-glucose, L-glucose, 3-O-methylglucose, or saline were therefore infused into the carotid artery, each at a dose of 1 mg X kg body wt-1 X min-1 for 3 min, and the pancreatic and islet blood flows were measured. None of these substances affected the systemic serum glucose level. The intracarotid infusion of D-glucose, however, caused a rapid increase in both the serum insulin concentration and IBF. The blood flow to the whole pancreas nevertheless remained unchanged, indicating a redistribution of flow within the gland. Carotid infusion of the other test substances or a similar amount of D-glucose given in a femoral vein did not affect these parameters. Both the increase in serum insulin concentration and the increase in IBF caused by D-glucose could be abolished by vagotomy or administration of atropine. When the systemic blood glucose concentration was increased by intraperitoneal glucose administration (2 g/kg body wt), vagotomy blocked the increase in islet blood flow but not the concomitant insulin release. These observations suggest that the glucose-induced increase in IBF is mediated by vagal cholinergic influences.


1987 ◽  
Vol 61 (5_supplement) ◽  
Author(s):  
A.C. Bonham ◽  
D.D. Gutterman ◽  
J.M. Arthur ◽  
M.L. Marcus ◽  
G.F. Gebhart ◽  
...  

Neurosurgery ◽  
1987 ◽  
Vol 21 (6) ◽  
pp. 843-848 ◽  
Author(s):  
Phillip D. Hylton ◽  
Howard O. Reichman ◽  
Roberta Palutsis

Abstract The early transient postirradiation effects in the central nervous system are well known; however, no specific means of objective follow-up have been devised. The xenon (133Xe) inhalation technique for measurement of regional cerebral blood flow (rCBF) is easily reproducible. Serial rCBF measurements corresponding to the clinical presentation and course of the early postirradiation syndrome have not been previously reported. It is our belief that the global decline in rCBF identified in these patients represents a generalized metabolic derangement induced by whole brain irradiation rather than primary vascular changes. A distinction between tumor recurrence and the early transient postirradiation effects can be made utilizing this technique. It also provides a reproducible monitor of the clinical and metabolic impact of radiotherapy for brain tumors. A series of seven such patients is presented with appropriate case histories and graphic representations of the serial rCBF measurements.


2009 ◽  
Vol 107 (1) ◽  
pp. 112-120 ◽  
Author(s):  
B. W. Hoffman ◽  
T. Oya ◽  
T. J. Carroll ◽  
A. G. Cresswell

Studying the responsiveness of specific central nervous system pathways to electrical or magnetic stimulation can provide important information regarding fatigue processes in the central nervous system. We investigated the changes in corticospinal responsiveness during a sustained submaximal contraction of the triceps surae. Comparisons were made between the size of motor-evoked potentials (MEPs) elicited by motor cortical stimulation and cervicomedullary motor-evoked potentials (CMEPs) elicited by magnetic stimulation of the descending tracts to determine the site of any change in corticospinal responsiveness. Participants maintained an isometric contraction of triceps surae at 30% of maximal voluntary contraction (MVC) for as long as possible on two occasions. Stimulation was applied to the motor cortex or the cervicomedullary junction at 1-min intervals during contraction until task failure. Peripheral nerve stimulation was also applied to evoke maximal M waves (Mmax) and a superimposed twitch. Additionally, MEPs and CMEPs were evoked during brief contractions at 80%, 90%, and 100% of MVC as a nonfatigue control. During the sustained contractions, MEP amplitude increased significantly in soleus (113%) and medial gastrocnemius (108%) muscles and, at task failure, matched MEP amplitude in the prefatigue MVC (∼20–25% Mmax). In contrast, CMEP amplitude increased significantly in medial gastrocnemius (51%), but not in soleus (63%) muscle and, at task failure, was significantly smaller than during prefatigue MVC (5–6% Mmax vs. 11–13% Mmax). The data indicate that cortical processes contribute substantially to the increase in corticospinal responsiveness during sustained submaximal contraction of triceps surae.


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