scholarly journals Activation of the retrotrapezoid nucleus by posterior hypothalamic stimulation

2009 ◽  
Vol 587 (21) ◽  
pp. 5121-5138 ◽  
Author(s):  
Michal G. Fortuna ◽  
Ruth L. Stornetta ◽  
Gavin H. West ◽  
Patrice G. Guyenet
1976 ◽  
Vol 231 (6) ◽  
pp. 1708-1715 ◽  
Author(s):  
RD Bunag ◽  
E Riley ◽  
M Montello

Whether or not pressor responsiveness changes in unanesthetized rats during recurrent sympathetic excitation was determined by recording blood pressure and heart rate continuously while the posterior hypothalamus was stimulated repeatedly with constant currents. Because preliminary tests showed that telestimulation with a radio-controlled stimulator produced erratic responses, awake rats were routinely stimulated in a conventional manner by connecting them through wires to a square-wave stimulator. Although tachycardia was the most common chronotropic effect, bradycardia also occurred, and both responses were occasionally seen in the same rat at different times. Inhibition of chronotropic responses by combined pharmacologic blockage with propranolol and atropine did not affect corresponding pressure responses in normotensive rats. Renal and spontaneously hypertensive rats always had larger pressor responses than normotensive ones, and, in spite of individual variations, responsiveness generally remained unaltered during 3-6 h of repeated hypothalamic stimulation. These results indicate that in awake normotensive or hypertensive rats cardiovascular responses to posterior hypothalamic stimulation continue unabated even when stimulation is repeated for hours.


1975 ◽  
Vol 228 (3) ◽  
pp. 923-927 ◽  
Author(s):  
RL Verrier ◽  
A Calvert ◽  
B Lown

The effect of posterior hypothalamic stimulation on cardiac susceptibility to ventricular fibrillation (VF) was studied in 34 dogs. VF threshold was determined by inducing a sequence of early extrasystoles (R/T pulsing). Hypothalamic stimulation was associated with sinus tachycardia, systemic hypertension, and a 40% reduction in VF threshold. The effects of hypothalamic stimulation on the VF threshold persisted when heart rate acceleration and the pressor response were prevented. Cervical vagotomy and bilateral adrenalectomy were likewise without effect on fibrillation threshold changes. However, the decrease in threshold was abolished by beta-adrenergic blockade. It is concluded that the reduction in VF threshold associated with hypothalamic stimulation derives from the direct action of sympathetic nerves upon the myocardium, rather than from secondary hemodynamic effects.


Neurosurgery ◽  
2003 ◽  
Vol 52 (5) ◽  
pp. 1095-1101
Author(s):  
Angelo Franzini ◽  
Paolo Ferroli ◽  
Massimo Leone ◽  
Giovanni Broggi

Abstract OBJECTIVE To describe the results of deep brain stimulation of the ipsilateral posterior hypothalamus for the treatment of drug-resistant chronic cluster headaches (CHs). A technique for electrode placement is reported. METHODS Because recent functional studies suggested hypothalamic dysfunction as the cause of CH bouts, we explored the therapeutic effectiveness of posterior hypothalamic stimulation for the treatment of CHs. Five patients with intractable chronic CHs were treated with long-term, high-frequency, electrical stimulation of the posterior hypothalamus. Electrodes were stereotactically implanted in the following position: 3 mm behind the midcommissural point, 5 mm below the midcommissural point, and 2 mm lateral to the midline. RESULTS Since this treatment, all five patients continue to be pain-free after 2 to 22 months of follow-up monitoring. Two of the five patients have remained pain-free without any medication, whereas three of the five required low doses of methysergide (two patients) or verapamil (one patient). No adverse side effects of chronic, high-frequency, hypothalamic stimulation have been observed, and we have not encountered any acute complications resulting from the implant procedure. There have been no tolerance phenomena. CONCLUSION These preliminary results indicate a role for posterior hypothalamic stimulation, which was demonstrated to be safe and effective, in the treatment of drug-resistant chronic CHs. These data point to a central pathogenesis for chronic CHs.


1973 ◽  
Vol 3 (5) ◽  
pp. 385-385
Author(s):  
L. G. Paulo ◽  
R. S. McCuskey ◽  
G. D. Fink ◽  
B. L. Roh ◽  
J. W. Fisher

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