Stimulation of the Posterior Hypothalamus for Treatment of Chronic Intractable Cluster Headaches: First Reported Series

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


Neurosurgery ◽  
2018 ◽  
Vol 65 (CN_suppl_1) ◽  
pp. 115-115
Author(s):  
Nilson N. Mendes Neto ◽  
Jessika Thais da Silva Maia ◽  
Juliano Jose da Silva ◽  
Sergio Adrian Fernandes Dantas ◽  
Marcelo Rodrigues Zacarkim ◽  
...  

2020 ◽  
Vol 10 (12) ◽  
pp. 973
Author(s):  
Yousef Hammad ◽  
Allison Mootz ◽  
Kevin Klein ◽  
John R. Zuniga

Background: The trigeminocardiac reflex (TCR) is a brainstem reflex following stimulation of the trigeminal nerve, resulting in bradycardia, asystole and hypotension. It has been described in maxillofacial and craniofacial surgeries. This case series highlights TCR events occurring during sphenopalatine ganglion (SPJ) neurostimulator implantation as part of the Pathway CH-2 clinical trial “Sphenopalatine ganglion Stimulation for Treatment of Chronic Cluster Headache”. Methods: This is a case series discussing sphenopalatine ganglion neurostimulator implantation in the pterygopalatine fossa as treatment for intractable cluster headaches. Eight cases are discussed with three demonstrating TCR events. All cases received remifentanil and desflurane for anesthetic maintenance. Results: Each patient with a TCR event experienced severe bradycardia. In two cases, TCR resolved with removal of the introducer, while the third case’s TCR event resolved with both anticholinergic treatment and surgical stimulation cessation. Conclusion: Each TCR event occurred before stimulation of the fixed introducer device, suggesting the cause for the TCR events was mechanical in origin. Due to heightened concern for further TCR events, all subsequent cases had pre-anesthesia external pacing pads placed. Resolution can occur with cessation of surgical manipulation and/or anticholinergic treatment. Management of TCR events requires communication between surgical teams and anesthesia providers, especially during sphenopalatine ganglion implantation when maxillary nerve stimulation is possible.


1990 ◽  
Vol 259 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
K. W. Barron ◽  
C. M. Heesch

The overall purpose of this study was to examine the effect of sinoaortic baroreceptor denervation (SAD) on the cardiovascular and sympathetic outflow responses to electrical stimulation of the posterior hypothalamus. In anesthetized rats that had undergone SAD 7-10 days before experimentation, electrical stimulation of the posterior hypothalamus elicited greater increases in mean arterial pressure, iliac vascular resistance, mesenteric vascular resistance, and lumbar sympathetic nerve activity than in sham-operated baroreceptor-intact animals. Similarly, the pressor effects of intravenous norepinephrine were also augmented in the baroreceptor-denervated group compared with the baroreceptor-intact group. When posterior hypothalamic and intravenous norepinephrine pressor stimuli, which produced equivalent pressor responses in sham-operated baroreceptor-intact animals, were compared in baroreceptor-denervated animals, the pressor effects of the central hypothalamic stimulus were enhanced to a greater degree than the norepinephrine pressor effects. These data provide evidence that arterial baroreceptor reflexes exert greater buffering of pressor stimuli initiated from the central nervous system compared with pressor responses due to peripheral vascular vasoconstrictor agents.


1993 ◽  
Vol 43 (4) ◽  
pp. 473-483 ◽  
Author(s):  
Kanji MATSUKAWA ◽  
Tetsuaki SHINDO ◽  
Mikiyasu SHIRAI ◽  
Ishio NINOMIYA

2015 ◽  
Vol 43 (10) ◽  
pp. 1298-1306 ◽  
Author(s):  
Dheeraj Pelluru ◽  
Roda Rani Konadhode ◽  
Narayan R. Bhat ◽  
Priyattam J. Shiromani

2010 ◽  
Vol 50 (7) ◽  
pp. 1164-1174 ◽  
Author(s):  
Mehdi Ansarinia ◽  
Ali Rezai ◽  
Stewart J. Tepper ◽  
Charles P. Steiner ◽  
Jenna Stump ◽  
...  

1994 ◽  
Vol 72 (1) ◽  
pp. 89-96 ◽  
Author(s):  
J. A. Thornhill ◽  
I. Halvorson

Experiments were designed to determine in the same animal whether electrical stimulation of the posterior hypothalamus and ventromedial hypothalamic nucleus could specifically evoke shivering and nonshivering (brown adipose tissue) thermogenesis, respectively, in anesthetized, normothermic rats. Urethane-anesthetized, male Long–Evans rats, kept at 37 °C, had colonic (Tc), gastrocnemius muscle (Tm), intrascapular brown adipose tissue (TIBAT), and tail (Tt) temperatures measured via thermistor probes, and electromyogram activity (differential multiunit activity from bipolar recording electrodes within gastrocnemius muscle) recorded, before and after unilateral electrical stimulation (monophasic 0.5-ms pulses of 200 μA at 50 Hz for 30 s) of the posterior hypothalamus and ventromedial hypothalamic nucleus (via stereotaxically implanted concentric stimulating electrodes). Each rat showed shivering (increased electromyogram activity) following posterior hypothalamic stimulation, which caused an immediate rise in Tm values with no change in TIBAT or Tt values. Electrical stimulation of the ventromedial hypothalamic nucleus of the same animals elicited no shivering activity, but significant increases in TIBAT values occurred with no change in Tm or Tt values. Results confirm that stimulation of the posterior and ventromedial hypothalamic nuclei in rodents specifically activates shivering and nonshivering (brown adipose tissue) effector mechanisms, respectively, to raise core temperature.Key words: posterior hypothalamus, shivering thermogenesis, ventromedial hypothalamus, intrascapular brown adipose tissue thermogenesis.


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