Hello and Happy Holidays.  I am a CH suffer for over 30 years however I have been fourtunate to the point my ch would last only 3 to 5 months and then they vanish for 4 to 5 years.  That was past tense it has now been 6 months and the beast is relentless in wanting to stick around this time.  I have been put on every medication known in the Neurolgist list and even some that isn't on the list.  The Holidays sucked this year where the beast didn't want to go and when it did it was back shortly to remind me who was boss just hours later.

Has anyone had or heard about an implant similar to a pacemaker used in CHs  I meet with my neurologist next week and they are talking about using the implant.  It is called a DBS implant?

A couple of journal articles to print out for your doc.


Cephalalgia. 2008 Mar;28(3):285-95.
Hypothalamic deep brain stimulation for cluster headache: experience from a new multicase series.

Bartsch T, Pinsker MO, Rasche D, Kinfe T, Hertel F, Diener HC, Tronnier V, Mehdorn HM, Volkmann J, Deuschl G, Krauss JK.

Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany. t.bartsch@neurologie.uni-kiel.de

Deep brain stimulation (DBS) of the posterior hypothalamus was found to be effective in the treatment of drug-resistant chronic cluster headache. We report the results of a multicentre case series of six patients with chronic cluster headache in whom a DBS in the posterior hypothalamus was performed. Electrodes were implanted stereotactically in the ipsilateral posterior hypothalamus according to published coordinates 2 mm lateral, 3 mm posterior and 5 mm inferior referenced to the mid-AC-PC line. Microelectrode recordings at the target revealed single unit activity with a mean discharge rate of 17 Hz (range 13-35 Hz, n = 4).
OUT OF SIX PATIENTS, FOUR SHOWED A PROFOUND DECREASE OF THEIR ATTACK FREQUENCY AND PAIN INTENSITY ON THE VISUAL ANALOGUE SCALE DURING THE FIRST 6 MONTHS. OF THESE, ONE PATIENT WAS ATTACK FREE FOR 6 MONTHS UNDER NEUROSTIMULATION BEFORE RETURNING TO THE BASELINE WHICH LED TO ABORTION OF THE DBS. TWO PATIENTS HAD EXPERIENCED ONLY A MARGINAL, NON-SIGNIFICANT DECREASE WITHIN THE FIRST WEEKS UNDER NEUROSTIMULATION BEFORE RETURNING TO THEIR FORMER ATTACK FREQUENCY. AFTER A MEAN FOLLOW-UP OF 17 MONTHS, THREE PATIENTS ARE ALMOST COMPLETELY ATTACK FREE, WHEREAS THREE PATIENTS CAN BE CONSIDERED AS TREATMENT FAILURES.
The stimulation was well tolerated and stimulation-related side-effects were not observed on long term. DBS of the posterior inferior hypothalamus is an effective therapeutic option in a subset of patients. Future controlled multicentre trials will need to confirm this open-label experience and should help to better define predictive factors for non-responders.

PMID: 18254897 [PubMed]
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Lancet Neurol. 2006 Oct;5(10):873-877.
Deep brain stimulation in headache.

Leone M.

Department of Neurology and Headache Centre, Istituto Nazionale Neurologico 'Carlo Besta', via Celoria 11, 20133 Milano, Italy.

BACKGROUND: The therapeutic use of deep brain stimulation to relieve intractable pain began in the 1950s. In some patients, stimulation of the periaqueductal grey matter induced headache with migrainous features, indicating a pathophysiological link between neuromodulation of certain brain structures and headache. RECENT DEVELOPMENTS: Neuroimaging studies have revealed specific activation patterns in various primary headaches. In the trigeminal autonomic cephalgias, neuroimaging findings support the hypothesis that activation of posterior hypothalamic neurons have a pivotal role in the pathophysiology and prompted the idea that hypothalamic stimulation might inhibit this activation to improve or eliminate the pain in intractable chronic cluster headache and other trigeminal autonomic cephalgias. Over the past 6 years, hypothalamic implants have been used in various centres in patients with intractable chronic cluster headache. The results are encouraging: most patients achieved stable and notable pain reduction and many became pain free. All deep-brain-electrode implantation procedures carry a small risk of mortality due to intracerebral haemorrhage. Before implantation, all patients must undergo complete preoperative neuroimaging to exclude disorders associated with increased haemorrhagic risk. No substantial changes in hypothalamus-controlled functions have been reported during hypothalamic stimulation. Hypothalamic stimulation may also be beneficial in patients with SUNCT (short-lasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing)-a disorder with close clinical and neuroimaging similarities to the cluster headache. WHERE NEXT?: Neuroimaging findings in patients undergoing posterior hypothalamic stimulation have shown activation of the trigeminal nucleus and ganglion. This evidence supports the hypothesis that hypothalamic stimulation exerts its effect by modulating the activity of the trigeminal nucleus caudalis, which in turn might control the brainstem trigeminofacial reflex-thought to cause cluster headache pain. Future studies might determine whether other areas of the pain matrix are suitable targets for neuromodulation in patients with cluster headache who do not respond to hypothalamic modulation.

PMID: 16987734 [PubMed

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