Bob Johnson
CH.com Alumnus
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"Only the educated are free." -Epictetus
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Kennett Square, PA (USA)
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There has been research on this approach for several years but no technique has gained wide use because of issues around side effects, cost, etc.
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Brain. 2005 Apr;128(Pt 4):940-7. Epub 2005 Feb 2.
Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action.
Schoenen J, Di Clemente L, Vandenheede M, Fumal A, De Pasqua V, Mouchamps M, Remacle JM, de Noordhout AM.
Headache Research Unit, University Department of Neurology, CHR Citadelle, Bd du XIIeme de Ligne, B-4000 Liege, Belgium. j.schoenen@ulg.ac.be
We enrolled six patients suffering from refractory chronic cluster headache in a pilot trial of neurostimulation of the ipsilateral ventroposterior hypothalamus using the stereotactic coordinates published previously. After the varying durations needed to determine optimal stimulation parameters and a mean follow-up of 14.5 months, the clinical outcome is excellent in three patients (two are pain-free; one has fewer than three attacks per month), but unsatisfactory in one patient, who only has had transient remissions. Mean voltage is 3.28 V, diplopia being the major factor limiting its increase. When the stimulator was switched off in one pain-free patient, attacks resumed after 3 months until it was turned on again. In one patient the implantation procedure had to be interrupted because of a panic attack with autonomic disturbances. Another patient died from an intracerebral haemorrhage that developed along the lead tract several hours after surgery; there were no other vascular changes on post-mortem examination. After 1 month, the hypothalamic stimulation induced resistance against the attack-triggering agent nitroglycerin and tended to increase pain thresholds at extracephalic, but not at cephalic, sites. It had no detectable effect on neurohypophyseal hormones or melatonin excretion. We conclude that hypothalamic stimulation has remarkable efficacy in most, but not all, patients with treatment-resistant chronic cluster headache. Its efficacy is not due to a simple analgesic effect or to hormonal changes. Intracerebral haemorrhage cannot be neglected in the risk evaluation of the procedure. Whether it might be more prevalent than in deep-brain stimulation for movement disorders remains to be determined.
Publication Types:
Evaluation Studies
PMID: 15689358
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Neurol Sci. 2005 May;26 Suppl 2:s138-9.
Deep brain stimulation and cluster headache.
Leone M, Franzini A, Felisati G, Mea E, Curone M, Tullo V, Broggi G, Bussone G.
Headache Centre, C. Besta National Neurological Institute, Via Celoria 11, I-20133, Milan, Italy. leone@istituto-besta.it
In recent years, neuroimaging data have greatly improved the knowledge on trigeminal autonomic cephalalgias' (TACs) central mechanisms. Positron emission tomography studies have shown that the posterior inferior hypothalamic grey matter is activated during cluster headache attacks as well as in short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT). Voxel-based morphometric MRI has also documented alteration in the same area in cluster headache patients. These data suggest that the cluster headache generator is located in this region and leads us to hypothesise that stimulation of this brain area could relieve intractable cluster headache just as deep brain stimulation improves intractable movements disorders. This view received support by the observation that high frequency stimulation of the ipsilateral hypothalamus prevented attacks in an otherwise intractable chronic cluster headache patient previously treated unsuccessfully by surgical procedures to the trigeminal nerve. So far, 16 patients with intractable cronic cluster headache (CCH) and one intractable SUNCT patient have been successfully treated by hypothalamic stimulation. The procedures were well tolerated with no significant adverse events. Hypothalamic DBS is an efficacious and safe procedure to relieve otherwise intractable CCH and SUNCT.
Publication Types:
Review
PMID: 15926012 [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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