Publications

Beta-oscillations in the posterior hypothalamus are associated with spontaneous cluster headache attack

authors:

  • Nager, W.
  • ,
  • Münte, T.F.
  • ,
  • Marco-Pallarés, J.
  • ,
  • Heldmann, M.
  • ,
  • Dengler, R.
  • ,
  • Capelle, H.H.
  • ,
  • Lütjens, G.
  • ,
  • Krauss, J.K.
  • (2010)

Without Abstract

Dear Sirs,

The etiology of chronic cluster headache (CH), manifesting as episodes of severe head pain with cranial autonomic features is still unknown, but a central role of the hypothalamus has been discussed recently. For example, during acute CH attacks (but not during migraine) PET revealed activation of the ipsilateral posterior inferior hypothalamus (PIH). In addition, increased grey matter density of the ipsilateral PIH has been found. These findings have prompted the use of deep brain stimulation (DBS) of the ipsilateral PIH in CH, which has been shown to be a promising option in cases refractory to other therapies. Currently available series suggest that the procedure is working in about 50% of operated patients.

While suggestive, the previously described structural and functional changes of the PIH in CH leave open the question as to the neural events that precipitate and mediate spontaneous CH attacks within the hypothalamus. Spontaneous discharge properties of hypothalamic neurons have been characterized by intraoperative microelectrode recordings to be dominated by 25 Hz oscillations outside of active cluster episodes. In addition, a recent report described changes of local field potentials (LFP) recorded from a DBS electrode during an acute attack with a power increase at 20 Hz at the onset of the attack. Here, we extend this observation with data from an additional case. A 52 year old man had suffered from right-sided chronic CH since age 41 and had received prolonged but unsuccessful courses of all standard treatments (including oxygen, sumatriptan, verapamil, corticosteroids). The target in the PIH was defined by CT-stereotactic surgery refined by microelectrode recording. The DBS electrode (Medtronic model 3389) was externalized for several days for test stimulation. Bipolar recordings (1,000 pts/s) between the two contacts with the greatest distance as well as surface EEG activity were obtained. During a recording session (no stimulation) the patient complained about an acute severe right-sided CH episode accompanied by slight ipsilateral ptosis but no conjunctival ingestion. Coinciding with the onset of the attack, the LFP spectrum showed a pronounced peak at 20 Hz. There was no such activity in the scalp recordings (Fig. 1b). Only one attack was observed. DBS led to marked initial clinical improvement (90% decrease of attack frequency) followed by a gradual increase of attack frequency (to ~50% of baseline) at 2 year follow-up.