Despite several reports on symptomatic cluster-like headache, there is no clear explanation of how different lesions thought to be causative are related to cluster-like headache. On the basis of two additional cases of symptomatic cluster headache, we discuss the possibility that an acute imbalance of the autonomic nervous system, namely a net overactivity of the parasympathetic system, may be able to trigger these headache attacks in patients who probably have an additional individual predisposition to react with a cluster-like headache. Such an imbalance can be due to an increase in parasympathetic tone (e.g. stimulation of parasympathetic fibres) or to a reduction of the sympathetic tone (e.g. a lesion of the sympathetic fibres).
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
* A Straube,
* T Freilinger,
* T Rüther &
* C Padovan
*
Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-University Munich, Germany
----------------------------------
A chronobiological study of melatonin, cortisol growth hormone and prolactin secretion in cluster headache
Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.
* Guy Chazot11Unite Neurométabolique, Hôpital Neurologique. 59 boulevard Pinel, 69003 Lyon, France; ,
* Bruno Claustrat22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Jocelyne Brun22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Daniel Jordan33Laboratoire de Médecine Expérimentale, INSERM U. 197-UER, Médecine Alexis Carrel, rue Guillaume Paradin. 69008 Lyon, France; ,
* Geneviève Sassolas44Unite de Soins, Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France,
* Bernard Schott
Cephalalgia
Volume 4 Issue 4 Page 213-220, December 1984
Although migraineurs appear in general to be hypersensitive to external stimuli, they maybe also have increased daytime sleepiness and complain of fatigue. Neurophisiological studies between attacks have shown that for a number of different sensory modalities the migrainous brain is characterised by a lack of habituation of evoked responses. Whether this is due to increased cortical hyperexcitability, possibly due to decreased inhibition, or to an abnormal responsivity of the cortex due a decreased preactivation level remains disputed. Studies using transcranial magnetic stimulation in particular have yielded contradictory results. We will review here the available data on cortical excitability obtained with different methodological approaches in patients over the migraine cycle. We will show that these data congruently indicate that the sensory cortices of migraineurs react excessively to repetitive, but not to single, stimuli and that the controversy above hyper- versus hypo-excitability is merely a semantic misunderstanding. Describing the migrainous brain as ‘hyperresponsive’ would fit most of the available data. Deciphering the precise cellular and molecular underpinnings of this hyperresponsivity remains a challenge for future research. We propose, as a working hypothesis, that a thalamo-cortical dysrhythmia might be the culprit.
Is the cerebral cortex hyperexcitable or hyperresponsive in migraine?
* G Coppola11G.B. Bietti Eye Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, ,
* F Pierelli2,32University of Rome ‘La Sapienza’ Polo Pontino—I.C.O.T., Rome and 3IRCCCS-Neuromed, Pozzilli (IS), Italy, &
* J Schoenen4,5
