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Our group has previously reported significant changes in the incorporation of precursors into glycerophospholipids, particularly phosphatidylserine, in polymorphonuclear cells obtained from the peripheral blood of cluster headache patients, when compared with controls. The potential of these results led to further work using both the previous methodology and a modified isolation technique to obtain polymorphonuclear cells in as pure a state as possible. Neither the new results obtained using the original technique, nor the results with high purity polymorphonuclear cells from controls and cluster headache patients, confirm the marked changes in precursor uptake into glycerophospholipids originally reported.

A comparison of heat-induced forehead sweating and cutaneous temperature patterns has been carried out in 17 healthy individuals (a total of 54 measurements). Only minor asymmetries in facial sweating and temperature were observed. No significant correlation between sweating and cutaneous temperature was found. The reproducibility of the method was excellent.

Prostaglandins and leukotrienes have been implicated in the pathogenesis of various types of headache, mainly because some, but not all, cyclo-oxygenase inhibitors are effective in their treatment. We have therefore investigated whether a pathologically changed turnover of arachidonic acid (AA)-containing phospholipids can be seen in headache patients, using isolated polymorphonuclear cells (PMNs) from healthy controls and patients with chronic paroxysmal hemicrania (CPH) and cluster headache. PMNs from healthy controls incorporated 55% of the added (1-14C)AA into total lipids, and 0.5% +/- 0.14% of this radioactivity was found in the phosphatidylserine (PS) fraction. PMNs from a cluster headache and a CPH patient showed 300% and 900% increase in PS labeling from AA, respectively. No other phospholipids showed any difference between controls and patients. The results are discussed in connection with membrane signal transduction via the PS-dependent protein kinase C.

The case of a 42-year-old woman with a 31-year history of continuous unilateral, pulsating headache with occasional exacerbations is described. Complete relief was obtained with 150 mg indomethacin daily.

Cluster headache periods (bouts) have, at the lower end of the scale, been supposed to last for periods as short as 1-2 weeks. Patients who usually have bouts of ordinary duration occasionally have brief attacks in the remission phase ("abortive attacks"). The group described here had a temporal pattern, clearly at variance with both these patterns: The six patients had mostly or entirely bouts of less than 1 week's duration. We have termed such short-lasting bouts minibouts, on the supposition that such cases belong within the cluster headache cycle. All the patients were men and had a history of unilateral headache without side shift, and usually the solitary attacks had some autonomic accompaniments, although of a moderate degree. In four cases only mild attacks occurred, whereas in two cases the attacks were rather severe and not consistent with full working ability. The group as such may not be homogeneous. The nosologic status of patients with bouts lasting only 1-2 days is somewhat uncertain. As long as the substrate of cluster headache is not outlined, the lower end of duration of minibouts cannot be accurately identified. The fact that three patients recently have experienced bouts of ordinary length strengthens the view that such cases really belong to the cluster headache cycle.