The aim of the present study was to examine the ability of pericranial muscle tenderness and the second exteroceptive suppression period to distinguish chronic tension-type headache sufferers, migraine sufferers, and controls in a young adult population utilizing a blind design. The second exteroceptive suppression periods were assessed using the methodology recommended by the European Headache Federation and were scored with an automated computer software program designed in our laboratory to provide reliable, standardized, and precise quantification of exteroceptive suppression periods and eliminate any influence of experimenter bias that may occur with manual scoring. Our sample consisted of 45 subjects diagnosed according to IHS criteria: 25 with chronic tension-type headache and 20 with migraine without aura. Twenty-three headache-free controls were recruited. Consistent with our previous findings, abnormalities in pericranial muscle tenderness, but not in the second exteroceptive suppression period distinguished chronic tension-type headache sufferers from controls. The chronic tension headache sufferers exhibited the highest pericranial muscle tenderness and the control group exhibited the lowest tenderness (P < .001). Pericranial muscle tenderness was quite successful in distinguishing recurrent headache sufferers from controls, but failed to distinguish chronic tension-type headache sufferers from migraineurs. Our findings raise the possibility that pericranial muscle tenderness is present early in the development of chronic tension-type headache and migraine without aura, and thus might contribute to the etiology of headache disorders. Our findings also indicate that a shortened second exteroceptive suppression period is not a reliable marker for chronic tension-type headache in young adults.

The widespread use of the test for basal metabolism which has developed since 1910, when F. G. Benedict introduced his new apparatus, has opened up problems which were not anticipated while investigation was confined to physiologic laboratories. When this test became an adjunct of clinical practice, entirely new fields of research were opened. The test was performed not only on normal persons but on patients, and many conditions were found to influence metabolism.The body surface standards that were used for adult patients gave surprisingly accurate information but were not satisfactory for children. This was appreciated early by many pediatricians, who could not correlate their findings with those of clinical experience; but the worker with adults did not admit that the hard and fast rules applied to mature persons could not be used for children. The difference in point of view can be explained best by the main physiologic difference in the two age groups: Children are in the process of continual change, while persons of middle life are stabilized; the degenerative changes of old age occur only in a relatively small group.The question arose early in my mind as to which standard of metabolism gave the truest picture of what was taking place in the body, since it was found that there Avere groups of children for whom the various standards gave inconsistent results. It was not an uncommon experience to find that use of the body surface standard permitted one interpretation and that of the total calory standard another. How was one to decide whether a metabolism of minus 20 per cent according to one standard represented clinical facts, when use of another standard gave plus 2 per cent? DuBois has drawn attention to this in the third edition of his excellent book.1 Fifteen years ago I commenced to study this problem by comparing the metabolism in all mv cases with all the standards available to me, 1. Dubois, Eugene F.:

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False positive genetic results in these two unrelated cases were attributable to the presence of a rare single nucleotide variant that prevented ligation of the probe in the multiplex ligation-dependent probe analysis kit used and falsely indicated deletion of exon 10 within GCK. Both cases had clinical features that did not tally with the typical GCK-MODY phenotype. These cases emphasize the need to interpret the results of definitive genetic tests within the specific clinical context. Increased medical sequencing is likely to lead to more reports of novel mutations of uncertain significance. If genetic investigations do not agree with the clinical picture, clinicians should exercise caution when making therapeutic changes based on these results.