We report on 83 juvenile patients with idiopathic stabbing headache, subjectively perceived as lasting from a fraction of a second to a few minutes. This sample was selected from among 2543 outpatients referred because of recurrent headache to the Paediatric Neurology Services of Ferrara and Padua (Italy). Other painful syndromes were excluded by clinical examination and appropriate tests. Idiopathic stabbing headache in the pediatric age group, contrary to the adult form, is usually not associated with other primary headache syndromes. We suggest that this clinical picture should be more clearly defined in the future, in order to better understand its relationships with other primary headaches.

An 8-month, double-blind, placebo-controlled cross-over trial was carried out on the use of trazodone in pediatric migraine prophylaxis. It involved 40 patients aged 7 to 18 years old and suffering from migraine without aura, randomly divided into 2 groups. After a 4-week run-in period, Group A received oral trazodone (1 mg/kg a day divided into 3 doses) for 12 weeks, while Group B received a placebo. After a further 4-week washout period, Group A was given the placebo and Group B was treated with trazodone for a further 12 weeks. The trial was completed by 35 patients, the number of drop-outs being comparable in the two groups. During the first treatment period, both the frequency and the duration of the migraine episodes were significantly reduced in both groups. During the second, a significant further improvement in both parameters was only observed in Group B. No side-effects were observed at any time. Our results showed that, like other antidepressants, trazodone is a valid prophylactic agent for juvenile migraine.

Interictal serum levels of serotonin and plasma and mononuclear cell concentrations of beta-endorphin were measured in 20 juvenile patients (13 suffering from migraine without aura and 7 from episodic tension-type headache) before and after 3 months of L-5-hydroxytryptophan treatment (5 mg/kg/day) and compared with a control group of 17 headache-free healthy subjects. While no significant differences in serum serotonin levels emerged between the three groups (migraine 104.6 +/- 26 micrograms/L, tension-type headache 90.7 +/- 26.2 micrograms/L, controls 96 +/- 32.9 micrograms/L), significantly lower plasma and mononuclear cell concentrations of beta-endorphin were found in both patient groups by comparison with the healthy controls (beta-endorphin in plasma: migraine sufferers 16.2 +/- 4.2 pmol/L [P < 0.05], tension-type headache subjects 14.5 +/- 1.7 pmol/L [P < 0.001] vs controls 21.3 +/- 4.6 pmol/L and respectively, beta-endorphin in mononuclear cells: migraine sufferers 110.5 +/- 16.4 pmol/10(6) GB/L [P < 0.001], tension-type headache subjects 142.3 +/- 22.7 pmol/10(6) GB/L [P < 0.001] vs controls 359.3 +/- 31.6 pmol/10(6) GB/L). No differences emerged between the two clinical forms of headache for the plasma and mononuclear cell concentrations of beta-endorphin. After L-5-hydroxytryptophan treatment, serum serotonin and both plasma and mononuclear cell beta-endorphin levels tended to be higher, though not significantly so, than prior to treatment, and the clinical score (frequency x intensity of headache attacks) was significantly lower in both headache groups than at the baseline. This study supports the theory that opiate analgesic system function is abnormally low in juvenile primary headache as in adults, and confirms that administering serotoninergic precursor drugs increases beta-endorphin, even in the peripheral blood, and may favorably affect clinical symptoms.

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