Background Increasing evidence suggests that vasoactive neuropeptides such as pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38), substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide are involved in the pathophysiology of migraine in adults, but their role in pediatric migraineurs remains unclear. We prospectively investigated plasma levels of these vasoactive neuropeptides in pediatric migraine patients without aura and compared the results with those of age-matched healthy controls. Methods Thirty-eight children aged 6–18 years with migraine without aura and 20 age-matched control subjects were included in the study. Neuropeptides in plasma samples from the controls, and in either the ictal or interictal periods in pediatric migraine without aura, were measured using ELISA. Results PACAP-38 and vasoactive intestinal peptide levels in both ictal and interictal plasma were higher in the patients with pediatric migraine without aura than in the controls ( p < 0.001), although calcitonin gene-related peptide and substance P levels remained unchanged. Otherwise, no significant difference was determined between ictal and interictal periods in terms of all neuropeptide levels. Conclusions This study demonstrates increased plasma PACAP-38 and vasoactive intestinal peptide levels, but not calcitonin gene-related peptide and substance P levels, in pediatric patients with migraine during both attack and attack-free periods. The study findings suggest that PACAP-38 and vasoactive intestinal peptide may be implicated in the pathophysiology of migraine, particularly in pediatric migraineurs.

Supraphysiologic amounts of oxygen negatively influences brain maturation and development. The aim of the present study was to evaluate whether maternal ω-3 long-chain polyunsaturated fatty acid (ω-3 FA) supplementation during pregnancy protects the developing brain against hyperoxic injury. Thirty-six rat pups from six different dams were divided into six groups according to the diet modifications and hyperoxia exposure. The groups were: a control group (standard diet+room air), a hyperoxia group (standard diet+80% O₂ exposure), a hyperoxia+high-dose ω-3 FA-supplemented group, a hyperoxia+low-dose ω-3 FA-supplemented group, a room air+low-dose ω-3 FA-supplemented+group, and a room air+high dose ω-3 FA-supplemented group. The ω-3 FA's were supplemented as a mixture of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) from the second day of pregnancy until birth. Rat pups in the hyperoxic groups were exposed to 80% oxygen from birth until postnatal day 5 (P5). At P5, all animals were sacrificed. Neuronal cell death and apoptosis were evaluated by cell count, TUNEL, and active Caspase-3 immunohistochemistry. Histopathological examination showed that maternally ω-3 FA deficient diet and postnatal hyperoxia exposure were associated with significantly lower neuronal counts and significantly higher apoptotic cell death in the selected brain regions. Ω-3 FA treatment significantly diminished apoptosis, in the selected brain regions, in a dose dependent manner. Our results suggest that the maternal ω-3 FA supply may protect the developing brain against hyperoxic injury.

Considering that no specific treatment is available for PVL, maternal ω3 FA supplementation may provide a nutritional strategy to limit periventricular white matter damage caused by infections during pregnancy.

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The purpose of this study was to determine whether children with epilepsy undergoing valproate therapy and who are otherwise healthy have lower levels of serum and muscle carnitine. A total of 50 patients with epilepsy, 3 to 14 years of age, who were treated solely with valproate and free of abnormal neurologic findings or nutritional problems were selected. The control group consisted of 30 healthy children. The total carnitine levels in serum were 28.1 +/- 10.3 and 55.6 +/-7.3 microg/mL, and the free carnitine levels in serum were 16.5 +/-10.2 and 44.6 +/-7.3 microg/mL, the total carnitine levels in muscle were 12.1 +/- 1.8 and 45.3 +/- 5.9 micromol/g noncollagen protein and the free carnitine levels in muscle were 5.6 +/- 1.6 and 39.3 +/- 6.0 micromol/g noncollagen protein in the valproic acid-treated and control groups, respectively (P < .05). In conclusion, valproate monotherapy depletes both muscle and serum carnitine levels in otherwise healthy epileptic children.