Higher incidence of dVRs was found in children with headache and epilepsy. No association was found between localization of dVRs and symptomatology of different nervous system diseases except for large dVRs probably due to the pressure on the surrounding tissues.

Parry-Romberg syndrome is characterized by progressive unilateral facial atrophy affecting subcutaneous tissue, cartilage and bone structures. Headache attacks and epilepsy are commonly associated with this syndrome but the underlying pathophysiology is still unknown. A case of a 12-year-old boy with Parry-Romberg syndrome and syringomyelia suffering from severe headache attacks and epileptic seizures is reported herein. Headache attacks were associated with bilateral autonomic symptoms and hyperventilation and were usually followed by complex partial and sometimes by secondary generalized tonic seizures. Detailed neuroimaging examinations were performed (magnetic resonance imaging [MRI] of the head, orbits, and spinal cord, MR angiography, and MR spectroscopy of the cerebellum). The EEG pattern revealed localized discharges contralaterally to the affected side. Antiepileptic treatment with carbamazepine was instituted with minimal effect. Modification of treatment (replacement with oxcarbazepine) was successful. In the reported patient interesting correlation of headache attacks, autonomic symptoms and epileptic seizures was observed. Additionally we believe it is the first report of coincident syringomyelia and Parry-Romberg syndrome.

Increased activity of hypothalamic-pituitary-adrenal (HPA) axis and hypersecretion of corticotropin-releasing hormone (CRH) are known to be important factors in pathogenesis of some stress-related diseases. Some neurosteroids exert anxiolytic and antidepressant effects probably by inhibition of HPA axis activity. The aim of our study was to find out if neurosteroids can directly affect human CRH gene transcription. The effect of allopregnanolone (ALLO), allotetrahydrodeoxycorticosterone (THDOC), pregnenolone (PGL), PGL sulfate (PGL-S), dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEA-S) on CRH expression was determined in differentiated Neuro-2A cells stably transfected with plasmid containing a fragment of human CRH promoter (-663 to + 124 bp) linked to the chloramphenicol acetyltransferase (CAT) reporter gene. It was found that PGL (0.3-30 μM), ALLO (1-30 μM) and THDOC (1-30 μM) present in the culture medium for 5 days in the concentration-dependent manner inhibited CRH-CAT activity. These neurosteroids also inhibited forskolin-stimulated CRH gene transcription with similar potency. In contrast, PGL-S, DHEA and DHEA-S in a concentration from 0.01 to 10 μM had no effect on basal and forskolin-stimulated CRH activity. Further experiments revealed that wortmannin (an inhibitor of phosphatidylinositol 3-kinase; PI3-K) at concentrations of 0.01 and 0.02 μM did not change the inhibitory effect of ALLO (3 μM) and PGL (1 μM) on CRH gene transcription. Moreover, ALLO (3 μM) and PGL (1 μM) present in the culture medium for 5 days did not change the amount of active, phosphorylated form of protein kinase B (PKB, Akt) and extracellular signal-regulated kinase (ERK). The obtained results indicate that PGL, ALLO and THDOC inhibited basal and forskolin-induced CRH gene promoter activity in the differentiated Neuro-2A cells and that these effects did not depend on the activation of PI3-K/Akt and ERK-MAPK pathways.

Posttraumatic headaches usually have tension-type or migraine-like characteristics. A correlation between head trauma and cluster headaches (CH) has been previously reported. CH in children are rare and require thorough differential diagnosis. We present an original case of a 15-year-old boy with cluster headaches associated with allodynia probably evoked by a neck trauma. Severe headache attacks started one month after neck trauma. At the beginning clinical presentation of our patient's headaches was very misleading. Headaches were bilateral and associated with infection. Initial diagnosis of sinusitis was made. During further observation headaches have become unilateral with typical for CH associated symptoms and additionally with allodynia. Other causes of secondary CH like cervicogenic headaches, brain tumor and vascular malformation have been excluded. The boy has undergone prophylactic treatment based on flunarizine and gabapentin with good result. Possible pathogenesis of our patient's headaches has been proposed and diagnostic traps discussed.

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