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Biomedical subjects

G Patruno

Publications and source records attributed to G Patruno.

4 recordsLinked to original sources
PubMed1992

Dexamethasone suppression test, melatonin and TRH-test in cluster headache.

The origin of Cluster Headache (CH) is still unknown. The periodicty and presence of symptoms due to both sympathetic and parasympathetic activity suggest the involvement of central nervous system structures, particularly the hypothalamus. To investigate hypothalamic involvement in CH, we employed a neuroendocrinological approach. We observed a normal dexamethasone suppression test (DST) in all patients, increased cortisol plasma levels in remission patients at 8.00am before and at the end of the DST, while only in CH patients during cluster period did we find a reduced TSH response to TRH and a reduced night-time melatonin peak. The neuroendocrinological derangements found in CH may be consistent with hypothalamic involvement.

Adult↗
PubMed1990

Neuroendocrine dysfunction in cluster headache.

Current views on cluster headache pathogenesis indicate a primary central nervous system dysfunction, in particular a hypothalamic involvement. To confirm the hypothalamic involvement in cluster headache we evaluated the hypothalamic-pituitary axis responsiveness with the thyrotrophin releasing hormone (TRH) test. A dose of 200 micrograms of TRH was administered i.v. to nine healthy controls, 32 patients with cluster headache during cluster period and 16 in remission period. Delta maximum thyrotrophin (TSH) was significantly lower in patients with cluster headache during cluster period (p less than 0.05 versus healthy controls and cluster headache patients in remission). No difference was observed between healthy controls and cluster headache patients in remission. A monoaminergic dysfunction at the hypothalamic level is hypothesized.

Adult↗
PubMed1990

Is nimodipine useful in migraine prophylaxis? Further considerations.

Nimodipine is one of the most discussed calcium antagonists used in cerebrovascular diseases and, recently, in migraine prophylaxis. Its specificity in preventing cerebral arterial constriction has been invoked to explain nimodipine's efficacy in migraine. The discovery of neuronal receptors specific for dihydropyridines, however, favours a mechanism of action for nimodipine that is not exclusively vascular. This is in accordance with a view of migraine pathogenesis which implicates a primary neuronal event as the basis of the vascular changes observed in migraine patients.

Clinical Trials as Topic↗