[Urinary lead and iron levels in a group of workers exposed to the risk of lead poisoning].
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Biomedical subjects
Publications and source records attributed to M Alessandri.
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The proposed non-muscarinic pupillary action of echothiophate iodide (EI) was investigated in humans. In 10 healthy volunteers the variations of the pupillary area, induced by EI eye drops, were evaluated by using an electronic pupillometer. When instilled alone, as well as after homatropine, EI caused pupillary constriction. The reduction of the homatropine-induced mydriasis by EI was not accompanied by any increase in the almost abolished pupillary response to light, thus excluding that an enhancement of the parasympathetic activity contributes to pupillary constriction. These findings suggest a non-muscarinic component in the EI-induced miosis, the nature of which remains to be elucidated.
OBJECTIVE: Following the introduction of guidelines of rational drug use, the pharmacoepidemiology of psychotropic drugs was investigated in a sample of long-stay patients living in a Italian psychiatric hospital. DESIGN: A prospective, longitudinal two-year follow-up study was carried out. Information about sociodemographic and clinical characteristics of the inpatient population, and about medications prescribed, was collected at baseline and after one and two years of follow-up. SETTING: Three wards of the psychiatric hospital of Milan. MAIN OUTCOME MEASURES: Number of patients taking psychotropic drugs, number of patients taking more than one neuroleptic or benzodiazepine, mean neuroleptic dose, psychopathological status according to the Brief Psychiatric Rating Scale (BPRS). RESULTS: 70 patients were recruited and followed for two years. At follow-up a reduction in the number of patients taking neuroleptic drugs was recorded, together with a 50% decrease in the number of patients taking more than one neuroleptic. A reduction in the use of depot formulations was in addition shown. Patients taking benzodiazepines decreased of 50%. According to the BPRS, no psychopatological changes were observed during the study. CONCLUSIONS: These data suggest that education in psychopharmacology may guide towards a more rational use of drugs; longitudinal clinical audits should be implemented to monitor everyday practice.
Studies of regional cerebral blood flow in migraine with aura have shown that the aura phase is associated with hypoperfusion in the cortical area which relates topographically to the clinical symptoms. Thus, the previously hypoperfused area becomes hyperperfused. However, there is no strict association between hyperperfusion and headache. The mode of hypoperfusion propagation recalls the circulatory manifestations of experimental cortical spreading depression. In addition, there are no focal cerebral blood flow abnormalities in migraine without aura. During the headache phase of migraine, dilation of both the large extra- and intracranial arteries takes place. A bulk of biochemical evidence has suggested that the pain in migraine is caused by blood vessels which are dilated and sensitized by circulating pain-producing substances e.g. bradykinin, serotonin and histamine (sterile inflammation). Recently, perivascular trigeminal fibres (trigeminovascular system) which, when stimulated, release sensory peptides (substance P and the calcitonin gene-related peptide) capable of provoking marked vasodilation and plasma extravasation (neurogenic inflammation) have been identified. Thus, the activation of the trigeminovascular system is probably involved in the vasodilatative and nociceptive phenomena of the migraine attack. The finding of a reduced endorphinergic brain tonus in migraine patients supports the hypothesis of a central nociceptive derangement in migraine. Nonetheless, the exact relationship between vasodilation and headache remains to be defined. However, the potent antimigraine effectiveness of sumatriptan--an agonist of the serotonin receptors which selectively constricts dilated arteries during the migraine attack--once again stresses the fact that serotonin is probably the crucial factor in the link between vasodilation and headache.
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