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Biomedical subjects

G Lanzi

Publications and source records attributed to G Lanzi.

At least 109 records · Page 6Linked to original sources
PubMed1984

Benign paroxysmal vertigo in childhood: a migraine equivalent.

The two main problems in defining and classifying the syndrome of benign paroxysmal vertigo (BPV) in childhood are the vestibular function pattern and the relationship between BPV and migraine. 13 children suffering from this syndrome were submitted to complete otoneurological examination, including caloric and rotational labyrinthine stimulation with ENG recording, and to headache provocation tests with nitroglycerin, histamine and fenfluramine. Vestibular responses were normal in all except 2 cases which presented signs of central vestibular impairment at the level of the vestibulocerebellar pathways. Headache provocation tests were positive in 9 out of 10 children, and in 4 cases they induced a typical vertiginous attack instead of headache. In addition, several children had a positive family history for migraine, headache was frequently associated with the crisis and other signs of a 'periodic syndrome' (motion sickness, cyclic vomiting, abdominal pain) were present, unrelated to vertiginous attacks. During the follow-up period, some children responded positively to migraine treatment. BPV, like paroxysmal torticollis in infancy and the signs of the periodic syndrome, can be considered a migraine equivalent or a migraine precursor and could be due to the same vascular and/or biochemical mechanisms responsible for the migraine. In children, for anatomical or developmental reasons, these mechanisms could selectively affect parts of the brain stem, including the vestibular nuclei and vestibulocerebellar pathways.

Child↗
PubMed1984

Benign paroxysmal vertigo in childhood. Diagnostic significance of vestibular examination and headache provocation tests.

Sixteen children with benign paroxysmal vertigo (BPV) are presented. The great majority had a family history of migraine, neurological and autonomic signs associated with vertiginous attacks, and headache or other sign of the periodic syndrome (motion sickness, cyclic vomiting, abdominal pain) unrelated to the attacks. Vestibular examination, including bithermal caloric and rotational testing with ENG recording, showed normal or transiently decreased vestibular function. Headache provocation tests with nitroglycerin, histamine and fenfluramine were positive in 9 of the 13 patients examined, and in 4 cases induced a typical vertiginous attack instead of headache. BPV can be considered a migraine precursor or a migraine equivalent, attributable to the same vascular and/or biochemical disturbances responsible for migraine.

Child↗
PubMed1983

Cyclic vomiting and recurrent abdominal pains as migraine or epileptic equivalents.

A retrospective method was used to estimate the incidence of recurring motion-sickness, cyclic vomiting and abdominal pain considered as different manifestations of a so-called periodic syndrome in 100 migraine sufferers, 100 epileptics and 100 control subjects in the pediatric age group. Such recurrent symptoms are significantly more frequent in those suffering from migraine than in the other two groups. Examination of subgroups of patients affected by particular forms of migraine (classical and common) and of epilepsy (generalized seizures, simple partial seizures, complex partial seizures) contributed little new to our understanding of the nature of periodic syndrome. It is concluded that the above symptoms of periodic syndrome should generally be considered as manifestations of a migrainous rather than of an epileptic disorder.

Abdomen↗
PubMed1983

The periodic syndrome in pediatric migraine sufferers.

The present study takes into consideration some of the symptoms comprised in the Periodic Syndrome. These include motion-sickness, cyclic vomiting, recurrent abdominal pains and paroxysmal vertigo. Particular consideration is given to the chronological and long-term aspects of such symptoms. Among 247 migraine sufferers in the pediatric age group, 173 subjects who complained of at least one of these symptoms were chosen. Results of the data show that motion-sickness is the first to manifest itself (mean age of onset 2 years), and has a tendency to continue into the headache period; cyclic vomiting appears in the third year of life, and terminates sooner than the other symptoms. At the mean age of five years abdominal pains start, and at seven, paroxysmal vertigo. Headache is the final symptom in this group. The sequentiality of such disturbances in each subject leads to the assumption that the Periodic Syndrome is the expression of a single disorder which manifests itself polymorphously as a rather precisely timed process.

Abdomen↗
PubMed1983

Psychological aspects of migraine in childhood.

Experimental data indicate that certain unconscious emotions cause modifications of the brain stem neurotransmitters, inducing neurohumoral and vascular changes which underlie the migraine attack in biologically predisposed subjects. The present study investigates, with patient interviews, psychodiagnostic tests (Rorschach, Blacky pictures, Thematic Apperception test, drawings, Wechsler) and parental interviews in 20 pediatric migraine subjects. In 85% of the cases, a condition of repressed anger preceding the attack is seen. In 40% of the subjects, events such as a death in the family, separations, angry quarrels among parents, and scholastic problems, are seen just before onset of the disease. In conclusion, migraine may be considered a psychosomatic disorder, with the phenomenon of pain as a somatic extrinsication of psychological distress.

Adolescent↗
PubMed1981

Stimulation of neutrophil chemotaxis, adhesiveness, phagocytosis, and hexose monophosphate shunt activity by N-(2-mercaptopropionyl)glycine.

The effects of the sulfydryl donor drug N-(2-mercaptopropionyl)-glycine (MPG) on neutrophil chemotaxis, adhesiveness, phagocytosis, and hexose monophosphate shunt activity were investigated in vitro. The drug significantly enhanced all the neutrophil functions tested when used at appropriate concentrations. The results, which are in accord with the well known inhibition of neutrophil function by sulfydryl-blocking agents, suggest the possible therapeutic usefulness of the drug in clinical conditions with defective neutrophil function.

Amino Acids, Sulfur↗
PubMed1981

Cerebrospinal fluid IgG changes in subacute sclerosing panencephalitis in the various stages of the disease and during isoprinosine therapy.

The cerebrospinal fluid (CSF) levels of IgG and the separation of the CSF and serum proteins by isoelectric focusing (IEF) were studied in 5 patients with subacute sclerosing panencephalitis (SSPE). Oligoclonal IgG fractions were found in the CSF of all the patients. The CSF IgG, IgG-Index and IgG SYN values were higher in the patients observed in the earlier than in those seen in the later stages of the disease. 1 of the 3 patients treated with isoprinosine presented a partial clinical remission accompanied by an increase in the parameters of intrathecal IgG synthesis.

Adolescent↗
PubMed1981

Effects of N-(2-mercaptopropionyl) glycine on neutrophil locomotion.

The effects of the sulphydryl group donor N-(2-mercaptopropionyl) glycine on neutrophil locomotion were evaluated in vitro. The drug, when used at a concentration of 10(-3) M was found to stimulate the random migration and chemotaxis of normal neutrophils as a result of an enhanced rate of locomotion. The true chemotactic response was unaffected. N-(2-mercaptopropionyl) glycine appeared to exert its effect on the whole moving cell population.

Amino Acids, Sulfur↗
PubMed1981

Computerized cranial tomography in Wilson disease: report of a case before and after penicillamine therapy.

A patient with Wilson Disease presenting neurologic signs was treated with d-Penicillamine. Computerized cranial tomography (CT) performed before therapy showed symmetrical areas of low density in the region of the basal ganglia, enlargement of ventricles and bilateral increased density of the medial nuclei of the thalamus. This abnormality of the thalamus had not been reported previously in Wilson disease. After two years therapy there was an evident clinical improvement and at the same time a reduction of CT abnormalities. The reports on CT scanning in Wilson disease are reviewed.

Adolescent↗
PubMed1980

Reversal by cimetidine of histamine-induced inhibition of true chemotaxis in neutrophil polymorphonuclears.

The effects of histamine and cimetidine on neutrophil locomotion were studied in vitro in experimental conditions able to dissociate random from truly directional motility. Histamine 10(-4) mol/l inhibited the true chemotactic response. Cimetidine was able to reverse the histamine-induced inhibition of true chemotaxis. Since histamine-induced inhibition of neutrophil chemotaxis may play a role in allergic patients with repeated infections, and since cimetidine has been shown to enhance cell-mediated immunity in vivo, often impaired in such cases, the use of cimetidine is suggested for the prevention of recurrences in these patients.

Chemotaxis, Leukocyte↗
PubMed1980

Effects of ascorbic acid on neutrophil locomotion.

The effects of ascorbic acid on neutrophil locomotion were studied in experimental conditions able to dissociate random from truly directional motility. It was shown that the significant enhancement of chemotaxis achievable with high ascorbic acid concentrations was due to an increase of the true chemotactic response. With lower concentrations of ascorbic acid, chemotactic values were unaffected as the result of an increase in the rate of neutrophil locomotion with a concomitant inhibition of the true chemotactic response. Ascorbic acid appeared to exert its effect on the whole moving cell population.

Ascorbic Acid↗
PubMed1980

Evidence for a reversible functional state of neutrophil chemotactic deactivation.

Neutrophils pretreated with a chemotactic factor become deactivated, that is, unresponsive to a subsequent chemotactic stimulus. A decay of surface esterase activity, an increased adhesiveness, an auto-oxidative damage of the cell structures and microtubule hyperpolymerization have been previously proposed as the cause of the chemotactic deactivation. To further understand the cellular mechanisms involved in this process, we have studied the locomotory behaviour of deactivated neutrophils in an experimental system allowing differentiation among the various types of migratory cellular response to chemotactic factors. Thus, we have found that deactivated neutrophils retain a normal capacity of random locomotion, but entirely lose their true chemotactic responsiveness. Diamide, which disrupts assembled microtubules in concanavalin A-treated cells, was able to completely restore the true chemotactic response of deactivated cells. These observations suggest that neutrophil deactivation is a reversible cellular event dependent on the functional state of the microtubular system.

Cell Movement↗
PubMed1980

Prevention of neutrophil chemotactic deactivation by ascorbic acid.

The locomotion of human neutrophils deactivated by pretreatment with appropriate concentration of chemoattractant was investigated in experimental conditions capable of dissociating random from truly directional motility. It was shown that deactivated neutrophils lose true chemotactic responsiveness, being unaffected by the rate of locomotion. Ascorbic acid, when present in appropriate concentrations during the deactivation step, completely prevented the loss of true chemotactic responsiveness by cells--that is, their chemotactic deactivation.

Ascorbic Acid↗