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Biomedical subjects

E Martignoni

Publications and source records attributed to E Martignoni.

At least 91 records · Page 5Linked to original sources
PubMed1988

Investigation on cerebrospinal fluid opioids and neurotransmitters related to spinal cord stimulation.

The purpose of this study was to assess the biochemical mechanisms underlying spinal cord stimulation (SCS). Seventeen patients with chronic pain were investigated by measuring cerebrospinal fluid concentrations of endogenous opioids and biogenic amines before and during dorsal column stimulation. Basal cerebrospinal fluid beta-endorphin levels were below the normal range. No significant change of norepinephrine, epinephrine, dopamine, beta-endorphin, beta-lipotropin, or adrenocorticotropic hormone levels were found after SCS. A 50% increase of cerebrospinal beta-endorphin and beta-lipotropin levels occurred in 6 out of 16 patients, namely those where SCS gave the major pain relief. These data confirm the derangement of the endogenous opioid system in chronic pain conditions and suggest that the beta-endorphin response to SCS could have clinical value in predicting the success of treatment.

Adult↗
PubMed1988

Aging brain and dementias: changes in central opioids.

We evaluated the CSF levels of beta-lipotropin (beta-LPH), beta-endorphin (beta-EP) and ACTH, which are three neuropeptides expressed by the same gene encoding for pro-opiomelanocortin, in various groups of demented patients including degenerative (presenile and senile Alzheimer-type dementia, ATD) and vascular (MID) forms. Twelve sex- and age-matched subjects were taken as controls. Our data indicate that ACTH levels are significantly reduced both in ATD and MID patients, while beta-EP and beta-LPH are significantly reduced only in ATD. The low CSF ACTH levels can be considered typical of all demented processes (both degenerative and vascular), while the reduction of beta-EP and beta-LPH in CSF could be due to a degenerative process of CNS.

Adrenocorticotropic Hormone↗
PubMed1988

Transient failure of central opioid tonus and premenstrual symptoms.

In order to evaluate the relationships between endogenous opioid activity and premenstrual complaints, we subjected three groups of patients in the mid (days 8-12 prior to menses) and late (days 1-5 prior to menses) luteal phases of the cycle to a naloxone test and some of the patients to a luteinizing-hormone-releasing hormone (LHRH) test. The premenstrual syndrome (PMS) group was composed of nine patients complaining of dizziness, irritability and depression close to menses for at least three years. The menstrually related migraine (MM) group was composed of 15 patients complaining of premenstrually related migraine. The common migraine (CM) group was made up of 16 women suffering from common migraine for years whose attacks occurred independently of menstrual cycle events. A group of seven fertile women served as controls. Every two days the patients filled out the Menstrual Distress Questionnaire for evaluation of their complaints. After the evaluation of spontaneous LH pulsatility for one hour, 4 mg of naloxone was injected as a bolus, and samples were collected every 15 minutes for 2 hours. Both estradiol (E2) and progesterone (P) were measured in basal samples from each naloxone test. LH responsiveness to LHRH was similar in the mid and late luteal phases and did not change between groups. In the mid luteal phase the LH response to naloxone in PMS and MM patients was similar to that in normal subjects, while CM patients had impaired LH secretion. In the premenstrual phase only the controls maintained an LH responsiveness similar to that observed in the mid luteal phase, while both PMS and MM lost the naloxone-induced LH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Premenstrual fall of plasma beta-endorphin in patients with premenstrual syndrome.

Plasma beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and cortisol concentrations were measured by perimenstrual period in 11 patients affected by premenstrual syndrome (PMS) and in 8 asymptomatic healthy volunteers. Blood samples were collected every 2 to 3 days, for 1 month, starting from midcycle. The Menstrual Distress Questionnaire (MDQ) was administered during the testing period. Plasma beta-LPH and cortisol levels remain stable during the perimenstrual period, in both controls and PMS patients. On the contrary, PMS patients showed a decrease of plasma beta-EP in the week preceding menses and during the first days of menstrual flow. Beta-EP values of PMS patients regain normal levels during the next follicular phase. No changes of beta-EP levels were recorded in asymptomatic women. MDQ scores revealed that PMS patients complained of water retention, pain discomfort, and mood swings. The transient and reversible decrease of plasma beta-EP in PMS patients near to and at menses remains to be clarified.

Adult↗
PubMed1987

Ritanserin, a serotonin-S2 receptor antagonist, does not prevent 5-hydroxytryptophan-induced beta-EP, beta-LPH and cortisol secretion.

Ritanserin, a new serotonin antagonist selective upon S2 receptor subclass is available. Thus, in order to better define the positive control of serotoninergic pathway on proopiomelanocortin (POMC)-related peptide release, a group of 7 healthy male volunteers has been submitted to a 5-hydroxytryptophane (5-OH-TP) test (200 mg p.o.) before and after 4 days Ritanserin pretreatment. Plasma beta-endorphin (beta-EP), beta-lipotropin (beta-LPH) and cortisol levels were measured hourly for 4 h after each 5-OH-TP loading. Hormonal levels were measured by specific RIAs on extracted (cortisol) and chromatographed (beta-EP and beta-LPH) plasma samples. Basal plasma concentrations of the three hormones were unchanged by Ritanserin pretreatment. Similarly, the integrated areas of beta-LPH, beta-EP and cortisol release in response to 5-OH-TP remained unaffected by the receptor blockade. These data confirm that serotonin-acting drugs are able to stimulate POMC-related peptide release and indicate that such interaction is not mediated through S2 receptor subclass.

5-Hydroxytryptophan↗
PubMed1987

Postprandial and orthostatic hypotension in Parkinson's disease.

In this study, the 24-hour pattern of blood pressure (BP), heart rate, and urinary catecholamine (CA) excretion and the response of BP and plasma CA to the tilt test have been investigated in 13 untreated patients affected by Parkinson's disease (PD) and in 11 age-matched healthy controls. Seven of the 13 PD subjects showed a fall of supine systolic BP greater than that in controls (ie, exceeding 20% of the preprandial value). A significant relationship was found in the PD group between the degree of postprandial hypotension and the 24-hour mean value of dopamine excretion. Eight PD subjects also showed orthostatic hypotension during the tilt test (performed in the morning hours) and in the postprandial phase. Basal norepinephrine plasma levels of PD patients, as well as their percentage increases on standing, were within the range of the controls. These data suggest the existence of a subtype of PD patient, characterized by a widespread impairment of cardiovascular responsiveness and bordering on syndromes of autonomic failure such as progressive autonomic failure or multiple system atrophy, or both.

Aged↗
PubMed1986

Abnormal dexamethasone suppression test in daily chronic headache sufferers.

The dexamethasone suppression test (DST) was administered in 48 daily chronic headache (DCH) sufferers, 37 of whom also suffered from mild to severe depression. In 14 of 48 subjects (29.2%), cortisol values at 1600h were greater than 50 ng/ml, despite normal suppression at 0800h. The escapers showed basal cortisol values and (Depression scale) scores on the Minnesota Multiphasic Personality Inventory higher than suppressors. Thus, a group of DCH sufferers appeared to share a biochemical defect often seen in endogenous depression. The escape from dexamethasone suppression could be a psychobiological indicator of vulnerability to develop depressive disorder and/or chronic pain complaints.

Adult↗
PubMed1986

Changes in the dopaminergic control of prolactin secretion and in ovarian steroids in migraine.

Prolactin (PRL) responses to dopamine (DA) blockers and to direct and indirect DA agonists have been studied in 23 healthy women, 17 women with catamenial migraine and 17 with non-catamenial migraine in both their follicular and luteal phases. PRL responses to the DA blockers were greater in the follicular phase of both migraine groups than in controls. The inhibitory effect of nomifensine on PRL secretion was dampened in the follicular phase of both migraine groups. These findings demonstrate an increased PRL reserve in migraine and suggest the existence of a dopaminergic supersensitivity of the lactotrophic postsynaptic DA receptors. The impaired inhibitory effect of nomifensine on PRL secretion hints at a decrease of the presynaptic DA content in tuberoinfundibular DA neurons. In migrainous women 17-beta-oestradiol levels are higher in both ovarian phases, whereas progesterone concentrations and the progesterone to oestradiol ratio are lower than in healthy subjects in the luteal phase. These data suggest the existence of a change in the oestrogen-dependent modulation of pituitary DA receptors.

Adult↗
PubMed1986

(-)Deprenyl in Parkinson's disease: a two-year study in the different evolutive stages.

Seventy-nine patients with idiopathic Parkinson's disease in various phases of evolution of the clinical picture were studied. All the patients, already under treatment with L-dopa + PDI, were treated with (-)deprenyl at the dose of 10 mg/day orally in two daily administrations. The mean follow-up was 8.7 months (range, 1-29). Overall, 47.6% of the patients improved, 27.4% showed a marked improvement, 38.1% showed evident modifications, and 27.4% worsened. Sixteen patients were excluded from the study for various reasons. In 53.2% of the cases it was possible to reduce the daily L-dopa dose by a mean of 30%. Overall, (-)deprenyl was effective in the treatment of our parkinsonian patients in the various conditions evaluated, and thus constitutes a new therapeutic strategy for Parkinson's disease.

Adult↗
PubMed1986

Autonomic disorders in idiopathic parkinsonism.

Clinical evidences and experimental data on various signs and symptoms of autonomic dysfunction in idiopathic parkinsonism are reported and their characteristics related to the effects of the drugs usually administered for the therapy of the extrapyramidal symptoms. The use of instrumental diagnostic criteria may sometimes help to detect alterations of autonomic functions (micturition disturbances, disorders of pupil reactivity, orthostatic and postprandial hypotension, temperature dysregulation), otherwise not easily identifiable. The existence of a large involvement of autonomic structures both at central and peripheral levels underlines the concept of Parkinson's disease being part of a wide spectrum of degenerative disorders where multiple nervous structures are at risk.

Antiparkinson Agents↗
PubMed1985

CSF beta-EP in headache and depression.

Cerebrospinal fluid (CSF) levels of beta-endorphin (beta-EP) were measured in 9 migraineurs with interparoxysmal headache (MIH), in 13 patients with major depression in an active phase (5 suffered from MIH), and in 16 age-matched controls. beta-EP was measured by specific RIA after gel-chromatography. While beta-EP levels of depressed patients (58.5 +/- 21.0 fmol/ml, M +/- SD) were similar to those of controls (65.8 +/- 26.6), those of migraineurs (15.0 +/- 11.1) were significantly reduced (p less than 0.01). In depressed patients also suffering from MIH, beta-EP concentrations (22.8 +/- 7.2, p less than 0.05) were half those reported in depressed patients without pain problems. The reduced CSF beta-EP levels in patients whose headache and depression coexist support the notion that this neuropeptide is concerned with chronic pain, independently of the affective state.

Adult↗