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Biomedical subjects

M Nicolodi

Publications and source records attributed to M Nicolodi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Nostril capsaicin application as a model of trigeminal primary sensory neuronal activation.

Capsaicin was applied unilaterally to the nostril mucosa of 18 episodic cluster headache sufferers in remission. Plasma and saliva levels of substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay. Increase of salivary SP-LI and CGRP-LI as well as of plasma CGRP-LI occurred after capsaicin stimulation. Capsaicin-induced neurochemical changes in saliva and in plasma were compared to the changes observed during cluster headache attacks measured in a separate study. The comparative changes in SP, CGRP and VIP characterizing these two conditions suggest that trigeminal capsaicin-sensitive sensory neurones are unlikely to play any fundamental role in the mechanics of cluster headache.

Administration, Intranasal↗
PubMed1994

Visceral pain threshold is deeply lowered far from the head in migraine.

A short-lasting over-distension of the hand-forearm veins, obtained through a non-invasive original maneuver (Hand Arm Vein Distension test) induces local pain when applied to migraine sufferers in inter-critical period. Conversely, subjects with an absolutely negative personal and family history for any type of idiopathic headache do not report any pain or only an uncertain, slight one. The injection of 1 mL of 2% to 8% (i.e. 0.34 mol/L to 1.36 mol/L) hypertonic saline into the antecubital vein during an extemporary short (1 minute) circulatory blockage (ischemia induced to guarantee a strictly local action of the chemical stimulus) provokes moderate, strong or unbearable local (arm vein) pain in migraine sufferers but not in subjects with a personal and family history absolutely free from any type of headache. These results show for the first time that migraineurs show a proneness to visceral pain in viscera (veins) distant from the head (arm-hand). Such a finding is consistent with the theory that migraine pain is due to a central derangement of the viscerosensory system.

Adult↗
PubMed1993

Possible long-lasting inhibition of converting enzyme by enalapril in human cerebrospinal fluid.

1. Converting enzyme and neutral endopeptidase activities were both measured every 3 h by a fluorimetric method in plasma and cerebrospinal fluid of patients diagnosed as migraineurs with aura after lumbar puncture, which was performed 9 h after an acute oral dose of enalapril or placebo. 2. A reduced converting enzyme activity, as compared with placebo, was observed in patients who were given enalapril. On the other hand, neutral endopeptidase activity detected after enalapril did not differ from that measured after placebo. 3. The results seem to indicate that enalapril penetrates the blood-brain barrier in sufficient amounts to reduce converting enzyme activity. Moreover, neutral endopeptidase was not affected by enalapril. Therefore, those clinical effects of the drug which have been attributed to the involvement of central opioid mechanisms may depend on the inhibition of brain converting enzyme but not the inhibition of brain neutral endopeptidase.

Adult↗
PubMed1993

Hypothalamic modulation of nociception and reproduction in cluster headache. I. Therapeutic trials of leuprolide.

A slow-release gonadotropin-releasing hormone (Gn-RH) analogue was administered to 30 males suffering from chronic cluster headache (CH) in a placebo-controlled study with the aim of enhancing neurotransmission in the pain-suppressing systems of the hypothalamus through a feedback action involving neuroendocrine functions too. A significant improvement in the severity of the pain occurred together with the expected lowering of the libido and serum levels of testosterone and luteinizing hormone. We postulate that the benefit of the Gn-RH analogue relates to an impairment of neuronal modulation in cluster headache.

Adult↗
PubMed1993

Hypothalamic modulation of nociception and reproduction in cluster headache. II. Testosterone-induced increase of sexual activity in males with cluster headache.

Short-lasting chronic testosterone administration did not change the course of cluster headache in seven chronic sufferers, whereas it enhanced sexual excitement in comparison with male control subjects who received the same treatment. We postulate that the sexual excitement induced in cluster headache sufferers by chronic treatment with testosterone relates to an impairment of neuronal modulation in this disorder.

Adult↗
PubMed1993

Phantom tooth diagnosis and an anamnestic focus on headache.

The cause of atypical odontalgia has been related to many factors, including psychological ones. Animal experiments indicate that tooth pulp extirpation provokes a deafferentation, which may or may not induce pain, depending on unknown factors. The research described here showed that human tooth avulsion induces atypical odontalgia when it is carried out in migraine and cluster headache sufferers. Conversely, no sensation is reported by personally and familiarly headache-exempt subjects who underwent the same type of tooth extraction.

Case-Control Studies↗
PubMed1992

Chronic naloxone administration, a potential treatment for migraine, enhances morphine-induced miosis.

The degree and duration of miosis, induced by low doses of parenteral morphine (65 mcg/Kg i.m.) before and after ten days of naloxone treatment, were evaluated in eleven volunteers affected by migraine without aura. Morphine induced miosis was significantly more intense and persistent after chronic naloxone treatment than before the drug was administered. In another group of seven volunteers suffering from migraine without aura, no differences between morphine-induced miosis, prior to and after a ten-day treatment with placebo, were observed. In addition, a third group of fifty-four subjects, suffering from migraine without aura, underwent three-month naloxone treatment (150 mcg/Kg/i.m./day). All subjects included in the third group, were partially or totally refractory to conventional therapy. Pupillopharmacological results indicate that the benefit gained from chronic administration of the opiate antagonist may be related to some type of naloxone-induced supersensitivity of the opioid receptor population.

Adult↗
PubMed1991

Idiopathic headache as a possible risk factor for phantom tooth pain.

Following tooth pulp extirpation, some subjects suffer from persistent pain which affects edentate sites in absence of any local pathology. As regards this peculiar pain, called phantom tooth pain (PTP), what is puzzling is the fact there is a low prevalence of PTP in a very large population showing identical conditions of tooth pulp extirpation. The present investigation indicates that PTP mainly affects migraine (M) and cluster headache (CH) sufferers, whereas it does not affect subjects who have a negative personal and family history for idiopathic headache (IH). These results circumscribe the presence of PTP to a specific section of the population. The present results, besides indicating that PTP may be the result of a peculiar neuronal predisposition relating to IH pathogenesis, suggests some practical therapeutic hints. In fact, successful anti- M and anti-CH prophylactic treatment greatly improve PTP syndrome.

Cluster Headache↗
PubMed1991

Visceral and somatic profiles of needless pain and nonpainful sensations in idiopathic headache.

The syndromes commonly called idiopathic headaches (IH) are the most frequent painful pathologies. The term derives from the fact that the IH necessarily but not exclusively involve the head area. Having abandoned the etiopathogenetic criterion of classification (vascular and tension headaches) which was proposed many years ago, The International IH Society has introduced a phenomenonological/descriptive classification, which is logically sound considering the idiopathy and clinical multiformity of IH. This classification may be useful until it is possible to substitute it with a nosography based on sure etiological data. The distinction between "chronicized" migraine (migraine attacks with daily intercritical headache) and tension-type headaches perhaps represents the greatest diagnostic difficulty, since the two forms require different therapeutic tools even though they have clinical analogies. In our center we are developing a nosological method to differentiate tension-type headaches from chronicized migraines on the basis of a criterion that is theoretically sound because it draws on the anatomofunctional features of these IH, and practical because it is easy to apply. This method is founded on solid algological knowledge. In fact, the IH are simply the most common manifestations of the spontaneous activation of the sensory/pain transmitting afferences, decodified at the level of the integrative areas as "useless" painful and nonpainful sensations of either a visceral or a somatic type, according to the type of IH. The adjective "idiopathic," attributed to the IH, refers to the uselessness of the sensations which dominate these syndromes. They are useless because they are not induced by harmful, environmental, or endogenous stimuli, and do not culminate in a passive or active defensive reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Headache↗
PubMed1991

Links between headache mechanisms and new medications.

A milestone in migraine (M) treatment was the discovery of the dramatic analgesic action of a nonanalgesic drug, ergotamine. The second step consisted in the identification of the prophylactic power of serotonin antagonists, particularly methysergide, in support of the serotonin theory of M. A growing number of drugs has widened the therapeutic resources in this area and at the same time has raised more and more complex and fascinating pathogenetic questions. According to the personal theory, pain in idiopathic headaches (IH) is the clinical expression of an automatism of transmission of painful signals along the neuroaxial sensory pathways. This automatism is in turn linked to a fault in the suprespinal pain modulating systems. This is a similar, but obviously not identical, situation to that of automatic pain transmission in organic deafferentation. As animal experiments have shown, the activation of the afferents may cause the retrograde (antidromic) release of substance P (SP) (and of the neurokinins related to it). This substance is devoid of algogenic capacity but endowed with a high capillary permeabilizing power, with consequent neurogenic edema (NGE) due to plasma overflow. The heavy and lasting edema provoked in both the forearm and the hand by injection of both SP and releasing histamine 48/80 b.w. into the humeral artery, is by no means painful, unlike that induced by injection into the superficial temporal artery (moderate urent pain), probably because of the greater sensitivity of the vascular structures of the head. It may be postulated that the repeated episodes of NGE may lead to a "sterile" phlogosis (neurogenic inflammation) which is capable of increasing and prolonging the pain in the periphery.(ABSTRACT TRUNCATED AT 250 WORDS)

Cluster Headache↗
PubMed1990

Sensory neuropeptides (substance P, calcitonin gene-related peptide) and vasoactive intestinal polypeptide in human saliva: their pattern in migraine and cluster headache.

Substance P, calcitonin gene-related peptide and vasoactive intestinal polypeptide-like immunoreactivities have been evaluated in the saliva of 15 subjects suffering from migraine without aura and 16 control subjects. All three peptides were also measured in the symptomatic/non-symptomatic side saliva sampled from 10 cluster headache sufferers during the cluster period, 5 cluster headache sufferers out of the cluster period, as well as in the right and left side saliva of 18 control subjects. The most interesting result gives a clear difference in common migraine and cluster headache salivary vasoactive intestinal polypeptide-like immunoreactivity contents. In fact, these are enhanced during cluster headache attack and decreased during migraine attack when compared with the interictal period vasoactive intestinal polypeptide-like immunoreactivity levels. Another remarkable finding concerns the significant increase of substance P-like immunoreactivity and calcitonin gene-related peptide-like immunoreactivity levels, from basal values, in the saliva sampled during both migraine and cluster headache attacks. Control subjects showed a calcitonin gene-related peptide-like immunoreactivity and substance P-like immunoreactivity salivary contents significantly higher than migraine sufferers' saliva sampled in basal conditions. Conversely, calcitonin gene-related peptide-like immunoreactivities levels in controls were lower than in cluster headache sufferers' saliva obtained during intervals. Finally, during cluster headache attacks the enhancement of substance P-like immunoreactivity and vasoactive intestinal polypeptide-like immunoreactivity salivary contents interest the non-symptomatic side, whereas the symptomatic side salivary substance P-like immunoreactivity and vasoactive intestinal polypeptide-like immunoreactivity contents remain unchanged. These findings do not allow any final conclusion. However, this biochemical evaluation indicates relevant changes of the salivary neuropeptides in diseases, such as migraine and cluster headache, in which pain transmission is surely involved.

Adult↗
PubMed1990

Substance P theory: a unique focus on the painful and painless phenomena of cluster headache.

These studies of cluster headache (CH) focus on two key features of pain transmission: a) sensory nerves when stimulated, as well as the expected afferent transmission, also display an efferent function which affects capillaries, glands, and smooth muscle (of the iris in CH); substance P (SP) and allied transmitters such as Vasoactive Intestinal Peptide (VIP) and Calcitonin Gene-Related Peptide (CGRP) are the main agonists of this dual afferent-efferent function; b) impaired pain transmission (deafferentation-like condition) provokes a rostral spread of neuronal irritability and automatic firing ("quasi epileptic foci") producing a clinical predilection for pain with the generation of "spontaneous" pains along the sensory pathways. The substrates studied in the present experiments are the iris, salivary glands, and nasal mucosa. 1) Iris: the conjunctival instillation of SP induces isocoric miosis both in CH sufferers and in normals, thus excluding gross SP receptoral dysfunction of the iris muscle in CH. Electrical stimulation of extraocular (infratrochlear) endings of the first branch of the trigeminal nerve provokes a miosis, which is significantly less in the symptomatic eye than in the contralateral one. This miosis is ascribed to a retrograde release of SP, induced by electrical stimulation of the trigeminal ophthalmic branch. The relatively poor miosis in the painful eye could correlate with a deficient release of SP from the sensory terminals in the iris. 2) Salivary glands: an increase of substance P-like immunoreactivity is found in the saliva taken from the asymptomatic side, but not from the painful side during a cluster headache attack, thus showing at this level also an asymmetry as previously shown in other head structures. 3) Nasal mucosa: intranasal application of capsaicin, a powerful releaser of SP from sensory terminals, evokes an immediate burning pain in the ipsilateral nasal, ocular, and temporal areas, as well as lacrimation and rhinorrhea. A gradual decrease (tachyphylaxis) of these phenomena is consistently observed after few days of daily nasal administration of capsaicin. When this treatment is applied to CH patients, a rapid decrease in the number and intensity of attacks, and even disappearance of symptoms accompanies the decline of the capsaicin-induced manifestations. Local (nasal) capsaicin, in spite of evoking immediately the same vegetative (rhinorrhea, lacrimation, conjunctival congestion) and in part nociceptive (transient nasal, ocular, temporal burning) phenomena of CH, never has been able to provoke delayed spontaneous-CH like attacks. Such delayed provoked attacks, one of the most pregnant phenomena in CH investigations, are almost constantly evoked by systemic stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Capsaicin↗
PubMed1989

Cluster headache in the male: sex steroid pattern and gonadotropic response to luteinizing hormone releasing hormone.

Serum testosterone, dihydrotestosterone, delta 4-androstendione and 17 beta-estradiol, sex hormone binding globulin (SHBG) and gonadotropic response to luteinizing hormone releasing hormone (LHRH) were studied in 34 male subjects with episodic or chronic cluster headache (CH). The sex steroid free fractions and those bound to SHBG and albumin were determined by a simulatory computerized method based on the mass action law. Individual steroid values were dispersed over a wide range in CH patients. Total, free and carrier protein-bound testosterone levels were significantly diminished only in chronic CH, where luteinizing hormone (LH) peak values after intravenous administration of LHRH were also decreased. Basal and peak follicle stimulating hormone (FSH) levels were significantly increased in episodic and in chronic CH groups, in comparison to healthy controls.

Adult↗
PubMed1988

Substance P in the human iris: possible involvement in echothiophate-induced miosis in cluster headache.

Substance P-like immunoreactivity (SP-LI) was measured by radioimmunoassay in iris, choroid, and retina obtained from men after death. Although present in different amounts, SP-LI, eluting as authentic SP or SP sulfoxide in the high-performance liquid chromatography system, was found in the three ocular structures. The retina contained higher concentrations of SP-LI than the iris and choroid. The possible functional involvement of iris SP was studied in 22 episodic cluster headache (CH) patients by using the anticholinesterase agent echothiophate iodide (EI), which also induces an atropine-resistant miosis, putatively due to release of SP from trigeminal sensory neurons. In CH patients EI eye drops instilled into both eyes provoked a prolonged miosis with a more marked response in the pupil of the symptomatic eye. It is proposed that the hyperfunction of SP-containing neurons may coexist with the previously documented sympathetic hypofunction in the innervation of the symptomatic pupil of CH.

Adult↗
PubMedDate not supplied

Possible non-muscarinic miotic action of echothiophate iodide in humans.

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.

Adolescent↗