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Biomedical subjects

F Sicuteri

Publications and source records attributed to F Sicuteri.

At least 73 records · Page 4Linked to original sources
PubMed1985

Substance P mechanism in cluster headache: evaluation in plasma and cerebrospinal fluid.

Substance P (SP), present in sensory afferent neurons, seems to process nociceptive information in the trigeminal system. SP, released from peripheral trigeminal endings, causes typical cluster headache (CH) signs, e.g. vasodilatation, conjunctival and nasal edema and miosis. Opiates and somatostatin (SRIF), both active in relieving CH attack, inhibit SP release from the central and peripheral trigeminal system. In the present study, plasma and cerebrospinal fluid (CSF), SP-like immunoreactivity (SPLI) and enkephalinase activity (EKA), and plasma SRIF-like immunoreactivity (SRIFLI) have been evaluated during spontaneous and histamine induced attacks in the cluster phase. During the histamine provoked attacks, CSF SPLI and plasma SRIFLI and EKA were unchanged, while plasma SPLI decreased significantly. During spontaneously occurring attacks, plasma SRIFLI was found to be unmodified and a significant lowering of SPLI was detected when compared with controls. Moreover, both during and between attacks in the cluster phase, plasma EKA was increased in comparison with the values in controls. It remains to be seen whether variations of plasma SPLI and EKA levels play a role in the CH mechanism.

Adult↗
PubMed1984

Pain relief by somatostatin in attacks of cluster headache.

The pain relieving effect of somatostatin treatment during 72 attacks of cluster headache in 8 male patients was compared to treatment with ergotamine or placebo in a double-blind study. Infusion of somatostatin (25 micrograms/min for 20 min i.v.) reduced the maximal pain intensity and the duration of pain significantly compared to placebo treatment, and to a degree comparable to ergotamine tartrate treatment (250 micrograms i.m.). The results obtained provide new information concerning the possible mechanism of cluster headache attacks and suggest a new therapeutic approach.

Adult↗
PubMed1984

Coexistence of pupillary and heart sympathergic asymmetries in cluster headache.

Ten cluster headache patients and 10 healthy controls were subjected to electrocardiographic and pupillometric procedures in a search for cardiac and pupillary sympathergic asymmetry. Sympathergic stimulation was provoked by hyperventilation and by instilling tyramine into both eyes. In the control group, hyperventilation changed neither the T-wave form and polarity nor the QTc. Tyramine provoked an equal mydriasis on the two sides. In cluster headache sufferers, hyperventilation produced changes in the T-wave form and polarity as well as an increase of the QTc due to a disproportionate shortening of the R-R and Q-T intervals. An unequal mydriasis was noted after tyramine instillation due to less marked response on the symptomatic side. The observed electrocardiographic abnormalities are considered an expression of an asynchronous repolarization attributed to a sympathergic asymmetry. It is postulated that both the cardiac and pupillary sympathetic imbalance associated with cluster headache are central in origin.

Adolescent↗
PubMed1984

Venospastic activity of somatostatin in vivo in man: naloxone reversible tachyphylaxis.

When the dorsal hand vein (DHV) is locally injected with somatostatin (SS) it spasms visibly. These spasms can be measured using the computerized venospasm technique. Acute, complete long-lasting tolerance (tachyphylaxis) develops following 2-4 injections of somatostatin. A revival of sensitivity to SS is induced in the fatigued vein by the local injection of naloxone. This suggests that endogenous opioids could participate partially or totally in SS tachyphylaxis. The analgesic effect displayed by somatostatin on the dramatic pain of the cluster attack is quantitatively similar to that of ergotamine; the therapeutic mechanism of both drugs has until now remained undefined.

Adult↗
PubMed1984

Asymmetric mydriatic response to topical tyramine in cluster headache relatives.

A pupillometric study was performed to evaluate the mydriatic response to tyramine, a noradrenaline releaser. There were three groups of subjects: (a) 10 cluster headache patients, in an asymptomatic period; (b) 20 of their close relatives, exempt from this disease; (c) 10 healthy controls. The tyramine was instilled into both eyes of each subject. The controls displayed an isocoric tyramine-induced mydriasis but the cluster headache sufferers and their relatives showed an anisocoric mydriasis. This anisocoric mydriasis was caused by a deficient mydriatic response on one side, which in the cluster patients corresponded to the symptomatic side. The sympathetic abnormality of the iris may be the expression of a functional asymmetry in the hypothalamus. Central sympathetic asymmetry could thus represent a dysgenetic family predisposition to lateralized headache attacks.

Administration, Topical↗
PubMed1983

Impaired 5-hydroxytryptamine tachyphylaxis in migraine.

Tachyphylaxis (TPX) to the spasmogenic activity of 5HT can be demonstrated in vivo in the superficial hand dorsal veins in man by the computerized venotest. The 5HT-TPX is reverted by previous local naloxone administration. Tachyphylaxis to 5HT is usually absent in the migraineur. The restored 5HT spasmogenic effect by naloxone suggests the possibility of local opioid apparatus participation in TPX to 5HT.

Adolescent↗
PubMed1983

Is acute tolerance to 5-hydroxytryptamine opioid dependent? Its absence in migraine sufferers.

The human dorsal hand vein, exhausted in vivo (tachyphylaxis) by repeated inoculations of 5-hydroxytryptamine, recovers its capacity to contract in response to the 5HT when naloxone (per se ineffective) is inoculated into the same vein. It would seem, therefore, that in the 5HT tachyphylactic mechanism a role could be played by the progressive excitation of a local opioid modulator apparatus (silent in basal condition); naloxone's capacity for neutralizing the vein's fatigue could be indirect evidence of this. This postulation of an opioid role in the tachyphylactic mechanism differs from the conventional thesis, which explains tachyphylaxis as a progressive exhaustion of NA released from the sympathetic neuron by 5HT (see Table 1). Tachyphylaxis is poor, delayed or absent in migraine sufferers; this anomaly is present even in the period between attacks. The anomaly of inverted tachyphylaxis appears amplified during attacks. The loss or inversion of 5HT-tachyphylaxis is constantly observed in heroin addicts during acute abstinence. The fact that the clinical phenomena of acute heroin abstinence are comparable with those of a migraine attack could be a matter for further investigation.

Endorphins↗
PubMed1983

Naloxone reversal of 5-hydroxytryptamine tachyphylaxis in humans.

The dorsal hand vein, a suitable substrate for testing the effects of spasmogenic amines in vivo, exhibits a rapid tachyphylaxis to 5-hydroxytryptamine (5-HT)-induced vasoconstriction in healthy subjects. In the tachyphylactic vein, naloxone promptly restores and sometimes potentiates the sensitivity to 5-HT. The local opioid system could be excited by the 5-HT-induced release of noradrenaline (NA) into the neuromuscular junction, thereby participating in the 5-HT tachyphylaxis. Naloxone, antagonizing this mechanism, restores the 5-HT spasm. Therefore, the 5-HT tachyphylaxis could be due to an increased opioid modulation and not (or perhaps partially) to a depletion of the NA in the sympathergic neuron.

Adult↗
PubMed1983

Substance P and endogenous opioids: how and where they could play a role in cluster headache.

Substance P appears to be involved in the transmission of pain signals from the periphery to the spinal cord and brain stem. Substance P containing neurons are responsible for the neurogenic vasodilation identical to that obtained by substance P release evoked by antidromic stimulation of these fibres. Both endogenous opioids and somatostatin inhibit the release of substance P from central and peripheral endings. Present pharmacological investigations conclude that morphine and somatostatin are as effective as ergotamine in reducing the pain of CH. All three drugs are significantly more active than placebo. Somatostatin and opiates could act by inhibiting the release of substance P.

Adult↗
PubMed1983

Clinical pharmacological aspects of dihydroergotamine timed release: activity on monoamine venospasm.

Using the computerized venotest, it is possible to evaluate both the venospastic activity of the vasoactive monoamines (NA,5-HT, DA) and the effects of the relative agonistic and antagonistic drugs. The ergot-derivatives are 5-HT and NA agonists at low doses, and are 5-HT antagonists at high doses. Dihydroergotamine timed release (DHE-TR) administered orally is capable at 12 hours following the last administration of producing a significant increase of 5-HT and NA venospasm. It is hypothesized that 12 hours after the last administration of DHE-TR, hematic concentrations, corresponding to clinical and therapeutic levels, capable of potentiating the monoamine venospasm still exists.

Adult↗
PubMed1983

Concluding remarks on the Capri symposium: myths, facts and new trends in migraine.

The speculative efforts of the scientists who research the atavistic enigma of the "spontaneous" aches which affect the head, nuc and neck of a great number of people, seem to be driven by the conviction that they are faced with a systemic autonomic illness rather than a local one. Pain is an obligatory phenomenon which dominates this ailment, and is more or less patently paralleled by a constellation of autonomic functions such as nausea, vomiting, vaso-constrictor dilation and arterial hypotension. An analogous vegetative constellation emerges at "cascades", that is, a stereotypical succession, following upon intense physiological (induced) pain. In a migraine attack, the autonomic hyperfunctions are the same in quality but their chronology is completely disrupted: the usual vegetative "cascade" being deeply perverted. In spite of concentric assaults by clinicians, biologists, rhythmologists and psychologists this species of medical sphynx has remained throughout the centuries. The core of the dilemma is in essence the following: are we dealing with a physiological or a pathological pain? The former (physiological pain) should be symptomatic of vascular (migraine) or psychic (muscle contraction headache) disorder; the latter (pathological) should be symptomatic of a malfunctioning of the nociceptor system.

Brain Chemistry↗