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1. 1. The anticonvulsive efficacy of flumazenil 10 mg/kg i.V., a BDZ antagonist, was studied in two models of experimental epilepsy electrically induced. 2. 2. The EEG after-discharge, which was induced by the electrical stimulation of selected brain regions [(notably the dorsal hippocampus (Hip) and the amygdala (CAm)] was evaluated in rabbits pre- and post-drug administration. 3. 3. In the animals submitted to electrical stimulation of the amygdala, flumazenil exerted a protective action, thereby inducing an increase in the after-discharge threshold and/or a decrease in after-discharge duration. 4. 4. In the animals submitted to electrical stimulation of the hippocampus, flumazenil did not induced changes statistically significant. 5. 5. Finally, the paper discusses the two possible mechanisms of action of flumazenil (a “per se” partial BDZ activity and/or a BDZ agonistic activity, which displaces the inverse agonist-like ligand) and the differencies in GABA distribution in the hippocampus and the amygdala.

A photochemical method using the Rose Bengal dye as thrombogenic agent was employed to induce focal cerebral ischemia in frontoparietal cortex of rats. A transcerebral microdialysis probe was used to collect samples from ischemic cortical area. An increase in glutamate (6-fold) and in taurine (4-fold) within the first hour occurred. Neuropathological investigations demonstrate a reproducible damaged area surrounded by a thin peripheral area showing neuronal apoptotic phenomena. The method represents a reproducible model of focal cerebral ischemia with neuropathological aspects superimposable to those characteristic of thrombogenic stroke in man. This method could also be relevant in the study of neurotransmitters during the evolution of ischemia. Furthermore, the presence of apoptotic phenomena in the perilesional halo confirms an ischemic penumbra suggesting the significance of preclinical pharmacological trials.

We examined 8 cases of familial ALS (amyotrophic lateral sclerosis) in three different families from our province, admitted to our hospital between 1970 and 1989. Clinical criteria for diagnosis were satisfied in all cases; EMG was performed in 6 out of 8 patients. 4 cases showed classical onset and 4 cases bulbar onset. The average age at onset was 65.7 + 10.6 years. The average survival was 19.1 + 9.2 months. In two families two generations were affected, in the other only one. The mode of transmission was found to be autosomal dominant with variable penetrance. Neither environmental nor toxic factors seemed to be involved in the development of the illness. Genetic investigations may help to elucidate the pathogenesis of familial ALS.

Ethanol is known to alter central neurotransmission and endocrine functions. Urine melatonin was studied in 10 male chronic alcoholic patients, before and after two weeks of controlled alcohol abstinence, and in sex and age matched healthy controls. In both groups, 24-hour urines were collected in two fractions corresponding to day- (D) (08:00-20:00) and night- (N) (20:00-08:00) time. Urine melatonin was assayed by RIA after methylene chloride extraction. Twenty-four hour urine melatonin levels were calculated adding up D and N values. In patients during alcohol intake, the 24-hour urine melatonin levels were significantly higher than in controls (p = 0.004, Student's t test). A disruption of the physiological ratio between N and D values was also observed, since the higher melatonin levels occurred in the D fraction. In drinking alcoholics, melatonin D values were significantly higher than the D values found in controls (p less than 0.01, Student's t test) and in the same patients after alcohol withdrawal (p less than 0.05). The N/D ratio approximated 1 during alcohol intake and became larger than 1 after alcohol withdrawal, as in the controls. The melatonin data were correlated with the suppressive effects of dexamethasone (DXT) on cortisol secretion evaluated both during alcohol intake and during abstinence. After alcohol withdrawal, the two (out of 10) patients, who remained unresponsive to the DXT suppression test, showed high D melatonin values and a low N/D ratio. These preliminary data indicate that in chronic alcoholism the pattern of urinary "melatonin- like immunoreactivity" is altered.

Within the framework of a research carried out at the Neurological Institute of Pavia on experimental cerebral ischemia some biohumoral determinations were done on two groups of rabbits: one kept on a standard diet and the other on an atherogenic diet to induce dyslipemia. The aim was to find out whether induced ischemia produces an activation of the hemocoagulation processes and whether hyperdyslipemia constitutes an aggravating factor. In the animals on a standard diet there was a statistically significant increase in factor X A and a nonsignificant increase in parameter (r + k) on TEG (thromboelastogram) and of factor VIII C after embolization. In the hyperdyslipemic group the changes were definitely more marked and, in the case of factor VIII C and parameter (r + k), statistically significant, accompanied by slight variations in APTT and factor IX pointing in the same direction. We discuss the meaning of our findings.

1. The interactions between selective D1 and D2 antagonists (SCH 23390 and raclopride) and methamphetamine on EEG arousal and behaviour was studied in rabbits. Haloperidol, a “classic neuroleptic” was used as reference drug. 2. Both 23390 and raclopride, which were used at low dosage (0.03–0.09 mg/kg iv for the former and 1–3 mg/kg for the latter), were able to block completely the behaviour induced but do not inhibit completely the EEG arousal pattern induced by methamphetamine. 3. The blockade of both behaviour and EEG arousal took only when the two drugs were administered concomitantly at the lower dosage. 4. The antagonistic effects obtained with the concomitantly administration of the two drugs were of higher degree in confront of those obtained with the pretreatment with haloperidol 0.3 mg/kg iv. 5. Our data indicate that both D1 and D2 antagonists are able to block, at the dosage used, motor hyperactivity and stereotyped behaviour typically induced by methamphetamine and that SCH 23390 and raclopride are potentiated also in this experimental model.

Fifty-nine depressed female inpatients were treated with 100 mg amitriptyline (AMT) IM for 4 weeks. Depression ratings and determinations of the parent drug and nortriptyline (NT) were performed weekly. No direct relationship between plasma AMT + NT concentrations and therapeutic response was apparent, but beneficial therapeutic responses and significantly lower side-effect scores were more frequently noted in subjects with concentrations in the 100-200 ng/ml range. AMT + NT concentrations were significantly correlated with age. No significant difference was found in the number of responders between younger and older subjects with two clinical improvement criteria; however, a significant difference emerged when a third more restrictive clinical outcome criterion was adopted. The implications of the present findings for patient treatment and for the interpretation of previous studies are discussed. The data collected point to a possible usefulness of monitoring AMT and NT plasma levels, even if further investigations are needed.

Migraine is a common and disabling neurological disease of unknown origin characterized by a remarkable clinical variability. It shows strong familial aggregation, suggesting that genetic factors are involved in its pathogenesis. Different approaches have been used to elucidate this hereditary component, but a unique transmission model and causative gene(s) have not yet been identified. We report clinical and molecular data from a large Italian pedigree in which migraine without aura (MO) segregates as an autosomal dominant trait. After exclusion of any association between MO and the known familial hemiplegic migraine and migraine with aura loci, we performed a genomewide linkage analysis using 482 polymorphic microsatellite markers. We obtained significant evidence of linkage between the MO phenotype and the marker D14S978 on 14q22.1 (maximum two-point LOD score of 3.70, at a recombination fraction of 0.01). Multipoint parametric analysis (maximum LOD score of 5.25 between markers D14S976 and D14S978) and haplotype construction showed strong evidence of linkage in a region of 10 cM flanked by markers D14S1027 and D14S980 on chromosome 14q21.2-q22.3. These results indicate the first evidence of a genetic locus associated with MO on chromosome 14.

The non-invasive technique of transcranial magnetic stimulation (TMS) was used in 62 chronic alcoholics to assess the functional status of descending motor pathways. The main aims of this study were: to investigate asymptomatic upper motor neuron dysfunction in alcoholics as well as to assess its relationship with parameters reflecting the intensity of exposure to alcohol; and to evaluate a possible relationship between central motor conduction time (CMCT) prolongation and neuropsychological measures of alcohol-related brain damage. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of CMCT (23 out of 62 subjects). No significant correlation was found between CMCT prolongation and intensity and duration of abuse, presence of peripheral neuropathy, or brain atrophy on CT scans. Prolongation of CMCT from the upper limb correlated significantly with impairment of frontal skills on neuropsychological testing (p0.01). These findings suggest that TMS may be a sensitive method for the detection in alcoholics of subtle neurological dysfunction, not confined to motor pathways.

The role of alcohol consumption on pathophysiology of atherosclerosis is not completely well established. Past studies were conducted with different methodological approaches, sometimes leading to opposing conclusions. The aim of this study was to determine the weight of alcohol intake on carotid atherosclerosis in a group of subjects asymptomatic for cardio-cerebrovascular diseases. They were examined by ultrasonographic assessment during the period 1993 through 1997. Common risk factors of atherosclerosis and drinking habit were assessed by a standardized questionnaire. In this survey we confirm the J-shaped relationship between atherosclerosis and alcohol consumption. The effect of alcohol intake is more evident if we consider the presence of multiple internal carotid stenosis, or those greater than 25%, as outcome variables. These effects are independent from the other risk factors included in logistic regression paradigms (age, arterial hypertension, dyslipidemia, diabetes mellitus, family history of cardio-cerebrovascular disease, smoking and social status). Our study supported that a high level of alcohol intake plays a role as an independent factor in carotid atherogenesis.

1. 1. Aim of the work was to verify the following three hypotheses in alcoholics: a) right hemisphere; b) diffuse brain deficit; c) anterior brain deficit, by means of a neuropsychological and a neuroradiological assessment. 2. 2. 15 alcoholic right-hand male subjects and 15 matched controls were enrolled in the study. 3. 3. Specifically designed neuropsychological testing was performed to investigate logical abilities, selective attention and memory. 4. 4. Neurological investigation was performed by a standard CT scan to assess the degree and localization of brain damage. 5. 5. Alcoholics performed worse than controls on some neuropsychological Tests I.e. Attention Matrices Test, Verbal Judgement Test, Forward Digit Span, Story Recall and Remote Memory Test. The analysis of variance adjusted by the attentional score showed no significant differences between alcoholics and controls. 6. 6. Neuroradiological data showed a preminnent and a more frequent atrophy of the frontal region. 7. 7. No correlations emerged between neuropsychological and neuroradiological data. 8. 8. In conclusion, the hypothesis of anterior brain deficit seems to be confirmed by our study.

Various neurological disorders have been related to Streptococcus pyogenes infection. Only recently, and for the first time, it has been suggested that acute disseminated encephalitis may also complicate a streptococcal infection. The case reported in this paper seems to confirm this hypothesis.

1. The differential role played by blockade of D-1 or D-2 dopamine receptors in mechanisms underlying seizures was studied in a model of EEG after-discharge induced by electrical stimulation of selective brain regions (dorsal hippocampus and amygdala) in the rabbit. 2. The D-2 antagonist haloperidol (1 mg/Kg) increased significantly after-discharge duration after stimulation of either hippocampus or amygdala and lowered after-discharge threshold in few animals. 3. The D-1 antagonist SCH 23390 (0.3 mg/Kg) caused no changes following stimulation of amygdala and reduced after-discharge duration when hippocampus was stimulated. 4. Haloperidol exerted a proconvulsant action in this experimental model, having a clearer influence on D-2 receptors. SCH 23390 had no effect on amygdala whereas it exerted protection on the hippocampus. 5. The present data suggest that D-1 and D-2 receptors have different roles in generating and spreading the epileptic activity.

A controversial entity, Eagle's syndrome, is reviewed. After an anatomical description of the maxillo-vertebro-pharyngeal region we summarize the causative, diagnostic and therapeutic aspects of the syndrome. Two different conditions are often reported as Eagle's syndrome: one characterized by dysphagia and unilateral pharyngeal pain radiating to the ear and worsened by swallowing; the other characterized by pain in the head and neck region due to compression of the neurovascular structure by an elongated styloid process. The latter also includes typical cranial neuralgias (such as glossopharyngeal neuralgia) and carotidynia. We believe that the term “Eagle's syndrome” is legitimate only in the first case and in those “atypical” painful head and neck conditions related to an elongated styloid process and relieved by styloidectomy. We believe Eagle's syndrome deserves consideration in the International Headache Classification.

Repeated and excessive consumption of alcohol leads to pathophysiological disorders in skeletal muscles. A successful management of this syndrome requires a strict abstinence and a nutritionally adequate diet. We propose here a simple and noninvasive investigation using 31 P magnetic resonance spectroscopy (MRS) to monitor the recovery of the basal energy status of eminence thenar muscles from documented chronic alcoholic patients during a controlled 15-day period of abstinence. Cessation of alcohol abuse induced a significant recovery of the PCr(PCr + Pi) ratio otherwise depressed before the abstinence. On the contrary, the relative level of free inorganic phosphate decreased, whereas intracellular pH was not affected. These results demonstrate (a) the rapid improvement of basal muscular energy metabolism during abstinence for patients with a chronic and heavy alcohol consumption, and (b) the feasibility of a follow-up of this recovery by serial examinations using 31 P MRS.

Bo Paola, Enrico Marchioni, Debora Soragna, Rosanna Murelli and Faustino Savoldi:Eegraphic and Behavioural Effects of Ondansetron, a 5HT3 Antagonist, in Rabbits.Proq. Neuro-Psychopharmacol. & Biol. Psychiatr. 1993,17(5): 801–823. 1. 1. EEGraphic and bahavioural effects of ondansetron , a 5HT3 antagonist, have been studied in the rabbit. Subsequently we tested the neurophysiological and behavioural interactions between ondansetron and L-5-HTP induced serotonergic syndrome. 2. 2. The drug produced a dose-dependent (0.001 0.01 0.1 mg/kg i.v.) increase in the cortical power density spectrum, particularly in the range of the lowest frequencies bands. This effect is expression of cortical synchronization. 3. 3. The lowest and mild dose, but not the highest, failed to produce behavioural sedation and to inhibit the arousal induced by vibroacustical stimulation. 4. 4. L-5-HTP (10 mg/kg i.v.) administration generated a typical EEGraphic-behavioural pattern characterized by a decrease of cortical power spectrum density and stereotyped movements. The EEGraphic effects were significantly suppressed by administration of mild and higher doses of ondansetron, while the behavioural effects were inhibited by all doses tested. 5. 5. It is concluded that ondansetron acts with considerably efficacy on central nervous system. The administration of low and mild doses shows a singular dissociation between EEGraphic and behavioural actions. The inhibition of the L-5-HTP behavioural syndrome by ondansetron suggests that this drug acts on behaviour only when there is an alterated physiological pattern.

We assessed cognitive performance and its relationship with clinical and anatomic disease severity in MS with mild to moderate handicap; 34 definite MS and 18 healthy subjects matched for age and education were submitted to a neuropsychological test battery. Both groups were examined for anxiety. MS patients underwent magnetic resonance imaging examination. MS performed worse than controls on all WAIS-P subtests and had learning, short- and long-term verbal memory impairment. Cognitive deficits were not related to abnormal emotional states, but were found to be associated with attentional process and information-processing speed impairment. Cognitive impairment did not correlate with severity of physical disability. The most severe memory deficits were found in patients with extensive periventricular damage.

The neuroleptics SCH 23390 and raclopride, which interact selectively with either D-1 or D-2 dopamine receptor, were studied for their effects on electroencephalographic (EEG) activity in the rabbit. Haloperidol (0.3 and 1 mg/kg intravenously, i.v.), which was used for comparison, induced synchronization of the cortical EEG activity. Spectral EEG analysis showed increase of power in the whole frequency range (0.1–38.5 Hz) and in all frequency bands in the cortex, whereas a slight decrease of slow and fast theta activity (3.7—7.2 and 7.2–12.2 Hz) was observed in the hippocampus. Animals appeared sedated and arousal response to somatosensory stimuli was markedly inhibited. SCH 23390 (0.03 and 0.3 mg/kg i.v.) induced periods of cortical synchronization and changes of spectral power qualitatively similar to those accompanying haloperidol administration. The drug slightly reduced the duration of arousal elicited by stimuli. Raclopride (1 and 3 mg/kg i.v.) induced weak EEG changes and little effect on arousal response to stimulation. There was an increase of slow wave activity which was particularly evident in the hippocampus. The data indicate that, although to a lesser degree, the D-1 receptor antagonist SCH 23390 induced EEG effects similar to those of haloperidol, whereas blockade of D-2 receptors by raclopride resulted in different patterns of EEG activity.

The antipsychotic remoxipride, a selective dopamine D-2 receptor antagonist, was studied for its effects on sleep-waking patterns in the rat and electroencephalographic (EEG) activity in the rabbit. Haloperidol, which has lesser selectivity for D-2 receptors, was used for comparison. In the rat, remoxipride (1-10 mg/kg SC) did not affect either total sleep or non-rapid eye movement (non-REM) sleep. Only REM was slightly reduced by the high dose of 10 mg/kg. Haloperidol (0.1-1 mg/kg PO) enhanced duration of both total sleep and non-REM sleep. In the rabbit, remoxipride (3 and 10 mg/kg IV) induced no significant changes of the EEG power spectrum over 0.1-38.5 Hz or individual frequency bands. In both cortex and hippocampus the drug did not alter the arousal response to acoustic sensory stimuli. Plasma concentration of remoxipride 10 mg/kg IV in rabbits declined biexponentially and was 4 and 2 mumol/l at 30 min and 1 h, respectively. Haloperidol (0.3 and 1 mg/kg) slowed down the EEG activity, enhanced the power spectrum of the cortical and hippocampal activity, and significantly reduced the duration of arousal induced by sensory stimuli. The results indicate that, unlike haloperidol, remoxipride has weak or no sedative effects. The data also provide support to the notion that D-2 receptors are not involved in the regulation of states of sleep and sedation.

The eegraphic and behavioural changes induced by the administration of polyamines (spermine and spermidine) were studied in rabbits. Spermine and spermidine were administered at different doses (200–400 γ) into the mesencephalic ventricle (i.c.v.) both as a bolus and in constant perfusion (60 min. duration). We also studied the effects of methamphetamine (M.A.) in a group of rabbits pretreated with spermine and spermidine 200–400 γ i.c.v. as bolus. Spermine caused a dose-related cortical synchronization associated with a partial sedation; spermidine induced cortical synchronization at a low dose without any behavioural changes while at higher dose (after perfusion) cortical desynchronization with an arousal behavioural pattern. The possible interaction of these substances with mesolimbic dopaminergic system is discussed on the basis of their potential neuroleptic action.

A high‐power, lumped‐elements, interdigital bandpass filter is described which has been used to improve the isolation between decouple and observe channels of NMR spectrometers, and to ‘‘clean’’ the transmitter signals. With no calculations, and with the help of a sweeper or a spectrum analyzer, filters of this type can be easily assembled and tuned over the 90–400 MHz range, typical of the proton decoupling frequencies.

An in vitro study of the nuclear magnetic resonance (NMR) response of protons in normal and pathological human skeletal muscle is presented. Muscle biopsies from 34 patients with various neuromuscular diseases and five normal subjects were studied by proton NMR techniques and the results were compared with those of light and electron microscopy. Proton spin-lattice relaxation time (T 1 ) and recovery law for the nuclear magnetization have been determined at 37°C and 43.5 MHz. The T 1 s for normal tissues were in the 650 to 800 ms range and the recovery process was nearly exponential. Muscles with well defined neuromuscular diseases were associated with highly nonexponential relaxation processes. The relationship between morphological alterations of the muscle tissues and the proton NMR response may become the basis of a fast and simple method for the diagnosis of neuromuscular diseases.

Noradrenaline levels and platelet and free serotonin concentrations were studied in depressed women in-patients (n=78) before and during amitriptyline (n=41) or lithium treatment (n=37). Pronounced monthly differences in platelet serotonin level have been shown in these subjects before treatment. In all clinical subgroups (neurotic, involutional, manic-depressive patients) a significant fall in platelet serotonin level was observed with amitriptyline medication while an increase was noted with lithium. No significant correlations between serotonin concentrations and clinical outcome were found. Amitriptyline treatment also produced a decrease in peripheral noradrenaline concentration in all subgroups, while an increase was observed with lithium. Some correlations between noradrenaline level and degree of depression were noted in patients treated with amitriptyline or lithium. A more extended analysis of blood amine levels could supply meaningful information on the peripheral action of antidepressive drugs on noradrenaline and serotonin concentrations in depression.

There are reports in which multiple sclerosis (MS) seems to be associated with abnormalities in selenium (Se) metabolism and erythrocyte glutathione-peroxidase (GSH-px) activity. Ordinary experimental allergic encephalomyelitis (EAE), which reflects some features of human MS, was induced in guinea pigs maintained with high, low and normal levels of Se in the diet. Evidence was obtained to indicate the following results: 1. (i) a direct correlation between dietary Se levels and whole blood Se levels. 2. (ii) Erythrocyte GSH-px activity was not found to be correlated with the blood Se content. 3. (iii) The animals fed with low or normal levels of Se showed the same survival rates and developed EAE in a similar way and percentage. 4. (iv) The animals fed with high non-toxic levels of Se showed a high incidence of death and some developed EAE with a subacute course, when compared with the other experimental groups. The results are discussed on the basis of findings in the literature.

Electroencephalographic and behavioral effects of the following ACTH fragments: 1–4, 4–9, 4–11, 1–10, 4–10, 1–13, 1–17 and 1–24 were studied in rabbits. Sequences 4–9, 1–10 and 4–10 displayed some epileptic properties, i.e., they induced epileptic seizures (only electrographic or also behavioral) or increased hippocampal spiking. The 4–9 sequence seemed to be the common sequence responsible for these proconvulsant effects. The possible involvement of the enkephalinergic system is discussed.

In the present study, the plasma and erythrocyte Se concentration and the erythrocyte and leukocyte glutathione peroxidase (GSH-Px) activity in 20 patients affected by multiple sclerosis (MS) were compared with those of a group of healthy controls. The Se concentration in the food was also studied and found to be less than the minimum values suggested by the US Food and Nutrition Board. The erythrocyte Se levels were found to be similar in both MS patients and in controls, while the plasma Se values were higher in the MS patients. The Se-dependent GSH-Px activity in the erythrocytes was found to be lower in the MS patients while no difference was found in the two groups as far as the leukocytes were concerned. Our data confirm that of other authors and indicate that the modified GSH-Px activity found in erythrocytes of MS patients is independent from the Se concentration and probably due to genetic factors.

Cerebral ischemic lesions were induced in rabbits through internal carotid artery embolization by means of microspheres. Different models of stroke ranging from single focal cortical lesion to massive bilateral brain edema were reproduced and monitored up to the 24th hour by electroencephalogram (EEG and QEEG), somatosensory evoked potentials (SEPs), cerebral blood flow (CBF), platelet aggregation. The site and extent of the lesions were verified by histological examinations. Results obtained and physiopathological implications are discussed.

The effects of different levels of zinc (Zn) in the diet were tested in the animal model of acute experimental allergic encephalomyelitis (EAE), which is considered a prototype for cell-mediated autoimmune disease of the central nervous system (CNS). Acute EAE was induced in guinea pigs maintained with normal, high and low levels of Zn in the diet. The animals fed normal and Zn-supplemented diets showed the same survival rates; the incidence and severity of the disease was similar for both groups. Zn-deficient animals exhibited the expected symptoms of Zn deficiency and after sensitization did not develop neurological signs of EAE; some of them presented only focal inflammatory alteration in CNS.

One hundred and sixty-seven subjects (91 females and 76 males) aged 18 to 55 and suffering from recurrent headache, daily headache, and cluster headache, were studied. In order to collect detailed information about their clinical as well as social and environmental conditions, a multi-page card was used which had been specially prepared for this purpose. The patients’ personality patterns were assessed by the following methods: MMPI (the Hs, Hy, D, and Ma scales, in particular); EPQ (Eysenck Personality Questionnaire); and AS IPAT (Cattel's Anxiety Scale). The statistical analysis of the data obtained made it possible to define the personality patterns of both male and female subjects and then to differentiate between them in relation to the various types of headache. Furthermore, possible relationships between personality traits and headache suffering were investigated. If the personality patterns of females seem to have existed prior to the disease, those of males raise some questions. In cluster patients, in particular, the age of onset seems to be related to certain personality traits; in patients with daily headache, by contrast the association between the duration and severity of the disorder appears to play a major trigger role. Some of these correlations do not have a linear character and suggest new working hypotheses that go beyond the limits of standard correlations.Nous avons étudiés 167 sujets (91 femmes et 76 hommes) avec un âge variable entre 18 et 55 ans, atteints de céphalée par accès, céphalée chronique et céphalée à grappe. Les informations sur la situation clinique et sur l'environement des sujets traités, ont été recueillies à l'aide d'une fiche spéciale. On a étudié les profils de la personnalité des patients à travers les tests suivants: MMPI (en particulier les échelles Hs, Hy, D, et Ma), EPQ (Eysenck Personality Questionnaire), AS IPAT (Anxiety Scale Cattel's). L'analyse statistique des données obtenues a permis de determiner les profils de la personnalité soit des hommes que des femmes et ensuite de les differencier selon les différents types de céphalée. Nous avons étudié les corrélations entre le profil de la personnalité des patients et la maladie. Tandis que le profil de la personnalité des femmes semble préexister à la maladie, pour ceux des hommes nous n'avons pas pu obtenir des informations certaines. En particulier chez les patients avec “cluster headache” l'âge d'apparition semble être en relation avec certaines caractéristiques de la personnalité, tandis que chez les patients atteint de céphalée chronique, la durée et l'intensité de la maladie semblent avoir un rôle plus important. Certaines corrélations n'ont pas un cours linéaire et conseillent des nouvelles hypothèses de recherche qui vont au-delà des limites des corrélations standard.Sono stati studiati 167 soggetti (91 donne e 76 uomini) di età compresa tra 18 e 55 anni, affetti da cefalea accessuale, cefalea continua e cefalea a grappolo. Allo scopo di raccogliere informazioni dettaliate sia sulla situazione clinica che sulle condizioni socio-ambientali, é stata utilizzata una scheda di raccolta dei dati appositamente approntata. I profili di personalità dei pazienti sono stati studiati attraverso i sequenti tests: MMPI (in particolare le scale Hs, Hy, D, e Ma); EPQ (Eysenck Personality Questionnaire); AS IPAT (Anxiety Scale Cattel's). L'analisi statistica dei dati ottenuti ha consentito di delineare i profili di personalità sia degli uomini che delle donne e quindi di differenziarli a seconda delle diverse forme di cefalea. Inoltre sono state analizzate le possibili relazioni tra tratti di personalità e sofferenza propria della cefalea. Mentre i profili di personalità delle donne paiono preesistere alla malattia, quelli degli uomini pongono alcuni interrogativi. In particolare, nei pazienti con cefalea a grappolo l'età di inizio della cefalea sembra essere in relazione con certi tratti di personalità; nei pazienti con cefalea continua, al contrario, sembrano avere un ruolo più importante la durata e la severità della malattia. Alcune di queste correlazioni non hanno un andamento lineare e suggeriscono nuove ipotesi di lavoro che vanno oltre i limiti delle correlazioni standard.

Modulation mechanisms of nociception have several neurotransmission interactions that are impaired in the disorder of painful perceptions. Neurotransmission changes may show up in several ways on the clinical level. They also have endocrinological correlations, since the neurotransmission systems implicated in the nociception disorders share transmitters with the regulation system operating at the pituitary level. In this sense, nocipathies exhibit analogies and may be compared to disorders of motricity and behaviour that also show endocrine changes that may be likewise explained. Though specifically different in each instance, the neurotransmission alteration that is a common denominator of these disorders allows comparisons, especially in those situations, such as the nocipathic and behavioural ones, where correlations are relevant on clinical and interpretative grounds. Les mécanismes de modulation de la nociception ont des interactions multiples de la neurotransmission qui sont compromises dans les nocipathies. Ces altérations de la neurotransmission peuvent avoir différents aspects cliniques. Elles ont aussi des corrélations endocriniennes, du moment que le système de neurotransmission en question a des neurotransmetteurs en commune avec le système regulatoire de l'hypophyse. Donc, les nocipathies montrent des analogies avec les maladies de la motricité et du comportement, qui présentent de même des troubles endocrins sujets à une interprétation similaire. L'alteration de la néurotransmission, quoique spécifiquement différente chez chaque condition clinique, est un commune dénomiteur à ces disordres et permet de confronter entre eux situations où des corrélations peuvent avoir importance sur le niveau clinique et interprétatif. I meccanismi di modulazione della nocicezione hanno multiple interazioni neurotrasmettitoriali che sono compromesse nelle nocipatie. Le alterazioni neurotrasmettitoriali possono manifestarsi in modo diverso sul piano clinico. Esse hanno anche correlazioni endocrine, poichè il sistema neurotrasmettitoriale in questione è condiviso nei suoi elementi dal sistema regolatorio dell’ ipofisi. Così, le nocipatie mostrano analogie e possono essere paragonate con malattie della motricità e del comportamento, che danno anch'esse luogo a turbe endocrine di analoga interpretazione. L'alterazione neurotrasmettitoriale, benché specificamente diversa in ciascun quadro clinico, è un denominatore comune di questi disordini, consente paragoni specialmente in quelle situazioni, come nocipatie e disturbi del comportamento, in cui le correlazioni possono aver rilievo sul piano clinico ed interpretativo.

Memory performance, central monoaminergic function and sympathetic nerve activity were studied in patients with dementia of the Alzheimer type (DAT) or with multi-infarct dementia before and after 4 weeks with single or combined drug therapy (choline-piracetam). Analysis of the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG), 3-methoxy-4-hydroxyphenylacetic acid (HVA) and 5-hydroxyindolacetic acid in the cerebrospinal fluid (CSF) and also in urine (plus 3-methoxy-4-hydroxy mandelic acid) showed that the basal values of HVA in the CSF and urine were lower in the more severely demented compared with the mildly demented subjects in both groups. The combined drug treatment resulted in a statistically significant increase in the MHPG level in the CSF of mildly demented subjects of the DAT group, while it seemed not to influence the other monoamine metabolites. The sympathetic nerve activity was similar in both patient groups and was unchanged after therapy. These findings suggest a dopaminergic deficit in advanced stages of the disease and a possible enhancement of the central noradrenergic output with therapy. No effects of therapy on memory performance or correlations between monoamine levels and memory test scores were noted.

The measurement of the urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG) in 59 unipolar depressed women before and during administration of 100 mg amitriptyline (AMT) i.m. daily for four weeks showed that the patients could be divided into high or low MHPG excretors. An analysis of the excretion course of MHPG and 3-methoxy-4-hydroxy mandelic acid during therapy showed, in most patients, a lower urinary excretion of both these noradrenaline (NA) metabolites in comparison with basal values. Therapy also decreased plasma noradrenaline concentrations and blood pressure values both at rest and on orthostatic challenge. Available evidence seems to suggest that AMT administration caused a lower overall noradrenergic output that might be partially responsible for a diminished sympathetic nervous activity. The authors were unable to confirm that the baseline MHPG level can predict the clinical response to antidepressant treatment and they found no significant correlations between changes in bio-chemical or physiological variables and drug plasma concentrations or clinical response. The possibility that depressed patients might be grouped according to their different NA metabolism needs to be validated in a larger patient sample.

In the occlusion of the internal carotid artery, the change occurring in the internal-external carotid pressure gradient may cause flow reversal within the ophthalmic artery and its branches. Ophthalmodynamographic, Doppler directional sonographic and angiographic investigations were performed in 21 cases (11 total occlusions, 6 severe and 4 moderate stenoses of the internal carotid artery). The authors compare the results of these investigations and discuss the practical importance of Doppler directional sonography and the significance of flow reversal in the ophthalmic artery.

The effects of some neuropeptides infused into the cerebral ventricles on the spontaneous cerebral electric activity were studied in unanasthetized rabbits. The following peptides were investigated: physalaemin, caerulein, bombesin, litorin (supplied by Farmitalia). The rabbits were prepared according to Monnier and Gangloff's [10] method in order to record the spontaneous cortical activity. Each of these substances affects the electroencephalographic (EEG) records in a specific and dose-related way. Bombesin induces a biphasic pattern (synchronization followed by a partial activation), litorin is partially activating and physalaemin brings about a marked desynchronization. In spite of the marked structural analogy between bombesin and litorin, their EEG effects differ.

The di-carboxylated derivative of spermidine, N-carboxyethyl γ-aminobutyric acid (CEGABA) has been identified in bovine brain and human cerebrospinal fluid by HPLC. This discovery strongly suggests the existence of a metabolic pathway connecting polyamines and GABA via putreanine and CEGABA through progressive oxidative deamination of the amino terminal groups in spermidine.

Report of a study of primary myopathies in children conducted within the framework of our program to evaluate the diagnostic potential of 1H NMR in muscular diseases. There are substantial differences in the in vitro 1H NMR response of skeletal muscles between normal children and children with congenital non progressive myopathies and Duchenne muscular dystrophy.

The effects of i.c.v. administered thyrotropin-releasing hormone (TRH) on EEG, rectal temperature and behaviour were studied on rabbits in basal conditions and after different pretreatments. The effects of TRH on the EEG and behaviour do not seem to involve serotoninergic, catecholaminergic and cholinergic systems. A possible involvement of the GABAergic system is hypothesized.

Common migraine (CM) is an evolutive disease characterized by a progressive increase in the number of attacks and a consequent reduction in the free periods, eventually reaching a state of continuous migraine with interparoxysmal headache (MIH). To evaluate the role of central pro-opiocortin-related peptides in the pathogenesis of the disease, cerebrospinal fluid (CSF) levels of beta-lipotropin (beta-LPH), beta-endorphin (beta-EP) and ACTH were measured in two groups of migraine sufferers with increasing severity of the disease (CM and MIH), and in healthy controls. ACTH values were similar in the 3 groups, while beta-LPH levels were significantly lower (P less than 0.005) in patients affected by MIH (10.4 +/- 8.6 fmol/ml) than in patients with CM (35.7 +/- 8.3) and in controls (32.9 +/- 15.33). beta-EP levels were closely correlated with the severity of the disease: they decreased significantly from those found in healthy controls (86.1 +/- 37 fmol/ml) to those of CM sufferers (38.5 +/- 3.5; P less than 0.005) and showed a further significant fall (P less than 0.01) to the lowest levels which were found in MIH patients (14.8 +/- 9.8). These data showing that the progressive evolution of migraine is concomitant with a progressive impairment in the CSF levels of beta-EP, sustain the concept that non-organic central pain is related to a reduced activity of the neurons responsible for the CSF content of beta-EP.

SYNOPSIS In the light of Sicuteri's central theory of migraine, reserpine-induced attacks have been related to a central depletion of monoamine stores, 5HT and DA in particular. Reserpine is known to increase serum prolactin (PRL) levels. The PRL response to reserpine, before and after treatment with drugs affecting DA and 5HT pathways, has been used as a tool to clarify the role of central neurotransmitters in migraine pathogenesis. Twenty-nine migraine patients and a control group underwent i.v. reserpine tests under control of PRL levels. A retest was performed after thirty days of treatment with bromocriptine, DL-5HTP or methysergide. The reserpine-induced PRL increase was similar for migraine and control groups during the first 5 hours, with no relationship to occurrence and severity of headache. Only the control males, however, had returned to basal PRL levels after 24 hours. At the retest, only bromocriptine could prevent the PRL increase by reserpine and the onset of headache in nine out of ten patients. The value of the pharmacodynamic PRL secretions tests is emphasized in order to clarify the central mechanisms of various trigger factors in headache, and drug effectiveness in the management of migraine.