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Biomedical subjects

C Menini

Publications and source records attributed to C Menini.

At least 37 records · Page 2Linked to original sources
PubMed1990

Clinical efficacy of five filters specific for leukocyte removal.

The clinical efficacy of 5 filters specific for leukocyte depletion was evaluated retrospectively. The patient population was composed of 191 thalassemics who received about 15,000 units of filtered blood in 28 months. The frequencies of reactions to filtered blood varied significantly (p less than 0.0001) according to the type of filter and were as follows: Erypur, 0.7%; Imugard, 2.7%; Leucostop, 0.7%; Miropore, 2.1%; Sepacell, 0.6%. There was a notable concordance between the efficacy in the leukocyte removal and the clinical performance of the filters. The 2 polyester filters examined combined good clinical and laboratory results with superior flow properties.

Adolescent↗
PubMed1990

Non-A, non-B hepatitis and anti-HCV antibodies in dialysis patients.

To define the prevalence of non-A, non-B hepatitis, antibodies to HCV were detected in 193 patients on renal replacement therapy (52 transplant and 141 hemodialysis patients) and in 50 staff members of a Nephrology Department. Unequivocal seroconversion was documented in 5 transplant (9.6%) and in 26 dialysis patients (18.4%). In the dialysis population, the prevalence of anti-HCV antibodies was evaluated in patients grouped according to the number of blood transfusions and to the different sections of dialytic treatment. The most striking findings were the marked differences in the prevalence of anti-HCV antibodies among patients treated in different sections (from 0% to 70%), and the presence of a significant increase in alanine-amino-transferase (ALT) concentrations in 14 anti-HCV negative patients. The results suggest that the diffusion of non-A, non-B hepatitis is mainly transfusion-related, with the possibility of significant environmental diffusion related to the violation of infection-control measures. The current immunoassay is probably unable to detect the actual frequency of the infection.

Adult↗
PubMed1990

[Value of the monkey Papio papio for the study of epilepsy].

The baboon Papio papio is the only animal model showing a natural photosensitive epilepsy very similar to that observed in some human epileptic patients. In the baboon, intermittent light stimulation (ILS) induces bilateral and synchronous myoclonic twitches which are associated with paroxysmal discharges (PDs) predominating in the frontal cortex, and can be followed by generalized tonic-clonic seizures. We were able to demonstrate the motor cortical origin of all these manifestations since neuronal generators responsible for paroxysmal discharges are localized there and are activated by visual afferents from the occipital lobe. The corpus callosum is the structure determining the interhemispheric synchronization of PDs. An unbalance of neurotransmitter systems such as GABA or excitatory amino acids should be responsible for the hereditary predisposition of baboons to photosensitive epilepsy. Some Papio papio, either photosensitive or not, may show spontaneous truncular myoclonic twitches, different from those induced by intermittent light stimulation, and resembling the intention myoclonus as observed in some human neurological disorders (post-anoxic syndrome, degenerative encephalopathies such as Ramsay-Hunt syndrome...). Because of the absence of any abnormal electrographic discharge, this myoclonus is considered non epileptic. Until now, we were unable to determine the structure generating this myoclonus. The most probable origin is in the lower brain stem. Experimental data suggest that a local unbalance of the cholinergic neurotransmission could be responsible for the predisposition of baboons to show this type of myoclonus.

Animals↗
PubMed1989

Relationship between tolerance to GABAA agonist and bursting properties in neocortical neurons during GABA-withdrawal syndrome.

The interruption of intracortical, chronic GABA infusion is known to give rise to 'GABA withdrawal syndrome' (GWS) consisting of electroencephalographic paroxysmal focal activities, associated with behavioral epileptic signs. Neocortical slices were obtained from rats presenting the GWS (GWS slices), and intracellular recordings were performed in the vicinity of the gamma-aminobutyric acid (GABA)-infused site. Electrical stimulation of the underlying white matter induced paroxysmal depolarization shifts (PDSs) in virtually all neurons. Bath-applied GABA (1-10 microM) had no effect on these neurons, while the same dose range was found effective in blocking action potentials in saline-infused cortex slices obtained from control rats. In the GWS slices a population of neurons presented, in addition to synaptically induced PDSs, voltage-dependent and cobalt-sensitive PDSs and bursts of action potentials induced by depolarizing current injections. These intrinsic bursting neurons were unresponsive to high doses of GABA (100 microM). Dose-response curves of isoguvacine, a specific GABAA agonist, showed a shift to the right for the intrinsic bursting cells whatever the parameter measured (depolarization or conductance increase): the ED50 was 50-100 times higher for intrinsic bursting cells than for other non-intrinsic bursting cells, thus indicating that intrinsic bursting cells are tolerant to GABAA agonist. This tolerance may result from a decreased number of receptors or from a change in their properties as a consequence of the previous prolonged GABA infusion. The decrease in the GABA efficacy could lead to disinhibition and could thus give the appearance of epileptic events.

Animals↗
PubMed1988

The GABA-withdrawal syndrome: a new model of focal epileptogenesis.

A novel model of focal, cortical epilepsy is described. Chronic (6 h to 14 days), localized application of gamma-aminobutyric acid (GABA) into the somatomotor cortex of rats induces, upon withdrawal, the appearance of epileptogenic activity with maximal electrographic expression circumscribed to the infused site. This GABA-withdrawal syndrome (tested for a 100 micrograms/microliter/h dose) lasted from 24 to 168 h (mean values). A significant correlation was found between infusion time and duration of the excitability rebound, with the longer duration corresponding to the shorter infusion time. A distant lesion effect was observed in the thalamic area of cortical projection. The potential use of this neurotransmitter-induced phenomenon in the study of brain plasticity in general, and of epilepsy in particular, is discussed.

Animals↗
PubMed1988

Local asymptomatic status epilepticus induced by withdrawal of GABA infusion into limbic structures.

Most of the experimental models of status epilepticus result either from administration of a variety of excitatory neurotoxins or repeated electrical stimulation. Here we propose a new model based on the withdrawal of chronic gamma-aminobutyric acid (GABA) infusion into limbic structures via osmotic minipumps. Appearing with a latency of about 50 min, continuous pseudo-rhythmic EEG epileptic spiking was elicited for about 12-24 h after removal of GABA infusion in hippocampus or amygdala. No apparent distant brain damage was observed. This model differs from many others by several features and could result from different mechanisms.

Amygdala↗
PubMed1988

Anticonvulsant effects of localized chronic infusions of GABA in cortical and reticular structures of baboons.

We studied the effects of chronic (7 day) infusions of GABA (100 and 20 micrograms/microliter, 10 microliter/h) applied in different cerebral structures of baboons made photosensitive by a subconvulsant dose of allylglycine. The GABA infusion has partial anticonvulsant effects when applied to the motor cortex, reticular magnocellular nucleus (RMC), or substantia nigra (SN), but when directed to the prefrontal cortex (area 8) it has no effect. These anticonvulsant effects of GABA infusion are more important when GABA is infused into the motor cortex, where paroxysmal discharges (PDs) originate, than when it is infused into the RMC. In contrast, the anticonvulsant effects on light-induced generalized seizures are more pronounced when GABA is infused into the RMC than when it is infused into the motor cortex. GABA infusion into the SN has no effect on PDs and myoclonia and blocks seizures less effectively than the RMC infusion. These results are in accordance with the role of the motor cortex as a generator of PDs and of RMC in the generalization of seizures. Focal paroxysmal EEG and clinical activities, previously reported to appear at the end of the motor cortex GABA infusion, were not observed after RMC or SN infusions. However, behavioral hyperactivity occurring at the end of subcortical GABA infusions was observed. These behavioral signs could correspond to the clinical expression of a GABA withdrawal syndrome.

Animals↗
PubMed1987

Epileptogenic gamma-aminobutyric acid-withdrawal syndrome after chronic, intracortical infusion in baboons.

We studied the effects of chronic (7 days) infusion of GABA (100 micrograms/microliter) applied intracortically into the fronto-rolandic (FR) area of baboons, via osmotic minipumps. In photosensitive animals, bilateral GABA application produced a complete blockade of the paroxysmal discharges and associated clinical signs induced by intermittent light stimulation. Unilateral administration had similar effects, although these developed more gradually. At the end of the infusion period, both photosensitive and non-photosensitive animals showed a transitory state (3-4 days) of cortical hyperexcitability (spontaneous epileptogenic activity) localized to the infused area. The data indicate a role of GABA both in the natural photosensitivity of the epileptic baboon and in the withdrawal syndrome consecutive to the sudden interruption of chronically enhanced GABA levels in the FR territories of this monkey.

Animals↗
PubMed1987

Photic epilepsy problems raised in man and animals.

The data gathered in 30 years' study in man and in several animal species, but especially in the Papio papio baboon, tend to show that the cortex plays a decisive part in the seizure and interval discharges induced by intermittent light stimulation in photic epilepsy. Two regions of the cortex predominate: the frontorolandic and occipital regions. The cortical cortex can, indeed, transmit or control the visual input to the frontorolandic region and can cause intermittent discharges in certain specific conditions in baboons and in certain human patients. The corticocortical pathway conveys the visual impulses to the frontorolandic cortex and is certainly modulated by deep structures like the reticular systems and the thalamus. At present no more can be said since further research is needed.

Animals↗
PubMed1986

Stimulus-sensitive myoclonus of the baboon Papio papio: pharmacological studies reveal interactions between benzodiazepines and the central cholinergic system.

The baboon Papio papio develops a nonepileptic myoclonus 20 to 30 min after i.m. benzodiazepine injection. It is characterized by bilateral jerks involving mainly the neck and the trunk, by the absence of any correlative EEG paroxysmal discharge, and by its facilitation during movement or agitation. This myoclonus resembles the intention myoclonus of human patients as seen, for example, after anoxia. We found in experiments on 10 adolescent baboons that atropine alone induced the myoclonus for several hours, that physostigmine completely antagonized the benzodiazepine-induced as well as the atropine-induced myoclonus, and that the peripherally acting cholinergic antagonist, methyl-QNB, and agonist prostigmine had no action on the myoclonus, suggesting that the benzodiazepine-induced myoclonus in this species depends on a strong depression of the central cholinergic system by benzodiazepine. The benzodiazepine-induced myoclonus was mediated by benzodiazepine receptors as it was blocked by the specific benzodiazepine receptor antagonist, Ro 15-1788, which did not block atropine-induced myoclonus; latency to myoclonus after benzodiazepine was longer than after atropine. These facts suggest that benzodiazepines, by an as yet unknown mechanism, induce a depression of the cholinergic system which in turn leads to the development of myoclonus. Finally, the benzodiazepine-induced myoclonus of the baboon can be considered as a good model for testing drugs that act on the muscarinic cholinergic system and also for testing benzodiazepine-acetylcholine interactions.

Animals↗
PubMed1986

[Analysis of the multi-unit activity of the cortex and subcortical structures during paroxysmal discharges and grand mal seizures in the photosensitive baboon].

Cortical and subcortical multiunitary activities (MUA) and EEG were simultaneously recorded in baboons rendered photosensitive by a subconvulsant dose of DL-allylglycine. Intermittent light stimulation (ILS) trains induce in those animals fronto-rolandic (FR) paroxysmal discharges (PDs, constituted as spikes and waves) and grand mal seizures. During the induction of FR PDs by ILS trains, the visual structures (occipital cortex, colliculi superioris, pulvinar) show a significant MUA increase which is not related to the PD spike or wave but is correlated to the flashes. The first structure showing bursts of MUA that frequently precede the PD appearance is the FR cortex. When PDs appear, the bursts are related to the spikes of PDs and are followed by an inhibition during the slow wave. The pontine and mesencephalic reticular formations and the facial nuclei are activated in bursts after the FR PDs have reached a certain amplitude. The thalamic nuclei ventralis lateralis, centrum medianum and lateralis posterior are activated only later, when the FR PDs have reached an even greater amplitude. It is suggested that the activation of visual structures is necessary for FR PD appearance. The secondary pontine and mesencephalic activation could reinforce that of the FR cortex and then the thalamus, and could determine the myoclonus observed in unparalyzed animals.

Allylglycine↗
PubMed1986

[Myoclonia. From the myoclonia of Papio papio to various human myoclonias].

The baboon Papio papio is naturally predisposed to present several types of myoclonus, the study of which can help in understanding the various human myoclonic symptomatologies. The three types of myoclonus which are studied have been called A, B and C. Myoclonus A, which is induced by intermittent photic stimulation in photosensitive animals, is of epileptic nature: It is always preceded by spikes-waves predominating in the fronto-rolandic cortex (areas 4 and 6) and can be followed by secondarily generalized tonic-clonic seizures. Myoclonus B, which occurs when the animal is agitated, is facilitated by somatic stimulations. Since it is never preceded or accompanied by spikes-waves and since it is never associated with epileptic seizures, myoclonus B is considered as non-epileptic. Myoclonus C occurs during wave-sleep. They are associated with spikes-waves during the slow but not during paradoxical sleep. Myoclonus A, B and C can co-exist in the same animal when it is photosensitive. Myoclonus B and C can co-exist in the same animal when it is non-photosensitive. Clinically, the three types of myoclonus have different symptomatologies. Myoclonus A is bilateral and synchronous. It always involves initially the eyelids and face. It can secondarily become generalized to the whole body. Myoclonus B, which is also bilateral and synchronous, is limited to the truncular musculature and to the proximal part of limbs. It never involves the eyelids and face. It never becomes generalized. Myoclonus C has a variable symptomatology and can be parcellar. The nervous structures originating the three types of myoclonus in the baboon are not identical. Myoclonus A is originated in the fronto-rolandic cortex, where a neuronal generator is triggered by visual inputs induced by photic stimulation. It appears mainly due to a dysfunction of the GABA system, because it is suppressed by GABA agonists and by benzodiazepines. On the contrary, it is facilitated by GABA antagonists. Myoclonus B has probably its origin in the lower brain stem (ponto-bulbar reticular formation) and is favored by cerebellar lesions. It appears mainly due to a dysfunction of the cholinergic system and is considerably facilitated by atropine. Myoclonus C can also have its origin in the lower brain stem but, contrary to myoclonus B, it can involve the cortex and thus can be accompanied by spikes-waves. The 3 types of myoclonus which are distinguished in the baboon have different relationships with epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio.

The spread and persistence of epileptic seizures have generally been attributed to chemical synaptic interactions. Using ion-sensitive microelectrodes, we showed that in the allylglycine-treated photosensitive baboon, prolonged light-induced generalized seizures were accompanied by abnormally large decreases in the concentration of extracellular calcium ions, reaching values at which chemical synaptic transmission was certainly very reduced or blocked. This feature was observed in all cortical layers. Measurements of the concentration of extracellular potassium ions in the course of such light-induced seizures indicated that the observed low values of the concentration of calcium ions could not be ascribed to the occurrence of spreading depressions. These findings showed that nonsynaptic mechanisms play a prominent role in the persistence of epileptic seizures.

Animals↗