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S Calzolari

Publications and source records attributed to S Calzolari.

15 recordsLinked to original sources

Tactile evoked spikes in children.

Tactile evoked spikes (TES) are a well known EEG feature in children. We reviewed our previous studies concerning this phenomenon, with special reference to the influence of sleep and stimulation rate, the relation with middle-long latency somatosensory evoked potentials (MLSEP) and the relation between TES and spontaneous spikes in the same individual. New data were obtained by re-evaluating 566 children with TES, by assessing MLSEP from each finger, in 15 subjects with TES, and by studying MLSEP following posterior tibial nerve stimulation in 12 children with TES. TES appear to be enlarged components of MLSEP which are present in some children aged 4 to 14 years; they tend to increase during NREM sleep and to decrease during REM sleep; Their amplitude decreases at stimulation rates above 3 Hz. TES are associated with an increased risk of epileptic seizures, which usually have a benign prognosis. The possible neurophysiological mechanisms underlying this phenomenon are discussed.

Adolescent↗

Effect of acetyl-L-carnitine on hyperactivity and spatial memory deficits of rats exposed to neonatal anoxia.

The effect of acetyl-L-carnitine (ALC) on behavioral deficits following neonatal anoxia (N2 100% for 25 min at 30 h after birth) was studied in the rat. Transient hyperactivity at P20-P45 postnatal days and permanent spatial memory deficits were shown by anoxic rats. A chronic ALC treatment (50 mg/kg per die injected intraperitoneally from P2, after anoxia, to P60) significantly reduced the transient increase in sniffing, rearing and locomotory activity of anoxic rats, but, mostly, ameliorated the spatial memory performances in a maze at P30-P40 and in a water maze at P50-P60. No behavioral changes were seen in ALC-treated animals that received sham-exposure at birth. On the basis of these results, the use of ALC for the treatment of perinatal asphyctic insults in children is suggested.

Acetylcarnitine↗

Median nerve middle-long latency somatosensory evoked potentials in children with tactile evoked spikes.

It is known that hand tapping during electroencephalography (EEG) recording evokes centrotemporal spikes in some 4- to 12-year-old children. This phenomenon occurs in both healthy and epileptic children. The same children were reported to show giant middle-long latency evoked potentials (MLSEPs). To study the relationship between tactile evoked spikes (TES) and MLSEPs, we performed a neurophysiologic investigation in 25 children with TES and in 25 children without any EEG abnormality. Such an investigation included a MLSEP study after both electrical and tactile stimulation with simultaneous recording of digital EEG. MLSEPs consistently showed three negative (NI, NII, NIII) and two positive (PI, PII) peaks. Children with TES had MLSEPs of enlarged amplitude. The analysis of MLSEPs and TES characteristics led us to the conclusion that they are the same neurophysiologic event, with NII being the evoked spike and NIII the following slow-wave.

Adolescent↗

Psychiatric disorder in a familial 15;18 translocation and sublocalization of myelin basic protein of 18q22.3.

Two related patients with similar clinical features consisting of a few dysmorphic signs and psychiatric disturbance were reported to have a partial trisomy of chromosomes 15(pter-q13.3) and 18(q23-qter) deriving from a familial translocation t(15;18). One patient is affected by bipolar disorder and the other by schizoaffective disorder. Both cases have a predominantly affective course; nevertheless, a clear diagnosis is difficult in the first patient, who is 15 years of age, and only a longitudinal course will allow us to establish a definite diagnosis. The possibility that these two pathologies belong to a single category is discussed, and the presence of a susceptibility locus on chromosome 18 is hypothesized. Cytogenetic data, FISH, and DNA studies indicate that the myelin basic protein (MPB) gene is not involved in the translocation, and localize it centromeric to the breakpoint on chromosome 18(q22.3). Thus, it is unlikely to be involved in the disease.

Adolescent↗

[Cohen syndrome. A new case and review of the literature].

We report the case of a 12-year-old child suffering from mild mental retardation, hypotonia, long hands with tapering fingers, microcephaly, truncal obesity, particular facial features. The association of these abnormalities has been known as Cohen Syndrome since 1973. Such a dysmorphic syndrome is usually inherited as an autosomal recessive trait whose gene has not been yet localized. There is no biological marker and the diagnosis is made only on a clinical basis. The diagnosis is quite difficult because of the intrafamiliar variation and the lack of a symptom present in 100% of the cases. From the analysis of the literature it proves that the more frequent symptoms are: mental retardation, open mouth, short philtrum, high palate, hypotonia. Because of the diagnostic difficulties it is possible that this syndrome was underestimate. Moreover, it is usually diagnosed too late, (mean age: 12,9). Therefore, we think necessary to consider the possibility of Cohen Syndrome in the case of every mental retardation of unknown cause.

Abnormalities, Multiple↗

Neonatal anoxia induces transitory hyperactivity, permanent spatial memory deficits and CA1 cell density reduction in developing rats.

Physical and reflex development, spontaneous behavior in open field and spatial memory abilities have been studied in rats after neonatal anoxia. Histological analysis of the hippocampal fields have been carried out in selected animals at the end of the testing period. No differences between control and anoxic rats were recorded in the physical and reflex development. Hyperactivity in open field was present in anoxic animals only transiently between P20 and P45. Spatial memory abilities, tested at two developmental stages by means of a maze and a water maze, appeared to be defectual not only during the hyperactivity period but also in adulthood. The histological analysis of the different hippocampal fields demonstrated a significant difference between anoxic and control rats in the cell density of the CA1 field. The present data demonstrate that neonatal anoxia, besides determining only transitory defects in open field behavior, profoundly affects cognitive abilities and cell density in CA1 hippocampal field. These results might be of relevance in the interpretation of the substrate of the cognitive impairment seen in hyperactive children that are exposed to hypoxia at birth.

Animals↗

[Ossification of the posterior longitudinal ligament of the lumbar spine].

The ossification of the cervical posterior longitudinal ligament (OPLL) is widely known and studied in Japan where a roentgenological incidence of 2.06% adults affected has been found. Data concerning the ossification of the lumbar posterior longitudinal ligament are few and occasional. An epidemiological survey on lumbar OPLL was performed by the authors in Matsumoto, Japan, on a total of 792 subjects, 554 of whom over the age of 35, by means of X-ray of the lumbar spine. Ossification of the lumbar posterior longitudinal ligament was detected in 23 subjects (2.9%), with no significant difference between males (3.0%) and females (2.8). Lumbar OPLL was absent in the 238 subjects aged less than 34; it was the most prevalent after the age of 45 (5.1% in males and 4.5% in females). The ossification developed in two ways: continuous ossified layer extending over several vertebrae; circumscribed ossification of the ligament corresponding to the level of the intervertebral disk (retrodiscal type). The result of this epidemiological survey showed a roentgenological incidence of lumbar OPLL of the same magnitude than that of cervical OPLL.

Adult↗

The effect of GM1 ganglioside on cholinergic and serotoninergic systems in the rat hippocampus following partial denervation is dependent on the degree of fiber degeneration.

The partial lesion paradigm of the dorsal hippocampal afferents in the rat was used as a model to study the effect of GM1 ganglioside treatment on recovery of neurotransmitter markers of the cholinergic and serotoninergic activity in various hippocampal regions. It was found that the enhancement of recovery of acetylcholinesterase, choline acetyltransferase and serotonin uptake by GM1 treatment (30 mg/kg i.m., daily), as studied on the 6th and 21st postlesion day, was dependent on the degree of fiber degeneration. The results may be interpreted in terms of the relationship between the action of GM1 and that of neuronotrophic factors whose release also depends on the extent of the fiber degeneration. These data indicate that GM1 elicits the recovery of biochemical parameters, or fails to, depending on the specificity of the trauma. The result may explain why, after certain brain lesions, GM1 does not promote functional recovery.

Acetylcholinesterase↗

The functional recovery of damaged brain: the effect of GM1 monosialoganglioside.

In the present study the topology and the biochemical mechanisms underlying the functional recovery of the dopaminergic nigrostriatal system is further analyzed. Rats with unilateral hemitransection were treated with 30 mg/kg GM1 monosialoganglioside or with its internal ester derivative for different periods of time. GM1 enhances 3H-dopamine uptake in striatal synaptosomes of the lesioned side, and the enhancement of dopamine uptake precedes that of striatal tyrosine hydroxylase activity. The above biochemical effects are accompanied by changes in behavioral- and electrophysiological-related parameters. The effect of GM1 on striatal tyrosine hydroxylase of the lesioned side disappears when the ascending dopaminergic fibers are extensively lesioned. This suggests that the source of regrowing dopaminergic nerve terminals in the striatum of partially lesioned rats resides mainly in the intact axons remaining in the ipsilateral side. When GM1 is injected into partially lesioned rats kept in darkness, no effect on tyrosine hydroxylase activity is observed. This indicates that the mechanism through which GM1 acts involves a normal light-dark cycle.

Animals↗