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Biomedical subjects

G L Gigli

Publications and source records attributed to G L Gigli.

At least 19 recordsLinked to original sources
PubMed1992

EEG changes induced by carbamazepine therapy at rest and during mental processes.

The effects of carbamazepine (CBZ) on EEG background activity have been studied, at rest and during mental processes, in 18 epileptic patients suffering from focal epilepsy and starting antiepileptic treatment for the first time. The EEGs were recorded before and after CBZ therapy, at rest with eyes closed (EC), during blocking reaction (BR), fixation (FIX) and mental arithmetic (MA) tasks, and then evaluated by spectral analysis. All data underwent statistical evaluation utilizing the ANOVA and correlation coefficient. The following parameters were evaluated: mean absolute and relative power and mean frequency. The results have shown that CBZ induced a significant increase of slow activity at rest with EC, which was represented by delta potentials, and was correlated with CBZ plasma levels. In evaluating the different cortical activation patterns, a decrease of the alpha reactivity was noted during BR and FIX, while a significant increase of beta activity was observed during the performance of all tasks. The relationship between the increased beta power, possibly reflecting an increase of cognitive activity for processing information, and the lack of a significant decrease of alpha activity are discussed.

Adolescent↗
PubMed1992

Effect of carbamazepine treatment on EEG changes induced by different cortical activation patterns in newly referred epileptic patients.

Sixteen epileptic patients suffering from focal epilepsy who underwent antiepileptic drug treatment with carbamazepine (CBZ) for the first time were studied. The EEG was recorded at rest with eyes closed, during blocking reaction (BR), fixation (FIX) and mental arithmetic tasks. The computerized EEG study, performed before and after CBZ therapy, utilized spectral analysis. Data underwent statistical evaluation through Anova and correlation analysis. The parameters evaluated were the mean frequency and the mean absolute and relative power. The results have shown that after CBZ treatment there is a decrease in the alpha reactivity during BR and FIX, while a significant increase in beta activity was observed during all tasks. The effect of CBZ therapy on EEG activity during cortical activation patterns are discussed.

Adult↗
PubMed1992

Lateralization of the epileptogenic focus by computerized EEG study and neuropsychological evaluation.

The localization of the epileptogenic focus relies on different factors. In patients with partial seizures, asymmetries in EEG background activity were measured by a statistical evaluation of spectral data. Neurophysiological results were compared with neuropsychological findings and MRI. Fifteen of 22 patients showed asymmetries in EEG background activity. The most prominent abnormality was a statistically significant increase of slow activity observed in 59% of cases. Delta asymmetry coincided with the site of lesions, evidenced by MRI, in 83% of patients; with the site of decreased beta activity in 60% and with the maximum level of spiking activity in 58% of cases. Neuropsychological tests showed a lateralization of the hemispheric function which coincided with delta asymmetry in 33% of patients. These results suggest that the EEG background activity, when compared with other parameters, may represent a useful method in lateralizing the epileptogenic focus.

Adolescent↗
PubMed1992

Electroencephalography.

Recent advances in electroencephalography (EEG) research are presented. Particular emphasis is placed on sleep and epilepsy research in humans. In this context, among others, studies on the modifications of EEG epileptic activity during sleep are discussed in more detail. A large number of reports come from EEG monitoring during presurgical evaluation and surgical treatment of drug-resistant epilepsy; information provided by these studies is therefore considered with special attention.

Brain↗
PubMed1991

Effects of seizures and carbamazepine on interictal spiking in amygdala kindled cats.

We examined the influence of seizures and carbamazepine (CBZ) on spiking rates in kindled cats. In the first experiment, spiking rates were measured before and after seizures, with and without CBZ. CBZ was administered immediately after seizures in order not to affect them. Spiking rates were measured over 9 h during the different sleep stages. In a second experiment, CBZ was administered before and after seizures so as to affect seizure strength and thus measure its effect on spiking. Results confirmed earlier findings of a large increase in spiking following a stage 6 seizure in fully kindled animals. We also established that: (1) repeated daily seizures caused a further increase in spiking until a ceiling was reached; (2) increased spiking was not a direct effect of postictal alterations in sleep stages; (3) CBZ, despite its effectiveness as an anticonvulsant, did not reduce spiking but rather increased it; (4) postictal increases in spiking were related to seizure 'strength'. These findings support the hypothesis that spiking rates are primarily influenced by seizure occurrence, as was found in patients with temporal lobe seizures, and that anticonvulsants act differently on seizures and spikes. This emphasizes the possibility of distinct pathophysiological mechanisms for interictal spikes and seizures.

Action Potentials↗
PubMed1991

Interictal spiking during wakefulness and sleep and the localization of foci in temporal lobe epilepsy.

We examined variations in interictal spiking during sleep and wakefulness to assess differences in reliability for localizing epileptic foci. Forty patients were studied prospectively. Spikes were assessed for rates, field, and appearance of new foci. Final localization was determined by surgery, electrocorticography, and seizure onset. Comparison of interictal EEG foci with final localization was made. In 39 patients, slow-wave sleep activated spiking compared with wakefulness. Most patients showed maximal spiking in sleep stages 3 or 4. Restriction of field in rapid eye movement (REM) sleep and wakefulness, and extension of field in slow-wave sleep occurred. New foci appeared in non-rapid eye movement sleep in 53% of patients. Similar but not identical spiking rates, foci, and field distributions were seen in wakefulness and REM sleep. All REM foci were unilateral. Our findings suggest that localization of the primary epileptogenic area is more reliable in REM sleep than in wakefulness, and in wakefulness more than in slow-wave sleep.

Action Potentials↗
PubMed1990

Intracerebral metastasis in Ewing's sarcoma.

The evidence of CNS involvement in Ewing's sarcoma is uncommon and very often due to a direct extension of the tumor to extradural space and meninges. We report a case of a 14-year old girl with a primary ischio-pubic localization of Ewing's sarcoma. Body CT scan showed a bone lesion involving the left fronto-temporal region of the skull without affecting the brain. After chemotherapy radiological findings showed complete recovery. Ten months after treatment, the patient had neurological symptoms. Cerebral CT scan evidenced a large tumor mass localized in the right temporal lobe. Following radiotherapy the tumor mass was no longer visible. This case shows that late intraparenchymal CNS metastasis occurs independently from the previous skull lesion. Therefore these data, even through based on a single observation, lead to believe that in some cases prophylactic chemotherapy and radiotherapy of CNS may not be necessary.

Adolescent↗
PubMed1989

Evoked potentials suggest cranial nerves and CNS involvement in chronic relapsing polyradiculoneuropathy.

Brainstem auditory and visual potentials were recorded from 6 patients with chronic idiopathic polyradiculoneuropathy. Evoked potentials were either completely absent or their latency was prolonged suggesting slow conduction in visual or auditory pathways. The results of our study provide further evidence suggesting subclinical involvement of cranial nerves and central nervous system sensory pathways in chronic inflammatory demyelinating polyradiculoneuropathy.

Adult↗
PubMed1987

Non-invasive evaluation of input-output characteristics of sensorimotor cerebral areas in healthy humans.

The topography of scalp SEPs to mixed and sensory median nerve (MN) and to musculocutaneous nerve stimulation was examined in 20 healthy subjects through multichannel (12-36) recording in a 50 msec post-stimulus epoch. MN-SEPs in both frontal leads were characterized by an N18, P20, N24, P28 complex showing maximal amplitude at contralateral parasagittal sites. This was sometimes partly obscured by a wide wave N30 having a fixed latency, but a steep amplitude gradient moving toward the scalp vertex. A P40 component followed, having longer peak latencies, moving the recording sites from contralateral medial parietal toward the vertex and frontal ipsilateral positions. MN-SEPs in contralateral parietal leads contained a widespread N20 with a maximum source posterior to the Cz-ear line. The following P25 enveloped two subcomponents - early and late P25 - having different distributions. The late P25 showed a maximum - coincident with that of wave N20 - which was localized more posteriorly than that of the early P25. An inconstant wave N33 with progressively longer peak latencies from sagittal toward lateral positions was then recorded. MN-SEPs in contralateral central positions showed a well-localized P22 wave in which both the parietal early P25 and the frontal P20 were vanishing. Common or separate generators for frontal, central and parietal SEPs were discriminated by evaluating the influence of stimulus rate and intensity, as well as of general anesthesia and transient CBF deficits, investigated in 7 patients undergoing carotid endarterectomy. Unifocal anodal threshold shocks were separately delivered to each of the scalp electrodes and motor action potentials were recorded from the target muscle in order to delineate the scalp representation of the motor strip for the upper limb and, consequently, to monitor, through SEP tracings, the short-latency sensory input to the motor cortex for hand and shoulder muscles. This was characterized by a boundary zone separating the parietal N20-early P25 complex, from the fronto-central N18-P22 one. This zone had an oblique direction strongly resembling that of the central sulcus.

Adult↗
PubMed1987

Monitoring of subcortical and cortical somatosensory evoked potentials during carotid endarterectomy: comparison with stump pressure levels.

Monitoring of multichannel somatosensory evoked potentials (SEPs) has been performed in 40 cases of carotid endarterectomy (CEA). SEPs were obtained after median nerve stimulation at wrist, recording from 2nd cervical and from the scalp parietal (ipsi- and contralateral) and central (contralateral) positions. The reduction of CBF due to clamping of the carotid artery provoked SEP abnormalities in 10 of the 40 cases. None of the 30 patients with unmodified SEPs developed post-surgical neurological sequelae. SEP alterations were characterized exclusively by amplitude decrements and latency increases of the cortical components, the subcortical ones being unaffected. In 5 of these patients, SEPs returned to normal values before the end of the intervention and no neurological deficit was observed on awakening. In the remaining 5 cases SEPs retained their abnormalities and patients developed post-surgery neurological sequelae (4 immediately, 1 the day after). SEP alterations affected parietal and central components to a similar extent; however, in a few cases cerebral blood flow deficits provoked by carotid clamping modified differently the central P22 and the parietal N20-P25 waves. Comparisons with stump (back) pressure in the carotid artery revealed a higher sensitivity of the SEP technique in detecting vascularization problems due to carotid clamping. The time course of the appearance of SEP abnormalities seems to discriminate alterations secondary to collateral revascularization from those determined by embolization.

Adult↗
PubMed1987

Butoctamide hydrogen succinate and intensive learning sessions: effects on night sleep of Down's syndrome patients.

Mentally retarded children present a reduction in percentage of REM sleep and of oculomotor frequencies. These sleep patterns are probably relevant for their cognitive activities. The effects of butoctamide hydrogen succinate and intensive learning sessions on the night sleep of five Down's syndrome patients was studied by the authors. They found an increase in percentage of REM sleep after pharmacological treatment and an increase in oculomotor frequencies after learning sessions. The authors' hypotheses of REM sleep as a neurophysiological indicator of cerebral "plasticity" and of oculomotor frequencies as an indicator of "organization" abilities are discussed in this article. Pedagogical implications and therapeutical perspectives are also outlined.

Amides↗
PubMed1986

Sleep patterns of Down's syndrome children: effects of butoctamide hydrogen succinate (BAHS) administration.

Several investigators have described the altered sleep patterns in Down's syndrome subjects. The most relevant findings have been a reduction in percentage of REM sleep, a prolonged latency to the first REM episode, an increase in undifferentiated sleep, and a reduced ratio of the oculomotor frequencies. Because it is of interest to identify new drugs able to increase the percentage of REM sleep in mentally retarded subjects, we studied the effects of butoctamide hydrogen succinate (BAHS) on nocturnal sleep in eight young institutionalized Down's syndrome subjects. BAHS produced a significant increase in the percentage of REM sleep as well as a decrease in undifferentiated sleep and latency to the first REM.

Amides↗
PubMedDate not supplied

Sleep alterations after acute administration of carbamazepine in cats.

Little is known about the effects of carbamazepine (CBZ) on sleep despite the relationship between sleep and epilepsy and the common clinical use of CBZ. As part of a larger study on sleep and interictal activity in kindled cats, we performed sleep recordings in 11 normal cats before and after acute administration of CBZ. Epidural screws (frontooccipital) and depth electrodes (amygdala and hippocampus) were implanted bilaterally for EEG recording. Supraorbital screws and neck intramuscular electrodes were inserted for EOG and EMG. Ten days after electrode implantation, recordings were made of animals for 2 consecutive nights to assess baseline sleep patterns. Before the third night, cats received a single oral dose of 100 mg CBZ. After washout, a second similar drug administration was given before the fourth night. Recordings were scored for wakefulness, stage I and II of NREM sleep, REM sleep, number of stage shifts, awakenings, and REM onsets. The administration of CBZ produced a significant decrease in duration and percentage of REM sleep (p less than 0.001) and an increase in stage I NREM (p less than 0.05). Total sleep time was increased (p less than 0.05); awakenings were shorter (p less than 0.01), and stage I episodes were longer (p less than 0.01).

Animals↗
PubMedDate not supplied

Fragile-X syndrome: a particular epileptogenic EEG pattern.

A clinical and EEG study of 12 fragile-X syndrome subjects (six with epilepsy) is presented. All subjects had clinical-family history examinations, EEG evaluations, and karyotyping. Spikes were present in the sleep EEG of one nonepileptic and four epileptic subjects: these spikes were similar in location, occurrence, voltage, frequency, and morphology (and similar to those of the Rolandic spikes). These data, together with the clinical similarities (type of epilepsy, responses to drugs, ages of seizure onset, etc.), have resulted in the postulation of EEG characteristics of epileptic and nonepileptic fragile-X patients. However, further studies with fragile-X patients are needed to confirm this hypothesis.

Adolescent↗
PubMedDate not supplied

Eye closure sensitivity without photosensitivity in juvenile myoclonic epilepsy: polysomnographic study of electroencephalographic epileptiform discharge rates.

Two cases of juvenile myoclonic epilepsy (JME) presented with myoclonic jerks and EEG activation after eye closure, without sensitivity to intermittent photic stimulation. The effect of eye closure was computed by comparing discharge rates of polyspike-and-wave (PSW) complexes after eye closure and after eye opening. For one patient, never treated pharmacologically, a nocturnal polysomnograph was performed to study the variation of discharge rates of PSW complexes during wakefulness and sleep. The rate of PSW complexes was high during wakefulness before sleep onset, increased during spontaneous nocturnal awakenings, and became maximal during final morning awakening. Among nonrapid eye movement (NREM) sleep stages, EEG epileptiform activity was maximal during stages III and IV. Discharges were completely suppressed by rapid eye movement (REM) sleep. Awakenings following deep NREM sleep were very activating if no REM sleep was interposed. Awakenings from light NREM sleep were much less activating. There were no EEG abnormalities in awakenings immediately following REM sleep. Results suggest that REM sleep, similarly to eye opening, plays a role in inhibiting EEG manifestations of JME with eye closure sensitivity.

Adolescent↗
PubMedDate not supplied

Sleep microstructure and EEG epileptiform activity in patients with juvenile myoclonic epilepsy.

Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleep-wake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predominance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 +/- 0.98) and strong inhibition during phase B (0.06 +/- 00.6). Intermediate values were noted during NCAP (0.54 +/- 0.27). No correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges.

Activity Cycles↗