Biomedical subjects

M G Marciani

Publications and source records attributed to M G Marciani.

81 records · Page 5Linked to original sources

PubMedDate not supplied

Effects of drug withdrawal on location of seizure onset.

Fourteen patients with intractable epilepsy, candidates for surgical treatment, were investigated with intracerebral electrodes because of the presence of multifocal abnormalities in surface recordings. EEG and video monitoring was performed during a period of reduction and/or discontinuation of anticonvulsant medication performed to precipitate seizure occurrence. The clinical and electrical patterns of seizures recorded during the withdrawal of anticonvulsant drugs were compared to those of the patients' habitual seizures observed on full medication. For each patient, we determined a profile of the clinical and electrographic seizure activity observed before the withdrawal of medication or reported by the patient prior to hospitalization. Following the reduction or cessation of medication, an increase in partial seizure frequency was observed in all patients. All but one of these partial seizures had the same clinical pattern as the habitual attacks of the patients, and the EEG manifestations were compatible with the baseline data. Seven of the 14 patients had secondarily generalized seizures; for each patient, these seizures had the same clinical and electrographic onset as their partial seizures. Only one patient had a single partial seizure having an EEG onset different from the other seizures occurring around that time and having a clinical pattern never experienced before. In conclusion, the reduction of anticonvulsant medication extremely rarely causes the appearance of seizures having an electrical onset or a clinical pattern different from those observed on full medication.

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↗

PubMedDate not supplied

Neurophysiologic and neuropsychologic profiles of lamotrigine in epilepsy.

The anticonvulsant potential of lamotrigine (LTG) has been extensively assessed in open and double-blind clinical trials including patients with different types of epilepsy. In this review, the neurophysiologic and neuropsychologic profile of LTG is discussed. The electroencephalographic (EEG) findings reveal that the drug induces a decrease both in frequency and in probability of propagation of the EEG epileptiform abnormalities (interictal and ictal), whereas the background activity appears unmodified. In contrast with the traditional antiepileptic drugs (AEDs), LTG does not affect evoked responses (brainstem auditory evoked potentials and somatosensory and visual evoked potentials), indicating only a minor toxic effect on the nervous system. The neuropsychologic assessment shows that LTG does not alter the cognitive functions. In conclusion, the neurophysiologic and neuropsychologic data confirm the efficacy and safety of LTG and support its clinical use as monotherapy in epilepsy.

Anticonvulsants↗

PubMedDate not supplied

Toxic effects of high-dose deferoxamine treatment in patients with iron overload: an electrophysiological study of cerebral and visual function.

BACKGROUND AND METHODS: It is well known that deferoxamine (DFO) treatment in thalassemia major can produce ocular toxicity. In one experience, Visual evoked potentials (VEPS) to pattern reversal were formed to be altered in 4 out of 10 patients under conventional treatment with DFO, before supplementary high-dose i.v. deferoxamine. In all 4 cases the alterations consisted of bilaterally delayed P100 latency, always obtained by stimulation with high spatial frequency (15' checks) and associated in three cases with low spatial frequency (55'). Computerized EEG (cEEG) studies showed a generalized increase of slowing activity. All patients underwent high-dose DFO treatment. RESULTS: At the control performed at the end of treatment in all 4 cases with previous VEP alterations, a further delay in P100 latency was observed bilaterally while two of the six patients, without previous involvement, showed delayed responses when using checks of 15'. The EEG slowing activity was not modified. Three weeks after terminating i.v. DFO therapy, the patients were still under subcutaneous treatment (50 mg/kg/day); a more evident VEP recovery towards the initial values was observed in those patients without initial alterations. No significant changes were found between electrophysiological parameters and serum ferritin levels. CONCLUSIONS: Our results indicate that high-dose DFO therapy in patients with iron overload induces reversible visual impairment without significant changes in brain electrical activity. The employment of VEP in intensive chelation programs in thalassemia major is discussed.

Adolescent↗

PubMedDate not supplied

Non-clinical tests for the diagnosis of multiple sclerosis.

Liquoral, Neurophysiological and Nuclear Imaging data were investigated in 29 patients suffering from Definite (11 cases), Probable (11 cases) and Possible (7 cases) Multiple Sclerosis (MS). The most sensitive tests were: Visual Evoked Potentials (VEPs), altered in 75% of patients, Motor Evoked Potentials (MEPs), abnormal in 75%, Nuclear Magnetic Resonance Imaging (MRI) in 72.4%. Somatosensory Evoked Potentials (SEPs) were altered in 69.2% in PN-SEPs and in 53.6% in MN-SEPs, whilst Brainstem Evoked Potentials (BAEPs) were altered in 30.8% of cases. The results suggest that patients with suspected forms of MS should be submitted, as routine diagnostic protocol, to a battery of EPs, including as a first choice VEPs, MEPs and PN-SEPs. MRI should be performed to confirm a diagnosis not supported by EP data, or for a comprehensive localization of the demyelinating plaques.

Adolescent↗

PubMedDate not supplied

Protective effect of clonazepam on ischemic brain damage induced by 10-minute bilateral carotid occlusion in Mongolian gerbils.

A 10-min bilateral carotid occlusion (BCO) in a control group of Mongolian gerbils, induced a transient generalized epileptic activity both in the hippocampal and in the cortical regions, associated with motor manifestations. After recirculation, spiking activity persisted, reaching its maximum peak within 18-36 h and then slowly decreasing till its total disappearance on the 6th-7th day. On the 7th day, histological studies manifested a selective loss of CA1 hippocampal neurons. The treated gerbils (divided in 2 groups according to the dosage used) were administered clonazepam (CZP), a benzodiazepine receptor agonist, immediately after clamping and again every 24 h for the following three days at dosages of 0.05 and 0.1 mg/kg i.p., respectively. The drug inhibited epileptic activity in a dose-dependent manner, while it prevented CA1 neuronal loss at both doses. These results point to a possible derangement of the GABAergic system which probably in turn triggers an exaggerated excitation.

Animals↗

PubMedDate not supplied

[Update on cerebral monitoring and protective methods].

Clamping ischaemia is responsible for the 20-30% of the neurological complications during carotid surgery. It is impossible at present to determine preoperatively for certainty the patients who are at risk and the ones who are not at risk for clamping ischemia. Intraoperative monitoring is mandatory in all the cases to point out cerebral ischemia and to prevent neurological deficit with an adequate brain protection. Methods used to predict brain ischaemia include local anesthesia, EEG, SEP, stump pressure measurement, transcranial doppler, regional cerebral blood flow measurement and evaluation of venous blood gases from the internal jugular vein. Local anesthesia is a safe and simple method of assessing cerebral ischemia during carotid clamping but has some limits particularly in case of brain ischaemia for the technical difficulties to install an indwelling shunt in an awake and often troubled patient. Moreover the only possibility of cerebral protection under local anesthesia is an increase in systemic blood pressure with a resulting growth in cardiac morbidity and mortality. For these reasons operation should be performed under general anesthesia to assure a better farmacogical brain protection when preoperative evaluation demonstrates a reduction of cerebral vasoreactivity, with a consequent high risk of clamping ischemia. At present EEG is one of the most used technique of cerebral monitoring under general anesthesia with a sensibility and specificity in the diagnosis of brain ischaemia that is about 90%. The best cerebral protection is obtained with a selective shunting. Burst suppression, with high dose thiopentone, has recently demonstrated its reliability alone or in association with an indwelling shunt in patients at high risk for clamping ischaemia. Of course a systematic cerebral protection together with an accurate control of the blood pressure is necessary in all the patients. This behaviour allowed us to obtain good results in the last 500 patients with a morbidity and mortality respectively of 1% and 1.6% with no significant differences between patients who tolerated carotid clamping and those with clamping ischaemia.

Blood Pressure Determination↗

PubMedDate not supplied

Lamotrigine add-on therapy in focal epilepsy: electroencephalographic and neuropsychological evaluation.

The effect of lamotrigine (LTG) as add-on therapy on electroencephalogram (EEG) background activity was studied in 11 patients with refractory partial seizures with or without secondary generalization. The computerized EEG study was performed at rest with eyes closed (EC), during blocking reaction (BR), fixation (FIX), and mental arithmetic (MA) tasks. EEG spectral values were analyzed statistically using three-way ANOVA. The neuropsychological evaluation included a battery of six tests. Epileptic patients before LTG therapy, compared with control subjects, displayed at rest condition EEG changes consisting of higher delta and theta relative power coupled with lower alpha and beta power. During performance of attentive (BR) and cognitive (FIX) tasks, a decrease in alpha reactivity associated with a decrease of beta 1 and beta 2 power was found. The addition of LTG to previous therapy induced changes, although subtle, consisting of an increase in both alpha reactivity and beta power to attentive task. Neuropsychological evaluation did not evidence any impairment of cognitive functions. During LTG therapy, a decrease in seizure frequency occurred in 9 of the 11 patients whereas no changes were observed in the remaining 2. On the basis of these neurophysiologic and neuropsychological findings, LTG as add-on therapy does not seem to produce adverse side effects on mental activity; moreover, EEG data indicate a slight improvement in attentional processes.

Adolescent↗