Apomorphine and lisuride infusion. A comparative chronic study.
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Biomedical subjects
Publications and source records attributed to E Stefano.
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The pattern electroretinogram (PERG) was recorded at different contrast levels (96%, 71%, 47%) in 10 Parkinson's disease patients before and during dopaminergic monotherapy. The data were compared to a control group of 8 normal subjects recorded with the same procedure. PERG P50 latency progressively increased as contrast was decreased both in normal subjects and patients; however, this trend was much more pronounced in PD patients without therapy; consequently in this group the difference between P50 latency obtained with 96% and 47% contrast was statistically significant (P = 0.01, analysis of variance corrected by post-hoc Tukey test). By contrast this was not seen in the control group. Statistical analysis (Bonferroni's t test) showed at the 47% contrast level a significant P50 latency increase (P less than 0.01) in PD patients without therapy if compared with the control group. Dopaminergic monotherapy induced a P50 latency recovery in PD patients. We conclude that low contrast stimuli enhance PERG sensitivity to the visual dysfunction of PD patients. Moreover, the effects observed after therapy confirm that abnormal contrast response functions in PD patients are linked to dopaminergic deficiency.
We studied 18 multiple sclerosis (MS) patients affected by retrobulbar neuritis (RBN). The patients were subdivided into two groups. Group 1: 14 patients with RBN. Group 2: 4 patients with optic atrophy. An ophthalmological examination (visual acuity, fundus oculi, visual field) was carried out in all the patients. A simultaneous visual evoked potential (VEP) and pattern electroretinogram (PERG) recording at two spatial frequencies (45' and 15') was performed. All the data obtained in Group 1 were compared (Student T-Test) with those of a control group of normal subjects matched for age and sex. Group 1. VEP: a comparison of the data in MS patients affected by RBN with the control group revealed a statistically significant P100 latency delay with both spatial frequencies (P less than 0.001). PERG: no "b" wave latency change at 45' and 15' spatial frequencies were seen. A "b" wave amplitude reduction was observed; this reduction reached significant values at 45' (P less than 0.001). Group 2. In optic atrophies the PERG was absent in 4 eyes at 45' and in 5 eyes at 15'.
The neuropharmacological and neurochemical features of Progressive Supranuclear Palsy (PSP) are reviewed, together with the results obtained by various therapeutic trials. PSP is a neurodegenerative disease which often causes Parkinsonian symptoms but dopaminomimetic drugs have given rise to poor improvement, in spite of dopamine decrease observed in PSP patients' nigrostriatal region. The uselessness of L-DOPA therapy in PSP patients may explain the numerous failures encountered in PSP patients misdiagnosed as Parkinsonian. On the basis of the recent discovery of striatal dopaminergic receptor abnormalities and of interaction between various neurotransmitters, the authors suggest some possible therapeutic substances that might improve the outcome of the disease.
The authors review the neurochemical and electrophysiological features of insomnia, together with the results obtained by various substances. The literature data show that the benzodiazepines (BZ) should be administered for short periods of time, in order to avoid addiction and withdrawal symptoms. For this reason, the authors suggest that, before starting a therapy with such substances, an accurate clinical evaluation should be made and a good knowledge of the pharmacokinetics of the various BZ is essential.
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Short-latency flash visual evoked potentials (VEPs) and electroretinograms (ERGs) were recorded in 30 healthy volunteers and 14 patients (7 with retrobulbar neuritis and 7 with retinitis pigmentosa). Simultaneous recordings were performed by corneal, scalp, nasopharyngeal and retrobulbar (5 patients) electrodes. In 18 out of 30 healthy controls a brief sequence of oscillating wavelets was recorded between 15 and 40 ms on the scalp sites behind the vertex. In retrobulbar neuritis (RBN) patients normal responses were recorded by lens, retrobulbar, nasopharyngeal and frontal scalp electrodes. On the contrary none of these patients displayed short-latency activity behind the Cz scalp position. In 5 out of the 7 patients with retinitis pigmentosa, corneal, nasopharyngeal and scalp electrodes failed to detect any reliable waveform time-locked to the flash onset. In the remaining 2, a small lens ERG was recorded, while all other electrodes recorded a sequence of low-volted wavelets initiating 30 ms after the stimulus onset. In these patients an occipital VEP reduced in amplitude and with prolonged latency was also recorded. It is concluded that in presence of a normal corneal ERG because of the presence of volume spread oscillating retinal activity, it is hard to define while part of the scalp recorded, short latency, oscillating potentials is generated in subcortical visual structures.
The authors have studied, by means of pattern visual evoked potential (VEP) and flash electroretinogram (ERG) recordings, a group of 15 patients affected by definite multiple sclerosis. All of the subjects examined presented a clinical history indicating involvement of the visual pathways; VEPs were altered in a high percentage of eyes examined (93.3%), while a lower percentage of abnormal ERGs was seen (20% of eyes examined). The only type of ERG alteration found consisted of a pathologic b wave voltage increase, observed mainly with red flash stimuli. This finding could be attributed to an involvement of centrifugal optic nerve fibers having inhibitory functions on retinal cells.
The epileptogenic properties of cefazolin (CFZ) were utilized to induce an electrophysiological pattern of epilepsy in the rabbit. CFZ, cortically applied in different concentrations (2 or 4%), produced epileptic activity in a degree proportional to the concentration of the substance. In this experimental epilepsy model, we evaluated the effects of increasing doses (0.025, 0.05, and 0.1 mg/kg i.v.) of the calcium antagonist nimodipine (Bay e 9736). In the evaluation of nimodipine effects, the spike-and-wave burst frequency per minute was taken into account. These data were compared with those of placebo-treated (Bay e 9736 control test) control groups and statistically evaluated by two-tailed t test. In 2% CFZ-induced epilepsy, nimodipine at the 0.025- and 0.05-mg/kg doses did not produce significant changes in the EEG pattern. A statistically significant reduction (p less than 0.001) in epileptic activity was observed at the 0.1-mg/kg nimodipine dose. This reduction was seen first in the contralateral focus leads and persisted for the entire time of observation. In the more intense epileptic form (4% CFZ), nimodipine at the doses employed did not induce noteworthy EEG modifications. These data indicate that nimodipine exerts an antiepileptic effect. The possible mechanisms involved in this activity of a calcium antagonist are discussed.
Great interest has been recently raised by the discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a meperidine analogue capable of producing an irreversible Parkinson's disease. On the basis of papers published during the last years, we examined the structural features and the specific mechanism of action of this substance at the level of dopaminergic neurons. Furthermore, the clinical features of the experimental Parkinson model, obtained by means of MPTP inoculation in various animals and their similarities to the analogous human disease are described. We can conclude that the MPTP discovery enhances the hypothesis that Parkinson's disease can be also attributed to toxic factors.
Two cases of subcortical arteriosclerotic encephalopathy (Binswanger's disease) are reported. The two patients lacked a clinical history of hypertension, relevant pathogenetic factor in the development of the small and medium size cerebral arteries atherosclerosis, which is the main pathologic finding of the disease. The two subjects clinically showed a marked intellectual deterioration, together with mood depression and focal neurological signs, that were an expression of the multifocal neurologic involvement. In both cases CT scans evidentiated a mainly periventricular leucoencephalopathy associated, in the first patient, with small multiple ischemic lesions and, in the second, with a unique hypodense area in the centrum semiovale. A review of the literature on the subjects is proposed, together with an attempt of pathogenetic interpretation of our two cases.
6 patients suffering from migraine and consciousness disturbances occurring together in a significant chronologic association were selected retrospectively. Clinical, radiologic and electroencephalographic data are reported; the hypothesis of a common pathogenesis of the two syndromes is discussed by means of the "neural" theory of migraine and the results of cerebral blood flow studies in migrainous subjects. In addition, the therapeutic effectiveness of the pharmacologic association between calcium-antagonists and antiepileptic drugs in some patients is remarked.
Twenty-four patients affected by beta-thalassemia major were studied by means of combined EEG, VEP and BAEP recordings. All the subjects were treated with regular blood transfusions and chelating therapy (DFO). An elevated incidence of EEG abnormalities (70.8%) consisting of diffused slow waves and/or diffused small sharp spikes was seen. VEP P100 latency was abnormally prolonged in eight patients (33.3%). Furthermore, a voltage increase of N75-P100 (29%) and P100-N145 (33.3%) VEP components was observed. Mean latency and voltage values were significantly increased when compared with those of a control group. No BAEP alterations were observed. No correlations were found between electrophysiological data, serum ferritin levels and transfusional treatment duration. The possible mechanisms involved in provoking such electrophysiological abnormalities are discussed.