Altitudinal visual stimuli and the cruciform model of evoked potentials.
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Expert chess players can recall meaningful chess positions with extraordinary precision in comparison with inexperienced players. We hypothesized, therefore, that their mental performance during chess deliberation could be an appropriate target for single photon emission computerized tomography (SPECT) studies. We studied cerebral activation with 1110 MBq 99mTc-Bicisate SPECT in five expert male chess players during mental solution of a complex chess problem. Region of interest (ROI) analysis, in comparison with average weighted cerebellar counts, showed activation by 10% or more, of the non dominant prefrontal area (right in four dominant right handed players, left in one dominant left handed player) and by 2-6% in the non-dominant middle temporal areas. Maximum variability of ROI analysis versus cerebellar counts in test/retest evaluation is in our laboratory, as in others, 1.5%. Our results are in agreement with neuropsychological studies suggesting that the non-dominant hemisphere is specialized for chess skill, and show that non-dominant prefrontal and temporal lobe activation during chess deliberation can be detected by SPECT.
We recorded short latency somatosensory evoked potentials (SEPs) to median nerve stimuli in 40 patients affected by idiopathic Parkinson's disease (PD) classified from I to IV on the Hoehn and Yahr disability scale. SEPs were recorded before and after chronic administration of L-Dopa and bromocriptine, before and after acute administration of L-Dopa. Fourteen patients experiencing wearing off and dystonic-dyskinetic disturbances were recorded during the occurrence of these oscillations of their clinical status. Absent or reduced N30 components were found in 32.5% of patients. SEPs were not modified by acute or chronic administration of L-Dopa or bromocriptine or during off and dystonic or dyskinetic conditions. Multiple correlations of N30 with scores of the Unified Parkinson's Disease Rating Scale showed that N30 abnormality did not classify patients with prominent clinical features, nor did it predict the outcome of treatment.
Visual evoked potentials (VEPs) to pattern reversal vertical bar stimuli were recorded from 19 scalp, 2 zygomatic and 3 inion derivations referenced to digitally linked earlobes in 50 controls. 1, 2 and 4 cycles per degree (cpd) patterns were presented as full field (FF) stimuli, on upper and lower hemifields (UHF-LHF), upper and lower quadrants and with the occlusion of central and peripheral UHF and LHF. VEPs to octant stimuli were also recorded with 2 cpd patterns. N1, P1 and N2 components were recorded from posterior and inion derivations with FF stimuli, from posterior derivations with LHF stimuli, only from inion leads with UHF stimuli, from derivations ipsilateral to stimuli with quadrants and octants, and from midline derivations only with lower quadrants. Polarity inverted sequences (iP1-iN1-iP2) were recorded from the other scalp derivations, with similar latency and spatial frequency sensitivity as N1-P1-N2. The orientation of Equivalent Dipoles (ED) was orthogonal with surface coordinates of mesial and occipito-polar calcarine cortex, measured on Magnetic Resonance Imaging. A model of VEP generators is proposed, suggesting that the VEP sequence is elicited only in mesial and occipito-polar surfaces of calcarine cortex.
In 6 patients with lesions of frontal, parietal and temporal lobe, in 4 patients affected by primary progressive aphasia (PPA) and in 56 age-matched controls, event-related potentials (ERPs) to an auditory odd-ball paradigm were recorded with the linked earlobe reference (LER) and with a computer calculated average reference (AR), excluding the two linked earlobe derivations. Latencies, amplitudes and scalp distribution of the earlier ERP components (P1, N1, P2, N2) were within normal limits for both LER and AR recordings. P300 scalp distribution in patients was normal when LER was used. When P300 was recorded using AR, the scalp distribution was statistically different from normal distributions in all patients. A negativity, instead of the positive P300 observed in controls, was recorded in patients from leads corresponding to the affected hemisphere.
Magnetic resonance imaging of optic nerves was obtained in 13 patients with acute optic neuritis and in 13 patients with a previous history of optic neuritis (ON), assessed by clinical, visual fields and visual evoked potentials evaluations. Results of the conventional short tau inversion recovery (STIR) sequence obtained with short time echo (STE-STIR: 22 ms) were compared with long time echo (LTE-STIR: 80 ms) sequence. The conventional STE-STIR sequence revealed lesions in 78.5% of acute ON and in 58.8% of optic nerves affected by previous ON. The LTE-STIR sequence was diagnostic in 92.8% of acutely symptomatic nerves, in 94.1% of nerves with previous ON. The calculated length of optic nerve lesions was significantly longer in imaging obtained with the LTE-STIR sequence than with the conventional STE-STIR sequences, both in acute and previous ON.
Visual evoked potentials (VEPs) to central and lateral half field patterned stimuli of 1, 2 and 4 cycles per degree (cpd) were recorded in a patient with Dorsal Simultanagnosia due to bilateral lesions of parieto-occipital junction. VEPs consisted of the normal N1-P1-N2 components with same spatial frequency sensitivity as in controls. VEPs had similar latencies and amplitudes whether the patient could see or not the patterned stimuli. Event related potentials (ERPs) to visual and acoustic odd-ball paradigm were also recorded in the same patient. Visual ERPs consisted of an early NA-effect, and of N2-P3 components. P3 was recorded only from frontal, central and temporal derivations. The topographical P3 abnormality was, however, the same for visual and acoustic odd-ball paradigms. The amplitude of P3 was smaller when the patient missed visual stimuli. These findings show that severe bilateral lesions at the parieto-occipital junction, inducing Simultanagnosia, do not obliterate VEPs or ERPs components.
Visual evoked potentials (VEPs) to pattern reversal vertical bar stimuli were recorded from 24 scalp derivations (including zygomatic and inion) referenced to digitally linked earlobes in 50 controls. 1, 2 and 4 cpd patterns were presented as full field (FF) stimuli, on Upper Hemifields (UHF) and Lower Hemifields (LHF), upper and lower quadrants and with the occlusion of central and peripheral UHF and LHF. VEPs to octant stimuli were also recorded with 2 cpd patterns. N1, P1 and N2 components were recorded from posterior and inion derivations with FF stimuli, from posterior derivations with LHF stimuli, only from inion leads with UHF stimuli, from derivations ipsilateral to stimuli with quadrants and octants, and consistently from midline derivations only with lower quadrants. Polarity inverted sequences (iN1-iP1-iN2) were recorded from the other scalp derivations, with similar latency and spatial frequency sensitivity as N1-P1-N2. Single Equivalent Dipole (ED) calculations were performed on N1 and P1 recorded in the different stimulus conditions. Our findings contradict previous hypotheses on VEP generators and contradict the predictions of VEPs polarity and distribution based on the "cruciform model" of VEPs generators. In order to explain the distribution of VEPs to upper and lower half fields and to quadrant and octants, we propose a model based on the position of the medial and occipito-polar surface of visual cortex in man.
With ST200 as the commercial source of L-acetylcarnitine hydrochloride, 94 patients were enrolled in this study; 31 were assigned to placebo, 31 to ST200 at 0.5 g/die and 32 to ST200 at 1 g/die, the i.m. treatments being injected daily for 15 consecutive days. In general, concerning the efficacy assessment, the administration of ST200 at 1 g/die appeared to be better than ST200 at 0.5 g/die when compared with the placebo administration. Statistically significant differences were revealed by the comparison of ST200 at 1 g/die to placebo, for the following variables: a) total motility as rated at the end of the 15-day study and confirmed by intention-to-treat analysis, b) visual analogue scale for all the patients having observation at day 15, and c) the objective and subjective judgements on efficacy. Safety and tolerability were good over the entire course of the study.
Event related potentials (ERPs) to an auditory odd-ball paradigm were recorded with the linked earlobe reference (LER) and with a computer calculated average reference (AR), excluding the two linked earlobe derivations. The study was performed in 30 patients with lesions of frontal, parietal, occipital cortex, unilateral and bilateral lesions of the medial temporal lobe (MTL), in four patients affected by Primary Progressive Aphasia (PPA) and in 56 age matched controls. Latencies, amplitudes and scalp distribution of the earlier ERP components (P1, N1, P2, N2) were within normal limits for both LER and AR recordings. P3 scalp distribution in patients was normal when LER was used, with the exception of two patients affected by bilateral MTL lesions. When P3 was recorded using AR, the scalp distribution was statistically different from normal distributions in all patients. A negativity, instead of the positive P3 observed in controls, was recorded in patients from leads corresponding to the affected areas. This finding might have clinical applications, and confirms earlier studies suggesting that P3 is generated simultaneously from different cortical areas.
Somatosensory Evoked Potentials (SEPs) to median nerve stimuli were recorded in seven Cynomolgus monkeys before and after the induction of the MPTP-parkinsonian syndrome. SEPs recorded after the onset of parkinsonism showed a significant amplitude reduction of an anterior negative component peaking at about 15 ms (N15), independent of the severity of symptoms. The amplitude decrease was not reversed by the administration of I-dopa, despite clinical improvement, or cholinergic, noradrenergic and gabaergic agents. Amplitudes of N15 and of parietal P15 components were increased by the administration of the N-MDA antagonists ketamine and MK 801, and markedly increased when monkeys were given the anaesthetic agent etomidate. The present study shows that the reduced N15 SEP component of parkinsonian monkeys is similar to the reduced frontal N30 SEP component evidenced by other authors in patients affected by Parkinson's disease. The attenuation of N15 is not related to deficitary dopaminergic, noradrenergic, cholinergic and gabaergic systems. The implications of this finding and the role of glutamate toxicity are discussed.
We describe the MRI changes preceding the onset of myoclonus in two patients whose post-mortem examination confirmed the diagnosis of Creutzfeldt-Jakob disease (CJD). MRI showed changes in the striatum early in the course of CJD (2-6 months after the onset of apathy, interpreted as depression, and 1-2 months before the onset of further clinical symptoms). Only in one patient did electroencephalography record the typical triphasic sharp-waves, 1 month after MRI.
Two cases of Creutzfeldt-Jakob Disease (CJD) are reported. In both cases, pathologically confirmed, magnetic resonance imaging (MRI) showed bilateral altered signal areas in the basal ganglia, early in the course of the disease. The CT scan, although performed later than MRI, confirmed these findings. Only in one patient did electroencephalography (EEG) show typical triphasic sharp-waves, but this support to clinical diagnosis was obtained 1 month after the appearance of MRI alterations.
Delayed P3 ERPs were recorded with an acoustic oddball paradigm in 5 patients affected by unilateral thalamic hemorrhage. P3 latencies in these 5 patients were above the normal mean latency of age-matched controls +2/+3 S.D.s. The P3 delay was persistent in serial follow-ups at 6 months from stroke. Normal P3 latencies were instead recorded in 4 patients with paramedian hemorrhage not involving or only partially involving the thalamus.
Narcolepsy and cataplexy began one year before treatment of a left mid-temporal primary B-cells lymphoma in a HLA DR2 negative man. Treatment with radio therapy and immunosuppression induced regression of the lymphoma and disappearance of narcolepsy and cataplexy.
We recorded event-related potentials to an acoustic "oddball" paradigm from 19 scalp derivations in five patients (three women and two men; age range, 44 to 56) who had global amnesia following encephalitis. CT and MRI showed severe bilateral lesions of anterior and midtemporal lobes. A P3 component, with a peak latency within the normal limits for age-matched controls, was recorded to "target" stimuli in four patients from all leads except Fp1, Fp2, F7, F8, T3, and T4. In the fifth patient, the P3 peak was delayed.
24 juvenile strain 13 guinea pigs were sensitized with homologous spinal cord homogenate in complete Freund's adjuvant in order to obtain Experimental Allergic Encephalomyelitis (EAE) in the Chronic Relapsing (CR-EAE), Chronic Progressive (CP-EAE) and Acute (A-EAE) forms. Visual, Brain-Stem Acoustic, Somatosensory Evoked Potentials were recorded in these animals, prior to the sensitizing injection and during the course of the disease. The aim of our study was to observe modifications of Evoked Potentials during progression of a demyelinating disease. Latency delays of Evoked Potentials appeared 15 days after the sensitizing injection, preceding or simultaneously with clinical alterations and when demyelinated plaques were not detected in anatomical specimens.
Acetyl-levo-carnitine (ALC) protects against 1-methyl, 4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity in the nonhuman primate. ALC pretreated monkeys do not show signs of parkinsonism or electroretinographic changes typical of dopaminergic deficiency when given MPTP. In addition, pilot neurochemical and morphological data confirm a partial protection effect. While MAO-B inhibitors, like L-Deprenyl, are thought to protect dopaminergic neurons from MPTP-induced cell death by preventing the conversion of MPTP to its toxic metabolite MPP+, ALC is not known to have MAO-B affinity. Converging evidence suggests that ALC may affect directly mitochondrial respiration, which is known to be the target of MPP+ and affected in human neurodegenerative diseases, including Parkinson's disease. The results of this study point to new therapeutic avenues for the treatment of these nosologic entities.