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Experimental allergic encephalomyelitis (EAE) in its chronic relapsing (CR-EAE), chronic progressive (CP-EAE) and acute (A-EAE) forms was obtained in 24 juvenile strain 13 guinea pigs. Visual, brainstem acoustic and somatosensory evoked potentials (EPs) were recorded in these animals prior to the sensitizing injection and during the course of the disease. Delays in the EPs appeared 15 days post-sensitization (dps), preceding or simultaneously with clinical alterations: electron microscopy revealed myelin stripping and vacuolation in the animals sacrificed 25 dps. Decreases in EP latency were recorded 32 dps; when electron microscopy revealed myelin layers indicating remyelination, whereas light microscopy showed only inflammatory changes. When confluent plaques were revealed by light microscopy 120 dps, the EP wave shapes were distorted or absent. The discussion reviews the literature on early myelin and conduction changes during central demyelination.

MRI of the optic nerves was obtained in 13 patients with acute optic neuritis and 13 with a previous optic neuritis (ON), assessed by clinical features, visual fields and visual evoked potentials. Results of the conventional short tau inversion recovery (STIR) sequence obtained with a short echo time (STE-STIR; 22 ms) were compared with those of a long echo time (LTE-STIR: 80 ms) sequence. The conventional STE-STIR sequence revealed lesions in the optic nerves in 78.5% of acute and 58.8% of previous ON. The LTE-STIR sequence showed abnormalities in 92.8% of acutely symptomatic nerves and 94.1% of nerves with previous ON. The optic nerve lesions appeared significantly longer with the LTE-STIR sequence than with the conventional STE-STIR sequences, in both acute and previous ON.

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.

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 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.

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.

Event-related potentials (ERPs) to an odd-ball paradigm were recorded from 19 scalp derivations in a patient (47 years old, housewife) affected by complete amnestic syndrome following limbic encephalitis. CT scans and magnetic resonance imaging showed severe bilateral lesions of anterior, mid-temporal lobes and frontal lobes. A P3 component, with a peak latency inside normal limits for age-matched controls, was recorded to ‘target’ stimuli from all leads except Fp1, Fp2, F7, F8, T3 and T4.

We studied 10 patients with post-traumatic amnesia (PTA) and normal CT scans. P3 with an oddball paradigm, several neuropsychological tests and EEG were performed the day after the trauma and several times later until full recovery. In all patients, P3 latencies at admission were above normal limits (mean + 2 SDs) and decreased progressively during recovery from PTA. The latency reductions correlated significantly with improvement of neuropsychological tests.

The paper reports the results of recordings and maps of event-related potentials (ERPs) obtained in normal subjects. ERPs were recorded from 19 scalp electrode derivations using both visual and acoustic paradigms. In normal subjects, topographical distribution of all ERP components is described in detail. Our findings in normals suggest that the early modulation of stimulus-related potentials could be located in primary associative areas, and that N2, P3a, P3b, and SW have different distributions.

Bit mapped color imaging of SEPs was recorded from 19 derivations in 11 healthy volunteers after electrical stimulation of the median nerve at the wrist, index finger digital nerve stimulation, and mechanical stimulation of the index fingertips by an electromechanically driven vibrating thin metallic plate. The latencies of SEP components increased for the various stimulation modalities, being shortestafter median nerve stimulation at the wrist and longest after mechanical stimulation of the index fingertips. The scalp distribution of SEPs to mechanical stimuli was, however, the same as other SEPs, independently of the stimulation employed, and components corresponding to N20 and P22 were recorded only contralaterally to the stimulated side.

In a patient affected by locked-in syndrome, because of a lesion of the caudal-ventral pontine tegment, we recorded event-related potentials (ERPs) to an acoustic odd-ball paradigm. We did not record N2 and P3 components in the 50 days following the acute lesion although the patient was able to understand the task and communicate with blinking. 55 days after the acute lesion, N2 and P3 reappeared on scalp derivations. This findings suggest that brainstem structures are involved in P3 or N2-P3 generation.

In a patient affected by locked-in syndrome, because of a lesion of the caudal-ventral pontine tegment, we recorded event-related potentials (ERPs) to an acoustic odd-ball paradigm. We did not record N2 and P3 components in the 50 days following the acute lesion although the patient was able to understand the task and communicate with blinking. 55 days after the acute lesion, N2 and P3 reappeared on scalp derivations. This findings suggest that brainstem structures are involved in P3 or N2-P3 generation.

Twenty patients affected by optic neuritis (ON) underwent serial visual evoked potential (VEP) recordings, performed with multiple electrode arrays, and with stimuli of 1 and 3 cycles per degree (cpd) for 1 year. VEP findings were correlated with long time echo-short tau inversion recovery (LTE-STIR) magnetic resonance imaging (MRI) of optic nerves and with visual field tests. MRI showed lesions in 95.2% of acute ON and in 66.6% of the 1 year follow-up. VEPs were classified into really 'delayed' VEPs and 'pseudodelayed' VEPs, based on their scalp distribution. Furthermore, VEPs to 1 or 3 cpd could be 'delayed' or 'pseudodelayed' in the same patient. Real delays could be recorded at onset or shortly after ON, and indicated the possibility of recovery of visual functions and good functional prognosis. Pseudodelays, to 3 cpd, corresponded to prominent central scotomata and indicated poor prognosis for the recovery of visual function, unless a breakthrough of normal or delayed components appeared in the first 4 months following acute ON. Pseudodelayed VEPs clustered in patients with longer demyelinating lesions, as shown by LTE-STIR MRI. There was no correlation between latency of VEPs and length of plaques. Our study addresses some reconsiderations of the pathophysiology of conduction delay in acute optic neuritis.

Twenty patients with optic neuritis (ON) described in the previous study [23] underwent serial VEP recordings (using multiple electrode arrays) for two years. The VEPs could be correlated with the lesions revealed by MRI, Visual Field tests and other clinical findings. On the basis of their scalp distribution, they were classified as “really delayed” VEPs and “pseudo-delayed” VEPs. Real delays could be recorded at the onset of ON or shortly afterwards, and their appearance indicated the recovery of visual function and a good prognosis. Pseudo-delays indicated an alteration in the visual field and, unless a breakthrough of normal or delayed components appeared in the first three months, following acute ON, indicate a poor prognosis for the recovery of visual function. The pseudo-delayed VEPs were mainly observed in patients with longer lesions revealed by means of LTE-STIR MRI [23]; there was no correlation between VEP latency and the length of plaques. Our findings contradict previous theories on the timing of conduction alterations in ON and multiple sclerosis.

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.

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.

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.

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.

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.

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.

Event related potentials (ERPs) to auditory and visual oddball paradigms were recorded from 19 scalp derivations in 10 controls. Three different reference systems were used: the linked earlobes (LE), the computer calculated mean reference (MR), and a calibrated sterno-vertebral extracephalic reference (EC). The distribution of ERPs was represented on single plane maps (quadratic interpolation, 4-NN method). With LE reference N2, P3a-P3b had no polarity reverted counterparts on the scalp. With EC reference a negativity was recorded on T3-T4 (and partly T5-T5) derivations with the same latency as P3a-P3b vertex component. With MR the N2, P3a-P3b components at vertex were paralleled by polarity reverted counterparts on anterior frontal, temporal and occipital derivations.

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 Fpl, 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.

Visual evoked potentials (VEPs) to pattern reversal vertical bar stimuli of 3 different sizes (1, 2, 4 c/deg) were recorded from 19 scalp derivations in 50 controls. The stimuli were presented on a full-field (FF) screen of 24 degrees visual angle, and on left and right half-fields (HF) of 12 degrees radius. In 15 controls partial HF stimuli were presented on the central 3 and 6 degrees and as hemiannular stimuli of 12 degrees with occlusion of the central 3 and 6 degrees. An antero-posterior polarity reversal of the N1-P1-N2 sequence was observed for FF VEPs. A tangential polarity reversal was observed for HF VEPs. Also with central or hemiannular stimuli polarity reversals of all VEP components were observed within the scalp. Variants of VEP distribution, absence or prominence of some of the ipsi- or contralateral VEP components were observed in 8-40% of controls. The FF and HF VEP distribution, and the variant VEP asymmetries were partly dependent on the pattern spatial frequency.

The paper reports the results of recordings and maps of event-related potentials (ERPs) in patients with Alzheimer’s disease (AD), progressive supranuclear palsy (PSP) and in subjects affected by dementia in multiple sclerosis (MS). ERPs were recorded from 19 scalp electrode derivations using both visual and acoustic paradigms. In 43% of AD patients, ERPs were normal; in 20%, although present, ERP components were delayed, while in the other 37% none of the N2 and P3 peaks could be recorded, because of abnormal topography of potentials on the scalp. In patients with PSP, the normal ERP sequence was not identified. In patients with MS delayed ERPs (50%), abnormal topography of ERPs (30%) and absence of ERPs (20%) were observed. The follow-up of AD patients showed a progressive alteration of ERPs. ERP topography alterations were observed in AD, PSP and MS patients with poorest cognitive performances.

This paper reports the results of recordings and maps of event-related potentials (ERPs) obtained in normal subjects, patients with Alzheimer's disease (AD), progressive supranuclear palsy, confusional states, and in subjects with homonymous hemianopsia. ERPs were recorded from 19 scalp electrode derivations using both visual and acoustic paradigms. In normal subjects, the topographical distribution of all ERP components is described in detail. In 45% of AD patients, ERPs were normal; in 35%, although present, ERP components were delayed, while in the other 20% the N2 and P3 peaks could not be recorded. In patients with progressive supranuclear palsy, the normal ERP sequence was not identified. Our findings in normals and in hemianopic patients suggest that the early modulation of stimulus-related potentials could be located in primary associative areas, and that N2, P3a, P3b, SW should have different origins.

This paper reports the results of recordings and maps of event-related potentials (ERPs) obtained in normal subjects, patients with Alzheimer's disease (AD), progressive supranuclear palsy, confusional states, and in subjects with homonymous hemianopsia. ERPs were recorded from 19 scalp electrode derivations using both visual and acoustic paradigms. In normal subjects, the topographical distribution of all ERP components is described in detail. In 45% of AD patients, ERPs were normal; in 35%, although present, ERP components were delayed, while in the other 20% the N2 and P3 peaks could not be recorded. In patients with progressive supranuclear palsy, the normal ERP sequence was not identified. Our findings in normals and in hemianopic patients suggest that the early modulation of stimulus-related potentials could be located in primary associative areas, and that N2, P3a, P3b, SW should have different origins.

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.

The authors briefly describe EEG, stimulus and event-related potential findings in two main subtypes of dementia (senile dementia of the Alzheimer type and multi-infarct dementia with lacunar state), suggesting the proper use of these electrophysiological techniques in the differential diagnosis and management of patients.

Systemic administration of L-acetylcarnitine HCl (LAC) increases in human subjects the amplitude of visual evoked potentials (VEPs) obtained with patterned elements of 7.5 min of visual angle, of steady-state VEPs obtained with intermittent luminous stimulation, of EEG theta, alpha and beta bands. The latency of the "cognitive" P300 potential obtained with an auditory "oddball" paradigm was also reduced by LAC injection, while the amplitude of this potential was increased. These results were obtained in control volunteers and in patients affected by different forms of dementias. The modifications induced by LAC appear 10-15 min after the i.v. injection and last for 50-90 min. These results parallel previously described findings of animal experiments and suggest an effect of LAC on cholinergic neurotransmission.

Magnetic resonance images of optic nerves were obtained in 20 patients with acute optic neuritis (ON), and assessed by means of clinical, visual field and visual evoked potential evaluations; the imaging was repeated 1 year later. The results of the conventional Short Tau Inversion Recovery (STIR) sequence obtained using short time echo (STE-STIR: 22 msec) were compared with those of the long time echo sequence (LTE-STIR: 80 msec). The conventional STE-STIR sequence revealed lesions in 57.2% cases of acute ON and in 42.9% of the optic nerves affected by previous ON; the LTE-STIR sequence was diagnostic in 95.2% of acute ON cases and in 85% of patients with previous ON. The calculated length of the optic nerve lesions was significantly longer in the images obtained using the LTE-STIR sequence than in those obtained using conventional STE-STIR sequences.