Black and white checkerboards (56′) of varying contrast levels were presented in the transient reversal mode (2 Hz). The transient Pattern Electroretinograms were recorded on four subjects with normal vision using DTL fibres. Across the contrast range 9–80%, the amplitudes of the response were linearly sensitive to contrast variation without saturation (P < 0.001). Two potentials on the major negative potential (N95) divided by a notch had different contrast sensitivities and contrast gains: the potential after the notch (a‐Nw) was strikingly less sensitive to contrast variation and had a lower contrast gain than the potential before the notch (Nw). a‐Nw had a linearity at contrast level over 23%. Nw showed a high similarity to P50 in both contrast versus amplitude function and contrast gain.The evident difference of the contrast gains between Nw and a‐Nw suggests that there are possibly some corresponding differences in their retinal origins. It is assumed that the major negative potential after the notch is functioned by the inner retinal neurones with low contrast sensitivity, which includes the ganglion cells, being possibly predominated by the retinal magnocellular cells; the potential Nw has some common retinal mechanisms with P50, probably representing the macular function.

Photosensitive epilepsy came to prominence in the 1950s with the advent of television. Photosensitive epilepsy occurs in 1 in 4000 of the population. The incidence is 1.1 per 100,000 per annum, however amongst 7-19 year-olds the incidence is more than five times as common. Photosensitive epilepsy is twice as common in females as in males. The onset is around puberty, but less than 25 per cent of patients lose their photosensitivity in their twenties. Patients are investigated in the EEG laboratory using intermittent photic stimulation. Peak sensitivity is between 16 and 20 flashes/s but 49 per cent of patients are sensitive to 50 flashes/s, explaining the sensitivity to PAL television systems. From 1993 the development of broadcast guidelines was developed restricting both flash rates and the areas of screen involved, as well as the use of long-wavelength red. Automatic analysis systems can now test material for compliance with guidelines in real time.

Flash visual-evoked cortical and subcortical potentials are studied in human albinos for evidence of optic nerve fibre misrouting. The relationships between the results obtained and the visual problems associated with albinism are discussed.

Nine patients who had epileptic attacks while playing computer games were studied in the laboratory. Patients had an EEG recorded as well as their response to intermittent photic stimulation (IPS) at flash rates of 1-60 fps. In addition, pattern sensitivity was assessed in all patients by a gratings pattern. Only 2 patients had no previous history of convulsions, and only 2 had a normal basic EEG. All but 1 were sensitive to IPS, and all but 1 were pattern sensitive. Most patients were male, but although this appears to conflict with previously published literature results regarding the sex ratio in photosensitivity, it was due to the male predominance of video game usage. We compared our results with those reported in the literature. Diagnosing video game epilepsy requires performing an EEG with IPS and pattern stimulation. We propose a standard method of testing.

The antiepileptic drug, vigabatrin, has been linked to a specific pattern of visual field loss. The majority of studies have not included the paediatric population due to difficulties assessing visual field function. This is a particular problem as vigabatrin is effective against infantile spasms. A field-specific visual evoked potential was developed which consisted of a central stimulus (0–5° radius) and a peripheral stimulus (30–60° radius). Both stimuli consist of black and white checks which increase in size with eccentricity. Responses are recorded from occipital electrodes O2 and O1 referred to frontal electrode Fz. Electroretinograms and perimetry was performed were possible as a comparison. Thirty-nine children with epilepsy treated with vigabatrin aged from 3 to 15 years were included in the study; 35/39 children complied with the field-specific VEP, 26/39 complied with the ERG and 11/39 performed perimetry. Of these results, 18 children had normal ERG responses and eight had abnormal response. Visual field testing revealed four children had abnormal and seven had abnormal visual field results. The Field-specific VEP identified three of four abnormal perimetry results and six of seven normal perimetry results, giving a sensitivity of 75% and a specificity of 85.7%. When comparing perimetry results with the ERG parameters only the 30-Hz flicker amplitude, with a cut-off amplitude below 70 µV, gave a useful sensitivity of 75% and a specificity of 71%. The field-specific VEP is a useful alternative method that is both well tolerated by young children and gives a reliable indication of likely peripheral visual field loss associated with vigabatrin. The defect appears to have a similar prevalence in children as it does in adults.

Vigabatrin is known to induce visual field defects in approximately one third of patients treated with the drug. It is apparent from electrophysiological studies that the cause of this defect is at retinal level probably as a result of the build up of GABA. Studies of electrophysiological retinal parameters such as the EOG and photopic, scotopic and 30-Hz flicker ERG have revealed changes in Arden Index, photopic a and b wave latency and amplitude, changes in oscillatory potentials, and changes in latency and amplitude of the 30Hz response. However, many of these changes such as the Arden Index, oscillatory potentials, latency and amplitude of photopic b wave appear to be related to current anti-epileptic drug treatment rather than visual field defects. Certain parameters, particularly the amplitude of the 30-Hz flicker response, do appear to correlate with the severity of the field defect. Paediatric patients treated with the drug at age 9 years or below cannot reliably perform visual field perimetry. To identify these patients a special VEP H-Stimulus has been developed to produce separate responses from central and peripheral field stimulation by alternating at slightly separate rates. Forty-five healthy children between ages 3 and 10 years have been used to develop a normal database. This technique has a sensitivity of 75% and a specificity of 87.5% in identifying the field defect and may be used in children with epilepsy from age 3 upwards.

and Sumnall (2002) to write to the Journal and welcome the opportunity to reply. Cole and Sumnall’s main point is that the Beck Depression Inventory (BDI) mean score (9.2) for our group of ex-chronic ecstasy users (MacInnes et al., 2001) coincided with that reported for the healthy volunteer control group (9.1) in a study by Tse and Bond (2001) in the same issue. This, they feel creates a dilemma in interpretation. Non-patient samples yield variable results on the BDI (Beck et al., 1988) and can differ according to age, gender and other demographic variables (Enns et al., 2000; Blanchard et al., 2001; Ostler et al., 2001). Indeed, we could cite the example of Reif and co-workers (2001) where control group BDI was only 2.7. Thus cross-study comparisons have very little meaning, the relevant comparison is within a study. Tse and Bond (2001) were able to use the experimental model with random allocation for the design of their comparison of citalopram with placebo, but investigations of users of illicit drugs are restricted to field-studies for ethical reasons. We matched our controls for age, gender, ethnicity and educational attainment and stand by our interpretation of the significant difference in BDI scores between our control sample (mean BDI 5.2) and ex-chronic ecstasy user group. Cole and Sumnall (2002) are not correct in assuming we believe the score BDI of 9.2 in our ex-chronic ecstasy users indicates ‘mild depression’. The purpose of the BDI is to establish symptom severity, not diagnostic status (Peirson and Herbert, 2000) and, as shown by the title of our paper, we suggest only that our former chronic users of methylenedioxymethamphetamine (MDMA or ecstasy) report ‘mild depressive symptoms’. Beck et al. (1961) emphasize that their instrument is ‘aimed at registering varying degrees of depression along a continuum, it is not designed to distinguish among standard diagnostic categories’. It is for this reason that it is a useful tool with which to examine depressive symptomatology in non-clinical samples. However, we did indeed include the subsidiary remark that Beck and co-workers suggest a score of 9 represents mild depression in our Discussion but the reference for this should have been the Beck Depression Inventory Manual (Beck and Steer, 1987), rather than Beck et al. (1961). Cole and Sumnall (2002) also claim there is no direct evidence to suggest that ecstasy users are at risk of ‘... developing “a more depressive syndrome” as a direct consequence of their ecstasy use’. We entirely agree. The control-group comparison was only one part of our study and we went on to investigate our ex-user group in some depth, finding that former chronic ecstasy users fulfil a vulnerability model of depression (Hammen and Cochran, 1981), including a negative attributional style or, as Beck (1991) would state, a negative cognitive shift, i.e. they perceive the outcome of future events as ending in failure or loss. Whether this is cause or consequence of previous use of ecstasy we cannot tell at this stage, but it is from this finding that we predicted a risk of our ex-users developing a ‘more depressive syndrome’.

Previous work has indicated recreational use of methylenedioxymethamphetamine (MDMA or ecstasy) is associated with elevated scores on self-report measures of depression. We sought to examine the long-term effects of consumption on depression in a group of individuals who had consumed large quantities of the drug in the past, but were now leading relatively drug free lives. Respondents to this study (n = 29) had consumed an average of 1.5 ecstasy tablets in the last month, 8.4 in the last 6 months and 23.3 in the last 12 months. The estimated total consumed was 527 tablets, indicating that these respondents were indeed former chronic users of the drug. None of the respondents had consumed ecstasy in the last 14 days. Levels of depression (Beck's Depression Inventory) were significantly (p < 0.01) elevated compared to a matched non-drug using control group. Within the group of former chronic users, these levels of depression were not significantly affected by current use of alcohol, cannabis or amphetamine, but were positively correlated with an external locus of control (p< 0.05), infrequent but severe- (p< 0.05) and frequent but mild- (p< 0.005) self-report measures of life stress. Multiple regression indicated that levels of frequent but mild life stress (p< 0.005) and the quantity of ecstasy tablets respondents consumed over a 12-h period (p< 0.05) were the only variables that were significant predictors of self-reported levels of depression. The results of this study indicate that former chronic ecstasy users report higher levels of depression than their matched controls.

An inverse problem needs to be solved in order to localise the brain activity that underlies the recorded MagnetoEncephalogram (MEG). However, this inverse problem is non-unique. The non-uniqueness can be reduced by constraining solutions to lie on and be orientated perpendicular to the cortical surface. In practice however, the accuracy to which the true position and orientation of the surface can be determined is limited by MEG-MRI co-registration errors. The FOCUSS [1] and constrained dipole fit algorithms used in this study incorporated constraints by means of a source space. This source space was constructed by placing equivalent current dipoles on a mesh defining a simulated cortical fold. The effects of the choice of the mesh-spacing and errors in the location and local orientation of the source space were examined. Simulated data were used so that the exact location of the target sources was known and the quality of the source reconstructions could therefore be objectively evaluated.

Although equivalent current dipoles (ECDs) are point source representations of the underlying neuronal currents they are in reality approximations to the true focus or foci of activity. The actual neuronal distribution is not point-source in nature, and may be distributed over a significant portion of the cortex. If an equivalent current dipole is a successful model for this distribution, either the neuronal current is localised or the spatial distribution is such that it is amenable to representation as an ECD. However, noise of all kinds will lead to an indeterminacy in the localisation of the ECD. Noise in the case of Magnetoencephalography (MEG) or Electroencephalography (EEG) refers to brain noise, signal noise, and experimental errors such as mis-registration of the detectors with the head. The estimation and display of positional uncertainties due to noise is the subject of this paper.

A patient in whom a variety of abnormal EEG findings can be elicited by elimination of central vision and fixation demonstrates fixation-off sensitivity. The underlying mechanisms of fixation-off sensitivity and its relationship with alpha rhythm remain unclear. To obtain a better understanding of this issue, we used a whole-head magnetoencephalograph to study an epileptic child with fixation-off sensitivity resulting in a 3-Hz, large-amplitude oscillation (300 microV) over the occipital regions on the EEG. Magnetic source localization revealed alpha activity around the calcarine fissure and surrounding parieto-occipital areas. Magnetic sources of abnormalities relating to fixation-off sensitivity, however, usually were located deeper in the brain, suggesting more extensively distributed sources, with involvement of the cingulate gyrus and the basomesial occipitotemporal region. Distributions of the sources of both types of activities show independent clusters but also an appreciable domain of overlap. Our findings indicate that abnormalities related to fixation-off sensitivity can emerge in thalamocortical networks, with larger and more anterior cortical distribution than those that generate alpha rhythm. Transition in the type of oscillation appears not only to depend on a change in cellular dynamics but also to be reflected in a different spatial distribution of the underlying neuronal networks.

The aim of this study was to compare MEG and fMRI localisations of primary sensory-motor cortex, in normal subjects and patients scheduled for neurosurgery. The study is a precursor to the development of a pre-surgical mapping program. The results indicate that in both normals and patients, fMRI and MEG localisations are confirmatory and match well with localisations obtained during surgery. However, in one subject, the MEG localisations were displaced significantly from the central sulcus. We discuss the implications and possible generating mechanisms of this displacement.

In the human visual system, segregation of information on a functional basis commences as early as the retinal ganglion cells. Both chromatic and luminance information is conveyed within the parvocellular pathway to the primary visual area V1. Descriptions of the chromatic evoked response tend to concentrate on the amplitude and latency of the principle response peak rather than to characterise its distribution or to determine its cortical origins. A more intensive investigation of both the cortical origins of the response and the spatial tuning properties of these chromatic sensitive cells was therefore considered appropriate. This study will examine the magnitude of the evoked magnetic response to isoluminant chromatic gratings over a range of spatial frequencies. Co-registration of MEG and MRI data will be examined to determine the cortical origin of the response.

Within the human visual system various hierarchical processing models indicate a clear dichotomy of colour and motion processing [1] with predominantly luminance information being input to cortical motion centres via the magnocellular pathway. This separation of information is consistent with reports of poor responses from cortical motion centres to isoluminant chromatic stimuli. Recent evidence suggests that chromatic information may be used in motion analysis [2]. This study will explore the temporal response characteristics of chromatic-sensitive parvocellular units in human visual cortex by examining the variation in magnitude of the evoked magnetic response to isoluminant chromatic stimulation. Co-registration of MEG and MRI data will be examined to determine the cortical origins of the response.

Purpose: Differences in methodology of intermittent photic stimulation within and between countries in Europe make collaborative research and interpretation of results difficult.Method: Experts in the field of photic stimulation from European countries have given an overview of methods used in routine photic stimulation. A consensus meeting was organized in May 1996 in the Netherlands.Results: Methodology, including specification of a photo stimulator, procedure of photic stimulation, and interpretation of EEG results, has been defined according to available scientific and clinical knowledge.Conclusions: Consensus was reached in setting up a safe, quick, simple and reliable method to determine whether or not patients are photosensitive. A specification of an international standard for intermittent photic stimulation in the routine EEG examination is given with the purpose of improving patient care and facilitating collaborative research.

Vigabatrin is an antiepileptic drug for the treatment of partial seizures. The anticonvulsant effect is achieved by irreversible inhibition of the enzyme GABA-transaminase which catalyses the inactivation of GABA. Vigabatrin has been associated with visual field loss and electrophysiological abnormalities. The purpose of the study was to determine any alterations in normal volunteers of the visual field and the visual electrophysiology resulting from a short exposure to vigabatrin. A three-way, double-blind study of placebo, carbamazepine and vigabatrin was undertaken at baseline and on days two, four and nine. Seven subjects completed all three cycles and 14 subjects (six females and eight males; mean age 27.3 years SD 6.7) completed at least one cycle. Static threshold automated perimetry comprised Humphrey Visual Field Analyzer Programs 30-2 and 30/60-2. Electro-oculography and electroretinograms were performed with undilated pupils using the Medelec Ganzfeld stimulator GS2000. The visual field was unaffected by placebo, carbamazepine or vigabatrin. The group mean amplitudes and latencies for the scotopic ERG, 30Hz flicker ERG and the oscillatory potentials remained unchanged for any cycle. The group mean photopic ERG b-wave latency increased from baseline (p < 0.05); no significant change occurred with carbamazepine or placebo. The group mean Arden Index for vigabatrin decreased from baseline to day 9 (p <; 0.01); no significant differences were present for carbamazepine or placebo. Vigabatrin has a rapid effect on both the photopic ERG and the EOG; however, the changes merely reflect alterations in retinal GABA levels secondary to concomitant blocking of GABA transaminase by existing vigabatrin therapy.