Ms In Normal Subjects Research Articles

The 3-Second Rule in Hereditary Pure Cerebellar Ataxia: A Synchronized Tapping Study

The ‘3-second rule’ has been proposed based on miscellaneous observations that a time period of around 3 seconds constitutes the fundamental unit of time related to the neuro-cognitive machinery in normal humans. The aim of paper was to investigate the temporal processing in patients with spinocerebellar ataxia type 6 (SCA6) and SCA31, pure cerebellar types of spinocerebellar degeneration, using a synchronized tapping task. Seventeen SCA patients (11 SCA6, 6 SCA31) and 17 normal age-matched volunteers participated. The task required subjects to tap a keyboard in synchrony with sequences of auditory stimuli presented at fixed interstimulus intervals (ISIs) between 200 and 4800 ms. In this task, the subjects required non-motor components to estimate the time of forthcoming tone in addition to motor components to tap. Normal subjects synchronized their taps to the presented tones at shorter ISIs, whereas as the ISI became longer, the normal subjects displayed greater latency between the tone and the tapping (transition zone). After the transition zone, normal subjects pressed the button delayed relative to the tone. On the other hand, SCA patients could not synchronize their tapping with the tone even at shorter ISIs, although they pressed the button delayed relative to the tone earlier than normal subjects did. The earliest time of delayed tapping appearance after the transition zone was 4800 ms in normal subjects but 1800 ms in SCA patients. The span of temporal integration in SCA patients is shortened compared to that in normal subjects. This could represent non-motor cerebellar dysfunction in SCA patients.

Comparison of static automated perimetry and semi‐automated kinetic perimetry in patients with bilateral visible optic nerve head drusen

Until now there has been no standardized, systemic approach to diagnostics in patients with optic nerve head drusen (ONHD). This study compares visual field (VF) results obtained with static automated perimetry (SAP) and semi-automated kinetic perimetry (SKP) in patients with bilateral visible ONHD. Visual fields in 26 eyes (13 patients) with ONHD were obtained by Humphrey Field Analyser II (SAP) and Octopus 101 (SKP) equipment and classified by three masked observers. Pairs of VFs were considered equivalent if the descriptions given by both methods matched. Individual reaction time (RT) was assessed during SKP. Fifteen healthy volunteers were examined as control material. Visual field pairs matched in 19 eyes (three normal VFs, 16 arcuate defects). In the remaining eight eyes SKP provided more information in concentric constriction of the VF (two eyes) and SAP provided more information on paracentral scotomas (five eyes). Sensitivity was 69% for SKP, 80% for SAP and 88% for both methods together. Mean RT assessed using SKP amounted to 909 ms in eyes with ONHD and 568 ms in normal subjects (p < 0.0003). The median examination duration was 13 mins with SKP and 11 mins with SAP (p = 0.05) in eyes with ONHD, and 8 mins in control eyes (p < 0.0001). In clinical practice it is necessary to perform both SAP and SKP in patients with ONHD because the VF defects are diverse. In SKP, RT is prolonged in eyes with ONHD compared with normal eyes and SKP takes longer than SAP in ONHD eyes.

Myocardial T2 quantitation in patients with iron overload at 3 Tesla

To investigate the feasibility of measuring myocardial T2 at 3 Tesla for assessment of tissue iron in thalassemia major and other iron overloaded patients. A single-breathhold electrocardiogram-triggered black-blood multi-echo spin-echo (MESE) sequence with a turbo factor of 2 was implemented at 3 Tesla (T). Myocardial and liver T2 values were measured with three repeated breathholds in 8 normal subjects and 24 patients. Their values, together with the T2 values measured using a breathhold multi-echo gradient-echo sequence, were compared with those at 1.5T in the same patients. At 3T, myocardial T2 was found to be 39.6 +/- 7.4 ms in normal subjects. In patients, it ranged from 12.9 to 50.1 ms. "T2 and T2(*) [corrected] were observed to correlate in heart (rho = 0.93, P [corrected] < 0.0001) and liver (rho = 0.95, P < 0.0001). Myocardial T2 and T2 at 3T were also highly correlated with the 1.5T measurements. Preliminary results indicated that myocardial T2 quantitation was relatively insensitive to B1 variation, and reproducible with 3.2% intra-exam and 3.8% inter-exam variations. Myocardial T2 quantitation is feasible at 3T. Given the substantially decreased T2 and increased B0 inhomogeneity, the rapid myocardial T2 measurement protocol demonstrated here may present a robust alternative to study cardiac iron overload at 3T.

Impairment of motor cortex activation and deactivation in Parkinson's disease

Objectives: To examine the time course of corticospinal excitability before and after voluntary movement in Parkinson's disease (PD). Methods: We studied 9 mild PD patients at least 12 h off medications and 11 healthy volunteers in a simple reaction time (RT) paradigm. Suprathreshold transcranial magnetic stimulation was delivered to the left motor cortex at intervals covering the periods before and after movement. Results: PD patients (284±90 ms) and normal subjects (282±56 ms) had similar median RT. The time courses of both the premovement increase and the postmovement decrease in corticospinal excitability were significantly different between PD patients and normal subjects. The increase in motor-evoked potential (MEP) amplitudes began earlier for PD patients (200 ms before electromyographic (EMG) onset) than for normal subjects (150 ms before EMG onset), but the rate of increase was slower in PD patients than controls. After EMG offset, MEP amplitudes were increased for about 150 ms in normal subjects, but in PD patients this period was prolonged to about 350 ms. Conclusions: Impairment of motor cortex activation and deactivation is an early feature of PD and may be a physiological correlate of bradykinesia. The normal RT in our patients may be related to the earlier occurrence of the premovement increase in corticospinal excitability compensating for the slower rate of rise.

Abnormal postexcitatory and interhemispheric motor cortex inhibition in writer's cramp.

Focal transcranial magnetic stimulation (TMS) of the motor cortex was used to study excitatory and inhibitory stimulation effects in 25 patients with writer's cramp and 25 healthy volunteers. We investigated excitatory and inhibitory corticospinally mediated motor effects in muscles contralateral to the stimulation side as well as interhemispheric inhibition of tonic motor activity in muscles ipsilateral to stimulation. Motor evoked potentials (MEPs) were recorded from both first dorsal interosseus muscles. Motor thresholds at rest and amplitudes and latencies of MEPs obtained during maximal contraction were always bilaterally normal. The duration of postexcitatory inhibition was significantly shortened (168+/-55 vs. 198+/-39 ms in normal subjects, P=0.001) and the duration of interhemispheric inhibition prolonged (30.3+/-6.6 vs. 26+/-3.9 ms in normal subjects, P < 0.001). Both observations would be compatible with a decreased inhibition of corticospinal and transcallosal outputs of the motor cortex. The results were not influenced by fatigue effects. Abnormal motor cortex inhibition seems to be a generalized phenomenon in writer's cramp since it was detected in both hemispheres and during a simple isometric motor task which did not evoke dystonic symptoms.

Transcallosal inhibition and motor conduction studies in patients with schizophrenia using transcranial magnetic stimulation.

Transcranial magnetic stimulation of the motor cortex may not only elicit excitatory responses in hand muscles contralateral to the stimulated hemisphere, but may also suppress tonic voluntary electromyogram activity in muscles ipsilateral to the stimulation. This inhibition is mediated between the motor cortices via the corpus callosum. To investigate motor excitability and interhemispheric (transcallosal) connections in patients with schizophrenia. Transcallosal inhibition and motor conduction parameters were investigated in ten patients with schizophrenia and in ten age- and gender-matched healthy subjects. Transcallosal conduction time (TCT) and duration of the inhibition were significantly longer in patients with schizophrenia (mean (s.d.)): TCT, 12.4 (2.9) ms in normal subjects and 15.3 (2.6) ms in patients (P = 0.03); mean duration, 34.1 (4.9) ms in normal subjects and 51.9 (16.8) ms in patients (P = 0.01). Magnetic motor conduction parameters are unaltered in schizophrenia, but transcallosal inhibition is significantly delayed and prolonged. This may indicate abnormal function of the corpus callosum in these patients.

QT Dispersion: Comparison of Orthogonal, Quasi‐orthogonal, and 12‐Lead Configurations

BackgroundFull standardization of QT dispersion has not yet been established; the influence of lead combination is still disputed. This study evaluates the respective value of automated QTc dispersion in orthogonal (XYZ), quasi‐orthogonal I‐aVF‐V2 (IF2), and 12‐lead ECG configurations.Methods15‐lead digitized ECG recordings were collected in 92 normal subjects and in 71 patients following myocardial infarction. Each lead was processed by an automatic algorithm. QT dispersion was assessed by the range of individual QT intervals, both corrected by Bazett's formula. QTc durations from all configurations were comparable (post‐MI: 412 ± 27 vs 407 ± 29 msec for 12‐lead and XYZ). Whatever the set of leads, QTc interval was longer in post‐MI (in 12‐lead, 412 ± 27 vs 397 ± 19 ms in normals, P &lt; 0.001). QTc dispersion was larger on 12‐lead (post‐MI: 51 ± 19, 21 ± 13 and 28 ± 20 ms with 12‐lead, XYZ and IF2); however, it was significantly larger in post‐MI with all sets of leads (in XYZ, 21 ± 13 vs 9 ± 7 ms in normal subjects, P &lt; 0.0001).ConclusionIn conclusion, magnitude of QT dispersion depends on the set of leads considered; orthogonal configurations may still contain valuable prognostic information.

QT Interval and QT Dispersion Measured with the Threshold Method Depend on Threshold Level

Various computerized methods with multiple parameter options for measurements of the QT interval now are available. The optimum parameter setting for most algorithms is not known. This study evaluated the influence of the threshold level applied on the T wave differential on the QT interval and its dispersion measured in normal and abnormal electrocardiograms (ECGs). Seven hundred sixty ECGs recorded in 76 normal subjects and 630 in 63 patients with hypertrophic cardiomyopathy (HCM) (10 consecutive recordings in each individual) were analyzed. In each lead of each ECG, the QT interval was measured by the threshold method applied to the first differential of the T wave. The threshold level was varied between 5% and 30% of the T wave maximum in 1% steps, resulting in 26 different choices of QT measurements. With each choice the maximum QTc and the QT dispersion (QTd, standard deviation of the QT in all 12 leads) were obtained for each recording. The maximum QTc was significantly longer in HCM patients than in normal subjects (P < 0.001) at all threshold levels except between 5% and 7%. The QTd was significantly greater in HCM patients at all threshold levels. The QTc and QTd changed significantly with the threshold level. The maximum QTc varied up to 60 ms in normal subjects and up to 70 ms in HCM patients, depending on the threshold level. Thus, the QT interval and its dispersion measured with the threshold method applied to the first T wave differential depended significantly on the threshold level in both normal and diseased hearts. All programmable options of available automatic instruments should be examined carefully before any study, and all algorithmic details should by systematically presented.

T wave spectral variance: A new method to determine inhomogeneous repolarization by T wave beat-to-beat variability in patients prone to ventricular arrhythmias

Inhomogeneous repolarization is considered to be associated with increased risk of ventricular arrhythmias, but exact determination of the end of the T wave is difficult, and a single measurement of the QTc interval may be insufficient for risk stratification. A new algorithm was therefore developed to determine the beat-to-beat variability of the T wave in Holter electrocardiographic recordings. This algorithm, termed T Wave Spectral Variance (TWSV) uses the two-dimensional fast Fourier transform to determine the beat-to-beat variability of the T wave in Holter ECG recordings. The two-dimensional fast Fourier transform was calculated by use of a data matrix with 1,024 consecutive single beats (first dimension) and a 200-ms segment centered on the T wave (second dimension). The power spectra of the 2D-FFT revealed the frequency content of the T wave in the first dimension and the periodicity of these frequencies in cycles per beat in the second dimension. A TWSV index of periodicity was calculated by dividing total spectral energy by spectral energy at 0 cycles per beat. A TWSV index of 0 means a constant T wave from beat to beat; a TWSV index of 1 means a completely irregular T wave. Of the 200 patients investigated, all of whom had had myocardial infarctions, 50 had documented sustained ventricular tachycardia (VT) (<230 beats/min) (group 1), 50 had ventricular fibrillation (VF) (group 2), and 100 were without VT or VF (group 3); 10 normal subjects were also investigated. The visually determined QTc was 442 ± 62 ms in group 1, 402 ± 13 ms in group 2, 411 ± 26 ms in group 3, and 398 ± 43 ms in normal subjects (differences not significant). The TWSV index was 0.95 ± 0.14 in group 1, 0.90 ± 0.16 in group 2, and 0.64 ± 0.24 in group 3; it showed a highly constant T wave in normal subjects (0.52 ± 0.23). Differences between patients with VT and VF as against patients without VT or VF were significant ( P < .05), whereas no statistical differences between patients with VT and VF could be found. Thus, TWSV, a new method to assess beat-to-beat variability of the T wave, revealed increased heterogeneity of repolarization in patients prone to both VT and VF after myocardial infarction, whereas a single QTc interval measurement showed no significant differences.

Computer-assisted study of ECG indices of the dispersion of ventricular repolarization

A new computer-assisted method for the quantitative assessment of the dispersion of ventricular repolarization (DVR) has been developed. Through interactive editing of an averaged QRS-T cycle from a 15-lead electrocardiographic (ECG) record (12-lead ECG + XYZ leads), five ECG indices of DVR are automatically computed: they represent the maximal interlead difference of QT and the intervals from the J point to the T wave end, from the J point to the T wave apex, and from the T wave apex to the T wave end. The standard limits of these indices were then established in six clinical groups, including normal subjects and patients with left ventricular hypertrophy, with myocardial infarction, and with intraventricular conduction defect, all subjects being without ventricular arrhythmias and without interacting drugs. The mean values and percentile ranges of all DVR indices were lower in the normal group than in all pathologic groups. The 97.5th percentiles of the QT end dispersion and the JT end dispersion were, respectively, 65 and 76 ms in normal subjects, 84 and 86 ms in patients with inferior MI; 89 and 100 ms in those with anterior MI; 90 and 98 ms in those with left ventricular hypertrophy; and 94 and 99 ms in those with intraventricular conduction defects. This suggests that increased DVR is associated with the varieties of heart disease represented in this study, even in the absence of ventricular arrhythmias, and also that individual measurements of DVR used as predictors of future arrhythmic events should be referred to the standard range of their own clinical group.

Early and late respiratory-related cortical potentials evoked by pressure pulse stimuli in humans.

Although respiratory-related cortical evoked potentials (CEPs) have been obtained in humans, early-latency responses have been obtained only with direct electrical stimulation of respiratory afferents. We have recorded both early and late cortical activity in response to a relatively novel stimulus consisting of a 300-ms negative pressure pulse applied to the mouth near the start of selected inspirations, when mouth pressure attained a predetermined threshold. This stimulus caused highly reproducible and rapid changes in mouth pressure and was effective in eliciting CEPs to a wide range of applied pressures. Using pulses of approximately -2 to -25 cmH2O, we obtained an early positive component with a mean latency of approximately 20 ms and a subsequent negative component at approximately 30 ms in normal subjects. Peak-to-peak amplitude varied directly, and component latencies inversely, as a function of pulse magnitude. Using -5- to -10-cmH2O stimuli, we also measured a later positive-negative-positive response with mean component latencies of 96.7 +/- 15.1, 147 +/- 14.8, and 237.6 +/- 23.5 ms, respectively. The early-latency activity was resistant to manipulations of stimulus predictability, whereas the later waves were attenuated or disappeared when load presentation was made completely predictable. We validated our method by eliminating the possibility of tactile stimulation of the lips and teeth as the origin of the evoked responses. We propose that early-latency activity derives from precortical structures and may provide a window on the functioning of respiratory afferents in normal subjects and in patients with respiratory disease.

Die motorische Leitungszeit des Tractus corticospinalis bei spinaler Stimulation

A muscular action potential (MAP) following transcranial and spinal stimulation can be recorded from most of the striped muscles. The motor central conduction time after transcranial and spinal stimulation can be determined at cervical 6/7. It is at 5,0 ms in normal subjects. This was demonstrated in four normal subjects. After spinal stimulation at cervical 6/7 a motor evoked potential can also be recorded from the scalp. It has a latency that is comparable to motor conduction time. In animal experiments in examining ten rabbits a motor evoked potential to stimulation at several levels of the spinal cord could also be determined.

Echocardiographic analysis of left ventricular filling in isolated pure chronic aortic regurgitation

Left ventricular (LV) diastolic filling was assessed using digitized M-mode echocardiography in 12 patients with aortic regurgitation (AR) and in 12 normal subjects. Ten patients with AR were asymptomatic and 2 patients had congestive heart failure. LV chamber dimensions, fractional shortening and the rate of change of LV dimensions during systole and diastole were determined. In addition, the timing of the rate of change of LV dimensions in diastole (peak dD dt , 50% peak dD dt and 20% peak dD dt ) was also measured. Patients with AR had a significant reduction in dD dt (12.2 ± 3.5 cm/s in patients with AR vs 15.9 ± 1.9 cm/s in normal subjects, p < 0.01) and a delay in the timing of peak dD dt (160 ± 35.2 ms in patients with AR vs 86 ± 17.6 ms in normal subjects, p < 0.01) from the minimum LV dimension. These diastolic abnormalities were present in patients with symptomatic as well as those with asymptomatic AR, occurred even when the fractional shortening and peak systolic emptying rate (peak dD dt ) were normal, and showed no correlation with the calculated LV mass (r = 0.14). The delay in the diastolic filling velocities (peak dD dt , 50% and 20% peak dD dt ) was associated with a decreased rate of change of LV dimension in diastole, suggesting delayed early LV filling. These findings indicate an abnormality of LV diastolic filling in patients with symptomatic as well as asymptomatic AR and suggest that diastolic abnormalities may precede echocardiographic indexes of systolic LV dysfunction.

THE EFFECT OF REDUCED VIEWING TIME ON COLOUR VISION IN NORMAL SUBJECTS AND THOSE WITH ABNORMAL OCULAR CONDITIONS

The effect of restricting viewing time to 3.75 ms in normal subjects is to produce a tritan-like colour response on the City University colour vision test. This response pattern is consistent and is repeatable for standard illuminant C at 600 lx. Supplementary tests suggest that the effect is due to a defect of the blue/yellow opponent system rather than a true tritan defect. The same test when repeated on subjects with amblyopia or retinal pathology provides different results which may aid in the differential diagnosis of some visual disorders.

Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study

To study left ventricular relaxation and filling in different forms of left ventricular hypertrophy, echocardiograms of the left ventricle in 24 patients with hypertrophic obstructive cardiomyopathy and in 24 patients with chronic left ventricular pressure overload (due to aortic stenosis in 6 and to severe arterial hypertension in 18) were analyzed by computer and compared with those of 28 normal subjects. The relaxation time index (minimal left ventricular dimension to mitral valve opening) was 13 ± 15 ms in normal subjects. This index was prolonged in patients with cardiomyopathy (93 ± 37 ms) and overload (66 ± 31 ms). During the interval from minimal left ventricular dimension to mitral valve opening both groups with left ventricular hypertrophy showed a marked increase in left ventricular dimension of 4.0 ± 2.2 mm and 3.0 ±1.8 mm, respectively, which was significantly greater (p < 0.001) than in normal subjects (0.6 ± 0.5 mm). This was probably a result of an abnormal change in left ventricular shape during isovolumic relaxation. The rapid filling phase and the increase in dimension during this period were significantly reduced in hypertrophic obstructive cardiomyopathy and chronic pressure overload. In contrast to findings in the patients with cardiomyopathy, in those with pressure overload the reduced increase in left ventricular dimension during the rapid diastolic filling period was compensated for by a greater dimensional increase due to atrial contraction, resulting in a normal end-diastolic dimension. These data indicate that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.

Measurements of excitatory postsynaptic potentials in the stretch reflex of normal subjects and spastic patients.

The patellar tendon was tapped by random impulses of triangular waveform and motor unit spikes were recorded from the quadriceps femoris muscle. The cross-correlogram of the taps and the motor unit spikes revealed a primary correlation kernel, the width of which was interpreted as an indicator of the mean time-to-peak of excitatory postsynaptic potentials (EPSPs) elicited monosynaptically in an alpha-motoneurone by the triangular taps. The mean time-to-peak was 7.6 +/- 1.3 ms in normal subjects and 9.0 +/- 1.8 ms in spastic patients (P less than 0.005). The prolonged time-to-peak of EPSP in spastic patients is consistent with the hypothesis that as a result of degeneration of the corticomotoneuronal tract the Ia axons sprout and form more synaptic contacts on distal portions of the dendrites of alpha-motoneurones.