Search

Introduction: Electrophysiologic tests in hypoxic encephalopathy consist of EEG and evoked/event-related potential studies. In most studies the generalized periodic epileptiform complexes have been reported combined with other EEG patterns and were indicators of a poor outcome in different etiologies of hypoxic encephalopathy (HE), but these have rarely been examined independently., Methodology: We analyzed from 2000 to 2007 the outcome of patients with HE and generalized periodic epileptiform complexes. We abstracted and tabulated clinical information, imaging findings, and outcome from the medical records., Results: We found 52 patients in our database. Fourteen patients (eight BiPLEDs and six GPEDs) were associated with HE. Patients with BIPLEDs were 68+/-19.4 years old, 5 female (62%) and 3 (38%) men. GPEDs patients were 52.5+/-19.1 years old, 2 women (20%) and 4 (80%) men. Myocardial infarction and ventricular tachycardia were responsible of 57% of the HE cases. Neuroimaging studies in both groups showed cortical structural lesions in 84%. All patients were comatose and died. Two GPEDs patients developed status epilepticus., Conclusion: GPEDs and BIPLEDs after an anoxic insult carried a poor prognosis for survival. Aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.

Objectives: The location of electrical sources in the brain can be estimated by calculating inverse solutions in which the location, amplitude and orientation of the electrical sources are fitted to the scalp EEG. To assess localization accuracy of the moving dipole inverse solution algorithm (ISA), we studied two patients who had depth electrodes implanted for presurgical planning of epilepsy surgery., Methods: Artificial dipoles were created by connecting a single sine wave pulse generator to different pairs of electrodes in multiple orientations and depths. Surface EEG recordings of the resulting pulses were evaluated with the ISA using a 4-shell spherical head model and plotted on the subjects' MRI. Dipole localization errors were evaluated with respect to the number of averaged pulses, different electrode montages and different dipole locations and orientations., Results: Dipoles located at 40-57 mm from the scalp surface had localization errors that were greater than those located at 62-85 mm. Localization accuracy improved with increasing numbers of pulses and recording electrodes. Results with a standard 10-20 array of 21 electrodes showed an average localization error of 17 mm, whereas 41 electrodes improved this to 13 mm. Mean angular errors were 31 and 30 degrees, respectively., Conclusions: The ISA was able to differentiate between tangential and radial dipoles. We conclude that our implementation of the ISA is a useful and sound method for localizing electrical activity in the brain.

Electroencephalography (EEG) and evoked potential (EP) studies are neurophysiologic techniques which provide information on physiological state and response to therapy, and may aid diagnosis and prognosis. Serial studies or continuous monitoring may enable changes to be detected prior to irreversible deterioration in the patient's condition. Current computer technology allows simultaneous display and correlation of electrophysiologic parameters, cardiovascular state and ICP. Continuous EEG monitoring in the ICU has been shown to have a decisive or contributing impact on medical decision making in more than three-quarters of patients. In addition, continuous EEG monitoring has revealed previously unsuspected non-convulsive seizures in two-thirds of patients. Somatosensory and auditory EPs can provide useful prognostic information in coma patients, however, these tests are etiologically non-specific and must be carefully integrated into the clinical situation. Motor EPs offer a potentially useful tool for evaluating motor system abnormalities in the ICU. Thus, neurophysiologic tests are established monitoring tools in the neurological intensive care unit.

We examined the inhibitory effect of a brief train of digital (D2) electrical stimuli at 4 times perception threshold on transcranial magnetic motor evoked potentials (MEPs) recorded from abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles ipsilateral to the side of D2 stimulation. We compared this to the inhibitory effect of ipsilateral D2 stimulation on averaged rectified EMG recorded at 10% maximum voluntary contraction and on F-responses and H-reflexes recorded from these same muscles. We also compared MEPs recorded following D2 stimulation just above perception threshold to MEPs following higher intensity D2 stimulation. As well, we assessed the effect of preceding D2 stimulation on MEPs recorded from a relaxed versus tonically contracted hand muscle. D2 stimulation elicited a triphasic response of modest MEP facilitation followed by inhibition and further facilitation. The duration and onset of MEP inhibition correlated with those of the initial period of rectified EMG inhibition, however, the magnitude of MEP inhibition was generally less than the magnitude of EMG inhibition, consistent with a greater inhibitory effect of digital afferents on smaller motor neurons. MEPs were not facilitated during the rebound of EMG activity (the E2 period) that usually followed the initial period of EMG inhibition (I1 period). The behavior of H-reflexes and F-responses following ipsilateral D2 stimulation suggested that inhibition of both EMG and MEPs is not mediated via presynaptic inhibition of Ia afferents, and that inhibition is augmented by descending rather than segmental input to spinal motor neurons. Tonic contraction of the target muscle during D2 stimulation decreased the inhibitory effect of the preceding digital stimulus possibly due to recruitment of larger spinal motor neurons less likely to be inhibited by cutaneous input.

To determine whether motor evoked potential (MEP) amplitude and area are accurate measurements of the magnitude of response to magnetic cortical stimulation, we simultaneously recorded the twitch and MEP in the first dorsal interosseous muscle of 8 normal subjects. Consecutive stimuli were delivered at increasing stimulus intensities (SI) or with increasing levels of background voluntary muscle contraction (BVC). There was stimulus to stimulus variability in MEP amplitude, area and twitch force. At low SI and at low levels of background contraction, there was a good correlation between twitch amplitude and MEP amplitude and area (r = 0.6-0.96, P < 0.005). Increasing either variable caused the correlation to decrease significantly (r = 0.02-0.31, P > 0.01). With increasing SI, MEP amplitude and area plateaued but twitch force continued to increase. A similar pattern was observed with higher levels of background muscle contraction although in some subjects a second increase in MEP amplitude and area was seen. Collision experiments demonstrated that the amplitude of the EMG activity resulting from repetitive motoneuron firing increased as SI was increased. This is due to multiple descending volleys which result in repetitive firing of some spinal motoneurons. Rapid, repetitive firing of some motor units is likely to result in phase cancellation and, therefore, the MEP amplitude, and to a lesser extent area, do not accurately reflect the net motor output.

We studied the effect of stimulus intensity, coil size, mental alertness and prestimulus muscle contraction on the variability of motor evoked potentials (MEPs) produced by magnetic cortical stimulation (MCS). In 5 healthy subjects we delivered MCS either with a circular coil centered at the vertex or a figure-8 coil centered over the motor cortex hand area, recording from first dorsal interosseous. With the subject at rest or exerting 5% maximum voluntary contraction, 30 consecutive stimuli were given at 4 stimulus intensities (SIs) in 10% increments above resting motor threshold. Concurrent mental arithmetic constituted mental alertness. Spectral analysis was performed on data from 300 consecutive stimuli. The variability of MEP response size was inversely related to stimulus intensity, prestimulus voluntary muscle contraction, the recruitment of motoneurons and the size of the field generated by the magnetic coil. The MEP variability was larger than and not correlated with the variability of the H-reflex. Fast Fourier transformation and cross-correlation analysis did not identify a consistent dominant frequency, suggesting that the variability in MEP size is essentially random. We suggest that the variability in MEP response is caused by constant, rapid, spontaneous fluctuations in corticospinal and segmental motoneuron excitability levels. Any maneuver that raises this level or increases the probability of motoneuron firing will decrease MEP variability.

Voluntary contraction of a muscle greatly increases the amplitude and decreases the latency of the motor potentials evoked by electromagnetic coil brain stimulation (facilitation). Facilitation has also been observed with contraction of a nearby ipsilateral and a contralateral homologous muscle. We studied these facilitatory relationships in 5 normal subjects in small hand, forearm and upper arm muscles using surface-recorded compound motor action potentials, single motor unit recordings, and post-stimulus time histograms. There was no evidence for spread of facilitation between any pair of muscles if the muscle from which motor evoked potentials (MEPs) were recorded was completely at rest during brain stimulation, although this sometimes required training to accomplish or could not be achieved. Thus, although spread of facilitation has been observed by others under these conditions, we did not find this effect. There may be significant interindividual variations in the degree of facilitatory spread.

Reilly and Peters (1973) reported that photoparoxysmal responses (PPRs) that outlasted the stimulus correlated significantly with seizures as compared to self-limited PPRs. However, they defined a wide range of activity, including occipital spikes and slow wave bursts, as PPR. We examined EEGs of 3557 patients and 48 normal subjects for PPRs defined only as generalized spikes or spike-wave activity. None of the 48 normal subjects showed a PPR. PPRs were seen in 35 (1%) patients, 27 (77%) of these had a definite history of epilepsy, 3 (9%) had a questionable history, and 5 (14%) had had no seizures. PPRs were prolonged more than 100 msec beyond the stimulus in 11, and self-limited in 24. The incidence of seizures was not statistically different in these 2 groups. Furthermore, the classification of PPRs into these 2 groups could be influenced by the time at which the stimulus was stopped after the appearance of the PPR. PPRs are rare in normal subjects and non-epileptic patients and have a high correlation with seizures irrespective of their relationship to the strobe stimulus.

Knowledge of short-term EEG variability in computerized analysis is important before interpreting spectral EEGs or assessing changes that may be due to inherent variability and not necessarily related to a task (e.g., listening to a story), therapy or changes in underlying disease. Eighty to 120 sec of 14-channel, edited, bipolar EEG were recorded in normal subjects and analyzed using an FFT. Absolute and relative power in 5 standard frequency bands, and median and peak power frequencies were obtained for each 4 sec epoch, and the mean and standard deviation calculated for each parameter. The average variation of the mean power, absolute and relative, in the frequency bands was less than 10% although some parameters varied by up to 50% in an individual subject. Median and peak power had the least variability, about 3%. Changes in total power correlated positively with relative alpha power, but negatively or not at all with the other relative power measures. This suggests that interpretation of relative measures of delta, theta and beta in individual spectra may be dependent on total power or absolute alpha power. In addition, mathematical transformations were necessary to normalize the epoch data, suggesting that the mean and standard deviation of data from a series of epochs may not have maximal value unless a transformation is used. These results also indicate that caution is needed in interpreting changes in EEG frequency analysis data that are of the same magnitude as spontaneous EEG variability.

Determination of clinically significant temporal changes in P100 latency requires knowledge of the degree of normal intraindividual variability. Checkerboard visual evoked potentials using 3 check sizes (17', 35' and 70') were performed serially on 20 healthy volunteers. Each subject was tested at least twice an average of 6 months apart. The P100 latency was measured at Oz with a forehead reference (Pz, O1 and O2 channels were also recorded). The overall average P100 latency change between studies for all check sizes and both eyes was 2.9 msec. However, the maximum absolute latency change was 11 msec. There was no significant difference between the average latency change for the 3 check sizes. The P100 interocular difference changed a mean of 2.5 msec (maximum 9 msec). Amplitude was more variable, with a mean change of about 1.5 microV or 25% (maximum was a 60% decrease in amplitude). A P100 latency change of up to at least 11 msec needs to be acknowledged as normal when assessing the clinical significance of changes in P100 latencies in patients. Also, P100 latency changes greater than 11 or 12 msec are very suggestive of an abnormality in the visual pathway.

We studied monocular pattern ERG (PERG) in 10 normal subjects and a patient with optic neuritis. No clinically significant PERG could be recorded from the occluded eye with any reference (ipsilateral ear or temple, or midfrontal), indicating that cross-contamination is not present with binocular testing. Ipsilateral temple reference minimized VEP (P100/N100) contribution to the PERG N95 which occurred with ipsilateral ear or midfrontal reference. The conclusions were confirmed by results from the patient, who had marked monocular delay of a normal amplitude P100. Twenty-four subjects were tested with monocular and binocular stimulation using an ipsilateral temple reference. There were differences in PERG latencies and amplitudes although the interside amplitude ratio showed smaller differences with binocular stimulation. Increasing check size (17, 35 and 70 min) decreased P50 and N95 latencies and increased P50 amplitude.