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The effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial stimulation (tc-MERs) were studied in five healthy human volunteers. Each subject, in four separate sessions, received intravenous bolus doses of propofol 2 mg.kg-1, etomidate 0.3 mg.kg-1, midazolam 0.05 mg.kg-1, and fentanyl 3 micrograms.kg-1. Electrical tc-MERs (tce-MERs) were elicited with anodal stimuli of 500-700 V. Magnetic tc-MERs (tcmag-MERs) were elicited using a Cadwell MES-10 magnetic stimulator at maximum output. Compound muscle action potentials were recorded from the tibialis anterior muscle. Duplicate tce-MERs and tcmag-MERs were recorded before and up to 30 min after drug injection. Reproducible baseline tce-MERs (amplitude 4.7 +/- 0.43 (SEM) mV, latency 29.4 +/- 0.35 ms) and tcmag-MERs (amplitude 3.7 +/- 0.43 mV, latency 31.1 +/- 0.39 ms) were obtained in all subjects. Pronounced depression of tce-MER amplitude to 2% of baseline values (P less than 0.01) was observed 2 min after injection of propofol. Thirty minutes after injection of propofol, amplitude depression to 44% of baseline (P less than 0.05) was still present, despite an apparent lack of sedation. Midazolam caused significant (P less than 0.01) amplitude depression, e.g., tcmag-MER to 16% of baseline values 5 min after injection. Significant depression persisted throughout the 30-min study period. Fentanyl did not cause any statistically significant amplitude changes in this small population. Etomidate caused significant but transient depression of tc-MER amplitude. However, there was considerable intersubject variability. Latency did not change significantly after any drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Many technicians and electroencephalographers (EEGers), particularly those who attend meetings, have been dazzled, perplexed, and possibly excited by the appearance of many new devices displaying the EEG and its processed result in the form of maps that are now rather commonplace at conventions. Since most of these are costly devices (Bickford and Allen 1986) many EEGers will want to know whether they should consider buying one of these instruments, whether they are for research purposes only, or have a useful and cost effective application in a neurologic practice.These are difficult matters to evaluate partly because the attractiveness and utility of a new device is at least partly dependent on the sensibilities and clinical interests of the neurologist. However this article aims at providing some guidelines that can assist you in the choice and application of these devices in your clinical laboratory.

Electroencephalograms and case histories of 50 patients with triphasic waves were reviewed. EEGs were studied for slowed dominant activity, anteriorly dominant triphasic waves, anterior-posterior lag time and bursts of triphasic waves. Etiologies of triphasic waves were: hepatic (28), azotemia (10), anoxia (10) and hyperosmolarity (2). Sixteen hepatic and two azotemic patients showed all of these characteristic EEG features. Triphasic waves demonstrating all of these features are highly characteristic of but are not pathognomonic for hepatic encephalopathy. Prognosis correlated best with the type of hepatic injury and deteriorating renal function. We postulate that triphasic waves are generated by the same thalamocortical volleys which normally induce spindles.

The tape recorded EEGs of 127 patients anesthetized with large doses of opioids were retrospectively analyzed for evidence of opioid-induced seizures, and in particular, correlated with movements that occurred during induction and could be clinically interpreted as seizures. Bilateral EEG leads in patients receiving fentanyl (20), sufentanil (20), or alfentanil (87) were recorded. Forty-six of these patients from all opioid groups manifested intense rigidity, as assessed both clinically and by EMGs recorded from eight muscles in 69 of the patients receiving alfentanil. This intense rigidity often resembled seizures, in that the phenomenon entailed severe stiffness of both limbs and trunk, with an explosive onset of myoclonic limb movements, and associated vertical nystagmus. Electroencephalographic observations were extensive, entailing 69 h of paper recordings played back from the tapes, at paper speeds of 30 or 60 mm/s, with detailed annotations from the voice track. These paper recordings were examined in detail independently by three of the investigators, who were unaware of the clinical phenomena that had occurred. The only observed EEG activity that could have been interpreted as epileptiform consisted of small sharp waves related to muscle activity or other artifact. The EEG never indicated seizure activity during these drug-induced movements and rigidity. Reports of opioid-induced seizures are reviewed and a set of criteria is offered to help achieve future consistency and credibility in evaluating this phenomenon. The available evidence does not support the existence of opioid-induced seizures in the clinical setting.

SUMMARY Effects of acute and chronic paleocerebellar stimulation were evaluated in four experimental models of epilepsy in 24 adult cats chronically implanted with bilaterally symmetric parasagittal electrocorticographic electrodes and anterior lobe cerebellar stimulation electrodes. Pentylenetetrazol was given intraveneously in 50-mg increments or 4% enflurane was inspired until grand mal seizures occurred spontaneously or were triggered by photic or auditory stimuli. Alpha-chloralose, 50 mg/kg, was injected intraperitoneally to produce a model of stimulus-sensitive myoclonus and sodium penicillin G, 350,000 units/kg, was injected intramuscularly to produce a model of petit mal epilepsy. One- to 250-Hz electrical stimulation of paleocerebellar cortical surfaces was performed with constant-voltage or constant-current stimulators at threshold and suprathreshold intensities with average intensities of 8 V and 2.5 mA, respectively. Acute or chronic, threshold or suprathreshold paleocerebellar stimulation did not predictably alter the electrographic or clinical manifestations in any of these four models. RESUME La stimulation liminaire ou supraliminaire aigue ou chronique, des lobes cerebelleux anterieurs n'inhibait ni les decharges gpileptiformes sur l'EEG ni les crises cliniques dans quatre modules expgrimentaux d'epilepsie chez le chat. Les quatre modeles etaient: l'injection intraveineux de pentylenetetrazol; l'inhalation d'enflurane 4% jusqu'a la survenue d'une crise grand mal parfois facilitee par la stimulation lumineuse ou par des stimulations sonores; l'injection intraperitoneale de chloralose pro-voquant des myoclonies induites par des stimulations sensitives; l'injection intramuscu-laire de p6nicilline G, produisant une epilepsie de type petit mal. RESUMEN La estimulacion aguda o cronica de los lobulos cerebelosos anteriores, utilizando estimulos equivalentes o superiores al umbral, no inhibio la actividad epileptiforme en el EEG ni los ataques clinicos en cuatro modelos de epilepsyia en el gato. Los modelos se consig-uieron mediante el pentilentetrazol intravenoso o la inspiracidn de 4% de enflurane en aire, mantenida hasta que se produjo una convulsion clihica generalizada. Tamben se utilizo la epilepsia evocada por estimulos auditivos o luminosos, la administracion intraperitoneal de cloralosa para producir mioclonus sensible a los estimulos y la penicilina G para crear un modelo de epilipsia de pequeno mal. ZUSAMMENFASSUNG Die akute oder chronische Stimulation der vorderen KLeinhirnlappen mit Werten im Bereich der Krampfschwelle oder diese uber-steigend, verhinderte weder epileptiforme Akti-vitat im EEG noch manifeste Krampfe bei 4 Epilepsiemodellen der Katze. Die Epilepsie wurde hervorgerufen durch Pentylentetrazol i.v. oder 4% iges Enfluran als Zumischung zur Einatmungsluft bis ein grosser Krampfanfall ausgelost wurde; in anderen Fallen wurde er hervorgerufen durch Foto-oder Tonstimulation, Chloralose i.p. um einen reizempfindlichen Myoklonus hervorzurufen und Penicillin G ijn. um das Modell einer Petit-Mal-Epilepsie zu erzeugen.

In a series of 75 patients undergoing cardiac operations with the assistance of cardiopulmonary bypass (CPB), 15 patients were subjected to relatively large hypotensive stresses during CPB as measured by the depth and duration of the fall in cerebral perfusion pressure. Of these 15 patients, eight manifested cerebral dysfunction postoperatively ranging from temporary exacerbation of pre-existing focal neurological deficits to irreversible coma. In each of these eight cases, EEG disturbances which first appeared at the time of hypotensive episodes during CPB persisted postoperatively and correlated with the nature and evolution of the clinical deficit. In two of the patients who did not regain consciousness postoperatively, neuropathological studies revealed bilateral laminar cortical necrosis, primarily involving cerebral cortex in one case and cerebellar cortex in the other, with accentuation in arterial border zones. Of seven other patients who suffered comparable exposures to hypotension during CPB, none evidenced cerebral dysfunction postoperatively. The most important determinants of this selective vulnerability to low extracorporeal perfusion pressure appeared to be the "reperfusion" pressure established after the hypotensive episode, postoperative blood pressure and cardiac output, and brain temperature at the time of the hypotension. Advanced age and history of cerebrovascular insufficiency were the greatest risk factors among patient variables.

Bilateral midbrain cooling (5–15°C) was performed in cats pretreated with p-chlorophenylalanine (PCPA). This was done in order to examine the possible role of 5-hydroxytryptamine (5-HT) systems in the process of electrocortical synchronization which normally accompanies midbrain reticular deactivation. Prior to treatment with PCPA, midbrain cooling always produced tonic electrocortical synchronization and behavioral unresponsiveness. Cooling following PCPA treatment on the other hand produced behavioral unresponsiveness which was not accompanied by tonic electrocortical synchronization; in that case electrocortical desynchronization persisted in spite of midbrain reticular deactivation. These results lead to the hypothesis that two distinct, tonically active, desynchronizing systems exist. During the acute blockade of the classical midbrain reticular activating system it is proposed that 5-HT systems normally operate to inhibit or otherwise prevent the expression of the second brain stem electrocortical desynchronizing mechanism. It is proposed, therefore, that 5-HT acts indirectly to produce electrocortical synchronization. In the absence of 5-HT, midbrain deactivation is not sufficient to guarantee synchronization. It is argued that tonic electrocortical synchronization is assured only when both desynchronizing systems are inactivated as would be the case in the acute cerveau isole.

SUMMARY In 13 healthy adult cats chronically implanted with parasagittal electrodes applied to the dural surface, curarization was performed and baseline recordings of the visual evoked response (VER), auditory evoked response (AER).and brainstem auditory evoked response (BAER) were made. Following the procedure of Prince and Farrell (1969), the animals were then given intramuscular doses of 300,000 to 500,000 U/kg of penicillin with the subsequent development of diffuse, bilaterally symmetrical,-photosensitive spike-and-wave discharges in the EEG These data and the similarity of this model to human petit mal epilepsy argue against increased inhibitory impulses to the visual system during the ictal discharge being responsible for the subjective loss of visual information during petit mal absence. If the amplitude of the evoked response is directly related to the functional integrity of a sensory system, this suggests that the impairment of sensory input, or absence, during spike-and-wave paroxysm is due to interference with sensory processing rostral to the brainstem ascending auditory pathway, and probably does not occur in primary sensory cortex but rather in cortical or subcortical association tracts. RESUME Chez 13 chats adultes et sains, curarises, porteurs d'electrodes epidurales chroniques implantees dans la region parasagittale, on a enregistre comme controle, les potentiels evoques visuels (PEV), auditifs (PEA) et les reponses evoquees acoustiques au niveau du brainstem (BAER). Suivant la methode de Prince et Farrel(1969)les animaux recevaient ensuite des doses de 300.000 a 500.000 unites/kg de penicilline. Ceci produisait une heure a une heure et demi apres des decharges EEG de pointes ondes diffuses bilaterales et symetriques evoquees par la SLI et s'accompagnant de myoclonies faciales, arret du mouvement et des episodes de comportement a type “d'absence” chez les animaux non curarises. L es differents potentiels evoques VER, AER, et BAER etaient enregistres a des intervalles de 15 minutes pendant plusieurs heures durant lesquelles le VER diminuait significativement d'amplitude jusqu'au moment de l'apparition des premieres pointes ondes evoquees par la stimulation photique environ une heure apres 1'injection apres laquelle toutes les composantes precoces (0 a 200 milli-secondes) du VER augmentaient progressivement de 150 a 300 pour cent jusqu'a l'apparition constante de bouffees spontanees de pointes ondes (entre une heure et demi et deux heures). En coincidence avec cette modification, on a aussi observe des modifications des composantes tardives (200 a 500 millisecondes). Les deux phenomenes de la diminution precoce et de l'augmentation tardive du PEV etaient egalement evidents dans le cortex visuel et non visuel. Avec ce modele on a observe aussi des modifications du PEA semblables mais de moindre importance par rapport a celle du PEV. L'amplitude des ondes de 1 jusqu'a 5 augmentait de 28 a 88% avec un maximum une heure et demi apres l'injection de penicilline. Ces donnees et les analogies du modele experimental utilise et de l'epilepsie avec absences typiques de type Petit Mal chez 1'homme, sont contre l'hypothese de l'existence au cours d'une decharge critique de type Petit Mal, d'une inhibition du systeme visuel qui serait responsable de la perte subjective d'informations visuelles pendant une absence Petit Mai. Si l'amplitude de la reponse evoquee a une relation directe avec l'integrite fonctionnelle d'un systeme sensoriel, ceci suggere que le deficit ou l'absence de l'afference sensorielle pendant les decharges de pointes ondes sont la consequence d'une interference dans Integration du message sensoriel qui se situe rostralement aux voies auditives ascendantes et qui n'a pas lieu dans le cortex sensoriel primaire, mais plutot dans les voies associatives corticales ou souscorticales. RESUMEN Se implantaron electrodos parasagitales en contacto con la superficie de la dura en 13 gatos adultos y sanos. Tras la curarizacion se registraron los trazados basales de las Respuestas Visuales Evocadas (VER), de las Respuestas Auditivas Evocadas (AER) y de las Respuestas Auditivas Troncoencefalicas Evocadas (BAER). Siguiendo el procedimiento de Prince y Farell (1.969) los animales fueron inyectados con 300,000 o 500,000 Unidades/kg, de penicilina consiguiendose el desarrollo subsiquiente, en el E.E.G., de descargas punta-onda fotosensibles de presentacion difusa, bilateral y simetrica. Aparecieron entre los 60 y 90 minutos y, en los animales no curarizados, coincidieron con mioclonias faciales, interrupcion de las actividades motoras y “ausencias” con mirada fija en el espacio; Las VER, AER y BAER fueron monitorizadas, durante varias horas, con 15 minutos de intervalo, observandose que las amplitudes de los VER disminuian consistentemente hasta el momento en que la fotoestimulacion provocaba los primeros brotes de complejos punta-onda. Esto ocurrfa, aproximadamente, a los 60 minutos de la inyeccion y, a partir de este momento, todos los componentes precoces de las VER (0 a 200 milisegundos) aumentaban progresivamente del 150 a 300% hasta que los brotes de punta-onda se registraban de forma consistente (de 90 a 120 minutos). Coincidiendo co este cambio tambien se observo un marcado incremento de los componenetes tarios (200 a 500 milisegundos). Ambos hallazgos, la disminucion precoz y el incremento tardio de las VER, se observaron igualmente en las cortezas visuales y no visuales. Tambien se registraron cambios en las AER con el desarrollo de este modelo y fueron semejantes a los observados en las VER aunque en menor grado. Las amplitudes de las ondas I a V de las BAER aumentaron del 28 al 88%, siendo este aumento maximo a los 90 minutos de la inyeccion de penicilina. Todos estos datos y la semejanza de este modelo con la epilepsia petit-mal en humanos, ofrecen argumentos en contra de un aumento de los impulsos inhibidores de la corteza visual durante la descarga ictal, considerados como responsables de la perdida de informacion visual durante la ausencia de petit-mal. Si la amplitude de las respuestas evocadas esta relacionada directamente con la integridad funcional del sistema sensorial, hay que suponer que la alteracion del in-put sensorial, o su ausencia, durante los paroxismos punta-onda puede ser debida a una interferencia en el proceso de la informacion sensorial en zonas mas rostrales que las vias auditivas ascendentes del tronco cerebral. Probablemente no tiene lugar en la corteza sensorial primaria sino, mas bien, en vias asociativas corticales o subcorticales. ZUSAMMENFASSUNG 13 Gesunden, ausgewachsenen Katzen wurden auf die durale Oberflache parasagittal Elektroden chronisch implantiert. Die Tiere wurden curarisiert und Basisableitungen der visuellen evozierten Potentiale (VEP), der akustisch evozierten Potentiale (AEP) und der akustisch evozierten Potentiale des Hirnstamms (BAEP) durchgefuhrt. Entsprechend dem Vorgehen von Prince und Farell (1969) erhielten die Tiere intramuskulare Dosen von 300.000 bis 500.000 E/kg Penicillin und entwickelten darauf diffuse bilateral symmetrische fotosensible spike- und wave-Entladungen im EEG, die 1 bis 1 1/2 Std. spater auftraten und bei nicht curarisierten Tieren einhergingen mit facialem Myoklonus, Bewegungsruhe und “absenceahnlichem” Starren. Die VEP, AEP, BAEP wurden in 15 Min. Intervallen fur mehrere Stunden vom Monitor aufgezeichnet. Wahrend dieser Zeit nahm die Amplitude der VEP deutlich ab bis zu dem Zeitpunkt an dem die ersten spike- und wave-Ausbruche durch Fotostimulation ausgelost werden konnten; das geschah etwa 1 Std. nach der Injektion. Nach diesem Zeitpunkt traten alle fruhen Komponenten (0–200 Millisekunden) der VEP zunehmend vermehrt von 150 auf 300% auf, bis spontane spike-und wave-Ausbruche standig abzuleiten waren (nach 1 1/2 bis 2 Std.) Mit diesen Veranderungen einhergehend konnte auch eine deutliche Zunahme der spaten Komponenten (200–500 Millisekunden) beobachtet werden. Sowohl die fruhe Verminderung und spatere Vermehrung der VEP waren gleichermassen im visuellen und nicht visuellen Cortex zu beobachten. Veranderungen der AEP wurden auch in der Entwicklung dieses Modells abgeleitet sie entsprachen den Veranderungen der VEP, waren aber geringer ausgepragt. Die Amplituden der Wellen I bis V der BAEP waren 1 1/2 Std. nach der Penicillininjektion von 28 auf maximal 88% angestiegen. Diese Ergebnisse und die Annlichkeit der Versuchsanordnung mit der Petit-Mal-Epilepsie des Menschen sprechen gegen die Annahme, dass wahrend der Krampfentladungen vermehrte inhibitorische Einflusse auf das visuelle System ursachlich verantwortlich sind fur den subjektiven Verlust visueller Information wahrend einer Petit-Mai-Absence. Wenn die Amplitude der evozierten Potentiale in direkter Beziehung zu der funktionellen Integritat eines sensorischen Systems steht, lasst dies vermuten, dass die Storung der sensorischen Einflusse oder ihr Fehlen wahrend der spike-und wave-Entladungen die Folge einer Interferenz mit der sensorischen Verarbeitung darstellt. Sie ist rostral der zum Hirnstamm aszendierenden Horbahn-wahrscheinlich nicht in den primaren sensorischen Cortex-zu lokalisieren sondern viel eher in corticale oder subcortical Assoziations-bahnen.

A study is reported in which the cortical responses to monocular and binocular scanning of patterned stimuli, both simple and complex, were recorded. In particular, the computer-summated parieto-occipital potentials, time-locked to eye movement (the lambda response), were used. No over-all asymmetries appeared between the hemispheres, whether the scanning was monocular or binocular, although responses were in general of greater amplitude for binocular than for monocular scanning. However, there were individual and other differences which were thought to be related to complex parameters of the lambda response itself.

A rhythm sometimes having the spurious appearance of alpha activity and associated with flutter of the eyelids occasionally is observed in records taken from the frontal and temporal leads of the electroencephalogram of normal persons and patients and is commonly seen when recordings are made from electrodes near the eyes. This rhythm is usually inhibited when the eyes are open and can be inhibited by holding the closed eyelids motionless. The rhythm is often increased briefly during mental activity. When recorded from electrodes placed close to the eyes, the rhythm was present in 8 of 14 normal persons used as controls and it appeared in 3 of 100 consecutive routine electroencephalograms. The rhythm is thought to be extracerebral in origin, probably resulting from oscillation of the electric field of the eyes produced by rapid ocular movements associated with flutter of the eyelids. It is suggested that flutter of the eyelids may be the source of kappa electroencephalographic waves.

In normal Ss, a parietal-occipital located response (lambda wave) is evoked by scanning a printed block and word material (colored, and black and white) of the Stroop test. When this response is summated with a computer triggered by the eye movement, a highly reliable triphasic wave appears which can be subjected to accurate latency and amplitude measurements. The shortest latency of this response was observed when blocks vs words were presented, but there were no differences in latency in spite of increasing difficulty of material. This indicates that the structure of the material rather than mental activity affected the latency. Likewise, no changes were noted with colored vs black material. There was, however, a small increase in amplitude of the lambda wave response in the most difficult (word interference) task—a result that could be attributed equally to increase of muscle potentials and to the effect of mental activity.

Summary The hepatic coma syndrome is significantly associated with elevation of arterial ammonia and an alkaline extracellular pH, which were also related. By contrast, depletion of body potassium was not related to the presence of neuropsychiatric changes, nor could it be related to the presence of extracellular alkalosis. In sequential studies, improvement or deterioration in the electroencephalographic findings, arterial ammonia concentrations, and body stores of potassium usually coincided; these changes probably reflected nonspecific alterations in hepatic function, since no significant relationship in the degree of change was demonstrated. Changes in serum potassium were unrelated to those in the electroencephalogram and in body potassium. The administration of chlorothiazide by vein to patients with hepatic disease resulted in reduction in the urinary excretion and concentration of ammonia, with a simultaneous increase in arterial ammonia concentration, despite relatively trivial changes in urinary excretion of potassium. No change in fasting arterial ammonia concentrations was found when chlorothiazide was given by mouth in the f asting state, but higher arterial ammonium concentrations followed an ammonium chloride load when chlorothiazide was given simultaneously. This was consistent with additional ammonia entering the circulation as a result of administration of chlorothiazide, rather than with impairment of the peripheral utilization of ammonia. It is concluded that, in the majority of patients we studied, depletion of potassium had relatively little influence on clinical and biochemical changes in hepatic coma.

Clinical experience has shown that the response to caloric stimulation may vary in the same person when the test is performed by different examiners, or even when the test is performed in the same manner by the same examiner on different days. The interindividual variations in response to caloric tests are even more striking.1This apparent inconsistency of response detracts greatly from the clinical usefulness of the caloric test. For this reason we set out to find factors that account for this variability of the caloric response, hoping that by a better understanding of these factors methods might be devised whereby caloric testing would produce more consistent results in practice. It is immediately apparent that certain anatomic differences exist between persons that could account for their failure to respond to caloric stimulation in precisely the same manner. These include differences in the structure of the temporal bone and the

In the course of investigation following implantation of depth multielectrode leads in an epileptic patient a fast discharge was observed in one electrode, located in the left occipital lobe, when the lights of the room were switched on and off. On the basis of roentgenographic evidence as well as the results of visual, photic and electric stimulation, the electrode involved in this phenomenon was estimated to be located in the anterior calcarine cortex or underlying white matter. Constant illumination (18 to 1200 foot-candles) provoked in this part of the brain a response characterized by an initial slow potential (“slow on-response”), followed by a fast discharge of around 50 c/sec. This evolved after a variable time into a discharge of 20 to 25 c/sec. that gradually declined and was usually over after 30 to 35 sec. (“fast on-response”). A pattern similar to the on-response, but of lower voltage and shorter duration, was observed when the stimulus was switched off (“slow” and “fast” off-response). The response was usually reduced by closure of the eyes and enhanced at their opening. The response was present and sometimes intensified during sleep. Various effects could be provoked by changing the duration and the intensity of illumination. There was some degree of similarity between the initial slow potential of the “on” and “off” response and (1) lambda waves and (2) responses to intermittent photic stimulation at low rate. These findings are discussed on the basis of previous animal experiemental studies.

(1969). Cortical Audiometry: Test Problems and Sources of Error. International Audiology: Vol. 8, No. 2-3, pp. 337-344.

Electroencephalograms of 71 normal children in one-year age groups ranging from 1 to 10 years inclusive were recorded. In all instances right and left parieto-occipital recordings were subjected to frequency analysis by means of the Ediswan Walter analyzer. The results of the analysis, presented in the form of a scattergram for each one-year age group, show (1) relative constancy (under basic conditions) of frequency analysis of one area and similarity of homologous areas; (2) great variability of analysis within single age groups; this has been illustrated by electroencephalograms representive of relatively mature (fast) and immature (slow) patterns in each age group; and (3) evidence of individuality of delta (1 to 3 c/sec.), theta (4 to 7 c/sec.) and alpha (8 to 12 c/sec.) which undergo complex changes with development. Four subjects (5.6 per cent) had grossly abnormal tracings. While 3 of these subjects had focal sharp-wave discharges, the fourth had a diffuse abnormality. Of the 3 subjects with focal sharp waves in their electroencephalograms, 2 had normal records 18 months later. It is concluded that sharp-wave foci in children may have a less serious prognostic significance than in adults. The relative merits of visual and automatic analysis are discussed together with suggestions for the practical application of automatic analysis in pediatric electroencephalography. It is suggested that combination of the automatic-analyzer tracing and the 8 traces of the standard recording may result in reaching or even exceeding the threshold of data saturation of the observer. Such a situation may require compromises aimed at simplifying the final presentation.

A study was made of the electroencephalograms of 50 children who had proved neoplasms of the brain. In 9 of 12 children who had tumors of the cerebral cortex, the localization afforded by the EEG was correct. In 8 children who had supratentorial tumors of or near the brain stem no localizing or consistent electroencephalographic pattern was observed. In 21 (70%) of 30 children who had tumors of the posterior fossa a bilateral abnormality was observed in the EEG recorded from the occipital region or occipital and contiguous regions. It is acknowledged that the abnormality found in this last group also is found occasionally in conditions other than in brain tumors of the posterior fossa. These conditions usually can be excluded by use of the history and other laboratory aids. Electroencephalography in the study of brain tumors in children should not be considered as an infallible test but rather as a diagnostic aid to be used and evaluated with the help of a clinical history and other diagnostic and laboratory aids.

SEVERAL investigators1-3have recognized that intermittent visual stimulation such as occurs when the eyes scan a picture is associated in man with the appearance of discrete electric discharges, lambda waves, in the parietal and occipital areas of the scalp. A previous communication4reported the findings of similar waves in the monkey, dog, cat, and rabbit. Others working with monkeys,5,6dogs,7and cats8also noted the occurrence of discharges in the occipital region, which they likewise considered to be the equivalent of lambda waves in the human. The studies to be reported represent an extension of those previously reported findings.4Not only were conventional scalp, extradural, and depth recordings made but computer summation techniques also were employed; in particular a Computer of Average Transients (CAT) was triggered by eye-movement potentials, and the succeeding brain activity was summed.9Thus, it was possible to sum

THE PRESENT study was part of a series of investigations into the human electroencephalographic response to visual patterns and "pattern sensitivity" at this laboratory 1,2 ; in particular, the investigations are concerned with λ-waves, 3 which occur as a response to scanning of patterned visual fields in the electroencephalograms of normal human subjects and which also have been found in many varieties of animals. 4 Remond and associates 5 first investigated λ-waves, using a computer-averaging technique. They called the response obtained the "lambda complex." In the parieto-occipital region, it consisted of four main components. The first was negative (N 1 ), followed by a positive wave (P 1 ), and then by a negative (N 2 ) and a positive deflection (P 2 ). In the present investigation, briefly reported 6 previously, a slightly different technique, using the Computer of Average Transients (CAT), was employed. The method was based on the observation 7,8 that each

1. 1. The effect of thiopental sodium (Pentothal) anesthesia and pentylenetetrazole (Metrazol) in changing the latency of the photic response at various levels of the optic system (optic nerve, geniculate and striate cortex) has been investigated. The anesthesia level has been quantitated by the method of cortical potential integration. With deepening thiopental anesthesia, there is progressive increase in latency at all three levels, with greatest increase at the cortex (for example, from 17 msec. to 36 msec. in one experiment). 2. 2. Pentylenetetrazole reversed more or less completely the increase in latency caused by thiopental sodium. 3. 3. The integrator rate is a more sensitive measure of depth of anesthesia than cortical photic latency, but the latter can be used at a depth of anesthesia which invalidates integrator readings owing to total suppression of cortical activity.

One of the main difficulties with the interpretation of evoked potential data is the question of how much noise is contained within the average. This question is crucial in deciding whether any particular peak component is a genuine signal, or whether it is a random occurrence due to noise. This is particularly crucial in abnormal cases, and with stimuli near sensory threshold. A simple method is described which allows on-line objective statistical determination of the presence of significant non-random peak components. It is shown that high signal-to-noise (S/N) estimates are seen with 'clean' and reproducible BAEPs and low S/N estimates are seen with poorly reproducible BAEPs. This provides an objective measure to judge the acceptability of any single BAEP, or to indicate that further averaging is required. The effect of noise on wave shape and peak latency is discussed. This can be quite marked, with gross distrotion of morphology and latency as a result. The technique lends itself to evoked response audiometry (ERA) and sensory threshold determination. Further, it can be applied to evoked potentials from other stimulus modalities.

We studied brainstem auditory evoked responses (BAERs) in 26 comatose patients after head injury, and long-latency auditory evoked responses (AERs) in 24 patients. BAERs-AERs were graded for abnormality to evaluate graded outcome. Only six patients had central BAER abnormalities. AERs were abnormal in 21, and all patients with abnormal BAER had abnormal AER, implying that the major site of injury affected the cerebral hemispheres. BAER was abnormal in only 5 of 12 with decerebration, suggesting that decerebration may occur with diffuse hemispheric injury. BAER (p less than 0.01) and AER (p less than 0.01) strongly correlated with outcome. Preservation of AER and normal BAER indicated good quality of survival; absent AER and normal BAER, survival; and absent AER and abnormal BAER, severe disability or death. BAER-AER predicted outcome as accurately as the detailed neurologic examination and occasionally added predictive power.

Cooling of the medial aspects of the midbrain tegmentum produces high voltage EEG rhythms and behavioral depression. This same procedure carried out in cats pretreated with parachlorophenylalanine between post-drug hours 20 and 60 produces a state exhibiting the tonic and phasic EEG, EOG, EMG and gross behavioral criteria of the paradoxical episode of sleep.

In this research, a quantitative study of the EEG from 5 subjects permitted a detailed analysis of the effect of 30 mg of flurazepam administered over 7 nights. Four placebo baseline nights and 3 placebo withdrawal nights were also recorded. For 4 of the subjects, a nondrug and nonplacebo follow-up record was obtained 4 to 6 weeks later. The subjects were 4 females, 1 male, age range 23-42. All complained of either sleep onset greater than 45 min, sleep length of less than 6 h, or two or more sleep awakenings. Compressed spectral analysis yielded a computer-generated somnogram on each of the 15 nights of sleep, and an automated spindle detector was used to count and measure the duration of spindle bursts with frequencies of 12.25-15.5 c/sec on baseline nights 3 and 4, drug nights 1, 2, 3 and 7, on the 3rd withdrawal night, and on the 4-6 week followup record. K-complexes were scored visually on the 4th baseline and 7th drug nights. There were no significant differences in spindle rate per minute among baseline nights and the follow-up record. By the 2nd drug night, spindle rate had significantly increased over the baseline rate. Linear contrast analysis indicated there was a significant increase of spindle rate over drug nights. All 5 subjects showed this pattern of increase. In contrast to the increase in spindle activity, the rate per minute of K-complexes significantly decreased during drug administration.

Analogies between brain waves and waves in physical systems suggest that EEG frequency may be partly determined by cortical surface area. Since a number of other physiological and anatomical parameters probably influence EEG frequency, only a weak correlation is to be expected. A study was made of 159 subjects, some of whom had either very large or very small heads. A single number representing head size was determined as the cube root of three linear measurements. Several characteristic EEG frequencies were determined for each subject by means of Fourier analysis. The data indicate that alpha frequency is significantly correlated with head size: larger heads tend to produce slower alpha rhythms. It was also shown that alpha frequency tends to be lower in all subjects above roughly age 60. Subjects above produced significantly less alpha rhythm than the younger group. It is suggested that analogies between brain waves and physical waves may explain a number of phenomena which are typical of EEG.

The averaged visual evoked potentials of 10 normal subjects were studied either with eyes fixated while a chequeboard reversed or when they moved their eyes across the stationary chequeboard. The resulting occipital potentials averaged using a computer of averaged transients were discrepant for the 2 conditions. The latency of the P100 component was similar allowing for the difference in latency in the computer triggering system but the resulting wave forms were different. There was a prominent negative component preceding the P100 in the lambda response and a prominent negative component following the P100 for the pattern shift. The possible reasons for the findings are discussed.

CODY and Bickford1have demonstrated that it is possible to measure hearing by means of electric currents from the cerebral cortex, known as cortical-evoked responses. This has provided an objective method (cortical audiometry) for testing hearing without the need of a conscious response by the patient. A similar test in laboratory animals could be significant in the evaluation of normal physiology, effects of various ototoxic drugs, acoustic trauma, and experimental operative procedures. The introduction of computer techniques which allow the isolation of potentials evoked by sensory stimuli from the electroencephalographic background has provided the otologist with both a useful clinical and research tool. Averaged responses evoked by click stimuli have been recorded from the dura over the auditory cortex in anesthetized guinea pigs.2However, it has been possible to obtain a small averaged cortical response to click stimuli in awake guinea pigs with scalp electrodes only during curarization.

The EEG is a screening method for organic focal lesions, particularly for cortical tumors, and to a lesser extent for subcortical and midline expanding lesions. With care in technic and interpretations, the neurologist and neurosurgeon are provided with a very useful and reliable method to supplement their clinical impressions.

The various types of electrodes used for intracerebral recordings in human beings have been reviewed. A multielectrode lead is described which can be introduced into the brain externally to the needle-introducer. It can be used for recordings in the operating room as well as for “chronic” implantation (as “chronic” is defined herein). Localization of the tip of the electrode in the roentgenograms of the skull is fairly easy.

IN PAST years the literature on subdural hematoma has been steadily increasing. Since Walter's1original description of a "silent area" over an extradural hematoma as evidenced in the electroencephalogram, and the description, by Jasper and co-workers,2of a "silent area" on the side of a subdural hematoma, several series of cases of subdural hematoma have been reviewed by various authors. These reviews have resulted in varied pictures. This discrepancy may be due to two factors: One is a matter of terminology. Both Walter and Jasper and co-workers employed the term "silent area," but Walter described under this term a delta focus, whereas Jasper and co-workers employed it for a marked lowering of the amplitude. A second factor is the small number of cases in most of the series. Glaser and Sjaardema3reported 3 cases; Cohn and co-workers,46 cases; Marsh and co-workers,513 cases; Smith

Portacaval anastomosis with diversion of all the portal blood from the liver (Eck's fistula) in dogs is followed by characteristic symptoms and death within a year. A similar surgical procedure performed on humans for the relief of bleeding esophageal varices does not produce similar symptoms. In this study we show that symptoms do not follow this operation in the dog if portal-systemic collateral circulation is present. Since the presence of excessive portal-systemic collateral circulation is one of the chief indications for this operation in man, the absence of symptoms similar to those of animals with Eck's fistula also may be related to this collateral circulation. The course and symptoms in animals with Eck's fistula were described adequately more than 60 years ago by Hahn and associates. 1 In our experience, the same symptoms have prevailed. If all the portal blood is diverted from the liver to the vena cava in