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The literature contains no references to electroencephalographic recordings during sleep of patients with hydrocephalus. All previous studies of animals and man considered only waking activity. Extremely high-voltage alpha waves were reported in hydrocephalic patients by Kreezer1 and mixed fast and slow activity by Gibbs and Gibbs.2 Williams3 suggested that the slow activity that occurs in patients with high intracranial pressure is due not to the intracranial pressure per se but to cerebral edema. Stuart4 produced experimental hydrocephalus in kittens and found large slow waves which did not correlate with the height of the intracranial pressure. He concluded that the slowing cannot be due to edema because it disappears too quickly when the intracranial pressure is reduced. Stein and Sonnenschein,5 in acute experiments on cats, found a general inverse relation between the height of the intracranial pressure and the frequency of cortical potentials. Levin and Greenblatt,

Patients subjected to frontal lobotomy may show after operation focal slow activity and seizure discharges. Such changes are to be expected from local cortical trauma and as an irritative reaction to injury. However, they are neither inevitable nor characteristic results of frontal lobotomy. In many cases, as will be shown in this report, the waking electroencephalogram remains normal. Lennox and Coolidge1 have reported an absence of frontal sleep spindles as a sequel of frontal lobotomy. In our experience the change, if any, consists of a reduction of frontal sleep spindles; in most cases this reduction is so slight as hardly to be evident even after close comparisons of pre- and postoperative recordings.We have observed an electroencephalographic alteration after frontal lobotomy which is constant and characteristic, but it takes many months to develop. We are now reporting this for the first time in print* because we have only recently

CURIOUSLY little has been written about the electroencephalographic changes found in association with encephalitis. A report of 1 case was published by Lindsley and Cutts,1 and the "Atlas of Electroencephalography"2 contains figures and several references to this subject. A more extensive report was published by Ross,3 but it was based on only 4 cases. Since encephalitis is a clinical condition of major importance, and since some of the most definite abnormalities that are seen in electroencephalography are encountered in patients with this condition, it seems appropriate to report on a larger number of cases. MATERIAL AND METHOD This investigation is based on 240 cases of a disorder clinically diagnosed as encephalitis, studied in different phases of the disease. Ideally it would be desirable to base such a survey on longitudinal data and on electroencephalograms prior to infection; but, for obvious reasons, this is exceedingly difficult if not

VALID quantitative data on the volume flow of blood through the human brain are of crucial importance for the solution of a variety of clinical and theoretic problems. The poverty of such data has been due chiefly to a lack of suitable technics. The thermoelectric flow recorder devised by one of us (F. A. G)1 does not yield qualitative data unless calibrated in situ, and this has not been done in man. Ferris2 has employed a method by which the bone-supported dural coverings of the brain and spinal cord are used as a plethysmograph. A trochar is inserted into the lumbar sac, and with an inflatable cuff the veins of the neck are compressed. The cerebral blood flow is estimated from the rate of displacement of spinal fluid. Kety and Schmidt3 have recently described a method based on the principle that the rate at which the brain

Students of cerebral function have, in general, paid too little attention to carbon dioxide. Procedures which alter the tension of carbon dioxide in the brain have a pronounced effect on cerebral function1 and on the electrical activity of the cortex.2 As shown by some of these experiments, extreme shifts in the carbon dioxide tension of the brain are disadvantageous. Therefore, a mechanism which would provide for the homeostasis of carbon dioxide would be advantageous. Such a mechanism appears to reside in the response of cerebral blood vessels to changes in alveolar or arterial carbon dioxide.An increase of carbon dioxide tension in the cerebral blood vessels causes dilatation of the cerebral arterioles, and a decrease causes constriction. In contrast, a maximal increase of oxygen tension produces only feeble constriction, and an extreme decrease in oxygen tension causes only moderate dilatation. These facts have been abundantly proved both for

Our reports on the electrical activity of the brain in epilepsy have thus far been almost entirely descriptive.1 Interpretation, we believed, could wait until a considerable body of data had been acquired. Now, after two and one-half years, we have electro-encephalograms for over four hundred patients. We have daily records for some patients extending over many days; others have been studied repeatedly at long intervals, and for others we have made long-continued records, the longest being thirty-four hours. Altogether, we have a total of approximately 60 miles (96 kilometers) of records. Most of these records were made with a multichannel instrument recording simultaneously from four parts of the head.The object of this effort has been to secure electro-encephalograms of patients during seizures, but we also wished to see what abnormalities, if any, occurred in the interval between seizures. We have records of the grand mal seizures of thirty

That epileptic seizures are caused by cerebral anemia consequent to a cerebral vascular spasm is a widely accepted and plausible hypothesis. It is, moreover, one that bears the respectability of age. In 1861 Reynolds1 in his book on epilepsy wrote:M. Bernard has shown that after division of the sympathetic nerve in the neck there is an elevation of temperature and vascularity, not only in the superficial parts of the head, but in the cranial cavity and the cerebral substance itself. Again, Donders and Van der Beke Callenfells have proved that irritation of these nerves causes contraction in the arteries of the pia mater; and the same observers, together with Dr. Brown-Séquard, have demonstrated that arteries of the brain-meninges contract through reflex stimulation; the centre of such reflextion being the medulla oblongata. Now, it has been shown experimentally by Astley Cooper, that compression of the brain will induce loss

Ever since Hippocrates expressed the opinion that epilepsy is a familial disease the inheritance of epilepsy has been a subject for debate. The principal evidence has been gathered from the family histories of persons subject to seizures. The most comprehensive data from extramural patients have been furnished by members of the Association for Research in Nervous and Mental Diseases and the American Neurological Association. The family histories of 2,130 patients have been tabulated by one of us (W.G.L.) and will be presented in detail later. The incidence of seizures among the 13,262 near relatives (parents, siblings and children) of patients in this group is 2.4 per cent. This is approximately five times the incidence of seizures in the general population. However, only 1 in 5 of these patients gives a history of any blood relative affected with seizures. The combined data of Rosanoff, Handy and Rosanoff1 and of Conrad

Overventilation is particularly effective in precipitating petit mal seizures, as has been pointed out by Gibbs, Lennox and Gibbs.1 Only rarely in their experience has any other form of epileptic seizure resulted from vigorous overbreathing. From this one can conclude that rapid induction of respiratory alkalosis gives rise to a physicochemical state of the fluids bathing the nerve cells in the brain which is favorable for the appearance of the petit mal attack. One cannot say, however, whether this physicochemical state in patients with petit mal epilepsy is different from that obtaining in nonepileptic persons when they overbreathe or whether the nerve cells of the epileptic brain are abnormally sensitive to a change in acid-base equilibrium which is within normal limits. The present series of experiments were performed in an attempt to answer the first alternative. They comprise a study of the adjustment of the acid-base balance during and

The observation that epileptic seizures can be precipitated by overventilation was reported by Rosett,1 and also by Foerster,2 in 1924. One of us (W. G. L.),3 in 1928, demonstrated that petit mal seizures can be temporarily abolished by breathing air containing an increased concentration of carbon dioxide. In spite of the numerous reports dealing with the effects of overventilation, there has been a curious lack of discrimination in regard to the types of seizures most readily influenced. Our studies have shown that overventilation will not precipitate all types of seizures with equal facility. In fact, overventilation seems to be almost specific for petit mal, although occasionally psychomotor seizures are precipitated. In several hundred trials, a period of overventilation which regularly produces petit mal seizures never precipitated a grand mal seizure. On the other hand, in 2 cases in which there were both petit mal and grand mal

Since the beginning of our work on the electrical activity of the cortex,1 we have attempted to distinguish between the different types of abnormal waves that are encountered in epilepsy. We have described the wave and spike of petit mal,2 the crescendo burst of fast waves of grand mal2 and the slow square waves and high voltage 6 per second waves of psychic equivalent seizures.3Characteristic examples of these various formations have been published,2d but for ease of reference they are shown again in figure 1. It will be noted that there are two kinds of wave and spike activity: (1) the approximately 3 per second wave and spike rhythm of the true petit mal seizure which is commonly accompanied by clonic muscle jerks, synchronous with the 3 per second rhythm, and (2) the slow wave and spike formation which repeats approximately twice a second and

It is well known that stoppage of the blood supply to the brain or the production of severe anoxemia results in unconsciousness and, if prolonged, in irreparable injury to nerve cells. In view of this fact, it is an easy assumption that all states of unconsciousness are due, wholly or in part, to a defect in the cerebral circulation or in the nutrition of nerve tissues. Although a subject of lively debate, the matter has remained largely in the field of speculation because of lack of direct information concerning physiologic disturbances of the cerebral circulation in the human subject. States of consciousness are difficult of determination in animals, even if anesthesia is not used.Two methods of direct approach to the study of cerebral circulation in unanesthetized persons are now available, viz., analysis of the oxygen content of the blood leaving the brain and observations of changes in blood flow

Recently a number of reports have appeared pertaining to a disturbance in the metabolism of the aromatic amines in the blood of schizophrenics. With such substrates as N,N'-dimethyl-p-phenylenediamine (MPD)1 or adrenaline,2 it has been possible to demonstrate a greater oxidation of these amines in the serum of schizophrenics. In both instances the oxidation was attributed to a copper-containing protein, ceruloplasmin. At the time the present work was completed we were not aware of the details of Akerfeldt's method except that MPD was a substrate. The present study reports findings on the ceruloplasmin activity of serum from patients with schizophrenia and a variety of other disorders; and the technique used, although similar to Akerfeldt's,1 appears to be somewhat simpler and subject to fewer errors. METHODS AND MATERIAL Details of our procedure were as follows: To 0.1 ml. of serum was added 1.0 ml. of tris (hydroxymethyl)aminoethane buffer