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Approximately one-third of the laboratory-confirmed cases of Western equine encephalitis occur in children under the age of 10. The present paper describes three instances of Western equine encephalomyelitis virus infection in infants under one year of age, together with the resultant sequelae. The difficulties associated with diagnosis of central nervous system disturbances in very young children are discussed, and it is pointed out that in view of the frequent occurrence of clinical infections with the arthropod-borne encephalitis viruses these agents should be given serious consideration as a cause of acute central nervous system infection in childhood and as the possible etiology for obscure, severe neurological disturbances in the pediatric age groups.

An antibody against neurones, which has previously been demonstrated by immunofluorescence, is present in the sera of patients with sensory carcinomatous neuropathy.. This antibody was demonstrated by a new technique, namely the use of purified peroxidase-labelled sheep anti-human γ-globulin. In cryostat sections of brain treated with a first Jayer of serum antibody followed by a second layer of peroxidase labelled ant -human γ-globulin, heavy coarse brown deposits in nerve cells only from different parts of the central nervous system indicated a positive reaction. The special technical precautions necessary to obtain, specific staining of neurones are outlined, [ABSTRACT FROM AUTHOR]

The paper summarizes 20 reported cases of transient diabetes of the newborn. Sex distribution is approximately equal with nine males and 11 females. Infection was suspected in a number of the reported cases. Fever, however, could have resulted from the dehydration. Central nervous system involvement has also been considered, but most cases showed no other related manifestations. Urinary excretion of ketosteroids and hydroxycorticosteroids were normal in our case and in four others, eliminating an adrenal cause. One assumption that neonatal transient diabetes may result from an insufficiency of pancreatic fetal beta cells secondary to a decreased blood sugar in the mother, such hypoglycemia being primary in nature or due to hyperinsulinism.

Previous authors have argued that the maintenance of the highly connected aggregates of nerve cells in the central nervous system in a stable state of intermediate activity presents something of a paradox. In the present paper it is shown that this is not so and that either a relatively large-scale structure of the aggregate or the presence of inhibitory connections makes a stable intermediate activity possible. It is suggested that large-scale structure can usefully be discussed from an information-theoretic viewpoint and that it is also related to the ergodic problem of classical mechanics.

Neurophysiological and psychophysiological studies have provided a substantial amount of data concerning the integration of autonomic and somatic responses. It is clear that this integration is primarily achieved within the central nervous system and that coordinated autonomic-behavioral activity is reflected, at the periphery, in the anticipatory and preparatory phases of movement. It is suggested that the central efferent organization of these preparatory responses is directly responsible for emotional experience. The demonstration that autonomic events are highly correlated with behavioral responses is regarded as providing further support for the view that the primary concern of the central nervous system is the production of adaptive behavior. [ABSTRACT FROM AUTHOR]

The article presents a paper "Chronic Postherpetic Neuralgia," by L.S. Van Blartcom and G. Horrax. Postherpetic neuralgia affects men and women equally and is very uncommon before the age of 40. Thirty-five patients with neuralgia of more than 3 years duration were studied and the response to many types of treatment was assessed. The precise mode of production of the pain is unknown, the authors suggest that the virus causes extensive and persistent inflammatory changes which are the original source of the pain, when the central nervous system is bombarded by pain impulses for too long a period a central pain mechanism is established with self-perpetuating circuits.

The article profiles Maurice L. Tainter, vice president of Sterling Drug Inc. and vice chairman of the Sterling Research Board. In 1943, he left professorship to organize and direct research activities of the Sterling-Winthrop Research Institute, Rensselaer, New York. During his teaching career, he did research on numerous field including metabolic actions of dinitrophenol, stimulating actions on the central nervous system of various chemical entities, basic actions of sympathomimetic amines along with investigations of their application to therapeutics.

The article presents an abstract of the paper "Experimental-Morphological Investigations Into the Action of the Sexual Hormone," by H. Hermann. In male guinea-pigs after an injection of proluton measurable changes were observed in the volume of cells or their nuclei in the anterior horns of the spinal cord, cerebral cortex, ganglia of the sympathetic chains, epithelium of the large and small bowel, liver, islets of the pancreas, epithelium of the tubuli contorti and of the urinary canals in the kidneys. The dosage was not within a physiological range.

An experiment is described which was designed to test the hypothesis that brief visual stimuli would not be perceived when they occurred during certain phases of the EEG alpha rhythm. The results agreed with the hypothesis. It was concluded that the alpha rhythm is a correlate of the activity of a 'neuronic shutter' which periodically prevents the reception or processing of visual information by the brain. The procedure used was such that there was no necessity for the subjects to pay attention to the stimuli; indeed, efforts were made to avoid such attention. This methodology was thought to be of importance in obtaining a positive result. [ABSTRACT FROM AUTHOR]

During the late embryonic period, cell death occurs in the central nervous system of Calliphora erythrocephala. The degenerating cells are small and rounded, contain a pyknotic nucleus, and selectively accumulate basic vital dyes such as nile blue sulphate and acridine orange. The number of degenerating cells is highest 13-15 hours after oviposition and decreases during the shortening of the ventral nerve cord. Nevertheless, these degenerating cells do not represent a morphogenetic phenomenon, since their number is too small to account for the 55% decrease in the length of the ventral nerve cord. In all probability the pyknoses seen in the central nervous system of this holometabolic insect are to be interpreted as phylogenetic degenerations of clearly vestigial neuroblasts that have lost functions they might have retained in the larvae of insects in lower orders, for instance the innervation of legs, wings, a larger number of abdominal segments, etc. About half of the pyknoses occur in pairs. [ABSTRACT FROM AUTHOR]

Evidence is presented to show that nicotine causes desensitization of certain cells of the snail brain. On cholinoceptive cells where the action of nicotine was excitatory (D-cells), nicotine (10 to 10 M) caused a dose-dependent depolarization and a decrease in input resistance. Firing rate was increased in pacemaker cells. On cholinoceptive cells where the action of nicotine was inhibitory (H-cells), nicotine (10 to 10 M) caused a dose-dependent hyperpolarization and a decrease in input resistance. Firing rate was decreased in pacemaker cells. Both the excitatory and inhibitory effects of nicotine were blocked by d-tubocurarine (10 to 10 M) or atropine (10 to 10 M). Hexamethonium (10 M) reduced the response to nicotine on D-cells but not on H-cells. The membrane potential of both D- and H-type cells returned to control in the presence of nicotine. The duration of the nicotine-induced depolarization of cell V7 was 15±0.8 min ( n=10). The duration of the hyperpolarization of cell V5 was 5±0.7 min ( n=4). The duration of the nicotine-induced hyperpolarization of H cells was consistently shorter than the duration of the nicotine-induced depolarization of D cells. The time course of changes in input resistance and firing rate paralleled the time course of changes in membrane potential in both cell types. The duration of the nicotine-induced change in membrane potential, input resistance of firing rate was not related to the concentration of nicotine. Similarly, the duration of the depolarization caused by acetylcholine, carbachol, lobeline or DMPP was not related to the drug concentration. At the time of repolarization after nicotine, the application of a second dose of nicotine had no effect or caused a depolarization that was low in amplitude and brief in duration. d-Tubocurarine (10 to 10 M) reduced the amplitude of the nicotine-induced change in membrane potential but did not affect the duration. Increasing the extracellular calcium concentration from 7 mM to 14 mM decreased the duration of the nicotine-induced changes. Also, increasing the pH from 8.0 to 10.0 decreased the duration. Elevating the extracellular magnesium concentration from 4 mM to 20 mM blocked spontaneous e.p.s.p.'s, i.p.s.p.'s and prevented orthodromic stimulation. In elevated magnesium, nicotine caused a depolarization-repolarization sequence similar to that in normal maguesium. It differed in that the amplitude of the depolarization was decreased and the duration increased. The results indicate that the cholinergic receptors of snail neurons closely resemble the cholinergic receptors of frog sartorius muscle. [ABSTRACT FROM AUTHOR]

A correlation was found between the amount of kinaesthetic figural after-effect experienced by individual subjects (which may be related to the sensitivity of the central nervous sytem) and the slopes of their brightness-estimation functions. These and related data suggest that part of the inter-subject difference that is found in psychophysical magnitude-estimation experiments is not random, but is due to differences in the way in which an individual's nervous system processes sensory information. Because the responses in magnitude-estimation and kinaesthetic after-effect tasks are different, it is unlikely that individual differences reflect response biases. [ABSTRACT FROM AUTHOR]

Heart rate (HR), respiratory rate (RR), blood pressure (BP). and motor components of responses to non-reinforced and reinforced auditory stimuli were studied in six dogs over a period of 20 months. The experiment consisted of several phases: habituation, orienting training, conditioning, extinction, and reconditioning. Differentiated non-specific motor reactions in four of six dogs developed quickly and before the differentiated specific motor conditioned response (CR) and consistent HR or BR conditioned responses. The form of the gross organismic CR pattern differed in each dog. Yet the animals reliably maintained, in each separate system, their rank-order positions across experimental phases, suggesting that the CR is determined in part by innate or earlier acquired differences in functioning. [ABSTRACT FROM AUTHOR]

1. The age-dependent deposition of sulfatide, glycolipids and phospholipids in the whole brain during the period of myelination in the normal rat has been estimated and expressed as lipid stored in the tissue per week per dry weight, per μg total protein or per mg DNA. 2. Deficiency in vitamin A during the period of myelination in the rat gives rise to a statistically significant decrease in the deposits of sulfatide per week in the whole brain. 3. The decreased weekly deposits of sulfatide in the vitamin A deficient rat brain is associated with a slight depression in the weekly storage of phospholipids in the whole brain. 4. The myelin fraction, isolated by gradient ultracentrifugation, showed a significantly lower sulfatide content in the deficient rats than in the group of rats fed and raised on an optimal diet. Expressed per dry weight of the myelin, the total content of the phospholipids was found to be increased in the vitamin A deficient group when compared to the myelin from the normal animals. 5. The vitamin A deficiency from birth resulted in half of the normal serum value of vitamin A within five weeks. However, no absolute lack of the vitamin could be induced by the deficiency. This is in agreement with previous studies, showing it impossible to deplete the liver completely of vitamin A. This lack of complete depletion may explain the decrease, but not the absolute lack, of sulfatide formation in the rat brain. 6. The formation of sulfatide from galactocerebroside and inorganic 35S-labelled sulfate in vitro was found to be highest in the sediment of 100,000 × g ultracentrifugation both in the normal and in the vitamin A deficient animals. 7. The vitamin A deficiency in the period of myelination heavily depressed the formation of 35S-labelled active sulfate and sulfatide in vitro compared to the activities of normal rats with an identical age (two months). [ABSTRACT FROM AUTHOR]

The article focuses on the tactual form perception or stereognosis in preschool children. By stereognosis is meant the ability to recognize an object solely by means of the mechanisms of active touch, without the aid of vision. In clinical neurology, astereognosis, that is, impairment of stereognostic capacity in the presence of a grossly adequate sensory substrate, in either hand is considered as evidence of a central nervous system lesion, usually one affecting the post-central gyms of the contralateral cerebral hemispher.

Discusses diagnostic and therapeutic considerations in neonates with spina bifida in Sheffield, England. Neurologic assessment of neonates at birth; Assessment of motor function, sphincter control, hydrocephalus and infection of the central nervous system; Meningomyelocele assessment; Complication of meningitis with ventriculitis.

This article presents a discussion of lead poisoning in children by pediatricians Ralph D. Feigin, Daniel C. Shannon, Stephen L. Reynolds and social case worker Lilian W. Shapiro. Reynolds stressed the importance of the medical history in the case of an 18-month-old boy who suffered from lead poisoning. Feigin discussed various typical features of lead poisoning, some of which are its occurrence in the 15 to 36-months age group and a concurrent viral or bacterial infection. The signs and symptoms of lead intoxication usually involve the gastrointestinal, hematologic and the central nervous systems.

Classically conditioned cardiac discrimination and reversal was observed in retarded and normal children. During initial conditioning (10 stimulus pairs) only the oldest normal group (6-11 yrs) evidenced significant stimulus discrimination. During subsequent reversal (10 stimulus pairs), both the oldest and an intermediate normal group (4-6 yrs) evidenced significant discrimination. Mongoloid children (4-11 yrs) and the youngest Normal group (2-4 yrs) evidenced no consistent cardiac discrimination during reversal, but in a manner inappropriate to the reinforcement contingencies. This behavior, unique in both CA and MA comparisons of incephalopathics with mongoloids and normals, may be related to a somewhat impaired conditioning and a more greatly impaired extinction process, or to a deficit in the Pavlovian postulated process of CNS mobility. [ABSTRACT FROM AUTHOR]

Examines the sequence of events leading to the acquisition of mature behavior. Pattern of development in the central nervous system; Procedure on manipulating longitudinal observations of behavior; Developmental process leading to coordinated locomotion ability.

This article analyzes the epidemiological distribution of dysfunctions of the central nervous system (CNS). Such dysfunctions are known to arise from the operation of a broad spectrum of causal variables during the prenatal, postnatal and the natal development changes. Brain damage maybe induced at any point in the life cycle from the earliest changes of embryonic development to the final stages of senescence. Some of the major causal variables of interest include such factors as genetic mutations and chromosomal aberrations. There are major biological and psychological determinants of brain damage. There is, however, another important group of causes, to which little systematic attention has so far been directed.