Rheoencephalographic and electroencephalographic measures of cognitive workload: analytical procedures.

This investigation demonstrates the feasibility of mental workload assessment by rheoencephalographic (REG) and multichannel electroencephalographic (EEG) monitoring. During the performance of this research, unique testing, analytical and display procedures were developed for REG and EEG monitoring that extend the current state of the art and provide valuable tools for the study of cerebral circulatory and neural activity during cognition. REG records are analyzed to provide indices of the right and left hemisphere hemodynamic changes that take place during each test sequence. The EEG data are modeled using regression techniques and mathematically transformed to provide energy-density distributions of the scalp electrostatic field. These procedures permit concurrent REG/EEG cognitive testing not possible with current techniques. The introduction of a system for recording and analysis of cognitive REG/EEG test sequences facilitates the study of learning and memory disorders, dementia and other encephalopathies.

Electroencephalographic scalp-energy analysis as a tool for investigation of cognitive performance.

In a new method of using electroencephalography (EEG) to monitor cognitive events, multichannel event-related potentials (ERPs) were used to estimate scalp distributions of surface energy densities of cortically generated electrical fields. Cross-subject regression analyses were then used to map sites and post-stimulus latencies, for which there is a high correlation of energy densities with subjects' performances. In a preliminary study, five right-handed young men were presented mental arithmetic tasks via a computer screen. A 21-channel ERP was computed for each subject and converted to show the scalp distribution of energy density at each sampling period (every 7.8 msec). Indices of subjects' task performances were regressed upon these estimates of potential energy at each electrode site and post-stimulus latency. High correlations were found at four distinct regions and latencies. These corresponded to the stages and sites of cortical localization for mental arithmetic inferred from studies of patients with localized cortical lesions. This correspondence suggests that the EEG procedure may offer an inexpensive, noninvasive method of investigating cortical localization of cognitive function in healthy subjects.

Cortical localization of cognitive function by regression of performance on event-related potentials.

This paper demonstrates a new method of mapping cortical localization of cognitive function, using electroencephalographic (EEG) data. Cross-subject regression analyses are used to identify cortical sites and post-stimulus latencies where there is a high correlation between subjects' performance and their cognitive event-related potential (ERP) amplitude. The procedure was tested using a mental arithmetic task and was found to identify essentially the same cortical regions that have been associated with such tasks on the basis of research with patients suffering localized cortical lesions. Thus, it appears to offer an inexpensive, noninvasive tool for exploring the dynamics of localization in neurologically normal subjects.

Corpus luteum progesterone secretion in rats undergoing pineal-mediated reproductive regression.

In nonseasonal breeders, such as the laboratory rat, the potentiation of the antigonadal action of light deprivation by olfactory bulbectomy is manifested, among other things, by a diminished secretion of testosterone in males and estradiol in females. Little is known about the actions of the pineal gland on progesterone secretion. Since secretion of the luteotrophic hormones (LH and PRL) decreases in blind-anosmic rats and because the rat corpus luteum exhibits different degrees of LH and/or PRL dependency, the purpose of these experiments was to study the corpus luteum progesterone secretion in both pseudopregnant and pregnant blinded-bulbectomized rats. Female rats blinded and bulbectomized at the age of 25 d showed at adulthood (75 d old) (1) estrous cycles longer than the regular 4-5 d in length exhibited by intact rats: 82.3 vs. 9.0% (P less than .01); (2) a decreased paired ovarian weight, 24.1 +/- 3.7 (nine) vs. 37.3 +/- 2.2 (ten) mg/100 gm BW (P less than .05), and lower plasma levels of LH on metestrus: 15.9 +/- 1.7 vs. 26.2 +/- 3.4 ng/ml (P less than .01). Pinealectomy, as previously reported, completely reversed the effects of dual sensory deprivation. In contrast to the clear antigonadal action of the pineal gland, which seems to affect the follicular component of the ovary through modifications in the rate of LH secretion, the production of progesterone by the corpus luteum remained almost unaffected. Although the duration of the diestrous phase in both pseudopregnancy and pregnancy was significantly longer in blind-anosmic rats than in intact ones (P less than .01), the serum levels of progesterone throughout both corpus luteum phases were identical.(ABSTRACT TRUNCATED AT 250 WORDS)

Different olfactory system deficits affect the antigonadal action of light deprivation differently in male rats.

Twenty-eight day-old male rats were subjected to: Blinding-olfactory bulbectomy, Blinding-peripheral anosmia, Blinding-accessory olfactory bulbectomy and Blinding-sham olfactory operation. A set of rats remained intact. Six weeks later, their pituitary-gonads-accessory sex organs were studied. Bulbectomy as well as peripheral anosmia exaggerated the antigonadal effects of blindness, while the accessory olfactory system impairment did not. It is suggested that olfactory bulbectomy potentiation of the antigonadal effects of light deprivation is due to a lack of sensory function rather than to bulbectomy itself and that the accessory olfactory system which is involved in the priming pheromonal effects does not play any role in the inhibition of the antigonadal effects of blindness.

Relation between body weight, growth rate, chronological age and puberty in male and female rats.

Body weight, growth rate, chronological age and puberty in female and male rats from litters of 8 and 12 offsprings/mother have been studied. Age and body weight at the moment of vaginal opening (VO) and balanopreputial separation (BPS) were analyzed. Results show that animals reared in smaller groups grew faster than others. After weaning there was an increase in growth rate. VO and BPS occurred at the same age in groups with different growth rates and different body weights. In conclusion this work evidences that external signs of sexual maturation are not linked to a "critical weight" or to a "growth rate".

Muscle water and electrolytes in uremia and the effects of hemodialysis.

The effects of acute uremia and hemodialysis on water and electrolyte distribution and intracellular pH (pHi) of skeletal muscle were studied in dogs. Acute uremia resulted in an increase in intracellular muscle water and Ca++ content, and a fall in both intracellular Na+ concentration and the calculated muscle membrane potential (EM). Muscle pHi did not change. The increase in muscle Ca++ content was prevented by previous parathyroidectony. The administration of parathyroid extract to previously parathyroidectomized uremic animals resulted in a rise in muscle Ca++ content to levels similar to those observed in intact uremic animals. Hemodialysis with standard dialysate resulted in a normalization of both muscle Em and Ca++ content but did not affect either muscle intracellular water, Na+ concentration, or pHi. Hemodialysis with hypertonic dialysate (glycerol or mannitol) resulted in a slight fall in intracellular muscle water content toward normal but did not change muscle intracellular Na+ concentration or pHi. The muscle membrand permeability of Na+ relative to K+ (PNa/PK) was not changed by hemodialysis with either standard dialysate or dialysate with mannitol added. Glycerol, however, appeared to increase PNa/PK to about 10 times the normal value. The observed changes in muscle water and solute content may be related to the increased muscle irritability seen in acute uremic patients. These changes, however, are only partially corrected by hemodialysis with standard or hypertonic dialysate.

Central nervous system pH in uremia and the effects of hemodialysis.

Rapid hemodialysis of uremic animals may induce a syndrome characterized by increased cerebrospinal fluid (CSF) pressure, grand mal seizures, and electroencephalographic abnormalities. There is a fall in pH and bicarbonate concentration in CSF, and brain osmolality exceeds that of plasma, resulting in a net movement of water into the brain. This syndrome has been called experimental dialysis disequilibrium syndrome. The fall in pH of CSF may be secondary to a fall of intracellular pH (pHi) in brain. Since changes in pHi can alter intracellular osmolality in other tissues, it was decided to investigate brain pHi in uremia, and the effects of hemodialysis. Brain pHi was measured by evaluating the distribution of 14C-labeled dimethadione in brain relative to CSF, while extracellular space was calculated as the 35504=/4 space relative to CSF. In animals with acute renal failure, brain (cerebral cortex) pHi was 7.06+/-0.02 (+/-SE) while that in CSF was 7.31+/-0.02, both values not different from normal. After rapid hemodialysis (100 min) of uremic animals, plasma creatinine fell from 11.8 to 5.9 mg/dl. Brain pHi was 6.89+/-0.02 and CSF pH and 7.19+/-0.02, both values significantly lower than in uremic animals (P less than 0.01), and there was a 12% increase in brain water content. After slow hemodialysis (210 min), brain pHi (7.01+/-0.02) and pH in CSF (7.27+/-0.02) were both significantly greater than values observed after rapid hemodialysis (P less than 0.01), and brain water content was normal. None of the above maneuvers had any effect on pHi of skeletal muscle or subcortical white matter. The data show that rapid hemodialysis of uremic dogs is accompanied by a significant fall in pH of CSF and pHi in cerebral cortex. Accompanying the fall in brain pHi is cerebral edema.

Effects of glycerol administration on experimental brain edema.

The effects of glycerol on brain water and solute distribution in cerebral edema are not well known. In brail edema induced in dogs by focal freezing, tissue underlying the necrotic lesion had an elevated water content but the remainder of the brain was unaltered. Administration of glycerol to maintain plasma glycerol at about 35 mM dehydrated normal white matter, but water and solute contents of the edematous white matter were not changed. During the initial 3 hours of glycerol infusion, CSF pressure fell, but when the infusion was continued for 6 hours or more, a gradual rise in CSF pressure was observed. In three animals, the final CSF pressure was higher than preinfusion values. At this time, brain water content was significantly less than normal, but both CSF osmolality and glycerol concentration were higher than plasma. The data show that glycerol infusion can decrease intracranial volume towards normal by dehydration of normal, but not damaged, brain tissue. The rebound rise in CSF pressure observed during the continuous administration of glycerol cannot be explained by rehydration of brain tissue but may be related to alterations in CSF dynamics.

Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain.

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.

Changes in the electroencephalogram in acute uremia. Effects of parathyroid hormone and brain electrolytes.

Studies were carried out in order to evaluate the effects of changes in brain calcium and the influence of parathyroidectomy and administration of parathyroid extract on the electroencephalogram (EEG) of normal and uremic dogs. Manual analysis of frequency and power distribution of the EEG in uremic dogs revealed a significant increase in both the percentage distribution and the area or power occupied by frequencies below 5 Hz. In addition, high amplitude bursts of delta activity were apparent in the uremic dog. These changes were largely prevented by parathyroidectomy before the induction of uremia, but the administration of parathyroid extract to either normal dogs, or to previously parathyroidectomized uremic dogs, induced EEG changes similar to those noted in uremic animals with intact parathyroid glands. In all groups of animals which showed EEG changes, brain content of calcium was significantly higher than in either normal dogs or previously parathyroidectomized uremic dogs. Changes in arterial pH and bicarbonate, or in the concentrations of Na+, K+, urea, or creatinine in plasma or cerebrospinal fluid were similar in uremic animals with intact parthyroid glands and in previously parathyroidectomized uremia dogs. The results indicate that the EEG changes found in dogs with acute renal failure require the presence of excess parathyroid hormone in blood, and they may be related to the observed changes in brain content of calcium.

Rebound phenomenon complicating cerebral dehydration with glycerol. Case report.

A patient with glioblastoma multiforme of the brain was treated with both intravenous and oral glycerol as well as intravenous mannitol in an attempt to reduce increased intracranial pressure. After an initial lowering of the cerebrospinal fluid (CSF) pressure to near normal values during continuous glycerol administration, a secondary rise in CSF pressure above the initial level occurred despite a persistent elevation of plasma osmolality (315 mOsm/kg) and glycerol level (30 mmole/l). Similarly, 4 hours after the administration of a single oral dose of glycerol, CSF pressure increased to levels higher (700 mm H2O) than the original baseline (400 mm H2O).