Search

The pupil light reflex has a long history of being able to indicate states of mental arousal, ranging from sleepiness to concentrated cognitive effort. Such mental states have usually been inferred from pupil diameter or pupil area movements relative to some reference; sleepiness, for example, is characterized by a smaller than average pupil while mental effort brings on a slightly larger pupil. But all pupil movements and associated states of arousal are accompanied by a persistent random pupil diameter motion which has previously been attributed to neurological noise, the noise apparently arising in the neurological controller of the pupil reflex control system. Our experiments and signal processing methods show that the amplitude of this pupil noise is an indicator of the sleeping disorder narcolepsy. Narcoleptics are found to have diminished pupil noise amplitudes relative to control subjects. Pupil noise is estimated by statistical procedures which yield unbiased noise measures in the form of six-dimensional Gaussian vectors. Each subject is associated with a Gaussian vector which is optimally projected onto a scalar axis so as to maximize the mean square distance between the narcoleptic and control samples. The Kullback-Leibler discrimination function is estimated and then evaluated for each projection as a means of discriminating narcoleptics from controls. The projected noise measures correctly classify 18 out of 20 subjects. The projected values also form the basis for supporting or rejecting a hypothesis of narcoleptic or control class membership. Parametric and nonparametric hypothesis tests suggest that, with probabilities close to one, narcoleptics and controls are distinguishable classes. To emphasize the importance of pupil noise as a diagnostic tool we present evidence from the neurophysiology literature indicating that Alzheimer's disease and narcolepsy have some of the same brainstem nuclei implicated. Further, Alzheimer patients and narcoleptics share some of the same disturbed sleep patterns. Index Terms - Attention state measures, narcolepsy, noise discriminators, pupillary noise.

A model of an asset market with noiseless price feedback is shown to achieve maximum profits for the market traders and also to achieve a point on the rate distortion function of the market input. A simplified version of the model, which is empirically more robust than the original, is shown to be a market operating with a fixed signal power. For this version it is found that there is a tradeoff between trader profits and price distortion. Unlike a pure communication channel, the market has its mutual information set by informed traders to maximize expected profits rather than set to minimize distortion. It is found that expected profits are maximized when there is just the right amount of price distortion. Index Terms - Market channel, price distortion, asset market price feedback codes.

Excitable tissues have been reported to respond to weak microwave (MW) fields, possibly by nonlinear perturbation of a cellular process such as ion conduction across membranes. We sought effects of MW (continuous wave, 2.45 GHz, specific absorption rates 12.5 or 125 mW/g) on input resistances and action potential (AP) intervals of neurons in ganglia of snails (Helix aspersa), at 20.9 plus or minus 0.1 degrees C. At 12.5 mW/g, input resistance did not change during irradiation, but increased (p < 0.05) afterward. At 125 mW/g, input resistance during irradiation was lower than in unirradiated controls. Serials correlograms changed marginally more frequently in MW experiments than in controls, but the changes had no consistent pattern. The AP firing rate was affected by MW, but the direction was not consistent across cells. When AP generation was modeled as being due to a neuronal input current, MW did not affect its mean, standard deviation, or autocorrelation. Unlike MW, temperature changes caused neurons to respond robustly and reversibly. Threshold for changing input resistance was 0.63 degrees C. The data suggest that MW may enhance degenerative effects such as metabolic rundown or loss of ion channel patency, but do not indicate a specific mechanism for MW interaction with neurons.

It has been reported that narcoleptics exhibit deficits in short-term memory, list recall, and stimulus frequency estimation compared with control subjects. It is also well-known that pupil dilation during cognitive tasks is a measure of subject attention state. Here we present results from six narcoleptics and six controls, a total of 360 experimental records in which pupillograms were made during cognitive tests, which indicate that narcoleptics begin pupillary dilations at a smaller diameter, begin dilating earlier poststimulus, attain higher pupillary diameter velocities, yet achieve the same equilibrium dilation diameter as controls. These findings are derived from statistical tests performed on the parameters of a nonlinear regression model of pupillary cognitive dilation as a function of time. In our experiments, the standard 1-s interdigit time between cognitive stimuli was increased to 2.3 s, which yielded pupillographic time records showing that the process of short-term memory overload sets in gradually at about four memory digits for controls and three memory digits for narcoleptics. We suggest our results can be partially explained by a narcoleptic stimulus-encoding deficit, which limits the time available for subjects to rehearse cognitive tasks. However, we also report the unexpected finding that the inferred encoding deficit is a transient one in that repeated tasks at the same memory load elicit a near normal naroleptic pupillary dilation. Index Terms--Cognitive response, narcolepsy, pupillometry.