Confusion points and constant-luminance planes for trichromats, protanopes and deuteranopes.

The confusion points of dichromats are derived from the constant-luminance planes of trichromats, protanopes and deuteranopes experimentally defined by heterochromatic-flicker photometry: (1) the zero-luminance planes of the observers considered in this experiment intersect almost exactly in a line that crosses the plane of the chromaticity diagram in the tritanopic-confusion point and confirm that the short-wavelength sensitive cones can be considered to have no contribution to luminance; (2) protanopic- and deuteranopic-confusion points are taken as being defined by the intersection of the tangent line to the long-wavelength region of the spectrum locus and the zero-luminance plane for protanopes and deuteranopes, respectively.

Effects of ethanol metabolism on PKC activity in isolated rat hepatocytes.

Isolated rat hepatocytes were exposed to increasing concentrations of ethanol. During exposure of cells to ethanol a moderate but significant modification in the level of hepatic PKC c-isoforms has been observed. The ethanol-induced effect on liver protein kinase C was reversed by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, indicating that the conversion of ethanol to acetaldehyde may be involved in the enzyme inactivation. The involvement of the alcohol metabolite in PKC modifications was confirmed by the exposure of hepatocytes or partially purified liver enzyme to acetaldehyde concentrations of pathological interest.

Color discrimination along the cardinal chromatic axes with VECPs as an index of function of the parvocellular pathway. Correspondence of intersubject and axis variations to psychophysics.

Chromatic information is carried only by the parvocellular pathway, giving the neurophysiologist the opportunity for eliciting specific responses. Further subdivision of the parvo chromatic system in two opponent chromatic mechanisms is potentially of great interest, given that the anatomical correlate seems to reside in subclasses of parvo ganglion cells that show differences both in size and in susceptibility to disease. We separately recorded responses arising from each chromatic opponent mechanism using visual stimuli chosen to belong to one of the "cardinal" chromatic axes. A calibrated color monitor, driven by a high resolution (14 bits/gun) computer board, was used for visualization of 1 c/deg isoluminant color gratings, sinusoidally modulated in time at 4 Hz. VECPs were recorded at several color contrasts along both cardinal axes, allowing extrapolation of contrast thresholds. Psychophysical thresholds were derived in the same stimulus conditions for comparison and found to correlate very well with the electrophysiologically derived values, both as intersubject and axis differences. The S-(L+M) opponent mechanism consistently yielded higher thresholds, smaller amplitude, and higher phase lag than the L-M mechanism. This finding was largely explained by the perceptual non-uniformity of the CIE chromaticity diagram. Correcting the VECP data for the perceptual differences yielded comparable responses, supporting the view that the two mechanisms are similarly represented in the cortex. In conclusion, recording of cortical responses to color contrast stimuli belonging to the cardinal chromatic axes seems a reliable procedure and may prove to be useful in performing clinical evaluations that refine the assessment of the physiology of the visual system.

Visual evoked cortical potentials and psychophysical determination of color contrast thresholds along different chromatic axes.

Color vision can be assessed by examining the color contrast threshold along various color axes. We investigated the possibility of determining these thresholds objectively by means of visual evoked cortical potentials. A color-calibrated flicker-free (112-Hz) monitor and a 14-bit-per-gun board allowed visualization of colors with specified xyY CIE 1931 coordinates. Horizontal grating, 1 c/deg were sinusoidally alternated at 8 Hz for both visual evoked cortical potential recordings and psychophysical determinations. Two healthy emmetropic 35 year-old subjects performed color brightness matching along each color axis, before any recording and reduction in color contrast. For each color axis, extrapolation to zero voltage of the visual evoked cortical potential amplitude versus log color contrast response allowed determination of the color contrast threshold. The visual evoked cortical potential-derived threshold changed considerably with the color axis, with evident intersubject differences. These differences were similar to those observed in the psychophysically determined thresholds. Visual evoked cortical potential responses to suitable chromatic stimuli allow determination of color contrast thresholds that correspond well to those determined psychophysically. Hence, with the visual evoked cortical potential, accurate objective assessment of color vision is feasible and may be useful in both research and clinical settings.

[Evaluation of intellectual functions in patients with Parkinson's disease. Bibliographic review]. / La valutazione delle funzioni intellettive nei pazienti con morbo di Parkinson. Rassegna bibliografica.

A literature review shows that patients affected by Parkinson's disease present an intellectual impairment more frequently than the comparably aged population. Such impairment has been related to several factors (age, arteriosclerosis, motor difficulties, depression, dopaminergic therapy, cortical and/or subcortical lesions). Parkinsonian dementia may be caused by the extent of the degenerative process. Our own results show that parkinsonian patients with dementia are different from nondemented ones with the following features: a) a more marked bradykinesia b) a more severe extrapyramidal picture c) a progressive unresponsiveness to levodopa in a shorter time. It seems possible that there is a Parkinson syndrome characterized, clinically, by an intellectual impairment with a poor prognosis quoad valetudinem, and, anatomically, with multiple cortical and subcortical lesions. Such syndrome may be a "transition" form between Parkinson disease and senile-presenile dementia.