The effects of anxiety and depression on frontal lobe functioning were tested in two groups of 9-11-year-old boys. Participants were screened for handedness, health, intelligence and classified as anxious-depressed or non-anxious, non-depressed based on scores from the A-State scale of the State-Trait Anxiety Inventory for Children and the Child Depression Inventory. Previous research in our laboratory has indicated that boys high in anxious-depression may have neuropsychological deficits [e.g., Emerson, C. S., Harrison, D. W., & Everhart, D. E. (1999). Investigation of receptive affective prosodic ability in school-aged boys with and without depression. Neuropsychiatry, Neuropsychology and Behavioral Neurology, 12(2), 102-109; Emerson, C. S., Harrison, D. W., Everhart, D. E., & Williamson, J. B. (2001). Grip strength asymmetry in depressed boys. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 14(2), 130-134]. In order to assess the effects of anxious-depression on cerebral functioning performance on the Trail Making Test (Forms A and B) and on the Concept Formation subtest of the Woodcock Johnson was compared between groups. As predicted, anxious-depressed boys demonstrated deficits in sequencing, alternation, and problem-solving tasks as evidenced by longer completion times and significantly more errors on the tests. These results provide supportive evidence for deficits in frontal lobe functioning.

Behavioral and physiological reactivity, and its relationship to cardiovascular disease has been studied in men for a number of years, and the expression of anger has been identified as a possible contributing factor. Few studies, however, have focused specifically on the reactivity of women, and those which have suggest that women are less reactive to laboratory tasks than men. For the present study, 45 undergraduate women, ages 19-21 were selected from a larger sample of 135 women to represent three discrete groups: (1) low anger/low denial, (2) high anger/low denial, and (3) low anger/high denial, based on their scores on the State-Trait Anger Expression Inventory, 1 and the Marlowe-Crowne Social Desirability Scale. It was hypothesized that the three groups would show reliable differences in heart rate and blood pressure during presentation of a stressful laboratory stimulus, the Stroop Color and Word Test. Each subject received three counterbalanced conditions: (1) no feedback, (2) error feedback without observer present, (3) error feedback with observer present. As hypothesized, women who reported a high level of denial and a low level of anger exhibited reliably greater systolic blood pressure to the no-feedback condition than subjects who reported low levels of denial and anger. The hypothesis that all groups°w ould display greater reactivity in a condition which T provided error feedback with observation was not supported. (Eliot, Buell & Dembroski, 1982;Obrist, 1981). The reasons for this are still somewhat unclear.Investigations of the etiology and effects of hyperreactivity have followed three independent, yet seemingly related, lines of research. As early as 1911, Walter Cannon addressed the association between anger and the neuroendocrine mediation of the "fight-flight" response, the physiological reactivity associated with the mobilization of energy. Much later, in the early 1950's, investigators studying the relationship between cardiovascular reactivity and hypertension found that Cardiovascular Reactivity 1 compared to normotensives, hypertensive individuals manifested larger systolic blood pressure increases to stimuli which elicited both pain and anger (Schacter, 1957).Concurrently, other researchers utilized a harrassment paradigm with men to study the effects of psychological stress on hypertension. They found that individuals could be grouped according to whether or not they expressed their feelings (especially those of anger and anxiety), and that these groups evidenced differential degrees of reactivity in blood pressure and heart rate (Funkenstein, King, & Drolette, 1954).A third line of investigation focused on coronary heart disease. Friedman and Rosenman (1961) (1982), Contrada (1984), and. A 1 portion of this data will be discussed here. (Glass, 1983;Eliot, 1979;Haft, 1974; Raab, Chaplin, & Bajusc, 1989; Ardlie, Glew, & Schwartz, 1968). These effects have been observed in animals (Manuck, Kaplan, & Clarkson, 1983a;1985a) and also in acute and chronic studies of humans (Franke...