Biomedical subjects

Walton T Roth

Publications and source records attributed to Walton T Roth.

23 records · Page 2Linked to original sources

PubMed2002

Reduced communication between frontal and temporal lobes during talking in schizophrenia.

BACKGROUND: Communication between the frontal lobes, where speech and verbal thoughts are generated, and the temporal lobes, where they are perceived, may occur through the action of a corollary discharge. Its dysfunction may underlie failure to recognize inner speech as self-generated and account for auditory hallucinations in schizophrenia. METHODS: Electroencephalogram was recorded from 10 healthy adults and 12 patients with schizophrenia (DSM-IV) in two conditions: talking aloud and listening to their own played-back speech. Event-related electroencephalogram coherence to acoustic stimuli presented during both conditions was calculated between frontal and temporal pairs, for delta, theta, alpha, beta, and gamma frequency bands. RESULTS: Talking produced greater coherence than listening between frontal-temporal regions in all frequency bands; however, in the lower frequencies (delta and theta), there were significant interactions of group and condition. This finding revealed that patients failed to show an increase in coherence during talking, especially over the speech production and speech reception areas of the left hemisphere, and especially in patients prone to hallucinate. CONCLUSIONS: Reduced fronto-temporal functional connectivity may contribute to the misattribution of inner thoughts to external voices in schizophrenia.

Adult↗

PubMed2002

High altitudes, anxiety, and panic attacks: is there a relationship?

People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to altitude and anxiety are apparent in all three leading models of panic, namely, hyperventilation (hypoxia leads to hypocapnia), suffocation false alarms (hypoxia counteracted to some extent by hypocapnia), and cognitive misinterpretations (symptoms from hypoxia and hypocapnia interpreted as dangerous). Furthermore, exposure to high altitudes produces respiratory disturbances during sleep in normals similar to those in panic disorder at low altitudes. In spite of these connections and their clinical importance, evidence for precipitation of panic attacks or more gradual increases in anxiety during altitude exposure is meager. We suggest some improvements that could be made in the design of future studies, possible tests of some of the theoretical causal links, and possible treatment applications, such as systematic exposure of panic patients to high altitude.

Adaptation, Physiological↗

PubMedDate not supplied

Salivary cortisol response during exposure treatment in driving phobics.

OBJECTIVE: Extensive research on the hypothalamic-pituitary-adrenal (HPA) axis response to stress has not clarified whether that axis is activated by phobic anxiety. We addressed this issue by measuring cortisol in situational phobics during exposure treatment. METHODS: Salivary cortisol was measured in 11 driving phobics before and during three exposure sessions involving driving on crowded limited-access highways and compared with levels measured in 13 healthy controls before and during two sessions of driving on the same highways. For each subject, data collected in the same time period on a comparison nondriving day served as an individual baseline from which cortisol response scores were calculated. RESULTS: Cortisol levels of driving phobics and controls did not differ on the comparison day. Phobics also had normal cortisol response scores on awakening on the mornings of the exposures but these were already increased 1 hour before coming to the treatment sessions. Phobics had significantly greater cortisol response scores during driving exposure and during quiet sitting periods before and afterward. These greater responses generally paralleled increases in self-reported anxiety. At the first exposure session, effect sizes for differences in cortisol response scores between the two groups were large. Initial exposure to driving in the first session evoked the largest responses. CONCLUSION: The data demonstrate that the HPA axis can be strongly activated by exposure to, and anticipation of, a phobic situation.

Adrenal Cortex↗

PubMedDate not supplied

End-tidal pCO2 in blood phobics during viewing of emotion- and disease-related films.

OBJECTIVE: Many patients with blood, injection, and injury (BII) phobia respond to specific stimuli with vasovagal dysregulation and fainting. However, little is known about the role of hyperventilation in the distress of these patients. Hyperventilation, defined by subnormal arterial pCO2 levels, induces anxiety and may promote the development of fainting. We studied end-tidal pCO2 in 12 patients with BII phobia and 14 nonanxious controls during presentation of emotional films. METHOD: Ten film clips were shown, two in each of 5 categories: pleasant, unpleasant, neutral, BII-related (surgery), and asthma-related (portraying labored breathing). For each subject, two subsets were created, each containing one clip from each category. For one subset, the instruction was simply to view the film, and for the other subset, to view the film while tensing the leg muscles. PCO2, heart rate, blood pressure, and leg electromyogram were recorded continuously during viewing, and self-report of symptoms and emotion was collected after each film. RESULTS: Patients reported the greatest anxiety and disgust during surgery films. PCO2 was relatively stable throughout all categories except surgery films, during which minima were below 30 mm Hg, indicating significant hypocapnia. Cardiovascular variables suggested biphasic patterns in two patients with BII phobia. These patients, together with one additional patient and one control who were close to fainting after or during one surgery film, also showed a marked fall in pCO2) Leg muscle tension raised heart rate and systolic blood pressure for all films, but was not related to near-fainting or endurance in surgery film viewing. CONCLUSION: Hyperventilation is part of the fear response of patients with BII phobia, but was transitory in experimental fear induction using surgery films. Its role in real-life exposure and fainting deserves further study.

Adult↗

PubMedDate not supplied

Psychophysiological and cortisol responses to psychological stress in depressed and nondepressed older men and women with elevated cardiovascular disease risk.

OBJECTIVE: The objective of this study was to compare psychophysiological and cortisol reactions to psychological stress in older depressed and nondepressed patients at risk for cardiovascular disease (CVD). METHODS: Forty-eight depressed participants and 20 controls with elevated cardiovascular risk factors underwent a psychological stress test during which cardiovascular variables were measured. Salivary cortisol was collected after each test segment. Traditional (e.g., lipids) and atypical (e.g., C-reactive protein) CVD risk factors were also obtained. RESULTS: At baseline, the groups did not differ on lipid levels, flow-mediated vasodilation, body mass index, or asymmetric dimethylarginine. However, the depressed patients had significantly higher C-reactive protein levels. Contrary to our hypothesis, there were no differences in baseline cortisol levels or diurnal cortisol slopes, but depressed patients showed significantly lower cortisol levels during the stress test (p = .03) and less cortisol response to stress. Compared with nondepressed subjects, depressed subjects also showed lower levels of respiratory sinus arrhythmia (RSA(TF)) during the stress test (p = .02). CONCLUSIONS: In this sample, older depressed subjects with elevated risk for CVD exhibited a hypocortisol response to acute stress. This impaired cortisol response might contribute to chronic inflammation (as reflected in the elevated C-reactive proteins in depressed patients) and in other ways increase CVD risk. The reduced RSA(TF) activity may also increase CVD risk in depressed patients through impaired autonomic nervous system response to cardiophysiological demands.

Age Factors↗