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1.
Curr Top Behav Neurosci ; 2: 229-50, 2010.
Article in English | MEDLINE | ID: mdl-21309112

ABSTRACT

Physiological symptoms are characteristic features of anxiety states. Presumably, specific psychophysiological profiles differentiate between anxiety disorders, which would offer potential for diagnostic purposes. Abundant evidence points to a causal relationship between panic disorder and instability of respiratory regulation. However, the specificity of most measures that indicate aberrant functioning of the respiratory system in PD can be questioned. Possibly, the traditional measures of respiratory functioning are too restricted. The underlying respiratory vulnerability in PD seems to constitute a subtle, unstable trait, which calls for more sensitive and sophisticated measures of respiratory variability and chaos. To increase the probability of finding parameters with diagnostic specificity, the application of disorder specific challenge paradigms is recommended.


Subject(s)
Anxiety Disorders/physiopathology , Respiratory Rate , Tidal Volume , Humans , Obsessive-Compulsive Disorder/physiopathology , Panic Disorder/physiopathology , Phobic Disorders/physiopathology , Respiratory Function Tests/methods , Stress Disorders, Post-Traumatic/physiopathology
2.
J Psychopharmacol ; 24(5): 695-9, 2010 May.
Article in English | MEDLINE | ID: mdl-19074540

ABSTRACT

Intuitively, phobic exposure would seem to be a very stressful experience. However, it is not clear whether the characteristic feature of a classic stress response, activation of the hypothalamic-pituitary-adrenal (HPA) axis, is present in phobic fear. Some instances of phobic fear have been found to be accompanied by robust increases in cortisol, whereas in other instances a dissociation between subjective-behavioural arousal and the HPA-axis has been found. The latter is referred to as desynchrony of fear. The aim of the current study was to test the hypothesis that phobic fear is similar to normal fear and, as such, is accompanied by a robust increase in cortisol values. In all, 16 spider phobic subjects and 16 healthy controls participated in the study. During and following a standardised stepwise exposure paradigm, saliva samples were collected for cortisol determination. In contrast to the controls, the spider phobics reacted with a strong fear reaction to the spiders. However, cortisol levels remained unaffected. The phobic response did not resemble the classic 'fight or flight' response. Some suggest that the HPA-axis response has become extinguished in modern man. Yet, it is possible that phobic fear is not a derivative of an ancient fear but rather a separate entity that relies on other neuroendocrinological systems.


Subject(s)
Fear/physiology , Phobic Disorders/physiopathology , Adolescent , Adult , Animals , Female , Humans , Hydrocortisone/analysis , Hypothalamo-Hypophyseal System/physiopathology , Male , Photic Stimulation , Pituitary-Adrenal System/physiopathology , Saliva/chemistry , Spiders , Stress, Psychological , Surveys and Questionnaires , Time Factors , Young Adult
3.
J Psychopharmacol ; 23(8): 975-8, 2009 Nov.
Article in English | MEDLINE | ID: mdl-18635711

ABSTRACT

Several reports have linked, among other aspects, the role of an opioid system in respiratory physiology with underlying mechanisms of panic attacks. The involvement of the opioid system in experimental panic is to be further probed. This study aimed to determine whether opioid blockade would increase panic-related symptomatology on provocation with 35% CO2 inhaled by healthy volunteers. Participants in a double-blind, randomised crossover design orally received either 50 mg of naltrexone or placebo. Most subjects undertook a double inhalation of 35% CO2 one hour after pre-medication, and a separate group did so after five hours. The reactivity to CO2 and the symptoms elicited by naltrexone alone were measured. Among other findings, naltrexone pre-medication alone elicited significant increments in panic-related symptoms. Responses to CO2 were not significantly different between conditions in either group. These preliminary findings suggest that exposure to opioid blockade alone can potentially elicit symptoms that resemble panic, however, without modifying the response to experimental panic provocation with 35% CO2.


Subject(s)
Carbon Dioxide/toxicity , Naltrexone/pharmacology , Narcotic Antagonists , Panic Disorder/etiology , Adult , Cross-Over Studies , Double-Blind Method , Female , Humans , Male , Receptors, Opioid/physiology
4.
Acta Neuropsychiatr ; 16(2): 94-100, 2004 Apr.
Article in English | MEDLINE | ID: mdl-26984002

ABSTRACT

BACKGROUND: The interaction between immune cells, neurotransmitters and the neuroendocrinological systems plays a role in affective disorders, especially depression. Although panic disorder (PD) shares a lot of features with depression, it is clearly a distinct disorder. Reports on immunological parameters in PD don't provide a clear picture of the immunological status of PD patients. This can partly be attributed to methodological differences between studies and small patient groups. OBJECTIVE: The present study aims to assemble all studies on immunological parameters in PD in order to combine all available data to gain a broader perspective on this matter. METHOD: PubMed was searched for studies describing immunological parameters in PD patients without comorbid disorders or medication use. All studies had to include a healthy control group and the outcome measures had to be shared by at least one other study. RESULTS: Fourteen articles were found. Although the T-lymphocytic branch and the innate immune system were normal, the B-lymphocytic branch showed some differences between PD patients and healthy controls. B-cell counts were increased in PD patients, which was underlined by increased human leucocyte antigen (HLA)-DR counts and increased immunoglobulin A levels. However, B-cell activity following mitogen stimulation was normal. CONCLUSIONS: PD patients show increased B-cell numbers. The finding that B-cell activity is not increased can possibly be attributed to functional exhaustion of these cells. The meaning of this finding remains unclear, although it may be potentially important in affective disorders as the same has been found in depression.

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