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Publications (7 of 7) Show all publications
(2018). [15O]-H2O-PET in Premenstrual Dysphoria.
Open this publication in new window or tab >>[15O]-H2O-PET in Premenstrual Dysphoria
2018 (English)Other (Other (popular science, discussion, etc.))
National Category
Obstetrics, Gynecology and Reproductive Medicine
Identifiers
urn:nbn:se:uu:diva-335001 (URN)
Note

Dataset till en artikel:

Eriksson, O, Wall, A, Olsson, U, Marteinsdottir, I, Holstad, M, Ågren, H, Hartvig, P, Långström, B, Naessén, T. "Women with Premenstrual Dysphoria show signs of an Asymmetric Frontal Brain Activity with R > L in both Phases of the Menstrual Cycle" (submitted March 2018).

Available from: 2017-11-29 Created: 2017-11-29 Last updated: 2018-03-16Bibliographically approved
Eriksson, O., Wall, A., Olsson, U., Marteinsdottir, I., Holstad, M., Ågren, H., . . . Naessén, T. (2016). Women with Premenstrual Dysphoria Lack the Seemingly Normal Premenstrual Right-Sided Relative Dominance of 5-HTP-Derived Serotonergic Activity in the Dorsolateral Prefrontal Cortices - A Possible Cause of Disabling Mood Symptoms. PLoS ONE, 11(9), Article ID e0159538.
Open this publication in new window or tab >>Women with Premenstrual Dysphoria Lack the Seemingly Normal Premenstrual Right-Sided Relative Dominance of 5-HTP-Derived Serotonergic Activity in the Dorsolateral Prefrontal Cortices - A Possible Cause of Disabling Mood Symptoms
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2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 9, article id e0159538Article in journal (Refereed) Published
Abstract [en]

Study Objective To investigate potential quantitative and qualitative differences in brain serotonergic activity between women with Premenstrual Dysphoria (PMD) and asymptomatic controls. Background Serotonin-augmenting drugs alleviate premenstrual mood symptoms in the majority of women with PMD while serotonin-depleting diets worsen PMD symptoms, both indicating intrinsic differences in brain serotonergic activity in women with PMD compared to asymptomatic women. Methods Positron-emission tomography with the immediate precursor of serotonin, 5-hydroxytryptophan (5-HTP), radiolabelled by 11C in the beta-3 position, was performed in the follicular and luteal phases for 12 women with PMD and 8 control women. Brain radioactivity-a proxy for serotonin precursor uptake and synthesis-was measured in 9 regions of interest (ROIs): the right and left sides of the medial prefrontal cortex, dorsolateral prefrontal cortex, putamen and caudate nucleus, and the single "whole brain". Results There were no significant quantitative differences in brain 5-HTP-derived activity between the groups in either of the menstrual phases for any of the 9 ROIs. However, multivariate analysis revealed a significant quantitative and qualitative difference between the groups. Asymptomatic control women showed a premenstrual right sided relative increase in dorsolateral prefrontal cortex 5-HTP derived activity, whereas PMD women displayed the opposite (p = 0.0001). Menstrual phase changes in this asymmetry (premenstrual-follicular) correlated with changes in self ratings of 'irritability' for the entire group (rs = -0.595, p = 0.006). The PMD group showed a strong inverse correlation between phase changes (pre-menstrual-follicular) in plasma levels of estradiol and phase changes in the laterality (dx/sin) of radiotracer activity in the dorsolateral prefrontal ROI (r(s) = -0.635; 0.027). The control group showed no such correlation. Conclusion Absence of increased premenstrual right-sided relative 5-HTP-derived activity of the dorsolateral prefrontal cortices was found to strongly correlate to premenstrual irritability. A causal relationship here seems plausible, and the findings give further support to an underlying frontal brain disturbance in hormonally influenced serotonergic activity in women with PMD. Because of the small number of subjects in the study, these results should be considered preliminary, requiring verification in larger studies.

National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:uu:diva-311612 (URN)10.1371/journal.pone.0159538 (DOI)000383653100001 ()27617751 (PubMedID)
Funder
Swedish Society of MedicineSwedish Society for Medical Research (SSMF)
Available from: 2016-12-30 Created: 2016-12-30 Last updated: 2017-11-29Bibliographically approved
Eriksson, O., Landén, M., Sundblad, C., Holte, J., Eriksson, E. & Naessén, T. (2012). Ovarian morphology in premenstrual dysphoria. Psychoneuroendocrinology, 37(6), 742-751
Open this publication in new window or tab >>Ovarian morphology in premenstrual dysphoria
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2012 (English)In: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 37, no 6, p. 742-751Article in journal (Refereed) Published
Abstract [en]

Ovarian cyclicity is a prerequisite for premenstrual dysphoria (PMD), as illustrated by the fact that this condition is effectively eliminated by ovariectomy or by treatment with a GnRH agonist. Despite the possibility of differences in ovarian function between women with and without PMD, no study comparing ovarian morphology in these two groups has ever been published. Fifty-two women were recruited for this study; 26 had premenstrual dysphoria, fulfilling criteria slightly modified from those of the premenstrual dysphoric disorder, and 26 were asymptomatic age-matched controls. Ovarian morphology was assessed using transvaginal 7MHz ultrasonography on day 5 after the start of menses, and venous blood was sampled for hormone analysis on days 3 and 8, the expected day of ovulation, and day -4 of the menstrual cycle. There were no significant differences between the groups with respect to the prevalence of polycystic ovaries (PCO), the total number of follicles, the total ovarian volume or serum levels of androgen hormones. In addition, serum free testosterone levels in late premenstrual phase showed an inverse association to premenstrual symptoms of irritability and a similar inverse association trend to symptoms of depressed mood. Unexpectedly, the prevalence of ovaries with fewer than five antral or growing follicles was significantly higher in women with PMD than in controls (p=0.016). While the results do not support a role for PCO or androgen hormones in eliciting late luteal phase irritability, the possible relationship between oligofollicular ovaries and PMD deserves further study.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-164890 (URN)10.1016/j.psyneuen.2011.09.005 (DOI)000303846800002 ()21974977 (PubMedID)
Available from: 2011-12-29 Created: 2011-12-29 Last updated: 2017-12-08Bibliographically approved
Eriksson, O., Wall, A., Marteinsdottir, I., Ågren, H., Hartvig, P., Blomqvist, G., . . . Naessén, T. (2006). Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria. Psychiatry Research: Neuroimaging, 146(2), 107-116
Open this publication in new window or tab >>Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria
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2006 (English)In: Psychiatry Research: Neuroimaging, ISSN 0925-4927, E-ISSN 1872-7506, Vol. 146, no 2, p. 107-116Article in journal (Refereed) Published
Abstract [en]

The cardinal mood symptoms of premenstrual dysphoria can be effectively treated by serotonin-augmenting drugs. The aim of the study was to test the serotonin hypothesis of this disorder, i.e. of an association between premenstrual decline in brain serotonin function and concomitant worsening of self-rated cardinal mood symptoms. Positron emission tomography was used to assess changes in brain trapping of 11C-labeled 5-hydroxytryptophan, the immediate precursor of serotonin, in the follicular and premenstrual phases of the menstrual cycle in eight women with premenstrual dysphoria. Changes in mood and physical symptoms were assessed from daily visual analog scale ratings. Worsening of cardinal mood symptoms showed significant inverse associations with changes in brain serotonin precursor trapping; for the symptom "irritable", r(s)=-0.83, and for "depressed mood" r(s)=-0.81. Positive mood variables showed positive associations, whereas physical symptoms generally displayed weak or no associations. The data indicate strong inverse associations between worsening of cardinal symptoms of premenstrual dysphoria and brain serotonin precursor (11C-labeled 5-hydroxytryptophan) trapping. The results may in part support a role for serotonin in premenstrual dysphoria and may provide a clue to the effectiveness of serotonin-augmenting drugs in this disorder but should, due to small sample size and methodological shortcomings, be considered preliminary.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-93101 (URN)10.1016/j.pscychresns.2005.02.012 (DOI)16515859 (PubMedID)
Available from: 2005-04-29 Created: 2005-04-29 Last updated: 2017-12-14Bibliographically approved
Damberg, M., Westberg, L., Berggård, C., Landen, M., Sundblad, C., Eriksson, O., . . . Eriksson, E. (2005). Investigation of transcription factor AP-2beta genotype in women with premenstrual dysphoric disorder.. Neurosci Lett, 377(1), 49-52
Open this publication in new window or tab >>Investigation of transcription factor AP-2beta genotype in women with premenstrual dysphoric disorder.
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2005 (English)In: Neurosci Lett, ISSN 0304-3940, Vol. 377, no 1, p. 49-52Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-68897 (URN)15722186 (PubMedID)
Available from: 2005-03-14 Created: 2005-03-14 Last updated: 2011-01-12
Landen, M., Eriksson, O., Sundblad, C., Andersch, B., Naessen, T. & Eriksson, E. (2001). Compounds with affinity for serotonergic receptors in the treatment of premenstrual dysphoria: a comparison of buspirone, nefazodone and placebo.. Psychopharmacology, 155, 292
Open this publication in new window or tab >>Compounds with affinity for serotonergic receptors in the treatment of premenstrual dysphoria: a comparison of buspirone, nefazodone and placebo.
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2001 (English)In: Psychopharmacology, Vol. 155, p. 292-Article in journal (Refereed) Published
Identifiers
urn:nbn:se:uu:diva-59311 (URN)
Available from: 2004-11-29 Created: 2004-11-29 Last updated: 2011-01-14
Cnattingius, S., Mills, J. L., Yuen, J., Eriksson, O. & Salonen, H. (1997). The paradoxical effect of smoking in preeclamptic pregnancies: smoking reduces the incidence but increases the rates of perinatal mortality, abruptio placentae, and intrauterine growth restriction. American Journal of Obstetrics and Gynecology, 177(1), 156-61
Open this publication in new window or tab >>The paradoxical effect of smoking in preeclamptic pregnancies: smoking reduces the incidence but increases the rates of perinatal mortality, abruptio placentae, and intrauterine growth restriction
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1997 (English)In: American Journal of Obstetrics and Gynecology, ISSN 0002-9378, E-ISSN 1097-6868, Vol. 177, no 1, p. 156-61Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: Smoking is associated with a reduced risk of preeclampsia, but what is the outcome of pregnancy when preeclampsia develops in women who smoke? STUDY DESIGN: Single births in Sweden from 1987 through 1993 to nulliparous women aged 15 to 34 years (N = 317,652) were included. Poisson regression analyses were used to calculate adjusted relative risks and rates of adverse pregnancy outcomes. RESULTS: Maternal smoking was associated with significantly reduced risks of mild and severe preeclampsia (relative risks = 0.6 and 0.5, respectively). In pregnancies with severe preeclampsia, smoking at least 10 cigarettes per day was associated with increased rates of perinatal mortality (from 24 to 36 per 1000), abruptio placentae (from 31 to 67 per 1000), and being small for gestational age (from 28% to 68%), whereas the corresponding smoking-related increases in rates in nonhypertensive pregnancies were considerably less. CONCLUSIONS: Smokers in whom preeclampsia develops have very high risks of perinatal mortality, abruptio placentae, and small-for-gestational-age infants.

Keywords
Abruptio placentae, perinatal mortality, preeclampsia, small for gestational age, smoking
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-53864 (URN)10.1016/S0002-9378(97)70455-1 (DOI)9240600 (PubMedID)
Available from: 2004-11-29 Created: 2004-11-29 Last updated: 2017-12-04Bibliographically approved
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