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orbitofrontal cortex (OFC), and anterior cingulate cortex (ACC), in response to unpleasant images during low hormones compared to presumed high estrogen levels. 12 Thus, it is possible that high estrogen levels may decrease activation to negative stimuli, and possibly reduce their salience. However, hormone levels were not obtained, limiting inferences based on ovarian hormone effects. In addition, it was hypothesized that decreases in activation to aversive stimuli specifically related to the stress response, 12 but estrogen has also been associated with enhancing hypothalamic–pituitary– adrenal (HPA) axis function. 13,14 More research is necessary to investigate the pathway of estrogen’s effects and to explore whether menstrual cycle phase may have influenced activation to unpleasant images through a mechanism not directly related to the stress response. In a recent study from our laboratory, we utilized an emotional go/no-go task to evaluate menstrual cyclerelated changes in response inhibition. 15 In each condition, participants were instructed to respond to one type of stimulus (e.g. positive words) but to ignore another type (e.g. neutral words). Compared with the follicular phase of low hormone levels, we found significantly increased activation in the ACC and dorsolateral prefrontal cortex (DLPFC) while inhibiting response to positive words (compared with when inhibiting response to neutral words) during the luteal phase of high estrogen and progesterone levels. 15 In addition, luteal phase DLPFC activation during response inhibition to positive words was significantly positively correlated with plasma estradiol level and activation in the caudate and inferior parietal gyrus during response inhibition to negative words was negatively correlated with estradiol. Thus, in healthy women, high estrogen levels during the latter half of the menstrual cycle may increase salience of positive stimuli and decrease salience of negative stimuli. In order to begin evaluating differences in brain activation during emotional processing in healthy women compared to women with PMDD, one previous fMRI study assessed activation in healthy women during the late luteal phase (when PMDD symptoms are evinced) and mid-follicular (non-symptomatic) phase. 16 A variation of the emotional go/no-go task was used in which participants were instructed to inhibit response to italicized words, including positive, negative, and neutral stimuli. Anterior-medial OFC activation to negative stimuli, compared with neutral stimuli, was increased in the late luteal phase while lateral OFC activation increased in the follicular phase. 16 There were no differences in activation to positive stimuli. Because ovarian steroids are likely to be declining in the late luteal phase and may therefore not be very different from follicular phase levels, hormone effects were not the primary PATHOPHYSIOLOGY II: NEUROIMAGING, GABA, AND THE MENSTRUAL CYCLE 101 focus of the experiment and levels were not obtained. Instead, these data serve to exemplify brain activation in healthy women at these timepoints in the menstrual cycle so that these patterns may be compared to those with PMDD. However, in an emotional processing task of this nature, mood is likely to have a significant impact on behavioral response and activation. Thus, it may be difficult to differentiate brain activation patterns resulting primarily from differences in mood between healthy women and those with PMDD and not the underlying disorder. Given that differences have been found between healthy women and women with PMDD even in the absence of symptoms (e.g. Epperson et al 17 ), identification of differences in brain activation during the follicular (non-symptomatic) phase may be more valuable than identification of emotional processing-related differences during the late luteal phase. In contrast to fMRI studies focusing on brain structures and cognitive processes that may be modulated by ovarian steroids, several PET, SPECT, and MRS studies have evaluated changes in neurotransmitter systems across the menstrual cycle in healthy women and in women with PMDD. For example, a recent SPECT study evaluated menstrual cycle-related changes in dopamine transporter (DAT) availability in the striatum and serotonin transporter availability in the brainstemdiencephalon (Table 11.2). 18 No differences were detected between the follicular and luteal phases, even after excluding two participants who experienced anovulatory cycles in which there was no progesterone increase in the luteal phase. However, it is possible that there was not sufficient power to detect small changes in transporter availability in the sample of eight participants. Similarly, one PET study found no differences in D 2 dopamine receptor density, measured by putamen to cerebellum ratios, between follicular and luteal or periovulatory phases. 19 Although phase was verified by ovarian steroid levels, sample size for this study was small, with only four women completing tests in two different phases (three women in the follicular and luteal phases and one woman in early follicular and periovulatory phases). A more recent PET study investigated the serotonin hypothesis of PMDD. 20 Changes in daily prospective ratings of mood significantly correlated with changes in brain trapping of 11 C-labeled 5hydroxytryptophan ( 11 C-5-HTP) in regions of interest across the menstrual cycle. While changes in irritability and depressed mood negatively correlated with changes in trapping of the labeled serotonin precursor, changes in happiness and energy in the follicular phase positively correlated with changes in brain 11 C-5-HTP trapping. 20 Thus, it appears that a more stable cycle, marked by little change in symptoms, is associated with an increase in 11 C-5-HTP trapping in the luteal phase, but
102 THE PREMENSTRUAL SYNDROMES Table 11.2 Neuroimaging studies examining the impact of menstrual cycle phase on neurotransmitter systems Study Sample Findings/comments Positron emission tomography Nordstrom et al19 4 healthy women scanned; follicular Differences in putamen to cerebellum ratios of D2 and luteal/late follicular phases receptor density did not exceed those reported in [ 11C]raclopride tracer test–retest analyses in men. Sample size extremely small Eriksson et al20 8 women with PMDD scanned; Changes in irritability and depressed mood follicular and late luteal phases; negatively correlated with changes in brain 11C-labeled 5-hydroxytryptophan 11C-5-HTP trapping and changes in happiness and (5-HTP) energy positively correlated with trapping. Hormone levels were not obtained to verify phases of interest Single-photon emission computed tomography Best et al18 10 healthy women scanned twice; No menstrual cycle variation in striatal DAT or follicular and luteal phases brainstem-diencephalon SERT availability. Hormone levels obtained, but Prog levels did not confirm luteal phase in two cases Magnetic resonance spectroscopy Rasgon et al21 5 women with PMDD and 7 healthy Ratio of N-acetyl-aspartate to creatine in the medial women scanned; follicular and prefrontal cortex was decreased in the luteal phase late luteal phases in both groups Epperson et al17 14 healthy women and 9 women Occipital cortex GABA concentrations fluctuate with PMDD scanned twice; across the menstrual cycle in both healthy women follicular and mid-late luteal phases and those with PMDD. Women with PMDD have signficantly reduced cortical GABA levels in the follicular phase compared with healthy controls Epperson et al56 6 smoking women Occipital cortex GABA concentrations were reduced in female smokers compared with non-smokers PMDD, premenstrual dysphoric disorder; GABA, �-aminobutyric acid; DAT, dopamine transporter; SERT, serotonin reuptake transporter. an increase in symptoms in the luteal phase is associated with decrease in 11 C-5-HTP trapping. Although preliminary, these findings suggest a relationship between serotonin availability and PMDD symptoms. Using 1 H-MRS to investigate the etiology of PMDD, Rasgon et al 21 found changes in neurochemistry across the menstrual cycle. While the ratio of N-acetyl-aspartate (NAA) to creatine in the medial prefrontal cortex was significantly lower in the luteal compared to follicular phase in all subjects, there was a non-significant trend toward higher myoinositol to creatine ratios in women with PMDD in the luteal phase. 21 However, it is difficult to interpret the meaning of these changing ratios. With relatively recent advances in MRS techniques, our laboratory has been able to examine the role of GABA, the brain’s major inhibitory neurotransmitter, in the pathogenesis of PMDD. Before we describe our findings, it is important for the reader to consider the preclinical and clinical evidence supporting the notion that altered GABAergic function contributes to the pathogenesis and perhaps treatment of PMDD.
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The Premenstrual Syndromes
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© 2007 Informa UK Ltd First publis
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vi CONTENTS 10. Pathophysiology I:
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viii LIST OF CONTRIBUTORS Uriel Hal
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Preface Somatic, affective, and beh
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1 History of the premenstrual disor
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and estrogen/progesterone imbalance
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Dalton’s PMS, new, more precise t
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Many other therapeutic areas have b
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2 The diagnosis of PMS/PMDD - the c
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section of gynecological disorders,
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Universal acceptance of a diagnosti
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Extremely severe Severe None Severi
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Table 2.5 Differential diagnosis of
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17. Halbreich U, Borenstein J, Pear
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22 THE PREMENSTRUAL SYNDROMES pharm
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24 THE PREMENSTRUAL SYNDROMES IS PM
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26 THE PREMENSTRUAL SYNDROMES 18. S
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28 THE PREMENSTRUAL SYNDROMES METHO
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30 THE PREMENSTRUAL SYNDROMES Table
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32 THE PREMENSTRUAL SYNDROMES DAILY
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34 THE PREMENSTRUAL SYNDROMES Table
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36 THE PREMENSTRUAL SYNDROMES to ot
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38 THE PREMENSTRUAL SYNDROMES prosp
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40 THE PREMENSTRUAL SYNDROMES exami
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42 THE PREMENSTRUAL SYNDROMES healt
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44 THE PREMENSTRUAL SYNDROMES deter
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46 THE PREMENSTRUAL SYNDROMES 35. B
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6 Comorbidity of premenstrual syndr
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Page 66 and 67: symptoms as well as worsening of co
Page 68 and 69: 7 The clinical presentation and cou
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Page 74: 40. WHO. International Classificati
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Page 81 and 82: 68 THE PREMENSTRUAL SYNDROMES REFER
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Page 93 and 94: 80 THE PREMENSTRUAL SYNDROMES 110.
Page 96 and 97: 10 Pathophysiology I: role of ovari
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Page 100 and 101: studied, reflecting in part interes
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Page 104 and 105: mid-luteal phases of the menstrual
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Page 108 and 109: 52. Osterlund MK, Halldin C, Hurd Y
Page 110 and 111: 135. Facchinetti F, Genazzani AD, M
Page 112 and 113: 11 Pathophysiology II: neuroimaging
Page 116 and 117: EVIDENCE OF ALTERED GABAERGIC FUNCT
Page 118 and 119: the preclinical data indicating tha
Page 120: 19. Nordstrom AL, Olsson H, Halldin
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Page 144 and 145: 15 Psychotropic therapies Meir Stei
Page 146 and 147: Table 15.2 Intermittent dosing (lut
Page 148 and 149: Table 15.3 Intermittent vs continuo
Page 150 and 151: clinical evidence that concomitant
Page 152: 46. Yamada K, Kanba S. Effectivenes
Page 155 and 156: 142 THE PREMENSTRUAL SYNDROMES Tabl
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Page 159 and 160: 146 THE PREMENSTRUAL SYNDROMES PMDD
Page 162 and 163: 17 Clinical evaluation and manageme
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prior to menses) compared with the
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anxiety, or bipolar disorders, post
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premenstrual cognitive disturbance,
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PMS, and bilateral oophorectomy alo
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69. Studd J, Leather AT. The need f
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162 THE PREMENSTRUAL SYNDROMES GABA
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164 THE PREMENSTRUAL SYNDROMES the
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166 THE PREMENSTRUAL SYNDROMES psyc
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168 THE PREMENSTRUAL SYNDROMES 28.
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170 THE PREMENSTRUAL SYNDROMES 105.
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172 THE PREMENSTRUAL SYNDROMES In t
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174 THE PREMENSTRUAL SYNDROMES incl
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176 THE PREMENSTRUAL SYNDROMES by g
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178 THE PREMENSTRUAL SYNDROMES REFE
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Index Note to index: PMS is used fo
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levonorgestrol, with estradiol 156
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