Premenstrual Syndromes : PMS and PMDD - Rutuja :: The site ...
Premenstrual Syndromes : PMS and PMDD - Rutuja :: The site ...
Premenstrual Syndromes : PMS and PMDD - Rutuja :: The site ...
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18 THE PREMENSTRUAL SYNDROMES<br />
late-luteal phase may be too strict for some women <strong>and</strong><br />
very permissive for others (who may have many mild<br />
symptoms which do not exist at mid-follicular phase).<br />
<strong>The</strong> same considerations apply also to the impairment<br />
items. However, there are women who do not have actual<br />
premenstrual impairment of their performance but maintain<br />
their function with a high level of distress. This<br />
should be considered as a measure of severity no lesser<br />
than impairment in function.<br />
For research purposes, regular menstrual cycles are<br />
obligatory: usually 21–35 days are considered to be<br />
‘regular’. However, currently there is no requirement for<br />
the limit of individual cycle-to-cycle duration stability<br />
within this wide range.<br />
FUTURE DIRECTIONS FOR RESEARCH<br />
ON THE DIAGNOSIS OF <strong>PMS</strong>/<strong>PMDD</strong><br />
<strong>The</strong> main diagnostic issues that, to my opinion, are still<br />
unsolved are:<br />
1. Are there multiple diversified premenstrual syndromes<br />
that also include diversified premenstrual<br />
dysphoric phenotypes? This issue is also of crucial<br />
importance for the underst<strong>and</strong>ing of the pathophysiology<br />
of <strong>PMS</strong> <strong>and</strong> effective treatment (beyond<br />
the current efficacy ceiling of 60%).<br />
2. If there are diversified phenotypes, can we move<br />
beyond the DSM-IV-style descriptive arbitrary<br />
cut-off points towards a diagnosis based on the<br />
pattern(s) of symptoms, past history <strong>and</strong> time course,<br />
biological changes (etiology <strong>and</strong> pathobiology),<br />
<strong>and</strong> treatment outcome? Once phenotypes are established,<br />
are they specifically associated with specific<br />
genotypes?<br />
3. If our present underst<strong>and</strong>ing of <strong>PMS</strong> involves the<br />
concept of vulnerability <strong>and</strong> menstrually related<br />
trigger(s) of symptoms, then is it justified to distinguish<br />
between premenstrual syndromes <strong>and</strong> PMEs<br />
or catamenial disorders? <strong>The</strong> difference may be the<br />
degree of the threshold <strong>and</strong> the magnitude of the<br />
trigger needed to cause expression of symptoms, but<br />
not necessarily a fundamental difference between<br />
premenstrual syndromes <strong>and</strong> PMEs. If the vulnerability<br />
level changes over time, <strong>and</strong> may increase or<br />
decrease according to life events <strong>and</strong> their perception,<br />
as well as repeated assaults (kindling <strong>and</strong><br />
dynamically evolving vulnerability), then there may<br />
be a continuum between at least some premenstrual<br />
syndromes, PMEs, <strong>and</strong> more chronic major<br />
disorders – this notion deserves investigation.<br />
4. What is a clinically relevant <strong>PMS</strong> (or <strong>PMDD</strong>)? When<br />
do women warrant <strong>and</strong> benefit from treatment?<br />
5. Can we develop clinically relevant diagnostic procedures<br />
that would not require prospective monitoring<br />
of symptoms for two consecutive menstrual<br />
cycles (which are too much of a burden for many<br />
women <strong>and</strong> their primary care physicians)?<br />
<strong>The</strong>re are many more unsolved diagnostic issues of<br />
<strong>PMS</strong>/<strong>PMDD</strong>, even before we tackle issues of underlying<br />
mechanisms that may vary from phenotype to phenotype.<br />
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