The Nosology of Dysphoria in Humans with late luteal Phases

BY
Ilesanmi Oluwatoyin Olatundun PhD Department of Behavioral Studies, College of Management Science, Redeemers University, Lagos/Ibadan Expressway, Ogun State, Nigeria. Phone:08052236377 / 08058009879 e-mail Address:toytundun@yahoo.com & Osiki Jonathan.O. PhD, National University of Lesotho, Dept. of Theology & Religious Studies, Faculty of Humanities, P.O.Roma 180,Lesotho, Southern Africa. E-Mail:jonathanosiki@yahoo.co.uk

ABSTRACT This study examined the nosology of dysphoria during the luteal phases of menstruating female humans. Dysphoria is a group of conditions that occurred prior to the onset of menses. It is characterised by disabling emotional, behavioural, and physical symptoms, which include irritability, tension, and lability of mood which seriously interfere with their family, social, work-related activities, and daily lifestyle. Propossed aetiological models associated with dysphoria were highlighted among which are biomedical Explanatory models, health belief model, socio-cultural model, Sin & Devil-causatory models, Socio-Environmental model, Psychosomatic influences and Psychological Explanatory models. This study concluded that the nosological classification of dysphoria following the on set of menstruation in women has therefore been on the categorical; dimensional; dichotomous; and unitary planes. Key Terms: Dysphoria, Female Humans, Late Luteal Phases & Nosology

Introduction Problem and Background

Dysphoria following the on set of menstruation is a condition in which, an individual has generalized feeling of distress; feels acutely hopeless, irritable, sad, depressed, and despondent; experienced apathy, lethargy, boredom, constant fatigue, pervasive loss of interest in food, drink, sex, and normal activities (work, school, hobbies), severe mood swings; difficulty concentrating; sleep problems, pervasive loss of interest or pleasure and variety of physical symptoms. It is evidently a gender specific condition as it affects millions of women during their reproductive years. Its symptoms typically begin between the ages of 25 and 35 years. The roots of dysphoria extends back into antiquity. Particularly in the sixth century B.C. (Brannon, 1996) to when Plato (c. 428-c. 347 bc) and Hippocrates (460-377 B.C.) documented the deleterious influence of the wandering womb and the concomitant emotional status of women (Veith, 1964). Hippocrates (460-377 B.C.) described it as a 1

group of conditions that occurred prior to the onset of menses, in which women develop suicidal ideation and other severe symptoms (Veith, 1964). Refering to Ernt Von-Feuchtersleben, Rubinow and Schmidt (1995) opined that "the menses in sensitive women is almost always attended by mental uneasiness, irritability, and sadness". Frank {1931} attributed the combination of physical and psychological symptoms occurring in the days immediately prior to menstruation, to accumulations of the female sex hormone estrogen and named it "Pre-Menstrual Tension" (PMT), while Green and Dalton {1965} modified it into Premenstrual Syndrome (PMS). Antai, Udezi, Ekanem, Okon, and Umoiyoho (2004) observed 85.5% prevalence rate of PMS in 200 nulliparous female undergraduate students of the University of Calabar Nigeria, whose age ranged between 16 and 31 years. Ilesanmi (2005) while using a 28% or greater Premenstrual Distress as an index of luteal variation, found 11% prevalence rate of Premenstrual Dysphoria in 445 randomly selected female humans whose age ranged between 15and 45 years from two market centers and three senior secondary schools in the southwestern part of Nigeria because they scored > 40 on the Premenstrual Distress Form. They also observed 71% prevalence rate of PMS because the subjects scored between 28 to 39, while 18% of the women scored < 28. Nosology is the discipline of classification and terminology of diseases. Thomas Sydenham (1692) founded the discipline of nosology by insisting that diseases had their own natural history and could be described and classified on the basis of their specific characteristics (Neurology,1997). This concept did not have a major impact until the latter part of the 19th century, when the observational techniques of physical examinationpercussion, auscultation, sphygmomanometry, and thermometryhad been developed (Neurology,1997). However, Sydenham (1692) defines nosology as classification of diseases (Neurology,1997). Nosology is therefore the systematic classification of diseases, or the branch of medical science that deals thereto. The adjective is nosologic. The term nosologicy is often used in connection with medical classification systems, and psychiatric nosology (Andreasen .N.C; 1987). Examples of the medical classification systems and psychiatric nosology are: International Statistical Classification of Diseases and Related Health Problems (ICD) originally began as the Bertillon Classification (1893) and later became the ICD. Work on ICD-10 began in 1983 and was completed in 1992; ICD-CM (Clinical Modification): The latest version (2001) of ICD-CM is ICD9-CM; Diagnostic and Statistical Manual of Mental Disorders (DSM) (1952; 1968; 1980; 1987; 1994); International Classification of Procedures in Medicine (ICPM) and Medical Subject Headings (MeSH).

From a scientific point of view, the two most up-to-date classification systems in use today are the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), and the International Classification of Diseases, 10th Revision (ICD-10). These two may be considered as the theoretical basis of current psychological nosology. Since their official introduction, the International Classification of Diseases, 10th Revision (ICD- 10), and the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), operational classification systems have largely become an integral part of the body of knowledge of psychologists throughout the world and instruments they constantly refer to. 2

Although there is "ongoing nosologic controversy and confusion" concerning "dsyphoria" (Neurology,1997;48:126), this paper however presents the instrumentally generated
DSM-IV and ICD-10 diagnoses of dysphoric disorder in conjunction with its medical classification. If medical

realistic, simple to use, and reliable, nosological systems must be based not only on established facts, but also on theoretical assumptions regarding the nature of disease. In view of the fact that no concise attempt has been made to present the varying nosological classification of premenstrual experiences, this study was therefore conducted. Purpose of Study
classification is to be

The main purpose of this study is to present a sound nosology of premenstrual dysphoric disorder that will enhance communication among psychological researchers and health care givers, and also influence academic authors who undertake writing definitions, diagnostic criteria, or staging systems for diseases. Significance of the Study The more knowledge we have about the aetiological and nosological classification of dysphoria, the better we can tailor psychological efforts to and direct rich resources to its amelioration, which will provide the most benefit. This study therefore attempt to stimulate further discussion about the aetiology and nosologic classification of dysphoria. Scope of Study Specifically the study was limited to the presentation of the aetiological and nosological classification of dysphoria following the onset of menstruation. Definition of Terms The following are the definitions of the terms used in the study: Dysphoria: This is a a condition in which, an individual has generalized feeling of distress; feels acutely hopeless, irritable, sad, depressed, and despondent; experienced apathy, lethargy, boredom, constant fatigue, pervasive loss of interest in food, drink, sex, and normal activities (work, school, hobbies), severe mood swings; difficulty concentrating; sleep problems, pervasive loss of interest or pleasure and variety of physical symptoms. Female Humans: This refers to women of fertile age. Luteal Phase (Day 15-30): The menstrual cycle is generally divided into four phases: the follicular phase, ovulation, the luteal (or secretory) phase, premenstrual and menstrual phases. The luteal phase is the period of time (usually 11-14 days) following ovulation {That is, the post-ovulation phase of the menstrual cycle, also called the progestational or secretory phase}. During this phase, the glands of the uterine lining become distended and tortuous, providing blood supply for the potential ovum. If pregnancy occurs, the pituitary gland secretes HCG hormones, which causes the increased production of progesterone to help maintain the pregnancy. The lutea phase isin three phases: Early Luteal Phase, Mid Luteal Phase and Late Luteal Phase. Early Luteal Phase: The Early Luteal Phase starts on the day of ovulation (the day after the LH peak) and ends when progesterone has reached its plateau. It is characterised by increasing progesterone and decreasing LH and FSH levels. The Mid Luteal Phase: The Mid Luteal Phase corresponds to plateauing progesterone levels. It is characterised by constant elevated progesterone and constant low levels of LH and FSH. The Late Luteal Phase: The Late Luteal Phase starts when progesterone decreases and ends on the day preceding the next menses. It is characterised by decreasing progesterone and increasing LH and FSH levels. 3

Nosology: This refers to that branch of medical science which deals with the classification of diseases and abnormal behaviour.

Terminologies of Dysphoria
There are three main features of terminology of dysphoria following the on set of menstruation in women of fertile age: the definition, diagnostic criteria, and a system for staging severity. The defining characteristics of dysphoria are the common properties specifying the group of women experiencing it (APA, 1994). These are etiologic agent, a specified disorder of structure or function, and or a consistent syndrome. Diagnostic criteria are features of the disorder that are found by empiric research to best distinguish it from other disorder that resemble it. Staging systems are based on clinical features, pathophysiology, pathology, or a combination of features. Varing terminologies for dysphoria following premenstrual experiences have flourished within the scientific literature, including premenstrual changes (PMC); premenstrual experiences; premenstrual tension (PMT) {Frank, 1931}; premenstrual symptoms (Dalton, 1965); premenstrual exacerbation (PME); premenstrual syndromes (PMS) (Dalton, 1965); Late Luteal Dysphoric Disorder (LLPDD) (APA, 1987); and Premenstrual Dysphoric Disorder (PMDD) ( APA, 1994). The variability in terminology can be traced to inadequate definitions and the attempts to refine definitions along with increased knowledge of the phenomenon (APA,1994). The term PMT originally used by Frank (1931) has been replaced by PMS mainly because the premenstrual experiences reported represent a much broader range of experiences than entailed in the term tension. The term PMC has been preferred to describe the non-distressing experiences of women that are not considered pathological. The most advanced state, originally defined in the revised third edition of the Diagnostic and Statistical Manual for Mental Disorder (DSM-III-R; American Psychiatric Association, 1987) and in the fourth edition (DSM-IV; American Psychiatric Association, 1994) is PMDD. Many researchers use the terms PMDD and PMS interchangeably (Sundstrm, 1997). There are however attempts in the literature to differentiate between the two. In a recent update of PMDD, Steiner (1996) differentiates between PMS and PMDD. According to Steiner (1996} the term PMS should primarily be reserved for mild somatic symptoms such as breast tenderness, bloating, headache and minor mood changes while PMDD should be reserved for the severe form of PMS.

Nosology of Dysphoria: A Dynamic Process

Nosology (Gr. vocros, disease, and Xoyos, science) is that branch of medical science which deals with the classification of diseases and abnormal behaviour on the basis of etiology (cause), pathogenesis (mechanism in which the agent causes disease), symptom or the organ. The nosologic status of Dysphoria is unresolved eventhough it emerges as a distinct affective syndrome with generalized feeling of distress; acutely hopeless, irritable, sad, depressed, and despondent; experienced apathy, lethargy, boredom, constant fatigue, pervasive loss of interest in food, drink, sex, and normal activities (work, school, hobbies), severe mood swings; difficulty concentrating; sleep problems, pervasive loss of interest or pleasure and variety of physical symptoms. In the absence of a generally accepted etiological classification of dysphoria following the on set of menstruation, the basis of its nosology has therefore been descriptive (Cantwell and Carlson, 1983). In view of the aetiological theories, the classification of Dysphoria has been categorical, dimensional dichotomous, and unitary in nature. Among British and American psychiatrists, the classification of Dysphoria is 4

based on the presenting symptomatology, previous history, family history, physiological and biochemical findings, response to treatment, natural history (acute or chronic); course (progressive or intermittent); cause and disturbed biological process. Some of these classification systems are official, such as the International classification of Diseases-9th Edition (ICD-9); Diagnostic statistical Manual of Mental Disorder-III (DSM-III); Diagnostic statistical Manual of Mental Disorder-III-R (DSMIII-R); Diagnostic statistical Manual of Mental Disorder-IV (DSM-IV) and Diagnostic statistical Manual of Mental Disorder-IV Text-Revision (DSM-IV-T-R). The official classification of LLPDD tends to be created by organizations such as American Psychiatric Association (APA) and World Health Organization (WHO). Categorical Approach The DSM nosology is a categorical model of diagnosis based simply on operationism. Hence, with American Psychiatrists Associations (APA, 1987, 1994 and 2001) approach, all of the official psychiastric nomenclature of LLPDD in DSM-III, DSMIII-R, DSM-IV and DSM-IV-T-R have been categorical. The authors of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994) subscribe to a philosophical approach known as criterion philosophy (Musgrave, 1993), the defining premise of which is that the meaning of a word is identical to the criterion for applying it (the assumption behind operationism). This assumption is what is at stake in the DSM's categorical approach. The DSM's operationism entails that the meaning of a disorder is exhausted by the way of recognizing the disorder. According to Klerman (1991), the philosophy underlying the DSM is "The criteria for assigning individuals to diagnostic categories [are] based on algorithms, which should be based, whenever possible, on operationally defined, observable manifestations of psychopathology, with minimal inferences as to presumed causation" (p. 75). DSM provides explicit ways of recognizing Dsyphoria in women during the late luteal phases of their menses. These classification systems emphasize Dysphoria as discrete entity. With the DSM nosology and nomenclature, it is therefore possible to categorize women as either having the "disorder" or not having it. Thus a client either has Dsyphoria or does not. Although, Dsyphoria displays intriguing similarities with other conditions, and in particular with panic disorder, Landn and Eriksson {2002} view that it is neither a variant of depression nor an anxiety disorder, but a distinct diagnostic entity, with irritability and affect lability rather than depressed mood or anxiety as most characteristic features. Operational diagnostic classification systems, such as the ICD and DSM classifications which are the official nosological groupings resulted from the mutual agreement of experts on clinical descriptions of the disorder and at times on the presence of biological markers. In many instances diagnoses of dysphoria are based on certain symptoms. In fact, the two most widely used official classifications DSM and ICDcame to be largely regarded as nosologically valid by medical doctors, official institutions, and even the public at large. Dimensional Approach Dimensional approach is derived from the notion that psychodiagnostic concepts are matters of degree (Costa and Widiger, 1994; Frances and Widiger, 1986; Pincus and Wiggins, 1990; Kendell, 1991, p. 13). On the continuous dimensional plane, Dsyphoria during the late luteal phases in menstruating females is viewed as subtypes of disorder with recurrence of a variety of common symptoms on cyclical basis despite the superficial differences. That is different symptoms might replace each other in the same client and that there may be uniform benign prognosis. For instance, Abraham (1983) 5

classifies Dysphoria sufferers into four distinct subgroups. Each subgroup is linked to specific symptoms, hormonal patterns, and metabolic abnormalities. Abraham's (1983) classifications are PMT-A (A = anxiety, irritability, and emotional instability which is the most common symptom category and is found to be strongly associated with excessive estrogen and deficient progesterone during the premenstrual phase), PMT-C (C = carbohydrate craving, increased appetite, craving for sweets, headache, fatigue, fainting spells, and heart palpitations), PMT-D (D = depression), PMT-H (H = hyperhydration, weight gain, abdominal bloating and discomfort, breast tenderness and congestion, and occasional swelling of the face, hands and ankles). Although, Abraham's (1983) system is very useful in quickly identifying possible causes in a given case of PMS. An alternative approach is the classification of Dysphoria sufferer according to the causative factor. The most common proposed causative factors as discussed under theoretical review of literature are Excess estrogen, Progesterone deficiency, Elevated prolactin levels, Hypothyroidism, Stress, endogenous opioid deficiency, and adrenal dysfunction, Depression, Nutritional factors, Macronutrient disturbances/excesses, Micronutrient deficiency, psychosocial, health-believe, socio-cultural, sin / devil causation, and psychological factors. Dichotomous Approach The dichotomous approach sub-divides Dysphoria into several discrete disorders: Premenstrual Tension (PMT), Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD). As initially stated, PMT referred to physical tension occurring from ten to seven days before menstruation. PMS describe a collection of physical, psychological and emotional symptoms that many women experience during the one to two weeks before a menstrual period. These symptoms disappear soon after the start of menstrual bleeding. PMDD encompass a variety of intense mood and physical symptoms that occur right before menses and interfere with daily functioning. For instance, Smith (1989) noted that several experts using the dichotomous approach have created classification systems that identify PMS sufferers into subgroups. For example, Abraham (1983) divides PMS into four distinct subgroups. Each subgroup is linked to specific symptoms, hormonal patterns, and metabolic abnormalities. Classification by Cause The classification-by-cause approach arose from the study of Frank (1931) when the diagnostic category of premenstrual tension (PMT) first appeared and Frank attributed the combination of physical and psychological symptoms occurring in the days immediately prior to menstruation, to accumulations of the female sex hormone estrogen (Frank, 1931). Green and Dalton (1953) first recognized Dysphoria as a psycho-physio-logical disorder, which is caused by an imbalance of female hormones estrogen and progesterone. Dalton believes that decreased levels of progesterone cause PMS. Abraham believes that an excess of estrogen causes PMS. Classification-by-cause presents dysphoria as either a disease or a disorder. Although to this day, the precise pathophysiology of dysphoria following the of set of menstruation has not yet been elucidated Kessel (2000) and Donnica (2000) classification-by-cause aetiologically linked dysphoria to any of the following already advanced causative factors:

 Biomedical Model The Biomedical Model presents dysphoria as a biological disease (Dalton 1987) on the basis of possible hormonal, dietary, infections, genetics, neuroanatomic pathology or malfunctioning biochemistry and psychosomatic components. For instance, Frank (1931) proposed that the combination of physical and psychological symptoms occurring immediately prior to menstruation was due to excessive accumulations of the female sex hormone estrogen in the blood. That is fluctuations in the circulating level of hormones or excessive levels of estrogen and inadequate levels of progesterone cause retention of sodium in the blood stream, resulting in edema in body tissues including the brain. The retention affects circulation of blood, reducing the amount of oxygen reaching the uterus, ovaries, and the brain. Greene and Dalton (1953) suggested an abnormal elevation of the estrogen/progesterone ratio. Dalton (1977) implicated inadequate levels of progesterone in the luteal phase of the menstrual cycle. Israeli (1938) proposed that the primary cause of premenstrual tension was deficient ovarian luteinization, with a decreased production of progesterone leading to unopposed estrogen effect (Walker, 1995)}. Biskind (1943) explained that estrogen rises whenever the liver could not adequately metabolize it, unless it had a sufficient amount of vitamin B. Robinson (1986) proposed that excess estrogen before the period increases brain activity, which in turn results in premenstrual syndrome. He also implicated eating red meat and dairy products in the hormonal imbalance of excessive estrogen levels and inadequate progesterone levels found in the blood during the late luteal phase. Boyle (1999) hypothesized that premenstrual headaches may be triggered by declining estrogen levels in the luteal phase. Abraham (1983) postulated that both vitamin B6 and magnesium were essential to the conversion of the active circulating form of estrogen into the inactive conjugated estrogen form. Freeman, Rickels, Sondheimer, and Polansky, (1999), and Frackiewicz and Shiovitz, (2001) also suggest that serotonin plays a role in the etiology of premenstrual mood changes. They observed that women with PMS and PMDD have abnormal serotonergic function during the luteal phase as evidenced by lower whole blood serotonin concentrations and decreased platelet uptake of serotonin. They viewed that other neurotransmitters has been aberrant in PMS, including the opioid, catecholaminergic and the y-aminobutyric acid (GABAergic) systems. The basic assumption of the Biomedical model is that Dysphoria in fertile age women has physical causes and should be amenable to physical treatments. This assumption ignores other major influences on psychological thinking such as psychoanalysis. The efficacies of pharmacological compounds for the treatment of Dysphoria are highly controversial. In fact with regards to the endocrine theory which states that women who have an increased secretion of cortisone are more prone to Dysphoria, Schiff and Smith (1993) noted that there is no scientific evidence for a specific reproductive endocrine catalyst to evoke the PMS symptoms reported by women. Abplanalp (1983) and other critics of the biomedical models regarding Dysphoria also noted that the assumption of a single syndrome means that medical researchers give equal weight to all symptoms experienced by subjects. This means that a woman experiencing a specific food craving is the "empirical equivalent" of a woman who is suffering from extreme breast tenderness and/or a woman experiencing out of control mood swings. The bio-medical classification and explanations of Dysphoria are therefore unsatisfactory for many obvious reasons. First, the approaches of the bio-medical 7

sciences and clinical practice to Dysphoria have generally been limited in relation to physicians pharmachotherapeutic decisions concerning disorders of the menstruum. If one embraces the bio-medical model, one would expect all symptoms of Dysphoria, physical and behavioral, to be universally applicable to all female humans. Thus, a purely biomedical approach to understanding Dysphoria is limited and does not account for all cases. More so, the plethora of causation theories is evidence of the lack of medical consensus (Johnson 1987). There will therefore be a problem in relying too heavily on the bio-medical model since there is more to Dysphoria than a causal relationship between some biological substrate, symptoms and behavior. Despite these, the biomedical models have been able to show that Dysphoria can be ameliorated, though not in absolute terms. Therefore, regardless of what the bio-medical explanations may be, one can still examine other nosologic and etiologic views of Dysphoria. Unilinear model This is a model that is increasingly being put forward by self-help PMS texts (e.g., Armstrong & Sutherland, 1987; Lever & Brush, 1981) to classify it and also give it and aetiologic backing. This meant that over the last twenty years, hundreds of studies have been conducted examining the relationship between individual biological (see Parry, 1994) or psychosocial correlates (see Goudsmit, 1988; Richardson, 1991) of PMDD and premenstrual symptoms. For example, in a study, which reported the positive benefits of fluoxetine, Menkes, Taghavi, and Mason (1993) reported findings that support the proposed role of serotonergic hypoactivity in the aetiology of PMS (p.101). However, the finding that a particular treatment reduces premenstrual symptoms does not necessarily have implications for nosology and etiology. Aspirin is an effective cure for headache, and inhalation of Co2 an effective treatment for panic attacks, therefore neither aspirin nor Co2 can be implicated in the etiology of either disorder. The very premise of a causal relationship is also flawed, as the discovery of a correlation between premenstrual symptoms, and a particular hormone does not mean that the hormone caused the symptoms. Each may be related to a third variable, such as stress, or not related at all (Gannon, 1981). It is probable that there is a complex and fluid interaction between different factors, which cannot be encapsulated within this narrow positivist frame. Health Belief Model One of the most widely accepted standards for understanding health seeking behaviour is this Model. It views dysphoria prior and during menstruation as deviations from the norm of measurable biological (somatic) variables (Parsons, 1975). Based on the cognitive process, this model states that Dysphoria affects womens thinking, feelings, and patterns their course of action. Parsons (1975) proposed further that Dysphoria hinders positive health behaviours during the late luteal phase. Socio-Cultural / Environmental Model To Ussher (1997), the socio-cultural model assumes that subjectivity, behaviour, and the very definition and meaning of what is Dysphoria is constructed within and shaped by sociol-cultural practices, rules, language, relationships, and roles. The socio-environmental model focuses on the life events that may influence the emergence of symptoms of Dysphoria. Brown, Harris, & Peto, (1973) proposed 8

that stressful events and factors in the womans environment, in conjunction with her constitution {heredity} precede the onset of Dysphoric symptoms. Klebanov & Ruble (1994) also proposed that Dysphoria is a result of the influences of social expectation or social stereotype of the premenstrual woman (and attributions of specific moods or behaviour) to the premenstrual phase of the menstrual cycle. This framework assumed that the structures and practices of society have definite consequences for peoples lives. Freund and McGuire (1991) stated that social forces act on women who continue to experience Dysphoria and may determine whether or not they get well. Though, this model has much to offer for the psychopathology of Dysphoria, its limitation is the linkage of Dysphoria to complex environmental factors. For instance, the amelioration of the womans dysphoric condition particularly following the late luteal phase may not always be environmental [otherwise social] in absolute terms. This is because Dysphoria is essentially an emotional reaction to the hormonal changes taking place within the woman. Consequently, the socio-environmental factors can only act, as its exacerbating stressors. Sin-Commitant & Devil-causatory models The sin-commitant model states that all problems are a result of one's own sin and the death that results from sin. Hence, Dysphoria is a result of sin. Within this paradigm a woman struggling with an emotional problem such as Dysphoria would need to find the sin, confess it, repent, and sin no more (Cloud, 2001). The sin model based on the concept of good and evil, purity and impurity appears to be an extension of the cultural model. For example, Judaism denies Hebrew women access into the Temple during their menstrual flow. Certain Christian sects in Nigeria prevent women from entering the church during menstruation. Muslim women are equally denied access into the mosque while menstruating. The monthly denial of access into Temples, Churches and Mosques based on the Biblical and Quranic assumptions that the menstrual flow is a result of sin and thus makes women temporarily unholy, could result into the cyclical phenomenon of Dysphoria through anxiety and dejection. Such denial, based on the sin-commitant religious belief that a menstruating woman will defile the holy place as well as any one who touches her, could be implicated in the etiology of Dysphoria. Closely associated with the sin model, due to the spiritual connotations of both, is the Devil-causatory model. According to Osiki (1996), this model assumes that whether disturbances are physical or mental {i.e., organic or psychogenic}, human beings are passive recipients of Satans actions. Demonization connotes a demoncaused passivity and a control other than that of the person who is demonized. That is, the influence and control by one or more evil spirit beings (demons) can result in the disorder that evolve. Viewing Dysphoria as a demon-induced disorder will therefore place the woman as being constantly under the influence of devils especially during the late luteal phase of her menses. It regards the woman as the submissive and unresisting recipient of demons actions on monthly basis. This model therefore negates the facts that Dysphoria is a psychogenic disorder experienced by women during the late luteal phase. Defective Parenting Model Defective parenting model states that poor and ineffective parenting causes dysphoria prior and during menstruation. It proposes a way of conceptualising parenting that takes into account adult development and the reciprocal parent-child, 9

childparent nature of parenting, as well as the social and contextual factors that impact on the parent-child relationship. Dysphoria and Vulnerability are defined in this model as states that exist when either child- or parent-related factors create a gap between what children need from their parents to facilitate optimal development and the parent's ability to adapt positively to those needs. There are three different variants of this model. First, is double-bind theory, which claims that in the double bind family situation, a child is put into a state where he has to make a choice between two alternatives, both of which will produce confusion. Next is schism' and 'skewed' family patterns theory which states that one parent gets overly close to child of opposite sex as a result of power struggle. The third is Psudohositle psedomutulal verbal communication theory, which states that emotional expression is suppressed by the consistent use of certain ways of verbal communication, in the family. To Strober and Humphrey (1987), Defective parenting model therefore implicated unhealthy parenting patterns such as poor parent-child relationship, paternal and maternal child rejections, unhealthy method of control and discipline, poor methods of child nurturance, maturity demands, a lack of parental affection; overly negative, hostile, and disengaged patterns of family interaction; and parental impulsivity as sources of Dysphoria. Even though defective parenting patterns could be implicated in Dysphoria, it is not the only mechanism or pathway of influence. Other mechanism abound. Hence, defective parenting pattern cannot be linked with Dysphoria because some women who enjoyed good parenting also experience it on monthly basis. Psychological Model This model views dysphoria as a form of behaviour disorder. Psychological theories, as proposed by Weyerer and Kupfer (1994), implicated factors like unpleasant cognitions, emotions, low self-esteem, poor self-perception and behaviour in the etiology of Dysphoria. Current discussion of the psychological aetiology of Dysphoria is the assertion of the continuity of mental processes from early childhood throughout the reproductive years of the woman. Severino (1996) even stated that the inclusion of Dysphoria in a major publication of the American Psychiatric Association implies a psychological correlation of the disorder. He added that the inclusion of Dysphoria as a depressive problem reinforces the psychological component to PMS. The psychological model has also linked Dysphoria to depression. A number of studies have revealed that depression (Bancroft and Rennie, 1995; Kuczmierczyk, Labrum, and Johnson, 1992), or a history of depression (Bancroft, Rennie, and Warner, 1994) is present in at least half of women who report disabling premenstrual symptoms. The psychosomatic theory states that psycho physiological stress is the major factor in the onset of Dysphoria in women of fertile age. A psychosomatic Illness is a condition in which the state of mind (psyche) either causes or mediates a condition of actual, measurable damage in the body (soma). This is a stress related model. Horney (1931) proposed the psychosomatic model (in Walker, 1995), which viewed Dysphoria as the manifestation of repressed sexual desire and power. Horney described premenstrual tension as a psychological response to the anxieties and fantasies associated with pregnancy, combined with frustration caused by the cultural restrictions surrounding the expression of female sexuality, with 10

symptoms triggered by the physiological processes of preparation for pregnancy (Horney, 1931). This model implies that ovarian hormones are not dysfunctional. Instead, there is something about the womans temperament or psychology, which causes intensification of cyclical changes in mood and wellbeing through a psychosomatic mechanism. The theory is in some way analogous to the biomedical one. It states that there is some default in women caused by an external event (stressor) that exarts mental or physical demand upon their body and mind through perception. Such stressor can be anything from a loud noise to an exam or workload to physical activity or the in-laws coming into town. In this instance it lies within the psychological rather than the biochemical sphere, and treatment is directed towards psychotherapy or stress management rather than drug therapy. Therefore, the provision of effective treatment for the amelioration of the emotional and psychological distress of the late luteal phase ought to be sought for in the realm of psychology. A number of psychological packages have been grouped under psychoanalytic, cognitive behavioural, eclectic, and humanistic theories to explain Dysphoria as an affective state. However, for the purpose of this study, the cognitive behavioural and psychoanalytic psychotherapeutic models will be considered. Classification by Course Classification by Course sub-divides Dsyphoria into 3 severity stages: mild / low level symptoms, moderate / PMS (regular or standard) symptoms, and severe states / premenstrual magnification (severe) symptoms (1, 2, 3). Mild / low level symptoms were reserved for individuals with PMT, moderate for PMS, and severe for PMDD. Severe Dsyphoria affects between 3-5% of women of reproductive age. Such severe Dsyphoria is classified under the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) asa mood disorder, "Depressive Disorder, Not Otherwise Specified" emphasizing its emotional and cognitive-behavioural symptoms. The DSM nomenclature for severe Dsyphoria is premenstrual dysphoric disorder (PMDD). DSM-IVs codes {F 39 [296.90]} are in agreement with the International Classification of Diseases, Ninth Edition, Clinical Modification (ICD-9-CM) (625.4-premenstrual tension syndrome). ICD-9-CM is based on the ICD-9, a publication of the World Health Organization. In the DSM-IV, the name was changed from LLPDD to PMDD with criteria that were almost identical to those of LLPDD (only one item was added). DSM-IV {1994} multiaxial classification system includes five axes, each of a different domain of information that may be used in the comprehensive and systematic evaluation of the subjects. It draws attention to the various major mental disorders (Axis I) and personality disorders (Axis II); to general medical conditions (Axis III); to psychosocial and environmental factors (Axis IV); and provides a global assessment of functioning (Axis V). In using DSM-IV criteria for Dysphoria a certain familiarity with the multiaxial system is assumed. Thus, for Dysphoria, criterion C is crucial in excluding any current Axis I, II, or III illness or episode. Other essential features of the DSM-IVs Dysphoria criteria are the on-offness of symptoms and the emphasis on core mood symptoms (criterion A), the requirement that the symptoms must interfere markedly with lifestyle (criterion B), and, most importantly, that the disorder must be confirmed prospectively by daily ratings for at least two menstrual cycles. Prospective daily rating of symptoms is now the only acceptable means of confirming a provisional DSM-IV diagnosis of Dysphoria. 11

Dysphoria is also included in Appendix B of the DSM-IV TR {2000} as an area needing further research Inclusion of Dysphoria in DSM-III/DSM-IV has conceptualized it as an identifiable condition. In the most recent edition of DSM (DSM-IV, 1994), the label reverted to PMDD in category F39 (296.90) as depressive disorder not otherwise specified and it is classified as a cycle-related affective disorder. Its ICD-9-CM code is 625.4 under disorder of menstruation (the International Classification of Diseases (9th revision), World Health Organization 1992). The International Classification of Primary Care (ICPC) has grouped LLPDD under Menstrual problems. The ICPC rubric for PDD is X09, while Its ICPC/ICPC2 PLUS label is premenstrual symptoms/complaint. Classification by Generic Term Dysphoric symptoms are also classified under the generic term premenstrual syndrome (PMS), which is listed in the International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10) under disorders of the genitourinary system. The symptoms included are menstrual migraine, menstrual molimen and premenstrual tension not otherwise specified. The Oxford Medical Information System dictionary (OXMIS) and Read codes (in Hollowell, 1997) are also being used to select the codes, which define premenstrual syndrome. The OXMIS codes are 6269a for Tension premenstrual; 6269f for Syndrome premenstrual and 6269mt for Tension menstrual. The Read codes are K584.00 for premenstrual Tension Syndrome ande K584.11 for Migrane menstrual. The OXMIS is an amalgamation of the eighth revision of the International Classification of Diseases (ICD-8) and the surgical operation codes used by the Office of National Statistics. The Read codes were developed by James Read in the early 1980s to enable General Practitioners (GPs) to code and record relevant information from a patient encounter. Read codes are crossreferenced to the main national and international classifications. Discussion:

Diagnostic Controvery Affecting the Nosology of Dysphoria

Extensive disagreement exists over the status of Dysphoria occuring in reproductive age ovulating women as valid diagnostic categories. The difficulty with the available diagnosis is that it is not officially recognized in psychiatric literature, which means it is difficult for clinicians to make an accurate diagnosis (http://www.wdxcyber.com/nmood06.htm). It is a diagnosis not yet supported by empirical work. Part of the controversy raised over its diagnosis (http://www.wdxcyber.com/nmood06.htm) views that formal recogniyion of Dysphoria will pathologize normal ovulatory functioning. Hence, many women do not want the disorder to be considered a mental or emotional problem Even where there was agreement about the diagnostic entity, there was disagreement about its name (APA, 1992). While preparing the 1987 revision of the American Psychiatric Associations Diagnostic and Statistical Manual for Mental Disorders (DSM-IIIR), the syndrome was variously referred to as "Premenstrual Dysphoric Disorder" (PMDD) and "Periluteal Phase Dysphoric Disorder" (PPDD), before the responsible committee settled on "Late Luteal Phase Dysphoric Disorder" (LLPDD). In the most recent edition of DSM (DSM-IV, 1994), the label reverted to PMDD. Some feminist professionals, including the APAs Committee on Women and the National Coalition for Womens Mental Health (http://www.wdxcyber.com/nmood06.htm), objected to the inclusion of such a syndrome under any label. From their point of view, menstruation is a normal bodily function, and any psychological changes associated with this function should be seen as 12

normal as well. Classifying Dysphoria as a mental disorder will therefore stigmatizes women, and may have other undesirable social consequences by laying additional foundations for disability claims and the insanity defense. Debates over Dysphoria raises questions about the social construction of mental illness. Caplan, McCurdy-Myers, and Gans (1992) review concluded that there was no compelling empirical justification for identifying any particular cluster of symptoms as Dysphoria, nor for considering Dysphoria a form of mental disorder (Feminism & Psychology, 2:27-44, 109). There was no link between the symptoms ascribed to Dysphoria and premenstrual changes in hormonal levels. And there was no evidence that any pharmacological adjustment of hormonal levels had any effect on Dysphoria. The fate of Dysphoria was put up to a vote of the Legislative Assembly of the APA which is an essentially political process. In the absence of objective criteria for diagnosing mental illness, framing the psychiatric nosology is inherently political, and making a psychiatric diagnosis is inherently biased. Setting ideology and politics aside, if the diagnosis of Dysphoria is not officially recognized, it will be difficult to categorize women as suffering it or not. It will also be difficult for psychologists and those in the helping proffesion to proffer adequate therapeutic treatment for its amelioration in sufferers. It is therefore high time for psychiatirsts, general medical practitionrs and those inthe helping professions to team up with clinical psychologists researching into this area of disorder in order to give the rest of the world a valid and acceptable nosologic and diagnostic label of Dysphoria occuring in reproductive age ovulating women. Recommendation There is the need for further research work to be carried out in the area of adeaquate psychotherapuetic programme for the ameleoration of dysphoria in humans with late luteal phases. There is also the need for studies focusing on the effects of Dysphoria on job performance and interpersonal relationships of sufferers. Conclusion Dysphoria, a gender specific condition which affects millions of women during their reproductive years has been as a group of conditions that occurred prior to the onset of menses, in which women develop suicidal ideation and other severe symptoms (Veith, 1964). The nosologic status of Dysphoria is unresolved eventhough it emerges as a distinct affective syndrome with generalized feeling of distress; acutely hopeless, irritable, sad, depressed, and despondent; experienced apathy, lethargy, boredom, constant fatigue, pervasive loss of interest in food, drink, sex, and normal activities (work, school, hobbies), severe mood swings; difficulty concentrating; sleep problems, pervasive loss of interest or pleasure and variety of physical symptoms. Even though there is "ongoing nosologic controversy and confusion" concerning "dsyphoria" (Neurology, 1997; 48:126), this paper noted that it has been classified in DSM-IV and ICD-10 diagnoses of dysphoric disorder in conjunction with medical classification system. Varing classification of Dysphoria (Cantwell and Carlson, 1983; Kessel, 2000 and Donnica, 2000) following the on set of menses have flourished within scientific literature. Examples of these as presented in this study are biomedical Explanatory models, the health belief model, socio-cultural perspectives, Sin & Devilcausatory models, Socio-Environmental model, Psychosomatic influences and the Psychological Explanatory models. In view of the aetiological hypotheses, its nosology 13

as presented in this study has been descriptive (Cantwell and Carlson, 1983), categorical, dimensional, dichotomous, and unitary in nature. Among British and American psychiatrists, the classification of Dysphoria is based on the presenting symptomatology, previous history, family history, physiological and biochemical findings, response to treatment, natural history (acute or chronic); course (progressive or intermittent); cause and disturbed biological process. Some of these classification systems are official, such as the International classification of Diseases9th Edition (ICD-9); Diagnostic statistical Manual of Mental Disorder-III (DSM-III); Diagnostic statistical Manual of Mental Disorder-III-R (DSM-III-R); Diagnostic statistical Manual of Mental Disorder-IV {DSM-IV} and Diagnostic statistical Manual of Mental Disorder-IV Text-Revision (DSM-IV-T-R). The official classification of Dysphoria tends to be created by organizations such as American Psychiatric Association (APA) and World Health Organization (WHO).

REFERENCE
Abraham G.E. (1983) Nutritional factors in the etiology of premenstrual tension syndromes. Journal of Reproductive Medicine; 28: 446 - 64. Abraham, G.E., & Hargrove, J.T. (1980). Effect of vitamin B-6 on premenstrual symptomatology in women with premenstrual tension syndromes: a double-blind crossover study. Infertility, 3 (2) 158165. Acton, G. S. (1998). Classification of psychopathology: Goals and methods in an empirical approach. Manuscript in preparation, Northwestern University, Evanston, Illinois. Adams F. The genuine works of Hippocrates, translated from the Greek, with a preliminary discourse and annotations. Vol. II: aphorisms iii-12 and iii-31. London: Sydenham Society; 1849. American Psychiatric Association (1952). Diagnostic and Statistical Manual of Mental Disorders (DSM-I). Washington, DC: American Psychiatric Association. American Psychiatric Association (1968). Diagnostic and statistical manual of mental disorders (2nd Ed.). Washington DC: American Psychiatric Press. American Psychiatric Association (1980). Diagnostic and statistical manual of Mental disorders (3rd Ed.). Washington DC: American Psychiatric Press. American Psychiatric Association. {1987}. Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised {DSM-III-R}. Washington, DC: American Psychiatric Association. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC; APA. American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (4th Ed.) Text revision. Washington DC: American Psychiatric Press. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th edition). Washington, DC: Author. Andreasen NC. Comprehensive Assessment of Symptoms and History (CASH). MHCRC, Department of Psychiatry University of Iowa College of Medicine, USA; 1987:155. Angst J: The etiology and nosology of endogenous depressive psychoses. Foreign Psychiatry 2: 1, 1973. Antai, A.B, Udezi, A.W, Ekanem, E.E., Okon, U.J & Umoiyoho A.U. (2004). Premenstrual Syndrome: Prevalence in Students of The University of Calabar, Nigeria. African Journal of Biomedical Research, ISSN: 1119-5096. 14

Armstrong J., & Sutherland, B. (1987). Menstrual wellness: Coping with PMS and other dsorders.Melbourne: Collins Dove. Bancroft, J., Rennie, D., & Warner, P. (1994). Vulnerability to perimenstrual mood change: The relevance of a past history of depressive disorder. Psychosomatic Medicine, 56, 225231. Biskind M.S. {1943}: Nutritional deficiency in the etiology of menorrhagia, Metrorrhagia, cystic mastitis and premenstrual tension: Treatment with vitamin B complex. Journal of Clinical Endocrinol Met 3:227-34. Boyle C.A {1999}. Management of menstrual migraine. Neurology 53:S14. Brannon, Linda (1996).Gender: Psychological Perspectives. 62. cited by Stephen Ray Flora, Melissa Sellers {May-June, 2003} in 'Premenstrual Dysphoric Disorder' and 'Premenstrual Syndrome' myths.Skeptical Inquirer. 2004 LookSmart, Ltd. All rights reserved. Brown, G. W., Harris, T. O., & Peto, J. (1973). Life events and psychiatric disorders. Part II: Nature of causal link. Psychological Medicine, 3,159-176. Cahill, C.A. (1998). Differences in cortisol, a stress hormone in women With turmoiltype premenstrual symptoms. Nursing Research, 47, 278-284. Cantwell, D. & Carlson, G. (1983), Affective Disorders in Children and Adolescents. New York: Spectrum Press. Coleman, M. C., (1986). Behavior disorders: Theory and practice (2 nd ed.). Needham Heights: Prentice Hall. Dalton, K. (1987). What Is This PMS? In M. R. Walsh (Eds.), The Psychology of Women. (p.131). Binghamton, NY: Vail-Ballou Press. Dalton, K. (1977). The Premenstrual Syndrome and Progesterone Therapy. London: William Heineman Medical Books, Ltd. DePirro, R., Fusco, A., Ben-David, M., Assael, M., & Bernstein, R. (1978).Insulin receptors during the menstrual cycle in normal women. Journal of Clinical Endocrinology and Metabolism, 47, 1387-1389. Donnica, Mary M.D. (2000). PMS". Often Joked About, But Not A Laughing matter. http://www.drdonnica.com?display.asp?article=189 Eysenck, H. J. (1986). A critique of contemporary Classification and diagnosis. In T. Millon and G. L. Klerman (Eds.), Contemporary directions in psychopathology: Toward the DSM-IV (pp. 73-98). New York: Guilford. Farrell, Molly & Kebbel, Rebecca {1998}. PMS: FACT OR FICTION. PMS PROPOSAL HAYS (farrelma@miavx1.muohio.edu.}http://jrscience. wcp.muohio. edu/Research/HnatureProposalsrticles/PMSPROPOSALHAYS.html. Frackiewicz, EJ and Shiovitz, TM. (2001). Evaluation and Management of premenstrual syndrome and premenstrual dysphoric disorder. Journal of American Pharmacological Association; 41:437-447. Frances, A., Widiger, T., and Fyer, M. R. (1990). The influence of Classification methods on comorbidity. In J. D. Maser and C. R. Cloninger (Eds.), Comorbidity of mood and anxiety disorders (pp. 41-59). Washington, DC: American Psychiatric Press. Frank, R. (1931). The Hormonal Causes of Premenstrual Tension, Archives of Neurology and Psychology. 26:1053-7. Freeman, E.W., Rickels, K., Arredondo, F., Kao, L.C., Pollack, S.E., & Sondheimer, S.J. 1999). Full- or half-cycle treatment of severe premenstrual syndrome with serotonergic antidepressant. Journal of clinical Psychopharmacology, 19, 3-8. 15

Freund, P.E.S., and McGuire, M.B. 1991. Healths, Illness, and the Social Body. New Jersey: Prentice Hall. Garrison FH. History of medicine. Philadelphia, NJ: W. B. Saunders; 1929. http://ajrccm.atsjournals.org/cgi/content/full/167/5/678) Gordon L. Snider, Nosology for Our Day Its Application to Chronic Obstructive Pulmonary Disease, American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 678-683, (2003). http://ajrccm.atsjournals.org/cgi/content/full/167/5/678) Goudsmit, E. M. (1988). Psychological aspects of premenstrual syndrome. In M. Brush, & E. Goudsmit(Eds.), Functional disorders of the menstrual cycle (pp. 159 175). Chichester: John Wiley. Green, R., & Dalton, K. (1953). The premenstrual syndrome. British Medical Journal, 1, 1007-10013. Halbreich, U. (1997). Premenstrual dysphoric disorders: A diversified cluster of vulnerability traits to depression. Acta Psychiatrica Scandinavica, 95, 169-176. Hammarbck S, Bckstrom T. {1988}. Induced anovulation as treatment of premenstrual tension syndrome. Acta Obstet Gynecol Scand 67:159-66. Hammerback, S., Backstrom, T., & MacGibbon-Taylor, B. (1989). Diagnosis of premenstrual tension syndrome: Description and evaluation of a procedure for diagnosis and differential diagnosis. Journal of Psychosomatic Obstetrics and Gynaecology, 10, 2542. Hollowell J: The general practice research database: quality of morbidity data. Population Trends 1997, 87:36-40. Horney, K. (1931). Die pramensstruellen verstimmungen. (Premenstrual syndrome). Zeitscher fur Psychoanalytische Padagogik, 5-7. As in Ussher, J.M. (1997). Premenstrual syndrome: Reconciling disciplinary divides through the adoption of a material-discursive epistemological standpoint. Annual Review of Sex Research, 7, 218-251. Ilesanmi, O.O. (2005). Two Psyhotherapeutic Programmes in the Treatment of Dysphoria in Girls with Late Luteal Phases. Unpublished Ph.D. Thesis, Submitted To University of Ibadan, Nigeria. Israel, S.L. (1938). Premenstrual tension. The Journal of the American Medical Association, 110. 1721-1723. Jablensky A: The conflict of the nosologists: views on schizophrenia and manicdepressive illness in the early part of the 20th century. Schizophr Res 1999 39:95100 Kaur, G., Gonsalves, L., & Thacker H. L. {2004}. Premenstrual dysphoric disorder: a review for the treating practitioner. Cleve Clinical Journal of Medicine; 71(4): 303305, 312-313, 317-318 Kessel Bruce{2000}. PREMENSTRUAL SYNDROME: Advances in Diagnosis and Treatment. CURRENT REPRODUCTIVE ENDOCRINOLOGY Obstetrics and Gyneacology ClinicsVolume 27 Number 3 September 2000Copyright 2000 W. B. Saunders Company. Klebanov, P. K., & Ruble, D. N. (1994). Toward an understanding of womens Experience of menstrual cycle symptoms. In V. J. Adesso, D. M. Reddy, & R. Fleming (Eds.), Psychological perspectives on womens health (pp. 183 221).Washington, DC: Taylor & Francis. Kuczmierczyk, A. R., Labrum, A. H., & Johnson, C. C. (1992). Perception of family and work environments in women with Premenstrual syndrome. Journal of Psychosomatic Research, 36, 787795. 16

Landn, Mikael, & Eriksson, Elias {2003} Theoretical Review: How does premenstrual dysphoric disorder relate to depression and anxiety disorders? Depression and Anxiety 17:122-129. 2003 Wiley-Liss, Inc. Lever, J., & Brush, M. (1981) Premenstrual tension. New York: McGraw-Hill Book Company. Maj M. Critique of the DSM-IV operational diagnostic criteria for schizophrenia. Br J Psychiatry.1998;172:458-460. Menkes DB, Taghavi E, Mason PA, & Howard, R. C.1993} Fluoxetines spectrum of action in premenstrual syndrome. International Journal of Clininical Psychopharmacol 1993; 8:95102 Millon, T. (1991). Classification in psychopathology: Rationale, alternatives, and standards. Journal of Abnormal Psychology, 100, 245-261. NOSOLOGY:LoveToKnow 1911 Online Encyclopedia. 2003, 2004 http://82.1911encyclopedia.org/N/NO/NOSOLOGY. Osiki, J.O. {1996}. Spiritual intervention and rational emotive therapeutic techniques in the treatment of demonologically attributed illness in some disturbed individuals. Ph.D Thesis. University of Ibadan, Ibadan, Nigeria. Parry, B. (1994). Biological correlates of premenstrual complaints. In J.H.S. Gold (Ed.), Premenstrual dysphoria: Myths and realities 4766. London: American Psychiatric Press. Parsons, T. (1975). The sick role and the role of the physician reconsidered. Milbank Memorial Fund Quarterly, 53, 257- 277. Popper KR. Alles Leben ist Problemlsen. Munich, Germany: Piper; 1994. Qureshi NA, Al-Habeeb T.A. {2004}. Making gynecological and Psychiatric sense out of premenstrual pains, tension and dysphoria. Saudi Med J. 2004 Jun; 25(6): 717-27 Rapkin A. {2003}. A review of treatment of premenstrual syndrome and premenstrual dysphoric disorder. Psychoneuroendo- crinology; 28(Suppl 3):39-53. Rausch, J.L., Janowski, D.S., Risch, S.C., Judd, L.L., & Huey, L.Y. (1982). Hormonal and neurotransmitter hypotheses of premenstrual tension. Psychopharmacology Bulletin, 18, (4), 2634 Reid R.L, & Yen S.S. {1983}. The premenstrual syndrome. Clinical Obstetrics & Gynaecology; 26(3):710-718 Richardson, J. T. E. (Ed.). (1991). Cognition and the menstrual cycle. New York: Lawrence Erlbaum. Rittenhouse, C. A. {1989}. The Emergence of Premenstrual Syndrome: The Social History of a Womens Health Problem. Bell and Howell Company: Ann Arbor. Robinson, G. {1986}. 'Legal Implications of Premenstrual Syndrome: A Canadian Perspective', Canadian Medical Association Journal, volume 135,15 December, p. 1340. Rubinow, D. R & Schmidt, P. J. (1995) The treatment of premenstrual syndrome. Forward into the past. New England Journal of Medicine, 332, 15741575 Scadding JG. Principles of definition in medicine. Lancet 1959;1:323325. Severino SK. (1996). Premenstrual dysphoric disorder: Controversies surrounding the diagnosis. Harv Rev Psychiatry. 3:293-295. Smith S {1989}. The premenstrual syndromeDiagnosis and management. Fertility Sterility 53:527-43. Steiner, M. (1996). Premenstrual dysphoric dysorder. An update. General Hospital Psychiatry, 18, 244-250. Steiner M, & Pearlstein T {2000}. Premenstrual dysphoria and the serotonin system: pathophysiology and treatment. Journal of Clinical Psychiatry; 61 Suppl 12: 17-21 17

Strober, M., & Humphrey, L. L. (1987). Familial contributions to the etiology and course of anorexia nervosa and bulimia. Journal of Consulting and Clinical Psychology, 55, 654-659. Strmgren E. Nosology and classificationfriends or foes? In: Ferrero FP, Haynal, AE, Sartorius N, eds. Schizophrenia and Affective Psychoses. Nosology in Contemporary Psychiatry. London, UK: John Libbey CIC srl; 1992:11-16. Sundstrm, I. (1997). GABAA-receptor Sensitivity. Studies During the Menstrual Cycle in Patients with PMS and Controls. Ume U. Medical Dissertations New Series No 528, Ume, Sweden Sydenham, Thomas (1624-1689) in Processus Integri (Advances in Healing, 1692), Microsoft Encarta Premium Suite 2005. 1993-2004 Microsoft Corporation. All rights reserved The American Heritage Dictionary of the English Language, Fourth Edition Copyright 2004, 2000 by Houghton Mifflin Company The American Heritage Stedman's Medical Dictionary Copyright 2002, 2001, 1995 by Houghton Mifflin Company Ussher, J.M. (1997). Premenstrual syndrome: Reconciling disciplinary Divides through the adoption of a material-discursive Epistemological standpoint. Annual Review of Sex Research, 7, 218-251. Veith, I. (1964). Hysteria: The story of a disease. Chicago: University of Chicago Press. Walker, Anne {1995}. "Theory and Methodology in PMS Research," Social Science and Medicine, 41(6): 793-800. Weyerer, S., & Kupfer, B. (1994). Physical exercise and psychological health. Sports Medicine, 17, 108116. World Health Organization (1992) International Classification of Diseases (10th edn) (ICD10). Geneva: WHO. World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders: Diagnostic Criteria for Research. Geneva, Switzerland: World Health Organization;1993. World Health Organization. Schedules for Clinical Assessment in Neuropsy-chiatry. Version 2.0. Geneva, Switzerland: World Health Organization; 1994.

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