My Chaos Narrative: 67 Years of Bipolar Disorder

[RonPrice]

if this post is either too long or not appropriate just delete it. From my point of view it could be a relevant post to some who come across this section of the site.-Ron Price, Tasmania

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1.2 This is a longitudinal, retrospective account going back to my conception in the last half of October 1943. The story continues up to the last half of October 2010. This statement, even at some 66,000 words, is still a work in progress, as they say these days, some 67 years. Neurobiological, neuropsychiatric and affective disorders like BPD are found in diverse forms as well as in a broad range of age of onset and in a specificity of symptoms. Little is still known about its pathogenesis, that is, the origin and development of the disease. What follows is one person’s story, one person’s life experience of BPD, an illness that silently and not-so-silently shaped my life. It is a focussed account on a part of my personal life-narrative with the many manifestations, the symptomology, of BPD as I experienced it. BPD shaped, but did not define all that has been my life. It was a medical affliction that made for a certain inconstancy in living, a certain impulsivity and much else. The story of that ‘much else’ is found here.

 

1.3 I make reference to a strong genetic contribution to the aetiology of BPD, a genetic predisposition, a genetic susceptibility as a factor in the pathogenesis of BPD. A family history, what is sometimes referred to as a family pedigree, of affective disorder in a first-degree relative, in my case my mother(1904-1978) is relevant to this narrative. My mother had a mild case of what may very well have been BPD, at least I have come to think of her mood swings as falling into a significantly high place in what is sometimes called the BPD or affective spectrum during her 75 year life. Her mood-swing disability or affective disorder, though, was never given the formal medical diagnosis manic-depressive(MD), a term which developed from several concepts as early as the 1850s if not centuries before. The term MD was replaced in 1980 after my mother died in 1978 by the term BPD. In retrospect my mother exhibited symptoms which may be more accurately labelled: (a) explosive disorder disability, (B) neurotic disorder: anxiety state or (d) depressive disorder. I know nothing of the mental health of my mother’s parents or grandparents and so am unable to draw on what could be a useful knowledge base to explain the origins of my BPD.

 

These episodes are usually separated by periods of "normal" mood, but in some individuals, depression and mania may rapidly alternate, known as rapid cycling. Extreme manic episodes can sometimes lead to psychotic symptoms such as delusions and hallucinations. BPD has now been subdivided into: bipolar I, bipolar II, cyclothymia, and some other types based on the nature and severity of mood episodes experienced. The range of types and experiences is often described as the bipolar spectrum. –See Bipolar Disorder, Wikipedia, the free encyclopaedia.

 

1.4 My father also suffered from what seems to me now, in retrospect, a mild case of what today is sometimes called intermittent explosive disorder(I.E.D.) or impulse control disorder(I.C.D.), as opposed to planned acts of violence or a simple temper. Given the rarity of I.C.D., it seems to me that my father had only a mild I.C.D. Other names for I.E.D. include: rage attacks, anger attacks and episodic dyscontrol. People with I.E.D. experience anger which is grossly disproportionate to the provocation or the precipitating psychosocial stressor. My father may have been exposed to this type of behaviour as a child and so his I.E.D. may have been learned rather than organic and brain-centred. There are also complications associated with the diagnosis of I.E.D. and they include job or financial loss. My father lost much money on the stock market in his late middle age, his late 50s and early 60s. My father was also genuinely upset, regretful, remorseful, bewildered or embarrassed by his impulsive and aggressive behavior. In my father’s late 60s, and perhaps at earlier stages in his life, his disorder also exhibited, or so it seems to me now in retrospect, co-morbidity perhaps due to his genuine sense of remorse, but I don’t know for sure. I know nothing, either, of the mental health of his parents or grandparents all born in the 19th century. My conclusions regarding my father’s emotional disability are largely tentative. Perhaps he just had a bad temper.

 

1.4.1 About half of all patients with BPD have one parent who also has some form of mood disorder. There is then, or so it seems to me, a clinical significance in my mother’s and father’s mood disorders in the explanation of the origins and diagnosis of my own BPD. The high heritability of BPD has been well-documented through familial incidence, twin and adoption studies. There is an unquestionable justification for the inclusion of my family in the understanding of my BPD. No specific gene has yet been identified as the one bipolar gene. It appears likely that BPD is caused by the presence of multiple genes conferring susceptibility to BPD when combined with psychosocial stressors.

 

1.4.2 Advanced paternal age is a risk factor for BPD in the offspring. Since my father was 55 when I was born, the hypothesis that advancing paternal age “increases the risk for de novo mutations in susceptibility genes for neuro-developmental disorders” has some relevance to my having BPD.”( Psychiatric News, November 7, 2008, V.43 No. 21, p. 18.) The offspring of men 55 years and older, that same article went on to say, were 1.37 times more likely to be diagnosed as having BPD than the offspring of men aged 20 to 24 years. The maternal age effect was less pronounced. For early-onset cases, that is BPD onset under the age of 20, and that was the case with me, the effect of paternal age was much stronger; whereas no statistically significant maternal age effect was found.

 

1.5 For an elaboration of the subject of the genetic connection of BPD and in utero BPD see: David Healy’s Mania: A Short History of BPD Johns Hopkins, 2008. A short history of BPD is also available on the internet. Genes may also contribute to the age of onset of BPD and this is analysed now in the context of a phenomenon called genetic anticipation. Anticipation refers to the phenomenon of an illness occurring in successive generations at earlier ages of onset and/or increasing severity. In a recent study using registry data of BPD subjects, age at onset of the first illness episode was examined over two successive generations. Subjects born from 1900 through 1939(my mother) and from 1940 through 1959(myself) were studied. The median age at onset of the first episode of BPD was lower by 4.5 years in subjects born during or after 1940. It was not until my mother was in at least her twenties that her first episode of BPD occurred, although this is somewhat of a guesstimation.

 

1.5.1 BPD, affective disorders of various kinds runs in the family. I am unable to trace my BPD back several generations. But, if I knew more about the many generations that preceded me in my birth family episodes of hearing voices, delusions, hyper-religiosity, and periods of not being able to eat or sleep—I have little doubt would be found. These episodes, these types of experiences were remarkably similar across generations and between individuals. With modern psychiatry and chemotherapy treatments are now available. This is the story of my BPD and my treatments.

 

1.6 The goal of what is sometimes called ‘personalized medicine’ is to utilize a person's genetic makeup for appropriate disease diagnosis and treatment, an idea conceptualized initially in the recent years of the Human Genome Project. The current conceptualisation of MD/BPD can be traced back, as I indicated briefly above, to the 1850s, although its history can be traced as far back as ancient history in Turkey. Both terms, MD and psychosis, were coined in 1875 by Jules Falret, a French psychiatrist and he recognized its genetic link. German psychiatrist Emil Kraepelin (1856–1926), the founder of modern psychopharmacology, also made a major contribution to the early understanding of MD/BPD, only one of the many disorders in the general mood disorder category, but a cyclical mood disorder associated with a circularity between D and euphoria.

 

1.7 About 37,000 years ago Neanderthals arguably intermingled with modern humans and thus a new gene entered the human genome, the DRD4 7R gene. This gene arguably originated from Neanderthals. This gene is associated with risk-taking, sensation-seeking and novelty-seeking, and correlated with openness to new experiences, intolerance to monotony, and exploratory behavior, features of Neanderthal behaviour. About 10% of the population have the activated DRD4 7R gene. So goes yet another theory on the genetic predisposition to BPD.

 

1.8 All manifestations of BPD share uncertain etiologies, with often opaque, obscure, relationships between genes and environment. Some medical experts and theorists in the field of such studies posit latent changes in the expression of specific genes initially primed at the developmental stage of life. Some studies and some experts emphasize that certain environmental agents disturb gene regulation in a long-term manner, beginning at early developmental stages in the lifespan perhaps even in utero. But these disturbances, these perturbations as they are sometimes called, might not have pathological results until significantly later in life. In retrospect, as I look back from these middle years(65-75) of late adulthood, the years 60 to 80 as some developmental psychologists call these years of the lifespan, these perturbations and pathological results were clearly manifested at the age of 18. I could easily theorize an earlier onset on the basis of behavioural perturbations manifested in early childhood and into adolescence and I do such theorizing later in this account(see sections 2.7.1 and 2.7.2 below).

 

1.9 I received two or three diagnoses between 1963 and 1980 from psychiatrists, friends, family, GPs and concerned others. The diagnosis that was made in 1980, namely, BPD, is a diagnosis that is standardized according The Diagnostic and Statistical Manual of Mental Disorders (DSMMD-IV) which provides diagnostic criteria for mental disorders. I use the term BPD not MD throughout this document and I use that acronym. In the DSM-IV MD is a 5 axis/level system of diagnosis that is used.

 

1.9.1 In my case, axis/level 1 is for clinical disorders that are mood disorders. Axis 3 in this system is for what they refer to as acute medical concerns that relate to BPD; axis-4 is for psycho-social and environmental problems that contribute to BPD and axis-5 is an overall caregiver’s assessment of my functioning on a scale 1 to 100. Most of the successful diagnoses and treatment of my BPD have come from psychopharmacology and its roots in physiological assumptions. In the last decade, say, 2000 to 2010, talking cures and behaviour modification techniques like cognitive behaviour therapy with their roots, their emphasis on assumptions in the domain of intrapsychic experience have also been successful as adjuncts to medications or separate from them.

-------I WILL POST MORE OF THIS NARRATIVE AND ANALYSIS OF PERSONAL EXPERIENCE IF INTEREST IS SHOWN---------