At the same time as psychologically orientated investigators have attempted to understand the psychological processes involved in extreme forms of negative emotion, biologically orientated investigators with an interest in depression have pursued their own research agendas, most of which are too complex to describe in any detail here. A few of these avenues have directly paralleled the research we have already considered. For example, Richard Davidson at the University of Wisconsin has attempted to measure the way in which different emotional states reflect interactions between cortical areas of the brain and deeper brain structures in the limbic system.78 Davidson’s studies raise a range of issues that lie beyond the scope of this book. However, it is interesting to note that, in an experiment carried out in collaboration with Lyn Abramson, he found that ordinary people with an optimistic attributional style showed increased neural activation in the left frontal cortex.79 Depressed people with a pessimistic style, on the other hand, showed greater activation in the right frontal cortex. Interestingly, these relationships seemed to be specific to attributional style; no such asymmetrical associations were found between dysfunctional attitudes towards the self and neural activity. If nothing else, these observations remind us that an adequate approach to psychopathology will eventually have to integrate psychological and biological findings within a single framework.
Other biological investigations have focused specifically on processes that may be responsible for some of the somatic symptoms reported by depressed patients. A particularly interesting although relatively neglected line of investigation concerns the effects of disrupting the biological rhythms that regulate our patterns of sleeping and waking. These circadian rhythms are reflected in subtle bodily changes (for example, changes in biochemistry and core body temperature) that occur throughout the day. Left to their own devices, they tend to become progressively longer, so that most people confined to a land without clocks or daylight would eventually settle down to a cycle of about twenty-five hours. (Readers who have experienced unemployment or other kinds of prolonged periods of inactivity may have noticed this effect, finding that they go to bed slightly later every day and that they get up progressively later in the morning.) However, our rhythms are usually kept in synchrony with the Earth’s rotation by activities that expose us to regular stimuli, such as alarm clocks, journeys to work and meals. These stimuli are known as Zeitgebers (a German term that means clock-setting stimuli).
By way of an analogy, the reader might like to think of a person who is forced to keep time with a slow running watch, but who, at certain times of the day, is able to obtain information about the correct time. On each of these occasions, she moves her watch forward, thereby ensuring that it is always accurate within certain limits. When first encountered, this system of circadian rhythms and Zeitgebers seems strangely maladaptive – it is not immediately obvious why we have not simply evolved internal time keeping devices that are more in tune with the rhythms of our planet. However, the system seems less maladaptive when we consider that, at most latitudes, human beings need to change their routines according to the seasons. It turns out that the circadian system has just the right degree of flexibility required to enable this to happen.
Now let us consider what happens if we are unable to access Zeitgebers, or if our exposure to them becomes somehow irregular, so that our circadian rhythms become markedly desynchronized with the cycle of light and darkness. Many readers who have travelled abroad will have experienced this as the unpleasant but happily temporary phenomenon of jet lag. The symptoms of jet lag include fatigue and listlessness, disturbed sleep, loss of interest in food, and all too noticeable cognitive effects such as difficulty remembering, concentrating and finding words. These symptoms are, of course, caused by our circadian rhythms being out of synchrony with the place that we have travelled to, and resolve as they shift to the new cycle of activity that we impose on them. (Typically, jet lag is especially bad when we travel from west to east. This is because our naturally slow-running internal clock has greater difficulty adapting to the earlier waking which this kind of journey necessitates, compared to the later waking to which we have to adapt when travelling in the opposite direction.)
David Healy, a psychiatrist at the University of Wales College of Medicine, has noted that stressful life events often lead to a disruption of routine. He has argued that, if this disruption is severe enough, the consequence can be a form of chronic circadian dysrhythmia, in which our biological rhythms are persistently out of synchrony with the demands of daily living. It is as if the patient develops permanent jet lag.80 This proposal goes a considerable way towards explaining those symptoms of depression – for example, sleep disturbance, fatigue, loss of interest in simple pleasures, and subjective cognitive difficulties – that are difficult to explain in terms of the psychological processes that we have considered earlier. Interestingly, as Healy himself notes, these are precisely the symptoms that are most prominent in non-Western descriptions of depression.81
Healy’s suggestion is that circadian dysrythmia is the primary cause of depression, and that the psychological changes that we have considered earlier are consequence so fit. He argues that people who experience persistent fatigue and the kinds of subtle cognitive deficits that follow from disrupted sleep will often fail to cope adequately with the demands of their work and social relationships, and will begin to blame themselves for these shortcomings. According to Healy, once the individual has made internal attributions for these negative experiences, all the other cognitive abnormalities that we have considered will follow.
Although this theory has not received the attention that it deserves, observations that many depressed patients suffer from sleep problems and have irregular rhythms of social activity82 are clearly consistent with it.83 Nonetheless, we should be suspicious of Healy’s assertion that circadian dysrhythmia is always the primary cause of depression. This proposal seems to assume that depression is a single, coherent entity, and that it must be the product of a single causal pathway. In fact, as we have seen, depression is a term used to describe a range of symptoms, only some of which are easily accounted for by Healy’s hypothesis.
In all likelihood, many dysphoric episodes start with the pessimistic interpretation of negative events and, if somatic symptoms are present, it is because patients respond to their dysphoric mood by withdrawing from social life and abstaining from the kinds of regular activities that would normally keep their circadian rhythms synchronized. In other cases, a loss of routine may indeed be primary, and loss of self-esteem may follow from the perception of persistent failure. (The example I gave earlier of George, the dysphoric engineer, fits this kind of pathway well; recall that his episodes of depression typically followed trips abroad, which presumably challenged his circadian system.) Even in such cases, however, we probably need to assume that some kind of cognitive vulnerability, for example a pessimistic attributional style or dysfunctional attitude towards the self, is present beforehand. Why else would people interpret their fatigue and lethargy as evidence of their own inadequacy, rather than as a natural consequence of stressful life events?
In short, it seems reasonable to assume that more than one pathway leads to the disturbances of cognition and emotion that we lump together under the label of ‘depression’. The sequence of cognitive changes that follows a pessimistic appraisal of an adverse life event constitutes one such pathway, the consequences of a severe disruption to routine another. There may be others that I am not aware of. Putting together what we have learned in this chapter into a single flow diagram, we arrive at the model shown in Figure 10.7.
In the following chapters we will see that many of the processes described in this diagram also contribute to other symptoms.
Figure 10.7 The final model of depression.
11
A Colourful Malady*
As an experience, madness is terrific…
Virginia Woolf1
An Unquiet Mind,2 written by the Am
erican clinical psychologist Kay Redfield Jamison, is probably one of the bravest books about madness ever published. The daughter of a meteorologist working for the US air force, Jamison suffered the frequent dislocations that are often the lot of families of armed forces personnel. Although moody during childhood, she first became manic during her senior year at high school, when she experienced a period of intense excitement and disorientation that was followed by weeks of depression and exhaustion. At the time, it did not occur to her that she might be suffering from a psychiatric disorder. Even years later, after qualifying as a clinical psychologist, and after further episodes of disturbed mood, she was unwilling to believe that she needed treatment. Her appointment to a position in the Department of Psychiatry at the University of California in Los Angeles was a turning point. Shortly afterwards, following a period during which she worked furiously and without sleep, she began spending wildly. She bought watches, unnecessary furniture, books and (for some reason) numerous snakebite kits. Eventually she became ‘ravingly psychotic’, an experience she described in the following way:
One evening I stood in the middle of my living room and looked out at a blood-red sunset spreading out over the horizon of the Pacific. Suddenly, I felt a strange sense of light at the back of my eyes and almost immediately saw a huge black centrifuge* inside my head. I saw a tall figure in a floor-length evening gown approach the centrifuge with a vase-sized glass tube of blood in her hand. As the figure turned around I saw to my horror that it was me and that there was blood all over my dress, cape and long white gloves. I watched as the figure carefully put the tube of blood into one of the holes in the centrifuge, closed the lid, and pushed a button on the front of the machine. The centrifuge began to whirl.
Then, horrifyingly, the image that previously had been inside my head now was completely outside of it. I was paralysed with fright. The spinning of the centrifuge and the clanking of the glass tube against the metal became louder and louder, and then the machine splintered into a thousand pieces. Blood was everywhere. It spattered against the windowpanes, and the walls and paintings, and soaked down into the carpets. I looked out towards the ocean and saw that the blood on the window had merged with the sunset; I couldn’t tell where one ended and the other began. I screamed at the top of my lungs. I couldn’t get away from the sight of the blood and the echoes of the machine’s clanking as it whirled faster and faster.
The main theme of An Unquiet Mind is Jamison’s struggle to come to terms with her diagnosis. As the story unravels, she tells of her reluctance to accept the fallibility of her own mind, and of the anxiety she felt when forced by circumstances to reveal her condition to other people. The decision to write about her experiences is portrayed as the culmination of a gradual and frightening processes of ‘coming out’, facilitated at various points by sympathetic colleagues, friends and lovers. Early in her career, she made use of her experiences by presenting her own story at conferences as if she had heard it from a patient. Only later, after finding a type of medication that seemed to suit her, was she able to admit publicly that her life had been punctuated by periods of madness so severe that they had necessitated hospital treatment.
Jamison’s research has mostly focused on the link between abnormal moods and creativity. (We considered some of her findings in Chapter 5.) She is such a good example of the triumph of ambition over adversity (and therefore an excellent role-model for psychotic patients) that it will probably seem uncharitable to pass judgement on her account. And yet, throughout An Unquiet Mind, Jamison accepts the Kraepelinian paradigm uncritically. She hints at difficulties in her own life (her father was prone to moods that became so extreme that they eventually made him unemployable; her parents divorced, as she did later; a lover died tragically) but, for reasons that are easily inferred, she says very little about how these events contributed to her psychosis. The ‘illness’ in An Unquiet Mind is an invading army that imposes its will upon her. She endures its occupation with dignity. It does not appear to be the product of her psychology, a response to circumstances, or the outcome of a process of development.
This attitude is very common among psychologists and psychiatrists, who regard mania as such an extreme phenomen on that it is assumed to be impenetrable to psychological analysis. And yet, given that mania is typically experienced by people who also have a history of depression, it is reasonable to ask whether processes similar to those we have considered in the last chapter could be implicated in manic episodes. To begin to answer this question we must look more closely at what happens in a manic episode.
A Paradoxical Condition
Surprisingly, in her account of her illness, Kay Jamison nowhere describes in detail what it is like to experience mania. The closest she comes is her account of a terrifying hallucinatory episode, which I have reproduced above. Perhaps mania is too frightening to recall. Or more likely there is something about the manic state that makes it almost impossible to portray in words. Although I have spent many hours listening to recovered manic patients attempting to describe their experiences, their accounts have often seemed curiously incomplete. It is as if the break from normal functioning during an episode is so severe that the mind, on returning to sanity, cannot comprehend it.
This amnesia may be explained by a phenomenon known as state-dependent memory. We are most likely to remember something if we are in a similar state to that in which we learnt it. Howard Weingartner and his colleagues at the US National Institute of Mental Health demonstrated this effect in bipolar patients by asking them to learn simple word lists when manic and when in remission, finding that they were better able to recall the lists when in the same mood state.3 In a case study that illustrates this effect more vividly than any experiment, J. Mark Williams and H. R. Markar have described a patient who hid several thousand pounds when manic. Recovering, he could not remember where he had put the money. Some months later, when manic again, he tried to hide something else and, choosing the same place, found it.4
The difficulty experienced by patients when attempting to recall mania is matched by the poor descriptions offered in the classic literature of psychiatry. Even modern researchers have harboured gross illusions about the manic state. For example, the term ‘bipolar disorder’ gives the quite misleading impression that mania lies at the opposite pole to depression on a spectrum of emotion. Interestingly, some ancient physicians were more acute observers than their modern counterparts. The second-century physician Aretaeus, who lived in Cappadocia in Asia Minor, was probably the first person to suggest that mania is an extreme end-state of depression,5 a hypothesis that is consistent with much of the evidence that we will consider shortly.
The symptoms of mania
One of Kay Jamison’s most remarkable achievements is her encyclopaedic textbook Manic-Depressive Illness, which she co-authored with American psychiatrist Frederick Goodwin.6 Within its pages, Goodwin and Jamison gather together data on the emotions reported by patients suffering from mania or its milder variant hypomania (defined in DSM-IV as a period of ‘abnormally and persistently elevated, irritable or expansive mood’ accompanied by at least three additional symptoms such as inflated self-esteem, non-delusional grandiosity, decreased need for sleep, flight of ideas, distractibility or ‘excessive involvement in pleasurable activities that have a high potential for painful consequences’). Collating the data from fourteen studies involving over 700 patients, they found that euphoria was reported by 71 per cent of the patients examined, a finding that at first seems consistent with the bipolar concept. However, 72 per cent of patients were described as depressed, and 80 per cent of patients were described as irritable. Simple arithmetic reveals that some patients must be both dysphoric and euphoric. The DSM system recognizes this phenomenon by describing three types of bipolar episodes: depression, mania, and mixed episodes in which both manic and depressive symptoms are evident. However, the concept of a mixed episode remains controversial.7 Some researchers have suggested that the apparent co-occ
urrence of depression and euphoria in fact reflects ultra-rapid transitions between one mood state and the other, so that patients are euphoric one moment and depressed the next. Others have suggested that different moods predominate as manic episodes unfold. Frederick Goodwin, for example, has argued that most manic patients progress through three distinct phases, with euphoria dominant only in the first, whereas depression, panic and irritability dominate in the third and most severe stage (see Figure 11.1).8
The paradox of co-existing euphoria and depression in manic patients becomes less paradoxical when viewed from the perspective of the circumplex model of emotions, described in Chapter 9 (pp. 215– 19). Recall that, according to this model, negative mood and positive mood are independent dimensions of emotion. Therefore, although we would expect these emotions to be negatively correlated for much of the time (because events which make us feel bad tend not to make us feel good and vice versa) there is nothing to stop both types of mood states occurring together under exceptional circumstances.
This explanation is consistent with the results of a factor-analytic investigation of manic and mixed episodes recently reported by Frederick Cassidy and his colleagues at Duke University in North Carolina.9 Prior to their analysis, they collected detailed information about the symptoms of more than 200 patients. They discovered that these symptoms fell into five separate groups. Two of the factors were dysphoric mood and ‘increased hedonic function’ (euphoric mood, increased humour and an increased interest in sex), which were therefore shown to be independent of each other. The remaining three factors were psychomotor pressure (racing thoughts, rapid speech and increased activity), psychosis (mainly grandiose and paranoid delusions) and irritability.
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