Archive for October 1st, 2010
Posted on October 1, 2010 - by David
I am working directly from the unpublished text of Liah Greenfeld’s forthcoming book, Mind, Madness, and Modernity: The Impact of Culture on Human Experience. All the original ideas, and all interpretations and analysis of primary and secondary source materials used to support the ideas are attributable to Liah Greenfeld. Read the introduction to the exposition here.
part 3 – Madness: A Modern Phenomenon
With all that has been written about schizophrenia and manic-depressive illness, the countless studies that have been conducted, and the growing list of medications used in treatment, it would be easy to mistakenly assume that we now understand the nature and cause of these ailments. The history of the separation of psychoses of unknown cause into these two categories leads us to Emil Kraepelin (1856-1926). This German psychiatrist believed that these were heritable brain diseases, and he led a revolution in classification in German-language psychiatry around the turn of the twentieth century, trying to discover just what kind of brain diseases he was dealing with. Kraepelin used a latin version (dementia praecox) of the French term demence precoce (coined in 1852 by Benedict Morel), to distinguish a form of insanity with an early onset and rapid development from the common geriatric dementia. Kraepelin then separated Dementia praecox from manic-depressive insanity (called by the French folie circulaire or folie a double forme). Up until that point, the two conditions were believed to constitute one general category of insanity.
Kraepelin’s use of the term dementia praecox, which suggested a progressive slowing of mental processes, to refer to a condition characterized largely by delusions and hallucinations, (which imply not mental lethargy but imaginative hyperactivity) may have contributed to the misinterpretation of schizophrenia, (still common today), as degeneration of cognitive/reasoning capacities. The evidence suggests that it is rather the strange character of thought, the inability to think in normal, commonly accepted ways, which distinguishes schizophrenia from geriatric dementia. The name “schizophrenia” (meaning “splitting of the mind”) was introduced to replace dementia praecox in 1908 by Swiss psychiatrist Eugen Bleuler. Bleuler saw the disease mainly in terms of four features: abnormal thought associations, autism (self-centeredness), affective abnormality, and ambivalence (inability to make decisions). Then in the 1930’s, another German psychiatrist, Kurt Schneider, contributed greatly to the diagnosis of schizophrenia by identifying “first-rank symptoms,” primarily related to hallucinations and delusions. Hearing voices speak one’s thoughts aloud, discuss one in the third person and describe one’s actions; feeling like an outside force is controlling one’s bodily sensations or actions and extracting, inserting, or stopping thoughts; believing that one’s thoughts are “broadcast” into the outside world – these are some of the experiences which Schneider found to be characteristic of the illness which Bleuler had recently renamed.
It should be noted that although Schneider’s first rank symptoms are essentially psychotic symptoms, (and schizophrenia is by definition a psychotic illness), very often those diagnosed with schizophrenia do not experience these symptoms. Diagnostic standards today distinguish between positive symptoms, (symptoms like hallucination and delusions which are not present in healthy individuals), and negative symptoms (e.g blunted affect, lack of fluent speech, inability to experience pleasure, lack of motivation). Anti-psychotic medications are often effective in treating some of the positive (i.e psychotic) symptoms of schizophrenia, but attempts to alleviate negative symptoms with medication have been largely unsuccessful, and the prognosis tends to be worse for sufferers who experience primarily negative symptoms.
By far the most authoritative and extensive work (over 1200 pages long) on that other half of madness is Manic Depressive Illness: Bipolar disorders and Recurrent Depression, written by Drs. Frederick Goodwin and Kay Redfield Jamison. The subtitle (Bipolar disorders and Recurrent Depression) added for the 2nd edition, (published in 2007), emphasizes the essential unity of all the major affective illnesses. In the introduction, the authors stress their reliance on Kraepelin’s model for their own conceptualization of mdi. (They, like Kraepelin, see it as a brain disease with genetics playing a significant causal role). But because Kraepelin’s major act of classification was to divide psychotic illness into two distinct disorders, any definition of mdi based on his work depends on having a clear definition of schizophrenia, which is clearly lacking. Kraepelin’s distinction between the two was based primarily not on differences in symptoms, but on course of illness and outcome, with schizophrenia (or in his terminology, dementia praecox) being much more malignant and causing significant deterioration over time. It was in fact Eugen Bleuler who first called mdi an “affective illness,” not because schizophrenia occurred without major mood disturbance, but because in mdi he saw it as “the predominant feature.” This characterization has proven to be extremely important for the current conception of major mental illness; the original distinction as between two psychotic illnesses has largely been obscured, and mdi is now viewed essentially as a mood disorder, with schizophrenia, by contrast, appearing to be essentially a thought disorder.
Though manic-depressive illness includes a variety of mood disorder diagnoses, the main distinction is between major depression and bipolar disorder (alternating episodes of depression and mania). A few decades ago, the bipolar label was split into bipolar-I and bipolar-II. Bipolar-I is the severe form of the disease in which both depressive and manic episodes are serious enough to require treatment. A diagnosis of bipolar-II may be given when a patient suffers from major depressive episodes and also experiences “hypomanic” episodes (meaning basically “mildly manic” and therefore lacking psychotic features). Even Goodwin and Jamison seem skeptical of the value of this and other divisions in classification.
In order to compare manic-depressive illness with schizophrenia, then, we should concentrate on descriptions of, (go figure), depression and mania. According to the DSM-IV, typical symptoms of depression include “loss of interest or pleasure in nearly all activity,” irritability, “changes in appetite and weight, sleep, and psychomotor activity; decreased energy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making decisions; [and] recurrent thoughts of death or suicidal ideation, plans, or attempts.” The description given by Goodwin and Jamison is along the same lines, though much more vivid:
Mood in all of the depressive states is bleak, pessimistic, and despairing. A deep sense of futility is often accompanied, if not preceded, by the belief that the ability to experience pleasure is permanently gone. The physical and mental worlds are experienced as monochromatic, as shades of gray and black. Heightened irritability, anger, paranoia, emotional turbulence, and anxiety are common. (MDI 66)
Further descriptions from patients and clinical observers add more layers to this general body of symptoms; among the most interesting, lack of facial expression, and a sometimes frightening sense of unreality. It is quite clear that depression is something altogether different from normal sadness, and even “abnormally low mood.” These descriptions show a huge variation in the level of emotion experienced, from almost no feeling at all, to unbearably acute anxiety. A depressed person’s thinking may be slowed almost to the point of paralysis, or he may alternately be unable to control an unending torrent of painful thoughts. All that seems consistent within descriptions and definitions of depressive episodes is that it is an extremely unpleasant experience.
There is such a diagnosis as psychotic depression, (featuring obvious delusions and hallucinations, in which case it is not clear how it can be diagnosed differently from schizophrenia) but even its more ordinary form, many of the symptoms of depression cannot be easily distinguished from the negative symptoms of schizophrenia, which include flat affect and paralyzed thought. And what good reason is there not to consider the firm belief in one’s utter worthlessness, the obsession with death, and the sense of the absolute necessity of ending one’s life as instances of delusion or thought disorder?
Just as depression is not just extreme sadness, mania is not an exaggerated form of joy. According to the DSM-IV, a manic episode is a period of “abnormally and persistently elevated, expansive, or irritable mood,” with typical symptoms being “inflated self-esteem or grandiosity, decreased need for sleep, pressure of speech, flight of ideas, distractability, increased involvement in goal-directed activities or psychomotor agitation, and excessive involvement in pleasurable activities with a high potential for painful consequences.” To be considered a manic (rather than merely “hypomanic) episode, “the disturbance must be sufficiently severe to cause marked impairment in social or occupational functioning or to require hospitalization or it is characterized by the presence of psychotic features.” Mood within a manic episode may be highly variable, and the frequent alternation between euphoria and irritability is noted.
Grandiose delusions are common – the extreme expression of the inflated sense of self-importance so typical in mania. (Again, one wonders why the beliefs which spring from the typical sense of worthlessness in depression – the polar opposite of the grandiose beliefs in mania – should not be considered delusions as well). Grandiosity often manifests in compulsive writing which the sufferer may believe has special significance but is usually characterized by “flight of ideas” and “distractability.” This behavior is not unique to mania, and has been well documented in patients diagnosed with schizophrenia.
Delusions may be not only grandiose, but, (as in schizophrenia), paranoid as well. In some severe cases, the sufferer may reach the stage of delirious mania, which the authors of MDI describe by quoting Kraepelin:
At the beginning the patients frequently display the signs of senseless raving mania, dance about, perform peculiar movements, shake their head, throw the bedclothes pell-mell, are destructive, pass their motions under them, smear everything, make impulsive attempts at suicide, take off their clothes. A patient was found completely naked in a public park. Another ran half-clothed into the corridor and then into the street, in one hand a revolver in the other a crucifix….Their linguistic utterances alternate between inarticulate sounds, praying, abusing, entreating, stammering, disconnected talk, in which clang-associations, senseless rhyming, diversion by external impressions, persistence of individual phrases are recognized. …Waxy flexibility, echolalia, or echopraxis can be demonstrated frequently. (36)
The descriptions of delirious mania provided by recent clinicians are similar to Kraepelin’s. Quite obviously, a patient in the condition described above is suffering from some of the most characteristic symptoms of schizophrenia. Of course for those following in Kraepelin’s footsteps, this similarity should come as no surprise, since (as was mentioned earlier) his distinction between the two psychotic disorders was not based on differences in symptoms. Indeed, the need to clarify the blurry boundary between psychotic mania and schizophrenia has resulted not in further distinction, but the creation of hybrid diagnostic categories like schizoaffective and schizo bipolar. In summarizing the findings of a number of studies over a thirty year span comparing thought disorder in schizophrenia and mania, Goodwin and Jamison are forced to conclude that there is no quantitative difference in thought disorder between the two conditions. Nevertheless, (needing to maintain the distinction between their area of expertise and the even more mysterious realm of schizophrenia) they maintain there are qualitative differences in thought disorder, though the studies used to support this claim point in a number of different directions. Of course, these studies were done only after patients received a particular diagnosis, so differences in thought disorder may also have been related to the effects of different medications. After considering the huge overlap between these two diagnoses, and the fact that differences seem to be more of degree than kind, it seems possible that perhaps they might not be two distinct diseases after all.
While the technological advancements of recent decades allow us to map the human genome and look at the brain on the molecular level, the enormous amount of data that has been amassed is virtually useless for psychiatrists trying to diagnose their sick patients because the assumed biological causes of schizophrenia and manic-depressive illness have not been found. No brain abnormalities that are specific to either illness or present in all cases have been identified. Nevertheless, the experts who study and treat schizophrenia and mdi keep the faith (quite literally) that a breakthrough is just around the corner.
For years, genetic research has appeared to be the most promising of the recently opened avenues, but the excitement seems unwarranted by the findings. The relatively large number of chromosomal regions which may be implicated in susceptibility for bipolar means that hope of finding a specific bipolar gene or even a small number of genes must be given up. Some researchers think the way to go is to narrow the search by looking for genes associated with specific aspects of the disease. Of course, this further refinement is only possible because of the huge variation in symptoms and experiences of those who fall under the mdi/bipolar umbrella, and we are once again reminded of the difficulty of defining what this illness or group of illnesses even is. Furthermore, even the distinction between schizophrenia and mdi seems to collapse in light of the genetic linkage data. Goodwin and Jamison write:
While the search for predisposing genes had traditionally tended to proceed under the assumption that schizophrenia and bipolar disorder are separate disease entities with different underlying etiologies, emerging findings from many fields of psychiatric research do not fit well with this model. Most notably, the pattern of findings emerging from genetic studies shows increasing evidence for an overlap in genetic susceptibility across the traditional classification categories. (49)
Genetic studies in the schizophrenia research community lead to pretty much the same hypothesis as with bipolar: genetic susceptibility is most likely polygenic, meaning dependent on the total number of certain genes which may contribute to vulnerability. It must be noted that genetic vulnerability is a condition, not a cause of schizophrenia and bipolar – something else must be acting on this vulnerability. In one way or another, this fact is usually noted in the literature that deals with genetic data, but it is often obscured by a tone of confidence which suggests the information may be more meaningful and explanatory than it truly is.
Even when a specific gene has been well studied across illnesses, its usefulness in understanding genetic susceptibility may be extremely limited. Some studies in both schizophrenia and mdi have found an increased risk of illness for those who possess the short form of the serotonin transporter promoter gene 5-HTT. The thing is, each of us has two copies of this gene, and over two-thirds of us have one long and one short form, meaning that having the normal variant of the gene is the risk factor! If most of us possess a gene which puts us at risk for an illness which only a small minority of people have, then this particular trait is obviously not much of a causal explanation.
Still today, the most important evidence for the heritability of schizophrenia and bipolar are traditional genetic-epidemiological studies – “genetic” research only in the sense that we know that relatives share genes. There is significantly greater lifetime risk of illness for people with a first degree relative who suffers schizophrenia, and studies of bipolar and major depression (i.e manic-depressive illness) have had parallel findings. However, the overwhelming majority of schizophrenics do not have parents or first-degree relatives with schizophrenia, and most of them do not have children themselves, making it difficult to establish the genetic component by looking at family history in a large percentage of cases.
Studies of twins are particularly important for the heritability argument. Calculations from these studies find a 63% risk of having bipolar disorder if an identical (monozygotic) twin has it. The risk for major depression is significantly lower. In schizophrenia the risk is under 50%. The ideal study design for attempting to separate the contributions of biology and environment involves identical twins, separated at birth, adopted, and raised apart, with at least one of them suffering from mental illness. As can be imagined, these cases are hard to come by (4 in mdi and 14 in schizophrenia), and the small number of cases makes generalization suspect (though generalizations are often still made). Another method, for which there is significantly more data, is to compare the risks of identical (monozygotic) and fraternal (dizygotic) twins. Because both kinds of twins are assumed to share the same environment, but fraternal twins only share 50% of their genes, the difference in risk between fraternal and identical twins is attributed to genetics. But this method depends on an extremely limited understanding of environment, reducing it to simply having the same parents. It’s likely that identical twins would be treated in very similar ways by their parents and society at large, but fraternal twins, being biologically different (perhaps even in gender) will likely be treated in very different ways. Therefore, it is highly doubtful that twin studies are able to separate the contributions of biology and environment to lifetime risk of mental illness to anywhere near the degree that is suggested. The fact that over one-third of identical twins are not affected by the disease from which their twin suffers reveals again that genetic susceptibility is at most a condition, and not a cause of schizophrenia and mdi.
The prevailing assumption that schizophrenia and mdi have biological causes naturally leads to the expectation of finding them distributed uniformly across cultures and throughout history. In the case of schizophrenia, this belief justifies the adoption of the standard worldwide lifetime risk of 1%, (a nice round number), extrapolated from an embarrassingly small number of studies – one from Germany in 1928, and two from the 1940’s in rural Scandinavian communities. However, there is a serious lack of evidence of the existence of these illnesses before the early modern period, and studies have consistently found significant differences in the rates of mental illness across cultures and between social classes within cultures. Nevertheless, (perhaps because the idea that serious mental illness may affect different populations at different rates does not sit well with us), variations are often explained away with charges of inaccurate reporting and under or over diagnosis. But epidemiological studies sponsored by the World Health Organization carried out over several decades have found that the illness identified as schizophrenia in poorer, “developing” countries tends to be less chronic (fewer psychotic episodes), causes less disability, and has a better prognosis than schizophrenia in more affluent, “developed” societies. Some of the data from Western nations suggests a lifetime risk of schizophrenia greater than 1%, while in poorer societies the number often appears lower. Multiple studies have found the rate of schizophrenia among Afro-Carribeans born in the UK to be higher than the prevalence in the islands from which their families immigrated. Both schizophrenia and mdi have been found to be less prevalent in Asian countries.
Overall, cross-cultural data supports the hypothesis that schizophrenia and mdi are diseases caused by modern culture, and more specifically, that the more anomic a society becomes, (i.e the more identity becomes a matter of individual choice and the less guidance is given by culture), the more mental illness will be found. Research in the U.S has shown a lower age of onset and higher rates of prevalence for manic-depressive illness in those born after 1944 compared to those born before, though this increase has been attributed to the inadequacy of earlier data-collection techniques, which systematically underestimated the true prevalence of affective disorders. Usually, when environment is allowed a causal role in mental illness, poverty and the stress of the urban environment is the safest target to blame, with studies as early as 1939 finding a higher incidence of schizophrenia in lower-class, urban areas. However, when studies began to consider social class of origin rather than merely the status of the patient when the illness was first recognized, the picture changed significantly. The social mobility of schizophrenic patients displays a “downward drift,” suggesting that their greater proportion among the lower class is due to the disability of the disease rather than the stress of this environment. Furthermore, it appears that the upper-class supplies more schizophrenics than could be predicted by the total upper-class share in the population. The majority of studies of manic-depressive illness show significantly lower rates in blacks compared to whites, but this, like so many other findings which make no sense within the biological framework, is dismissed for a variety of reasons as a mistake.
Finally, Goodwin and Jamison tell us that “the majority of studies report an association between manic-depressive illness and one or more measures reflecting upper social class.” (169) To explain this finding, they consider the possibility that certain personality traits associated with affective illness may contribute to a rise in social position. (One assumes they mean the occasionally “positive” aspects of mild mania, since it is unclear how crippling depression or delusional mania would aid in social climbing). A second hypothesis, that manic-depressive illness could be related to the particular “stresses of being in or moving into the upper social classes,” is deemed simply “implausible, because it assumes that, compared with lower classes, there is a special kind of stress associated with being in the upper social classes, one capable of precipitating major psychotic episodes.” Furthermore, they accuse such a hypothesis of ignoring genetic factors, though discounting genetic vulnerability as a condition for mdi is quite obviously not implied by this idea.
By now it should be quite clear that the belief that major mental illness is caused biologically has made it virtually impossible to reconsider what the empirical evidence actually tells us. Each time the research that is supposed to support this belief comes up short, it is another occasion for the reaffirmation of faith in a soon-to-come breakthrough. Where the data appears to blatantly contradict their hypothesis, they often simply discount its reliability. While many of the most important experts will freely admit how little we actually understand about mental illness, despite all efforts, it is hard to imagine the direction of these efforts will change much anytime soon. This is not a recipe for scientific progress.
The final post of this series will bring Greenfeld’s theory of the mind together with what we know about schizophrenia and manic-depressive illness, considering the two as one disease existing on a continuum of complexity of will-impairment.