A historical overview
12.2 Onset
12 Studying the natural history of psychopathology
William W. Eaton
Department of Mental Health, Bloomberg School of Public Health, John Hopkins University, Baltimore, MD, USA
to define and discern. The absence of firm data on the validity of the classification system enjoins us to be careful about operationally defining disease onset.
It is particularly difficult to establish the validity of a threshold for the presence versus the absence of disorder, because, from the clinical standpoint, subtle differences in a given clinician’s approach to treatment may suggest quite varied thresholds; from the epidemiologic standpoint, subtle differences in threshold may produce widely varying prevalences.
A simple definition is that onset occurs when the individual first enters treatment. A related definition is that onset occurs when a symptom is noticeable by a clinician. Another definition is the point when the symptom is first noticed by the individual. With the operational criteria of theDiagnostic and Statistical Manual(DSM), it is possible to conceive of onset as the time when full criteria are met for the first time in the life. This definition has been used in studies of incidence (e.g. [3, 4]). But it omits that part of the pathological process that takes place prior to meeting full criteria for disorder – the prodrome, as described below. Since the aetiological process may be extended in time, and the operation of aetiological factors distant, the definitions above, although capable of being operationalised, lack an explicit relationship to the pathological process.
Pathology occurs when the sociobiologic dynamics have become abnormal and signifies a distinct change in the relationship among variables, the new influence of variables that were not important beforehand or a new metabolism of some sort.
Onset is that point in time when the aetiological process becomes irretrievably pathological, that is, the point when it is certain that the full criteria for disorder will eventually be met. This point of irreversibility is difficult to observe. Focus on pop- ulation indicators for the force of morbidity leads to explicit consideration of the idea of a continuous line of development toward manifestation of disease with an as-yet-unknown point of irreversibility. At present we can only hypothesise where the disease begins, so that even the use of the word ‘symptom’
is problematic in the strict medical sense, since we cannot ascribe the complaint to the disease with perfect accuracy. Studying the natural history of psychopathology may, in the end, lead to the
conclusion that the disease concept is inappropriate or not useful, suggesting a shift to a more explicitly developmental framework [5, 6], with emphasis on normally distributed characteristics, and continuities in development, rather than rare dichotomies and discontinuities, which the disease model entails.
One way of thinking about the development toward disease is to focus on the increase in severity or intensity of symptoms. An individual could have all the symptoms required for diagnosis but none of them in sufficient intensity or severity as to meet the threshold for case definition. The underlying logic of this concept is that the relatively high frequency of symptoms at a mild level of intensity in the general population makes it difficult to distinguish normal and subcriterial complaints from manifestations of disease. For many chronic disorders, including psychiatric disorders, it may be inappropriate to regard the symptom as ever having been absent (for example, deviant personality traits on axis II of the DSM). This type of progression toward disorder is termed intensification and leads the researcher to consider whether a crucial level of intensity exists at which the development toward disorder becomes irreversible.
Figure 12.1 is an adaptation of a diagram used by Lilienfeld and Stolley [7, Figure 6.2], to visualise inci- dence as a time-oriented rate. The adaptation shows several distinct forms that onset can take when the disorder is defined by different levels of intensity or severity of symptoms. Compare cases No. 3 and No. 5, for example, which in the original diagram are situations of uncomplicated incidence. The bottom part of the figure shows how intensity represented by the vertical width of the bars, might be different for these two new cases. It also shows how there might be intensifications occurring that are stronger in mag- nitude than that associated with incidence, which would not be recorded as new cases (bottom two
‘cases’ in grey). Since the intensification of symptoms represents the force of morbidity in the population, use of a simple dichotomous measure of incidence will be misleading, unless the threshold of intensity is precisely where the pathologic process begins.
A second conceptual approach toward disease development is the occurrence of new groups of symptoms where none existed. This involves the
1 2
Wave 1 Wave 2
Existing chronic case
2 3
4
5
New case New case
New case with sudden onset 3
5 New case with gradual onset
Sudden onset but not a new case
1 Existing chronic, not new, case
Remitted case
with intensification For bottom of figure, let = Threshold of intensity for defining onset
New case, not discovered
Fig 12.1 Dichotomous view of onset (top) compared to symptom intensification (bottom).
gradualacquisitionof symptoms so that clusters are formed that increasingly approach the constellation required to meet specified definitions for diagnosis.
‘Present’ can be defined as occurrence either at the non-severe or at the severe level: thus, decisions made about the process of symptom intensification compli- cate this idea which focuses on symptom acquisition.
This leads the researcher to consider the order in which symptoms occur over the natural history of the disease and, in particular, whether one symp- tom is more important than others in accelerating the process.
Conceptualising the force of morbidity as time to a single dichotomous event (i.e. traditional concepts of incidence) is not flexible enough to deal with dimensional constructs, as shown in Figure 12.1.
It is also not flexible enough to deal with changes through time in the covariation of indicators, which can be an important aspect of the force of morbid- ity.Emergence is defined to be the development of new covariation of a group of symptoms to each other. Figure 12.2 shows a simplified view of this developmental phenomenon for the example of the depression syndrome. The vertical axis represents the intensity of mood disturbance, and the diagonal axis, slanting backwards from lower left to upper right, the intensity of somatic disturbance. Time is represented by the horizontal axis, passing from left to right.
At some early stage of development, the correlation
5 10 15 20 25
Disorder
Time (years)
Depressed mood
Precursors Prodrome
Somatic symptoms
R = 0.0 R = 0.2 R = 0.3 R = 0.4 R = 0.5
Fig 12.2 Acquisition of symptoms to covariation thresh- old of onset.
of mood to somatic disturbance is pictured as being 0.0 (round circle representing cross-sectional scatter plot with correlation equal to 0.0). Gradually the mood comes to be associated with the somatic dis- turbance, shown by the evolution of the circle into an ellipse. At this point, the normal and the abnor- mal have not split, and the disorder is not inevitable.
At this stage both mood and somatic disturbance predict imperfectly to later onset of major depressive disorder. Later, a group begins to emerge for whom mood and somatic disturbance are highly correlated.
Finally, there emerges a group with very high covari- ation of mood and somatic disturbance, and a second normal group where little covariation remains. An