When Kraepelin originally defined and described dementia praecox, he assumed that it was due to some type of neural mechanism. He hypothesised that abnormalities could occur in a variety of brain regions, including the prefrontal, auditory, and language regions of the cortex. Many members of his department, including Alzheimer and Nissl, were actively involved in the search for the neuropathological lesions that would characterise schizophrenia. Although Kraepelin did not use the term ‘negative symptoms', he describes them comprehensively and states explicitly that he believes the symptoms of schizophrenia can be explained in terms of brain dysfunction:

The existence of a definable and distinct negative syndrome within schizophrenia remains to be established (Barnes & Liddle, 1989). Addressing this issue, Sommers (1985) discusses three stages required to demonstrate validity for a syndrome. These are first, that the signs and symptoms must be shown to occur together. Second, operational definitions must be developed which will reliably identify and rate and features, and third, the relationships between the syndrome and other variables must be shown to be predictable. With respect to the second and third stages, this paper reports briefly on two recent studies which explored the relationship between negative features and other clinical features, specifically depressive symptoms and drug-induced movement disorder. The results of such studies (see also McKenna et al; and Lindenmayer & Kay, this volume) allow some assessment of the ability of the rating methods used to discriminate between negative symptoms and features such as drug-related bradykinesia and depressive features.

If negative symptoms represent a distinct class of schizophrenic symptoms, they should, to paraphrase Bleuler (1911), be more closely related to each other than they are to other schizophrenic symptoms. The first part of this statement, that negative symptoms are intrinsically related to each other, has received considerable experimental support (Andreasen, this volume; Mortimer et al, this volume). The second, that negative symptoms are unrelated to other schizophrenic symptoms, has been somewhat more unevenly investigated.

The relationship of depression with affect deficit in schizophrenic patients continues to challenge both the clinician and the researcher. Often there is considerable difficulty in differentiating these two affect states in a reliable and valid fashion. On the observational level, depressed affect often appears somewhat restricted, having lost the full range of the euthymic state. On a subjective level, schizophrenic patients often complain of anhedonia, a defect in pleasure capacity which is shared by patients who are depressed. On the prognostic level, there is a large body of literature that links depressive features in acute schizophrenics to favourable subsequent course (Astrup & Noreik, 1966; Vaillant, 1964). We were, therefore, interested in investigating the relationship of depression with impaired affect and with positive/negative symptoms in young acute schizophrenic patients. We used a systematic multidimensional study of affect impairment among 37 young acute schizophrenic patients in a prospective, longitudinal approach over a 2-year span. In addition to a detailed assessment of the affect profile, including depression, both at baseline and on follow-up, we rated patients clinically for a positive and negative syndrome as well as general psychopathology, and we conducted premorbid and outcome measurements.

The introduction of neuroleptic (or anti-psychotic) medication into clinical practice was a major advance in the treatment of schizophrenia. Numerous well-controlled, double-blind clinical trials have established the therapeutic efficacy of these agents in both the acute and long-term treatment of schizophrenia (Klein et al, 1980; Kane & Lieberman, 1987). In general, the therapeutic benefit of medication has been assessed in terms of the relative reduction in the more florid signs and symptoms of schizophrenia (e.g. hallucinations, delusions, thought disorder, agitation, and hostility) and the ability of maintenance medication to reduce the rate of recurrence of these symptoms and in turn rates of rehospitalisation. At the same time it has been quite apparent that anti-psychotic drugs do not necessarily eliminate some of the major chronic disabilities of patients with this illness, disabilities reflected in impoverished affect, lack of drive and ambition, impaired spontaneity, reduced ability to relate to others, and diminished pleasure capacity. These symptoms have at times been described as negative in that they reflect an absence of or reduction in certain aspects of psychologic, cognitive, and emotional functioning in an attempt to distinguish them from the distortions or exaggerations in normal function which characterise positive symptoms (Strauss & Carpenter, 1974; Jackson, 1904).

In recent years, exploration of the distinction between positive and negative symptoms of schizophrenia has provided a fruitful basis for attempts to relate the clinical features of schizophrenia to the accumulating evidence of brain abnormalities in schizophrenic patients. By 1982, there was an extensive body of evidence supporting the hypothesis that negative schizophrenic symptoms, such as poverty of speech and flatness of affect, were associated with substantial brain abnormalities, such as increased ventricular to brain ratio, and extensive cognitive impairment (Crow, 1980; Andreasen & Olsen, 1982). However, at that stage there were several fundamental unanswered questions about the nature of negative symptoms, and their relationship to indices of brain abnormality. This paper presents some findings of a series of studies initiated in 1982 to seek answers to some of these questions.

As is evidenced by this special supplement of the British Journal of Psychiatry, negative symptoms have become the focus of an increasing research effort. We have recently reviewed this overall body of research in an attempt to understand its current status and to suggest directions for future work from a broad perspective (Pogue-Geile & Zubin, 1988). In contrast, the aim of this paper is to review concisely one specific aspect of this research — namely the prognostic and longitudinal characteristics of negative symptoms. Research findings on this general topic will be reviewed by addressing a series of more specific subquestions, which are outlined below. Throughout, the potential importance of when in the course of the disorder (i.e. during an acute episode or afterward) negative symptoms are assessed will be emphasised (Kay et al, 1986b).

Our reintroduction of the concept of negative symptoms in schizophrenia (Strauss et al, 1974) has been followed by much productive research on this topic. As in the work of Andreason, Crowe, and others, the focus of most of this research has been on improving descriptive assessments of these symptoms (Andreason, 1982) and exploring their biological correlates (Crowe, 1981). This work has been extremely important, but psychological and social aspects of negative symptoms are also important (Barton, 1959; Wing & Brown, 1970; Gruenberg, 1967), and in these areas there has been little research. Nevertheless, it is crucial to explore possible psychological and social factors in negative symptoms in order to understand the symptoms more fully and to provide a basis for more adequate prevention and treatment. It is also important to clarify psychological and social factors in these symptoms to provide a basis for more effective biological research, since the heterogeneity of negative symptoms at a psychological level could hide significant biological correlates.

The subject matter of this paper is the psychological treatment of negative symptoms. However, before embarking on a review of the available literature, it is worthwhile considering some conceptual issues and distinctions which are relevant to research in this area.