Biological Psychiatry - Vol. 2

By Hugo D'Haenen; J.A. Den Boer et al. | Go to book overview

XIX-2
Aminergic Transmitter Systems

Neil McNaughton


INTRODUCTION

A fundamental goal of biological psychiatry should be the separation of symptoms from syndromes. It is clear, for example, that 'headache' is not an appropriate diagnostic category. You cannot use it to define the treatment of the underlying disorder giving rise to the symptom. Nor is the regular decrease in headache symptoms produced by aspirin or paracetamol evidence for common aetiology of the causes of headache or for an 'analgesic insufficiency' as the primary cause of headache.

This problem is particularly acute with mood disorders. In the case of depression, which at first blush seems more coherent as an entity than the spectrum of 'anxiety disorders',

'in the DSM-III the “choice principle” was introduced. For the
diagnosis of a particular syndrome the presence of X out of a
list of Y symptoms suffices, no matter which ones. Hence the
various disorders that are distinguished are symptomatologically
ill defined. In fact, many different syndromes carry the same
designation: major depression and dysthymia.… The utility of the
… discrete diagnostic entities characterized by multiple criteria …
is questionable. Our studies at least have failed to validate them.…
Another fundamental shortcoming … is the lack of an aetiological
axis [since] with today's methodologies, one can arrive at an
aetiological hypothesis with no less reliability as one can regarding
the presence or absence and severity of particular psychopathological
symptoms.… Another [problem] is that of [classification in the
presence of] comorbidity … For the diagnosis of major depression,
psychotic and organic conditions have to be ruled out. The diagnosis
of generalized anxiety disorder cannot be made in the presence of a
mood disorder.

This principle is not applicable in biological psychiatry. One can
and should not simply discart [sic] the possibility that a biological
variable observed in a psychotic condition is linked to a concurrent
depression, or one found in depression is in fact related to an anxiety
disorder.…

For [these] reasons I consider these concepts unsuited for [mood
disorder] research, particularly biological research, requiring as it
does well-defined and assessable diagnostic concepts.'

Van Praag (1995, p. 270)

The problem of comorbidity may be even more acute in the diagnosis of anxiety disorders. For example, panic and obsession, as disorders, may well have no necessary connection to anxiety as such. Rather, each may be an indirect cause of, essentially 'normal', anxiety when they occur (as unexpected, uncontrollable and bizarre events) in someone with a pre-existing sensitivity to threatening events. Conversely, both panic and obsession can occur as a simple, non-pathological, consequence of high levels of anxiety. Even this anxiety need not be pathological—consider the obsessive behaviour of a parent with a young and extremely mobile child at an airport.

Syndrome identification faces two additional problems. First, is a lack of connection between cause and treatment. A purely cognitively mediated post-traumatic stress disorder can nonetheless result in brain damage and require pharmacological treatment. Panic attacks resulting from a neural disturbance may be best treated psychologically—resolving the anxiety-related problems engendered by the panic attacks without completely eliminating the latter (Franklin, 1990). Other exclusion criteria, such as the exclusion by 'DSM-III-R [of] persons with socially phobic symptoms secondary to axis III conditions … [such as] disfiguring or disabling conditions [can lack] empirical basis.…[and cause] a patient group [to be] overlooked with regard to treatment options' (Oberlander, Schneier and Liebowitz, 1994).

A final problem for diagnosis is that the grouping of 'anxiety disorders' as a single class in DSM-III, DSM-IIR and DSMIV seems inappropriate from the point of view of pharmacology or preclinical analysis of brain systems. These suggest that the different symptomatologies and therapeutic responses of patients presenting with 'anxiety disorders' reflects a confusion of diagnostic categories. Diagnoses should, but currently do not, reflect the primary brain systems that are dysfunctional in any particular case. Symptomatology must often reflect the brain systems, whether functional or dysfunctional, that have extremes of activity. For both these reasons, brains systems will be the focus of the next section.

The most significant aminergic neurotransmitter systems for anxiety and the conventional grouping of anxiety disorders are the monoamines serotonin and noradrenaline. As discussed in the section entitled 'The Neuropsychology of the aminergic systems' basic research implicates them as modulators of the entire defense system with a clear contribution to anxiety — in the sense that this can be distinguished from fear (Blanchard et al., 1988, 1991, 1997). Drugs that manipulate them have therapeutic effects that usually span several of the different types of anxiety disorder (den Boer et al., Chapter XIX-13). Finally, disturbances of their metabolism appear to play a significant role in the generation of anxiety disorders (see below). A weaker case can, also, be made for dopamine. The preclinical review below will also include consideration of acetylcholine because, although not a monoamine, it shares many of the anatomical and functional features of the monoamines.

The primary conclusion is that the success or failure of treatment with a particular drug is likely to reflect the secondary impact of alteration in monoamines on primary brain systems more often than an original disturbance of monoamines was the primary basis of the symptomatology.


THE NEUROPSYCHOLOGY OF ANXIETY

The view of the neuropsychology of anxiety disorders in this chapter is justified at great length in Gray and McNaughton

-895-

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