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There is much to be said for Nissen’s (2017) model of “hypochondria as an actual neurosis,” which sees the genesis of hypochondriacal anxieties as the end-product of a long series of defensive operations and a sign of an autistoid dynamic between the self, a malignant introject, and the hypochondriacally cathected organ—a model that seeks to integrate concepts due to Freud (1895, 1896, 1911, 1914), Winnicott (1971, 1974), Bion (1959, 1962, 1970), Rosenfeld (1958, 1964, 1971, 1987), Baranger, Baranger, and Mom (1988), and others. However, Nissen regards his model as primarily applicable to severe forms of hypochondria and hypochondriacal anxieties as a final substitutive formation directed against the unbinding of encapsulated contents resulting from earlier instances of traumatic collapse. In the tradition of Freud (1895), Klein (1932), Bion (1962), and Rosenfeld (1964), Nissen assumes that, in hypochondriacal anxieties concerning the body, a failure of the mechanism of projection drastically impairs the symbolizing function of the individual, so that the hypochondriac can undertake little or no symbolic elaboration of his psychic experience.
As a contribution to a discussion of this model I should like to outline an alternative conception of hypochondria (Rupprecht-Schampera 2003), to present some clinical examples of my own, and to consider some consequent objections.
Let me begin by anticipating some fundamental theoretical objections. First, there is in my view little point in devising a specific genetic or psychodynamic explanation for individual clinical pictures of a pathology—e.g. “a particularly severe form” of hypochondria. Instead, the requirement is for consistent investigation and description of the various forms of a pathology that appear phenomenologically to belong together “with a view to establishing their common denominator.” That is ultimately the only way to delimit and validate the field of a given complex of symptoms or indeed of a nosological c