Phenomenology of acute confusional states

I read with great interest the paper by Dr Fleminger (2002) on delirium, and the relevant controversy raised by Dr Philpott regarding to whom should be attributed the first description of hypoactive delirious states (Philpott, 2002). May I suggest that this initial description was made around one century earlier than mentioned by both authors. In fact, as early as 1892 the French alienist Philippe Chaslin borrowed the term of ‘confusion mentale primitive’ from a previous description proposed by Delasiauve during the 1850s. He was probably one of the first authors who gathered under a unified entity what was previously described under separate clinical features as psychosis post-influenza, post-acute diseases, post-fever and epilepsy (Chaslin, 1892). He also clearly noticed its similarity with what Lasegue had described earlier as delirium tremens, in which perceptual disturbances were considered as a dream-like experience (Lasegue, 1881). In his later monograph, Chaslin describes the acute confusional state as ‘an acute brain disorder, consecutive to an organic significant disease, with cognitive impairment associated with delusions, hallucinations, psychomotor agitation, or reciprocally, with psychomotor retardation and inertia’ (Chaslin, 1895). Despite this very early description of what has since been called hyperactive and hypoactive subtypes of delirium, there have been very few attempts to test the validity and the relevance of these subtypes. To our knowledge, at this time only one empirical exploration of what are the constitutive symptoms of each dimension has been proposed (Camus et al, 2000). We would like to add, concerning what Fleminger cites as possible psychological consequences of confusional experience, that another French alienist described ‘permanent ideations’ and ‘chronic delusional states’ following the post-dream-like confusional experience (Regis, 1911). We agree with Fleminger's assumption that hyperactive subtypes are among the most stressful confusional experiences because of the possible persistence of memories of perceptual disturbances beyond the full recovery of consciousness and arousal, and beyond the normalisation of the sleep—wake cycle. But it remains unclear what factors are associated with such persistent difficulties in overcoming the dream-like experience. We hypothesise that they could be related to the implication of some specific neurobiological pathways, but their potential relationship with some premorbid personality traits should also be explored. Finally, as long as the pathophysiology of delirium is poorly understood, research into biological markers such as cerebrospinal fluid levels of neuropeptides (Broadhurst & Wilson, 2001) should be correlated to all different aspects of delirium phenomenology.