Chapter

Aetiologies and anatomy of confabulation

Armin Schnider

in The Confabulating Mind

Published on behalf of Oxford University Press

Published in print February 2008 | ISBN: 9780199206759
Published online February 2013 | e-ISBN: 9780191754487 | DOI: http://dx.doi.org/10.1093/med/9780199206759.003.0004
Aetiologies and anatomy of confabulation

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The reported data allow some consistent conclusions about confabulations in the different types of brain damage and about their anatomical basis.

There is no cause of brain damage and no known lesion area that always induces significant confabulation.

Overall, behaviourally relevant confabulation is a rare phenomenon. Even among the aetiologies generally regarded as the most important ones (ACoA aneurysm rupture, traumatic brain injury, avitaminosis), only a small proportion of patients, possibly three to five per cent, continue to confabulate notably beyond the confusional state.

Behaviourally significant confabulation (severe momentary, fantastic, and behaviourally spontaneous confabulation) is usually a transient phenomenon lasting days, weeks, or months. Amnesia often persists.

Provoked confabulations in the form of intrusions in memory tests have been reported in virtually all diseases discussed above, independently of the occurrence of other, behaviourally relevant confabulations. Their severity appears to increase together with the severity of cognitive and memory failures (Tallberg and Almkvist 2001; Cooper et al. 2006). Provoked confabulations do not appear to have anatomical specificity. It seems appropriate to treat intrusions (provoked confabulations in memory tests) as a non-specific sign of brain dysfunction, distinct from other forms of confabulation.

Fantastic confabulations of two different degrees have been described: 1. Wholly illogical, nonsensical confabulations defying any common concept of reality. Such confabulations have been described in the early literature in patients with advanced paralytic dementia (syphilitic general paralysis) and in patients with schizophrenia and other psychoses. In the latter cases, these confabulations were not normally associated with severe memory impairment. Early authors set this type of delusional fantastic confabulations apart from other confabulations and called them delusional interpretation (Wernicke 1900) or ‘illusions or hallucinations’ of memory (Bleuler 1923); 2. Similar confabulations, fantastic by their lack of connection with ongoing reality but intrinsically logic and composed of elements from the patients’ real past. Such confabulations were often described in the acute phase of diseases with known potential to induce severe confabulatory states (ACoA aneurysm rupture, traumatic brain injury). Some reported patients stopped confabulating once they were out of the confusional state, others then continued to produce behaviourally significant confabulations.

Elaborate momentary confabulation in the absence of a confusional state or advanced dementia has been described particularly often in diseases affecting the ventromedial prefrontal lobes (posterior medial orbitofrontal area and the basal forebrain), and the diencephalon, in particular the hypothalamus, occasionally the anteromedial thalamus (paramedian thalamic infarction). Specifically, many patients with severe and long-standing confabulatory states had suffered ACoA aneurysm rupture or traumatic brain injury. Fewer cases of similar severity and duration had herpes simplex virus encephalitis or surgery of a craniopharyngeoma. Patients with focal lesions of the anterior cingulate gyrus (Whitty and Lewin 1960) had only very transient states of de-realization. Lesions outside the area of the ventromedial prefrontal cortex and diencephalon (hypothalamus, paramedian thalamus) are not normally associated with marked momentary confabulation unless there is dementia or a confusional state.

The anatomical basis of behaviourally spontaneous confabulation has been explored across diverse aetiologies and in comparison with non-confabulating amnesics. The area of strongest lesion overlap was the ventromedial prefrontal area (posterior medial orbitofrontal and the basal forebrain, Figure 4.12). Other lesions involved other parts of the orbitofrontal cortex, the anterior hypothalamus, the amygdala on one side and the perirhinal cortex on the other side, and the genu of the right internal capsule. In summary, then, all lesions of behaviourally spontaneous confabulators included the posterior medial orbitofrontal cortex or other anterior limbic structures directly connected with it.

Chapter.  26451 words.  Illustrated.

Subjects: Psychiatry

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