Confabulation, sometimes called “honest lying” is a cognitive phenomenon that can be seen in several acquired neurological conditions as well as in some psychiatric disorders.

Although the term confabulation is currently used to refer to false perceptions of body states or the external world (non-mnesic confabulations), it has traditionally referred to false products of the memory (mnesic confabulations) [1].

Confabulation is a complex phenomenon that lacks a consensual definitionor well-established classification criteria of the different types that have been described and whose explanatory models are still under debate [1, 2].

This article is the first of two installments on the phenomenon of confabulation in which the phenomenology, neuropathology and cognitive mechanisms and theoretical models that have been proposed to explain it will be briefly reviewed. Theoretical models will be addressed in the second part.

What do we mean by confabulation? concept and classification

Since the term confabulation first appeared in the works of Kahlbaum [3] and Wernicke [4] towards the second half of the nineteenth century, there have been multiple definitions and interpretations of this concept, which has evolved over time and is linked to the debate regarding its etiology and other closely related cognitive phenomena [2].

Broadly speaking, three definitions of confabulation have been discussed in the literature, depending on which aspects is considered essential:

1. Mnemonic, related to memory.
2. Linguistic, in which the character of incorrect verbal statement or false narrative is emphasized.
3. Epistemic, in which the subject does not question the ill-grounded claim, and this claim is not necessarily of a linguistic nature [1].

A recently proposed working definition of confabulation [5] describes them as false memories due to a retrieval problem, where the patient is unaware that he/she is confabulating and has the belief that the memory is true. From this viewpoint, the core characteristics of confabulation are:

• They are false memories within the context of retrieval that often contain false details within its own context as well (some confabulations may be true memories displaced in time, while others seem to lack any basis in reality).
• Confabulations are not intentionally produced since the patient is not aware that he/she is confabulating, and often is not even aware of the existence of a memory deficit; thus, confabulations are probably not the result of compensatory mechanisms.
• Patients may act upon their confabulation, reflecting their genuine belief in the false memory.
• Confabulations are more apparent when autobiographical recollection is required; in addition, under certain conditions of testing, they may also appear on semantic memory tasks [1].

There have also been several proposals regarding the classification of different types of confabulation. Now, a widely accepted classification is the one suggested by Kopelman [6], who distinguished between spontaneous and provoked confabulations.

• Spontaneous confabulations are rare and related to an amnesic syndrome superimposed on frontal dysfunction.
• Provoked confabulations are common in amnesic patients when given memory tests

Another popular classification in the literature distinguishes between momentary and fantastic confabulations [1].

• Momentary confabulations are described as brief and fleeting; they are also“invariably” provoked by questions probing the subject’s memory, and consisting of “real” memories displaced in their temporal context.
• Fantastic confabulations are spontaneous, sustained, wide-ranging, grandiose, and readily evident in the subject’s everyday conversation.

Neuropathology of confabulations

Confabulations can be found in a wide variety of disorders, including acquired disorders (e.g., CVA, traumatic ABI, hypoxia, cardiopulmonary arrest, etc.), degenerative diseases (dementia), and even psychiatric disorders such as schizophrenia and other psychotic disorders. However, confabulation is most common among patients with Korsakoff syndrome and those with ruptured aneurysms of the anterior communicating artery (ACoA)[1].

Regarding the neuropathology of Korsakoff syndrome, it has been argued that in patients with this syndrome there are two dysfunctional systems: in the first system, the severe amnesia that characterizes this conditionis ascribed to the mammillary bodies and the anterior thalamic nuclei lesions, as these structures receive hippocampal afferents via the fornix; on the other hand, the dorsomedial thalamic nuclei are reciprocally connected with orbitofrontal and medial areas of the frontal cortex, and receive input from cortical and subcortical structures (the amygdala and the basal forebrain); these structures comprise a second dysfunctional subsystem, which may be more closely related to the production of confabulations[1].

With regards to the pathology of patients with ruptures of aneurysmsof the ACoA, studies with amnesic patients who confabulated found lesions in the basal forebrain and orbitofrontal and medial areas of the prefrontal cortex [1].

A recent review [1] concluded that damage tothe orbitofrontal and ventromedial areas of the prefrontal cortex appear to be sufficient for confabulation, while another review mainlyfocusedon spontaneous confabulations [2] concluding that current evidence identifies four areas involved in this type of confabulation: the medial orbitofrontal cortex and its connections withthe amygdala, the cingulate gyrus, the dorsomedial nucleus of the thalamus, and the medial hypothalamus.

Cognitive mechanisms of confabulations

In summary, three cognitive mechanisms have been proposed to explain confabulation:

1. Confabulation has traditionally been attributed to memory impairment alone.
2. Deficits in executive functioning are necessary and sufficient to produce confabulation.
3. Dual hypothesis: some authors have suggested that a combination of memory impairment and executive dysfunction is essential to produce confabulation.

Recent models favor the dual hypothesis [1], hence confabulations are not the result of compensatory mechanisms due to memory decifits or amnesia but the consequence of a certain degree of impairment in memory systems and a certain degree of dysfunction in executive processes.

However, the specific contribution of executive and memory deficits in the production of confabulation and their role in the different types of confabulation remains to be clarified.

One last issue to highlight is that several studies in this field have used different memory tests and executive tasks which evaluate different executive processes and different memory subsystems, making it virtually unfeasible to compare the results of the various studies to draw conclusions.

Bibliographical references

1. Lorente-Rovira E, Berrios G, McKenna P, Moro-Ipola M y Villagrán-Moreno JM (2011). Confabulaciones I: concepto, clasificación y neuropatología. Actas EspPsiquiatr, 39(4):251-9.
2. Glowinski R,Payman V &Frencham, K. (2008). Confabulation: a spontaneous and fantastic review. Australian and New Zealand Journal of Psychiatry, 42:932-940.
3. Kahlbaum K (1863). Die Gruppierung der psychischen Krankheitenund die Eintheilung der Seelenstörungen. Danzig: AW Kafemann (Part III, trans. Berrios GE, HistPsychiatry1996; 7:167181.)
4. Wernicke K(1906).Grundriss der Psychiatrie, 2nd edn. Liepzig: Thieme.
5. Gilboa A, Alain C, Stuss DT, Melo B, Miller S, Moscovitch M. (2006). Mechanisms of spontaneous confabulations: a strategic retrieval account. Brain, 129:1399-414.
6. Kopelman MD (1987). Two types of confabulation. JNeurolNeurosurgPsychiatry, 50:1482-7.