Recovery from spontaneous confabulations parallels recovery of temporal confusion in memory.

BACKGROUND: In previous studies, the authors found that patients with spontaneous confabulation differ from those with nonconfabulating amnesia by 1) temporal context confusion (TCC) in memory based on an inability to suppress intrusions of currently irrelevant memory traces into ongoing thinking; and 2) lesions involving the orbitofrontal cortex, basal forebrain, or amygdala and perirhinal cortex. OBJECTIVES: To study the long-term clinical course of spontaneous confabulations, determine whether TCC in memory also parallels the clinical course of spontaneous confabulations, and study the impact of lesion site on clinical course. METHODS: Eight patients with spontaneous confabulation were re-examined 18 months after onset. Tests of memory and executive functioning and measurement of TCC in memory were again applied. MRI according to a standard protocol was performed to determine areas of permanent damage. RESULTS: Seven patients eventually stopped confabulating. TCC, but not common memory or executive tests, precisely paralleled the course of spontaneous confabulations. Patients with isolated, less extensive, orbitofrontal lesions stopped confabulating first and had the best neuropsychological outcome. Patients with basal forebrain lesions continued to confabulate for several months and remained amnesic. One patient with extensive orbitofrontal damage and perirhinal cortex damage continues to confabulate after more than 3 years, continuing to confuse memory traces. CONCLUSIONS: Temporal context confusion in memory is not only the sole feature reliably separating patients with spontaneous confabulation from those with nonconfabulating amnesia in the acute stage, it is also the only feature that precisely parallels the clinical course of spontaneous confabulations. Most patients eventually stop confabulating but duration of confabulations depends on the lesion site.

The mechanisms of spontaneous and provoked confabulations.

Confabulation is a mysterious adjunct of amnesia. It remains unexplained why some patients invent untrue stories in response to questions (provoked confabulations) or even spontaneously with no apparent motivation (spontaneous confabulations). Hypothesized mechanisms range from a desire to fill gaps in memory to a loss of the temporal context in memory. We examined the mechanisms of confabulations in 16 amnesic patients. Patients were classified as spontaneous confabulators if they ever acted according to their confabulations. Provoked confabulations were measured as the number of intrusions in a verbal learning test. We found a double dissociation between the two types of confabulations, indicating that they represent different disorders rather than different degrees of the same disorder. Confabulating patients did not show an increased tendency to fill gaps in memory as measured by the number of fake questions concerning nonexistent items that they answered. Neither type of confabulation correlated with a failure to store new information as gauged with recognition tasks; pure information storage was even found to be normal in some patients. However, we found a positive correlation between several measures of verbal learning and verbal fluency with provoked, but not spontaneous, confabulations. In contrast, spontaneous, but not provoked, confabulations were associated with an inability to recognize the temporal order of stored information as measured by the comparison of two runs of a continuous recognition task. We suggest that provoked confabulations depend on an amnesic subject's search in his deficient memory and are the trade-off for increased item recollection. Spontaneous confabulations appear to be based on a failure to recognize the temporal order of stored information, resulting in erroneous recollection of elements of memory that do not belong together.

Disorientation in amnesia. A confusion of memory traces.

Disorientation is a common phenomenon in delirium and amnesia. It is thought to have an obvious explanation, i.e. disoriented patients fail to store the information crucial for the maintenance of orientation. In this study, we explored whether disorientation was indeed associated with a failure to learn new information or rather with a confusion of information within memory. Twenty-one patients with severe amnesia were examined. Orientation was tested with a 20-item questionnaire. Two runs of a continuous recognition task were used to test the ability to acquire information (first run of the task) and the tendency to confuse the temporal context of information acquisition (comparison of the second with the first run). We found that orientation was much better predicted by the measure of temporal context confusion (r = 0.90) than by the ability to simply acquire information (r = 0.54). Superimposition of neuroradiological scans demonstrated that increased temporal context confusion was associated with medial orbitofrontal or basal forebrain damage; patients with normal levels of temporal context confusion did not have damage to these areas. We conclude that disorientation more often indicates a confusion of memory traces from different events, i.e. increased temporal context confusion, than an inability to learn new information. Disorientation appears to reflect primarily a failure of the orbitofrontal contribution to memory.