Functional anatomical study of psychogenic amnesia

Abstract

Psychogenic amnesia is characterized by an inability to recall information already stored in the patient’s memory. It is usually related to a stressful or traumatic event that cannot be explained by manifest brain damage. To examine the underlying functional disturbance of brain areas in this condition, we performed a positron emission tomography (PET) activation study on a psychogenic amnesic patient and on 12 normal control subjects. A task requiring explicit retrograde memory of faces was compared with a control task. To assess functional modifications associated with the processes of recovery, a second PET study was performed on the patient 12 months after onset. During the task, activation of the right anterior medial temporal region including the amygdala was increased in the psychogenic amnesic patient. Activation of the bilateral hippocampal regions increased only in the control subjects. During recovery, the right anterior medial temporal region became less active while the right hippocampal region became more active. Activation levels also differed in the anterior cingulate cortex, prefrontal cortex and some other cortical regions between control subjects and the patient. These findings suggest that the changes in these limbic and limbic–cortical functions are related to symptoms of the psychogenic amnesia.

Introduction

Psychogenic amnesia is characterized by an inability to recall information already stored in memory, and is usually related to a stressful or traumatic event that cannot be explained by manifest brain damage (Markowitsch, 1995). The diagnosis usually relies on features such as circumstances of onset, loss of personal identity (rare in organic amnesia except in advanced dementia), and whether or not new learning is affected (often spared in psychogenic amnesia). Semantic knowledge often remains intact, but is occasionally implicated. Memory for skills is often preserved (Kopelman, 1987).

Which neuronal mechanism underlies psychogenic amnesia is questionable. The only reported neuroimaging study of a psychogenic amnesic patient during amnesia is that by Markowitsch et al. (1997). Their patient experienced retrograde amnesia following personal financial problems. They studied episodic memory retrieval by measuring PET blood flow in the patient 6 months after the onset of symptoms. Compared with the results of previous functional imaging studies on episodic memory retrieval, their findings suggested an underlying functional disturbance of brain areas known to be involved in episodic memory retrieval. Limitations of this research were that their patient had some evidence of an organic background, and that their episodic memory task was restricted to new learned matter and did not relate directly to retrograde memory retrieval. Furthermore, they did not have normal control individuals perform their task, thus making their results from the patient not strictly comparable to that of control subjects.

We describe a psychogenic amnesic patient who experienced retrograde amnesia following a stressful event, and who had no evidence of an organic background. To examine underlying functional disturbances of brain areas involved in this condition, we performed positron emission tomography (PET) activation studies on the patient and on 12 normal control subjects. A task requires explicit retrograde or semantic memory components (Kapur et al., 1995). We applied the same task and materials to both the patient and control subjects, so that the results could be directly compared. To assess the functional modifications associated with the processes of recovery from amnesia, a second PET study was performed on the same patient 12 months after onset.