PSYCHOGENIC AMNESIA IS a relatively rare disorder caused by psychogenic stress but accompanied by an unknown underlying neural mechanism, although it has been examined in several functional neuroimaging studies. In this report, we examined for the first time sequential changes in cerebral blood flow (CBF)-single photon emission computed tomography (SPECT) findings during the process of memory retrieval in a patient with psychogenic amnesia.
The patient in this report was a 31-year-old Japanese man who presented with psychogenic amnesia. He had just been released from prison after serving a 3.5-year sentence. He reported losing his wallet and concurrently becoming disorientated and not knowing who or where he was. Then he was admitted to our hospital on referral for treatment of amnesia. His neurological status and various laboratory investigations were unremarkable. A detailed psychiatric examination revealed psychogenic amnesia unaccompanied by other psychiatric conditions. His semantic memories were almost intact, but he lost all his life memories. About 1 month after hospitalization, he gradually began to recall his life memories. We conducted CBF-SPECT using N-isopropyl-p-[123I] iodoamphetamine (IMP) five times during the process of memory retrieval: (i) shortly after admission (10 days); (ii) early in the memory retrieval period (50 days); (iii) later in the memory retrieval period (86 days); (iv) soon after memory retrieval (114 days); and (v) later after memory retrieval (146 days). We then used 3-D stereotactic region of interest (ROI) template (3DSRT), fully automated ROI analysis software, to analyze the data. As detailed previously, we determined regional CBF (rCBF) in the corticosubcortical regions of each cerebral hemisphere for 12 ROI: callosomarginal, precentral, central, parietal, angular, temporal, posterior cerebral, pericallosal, basal ganglia, thalamus, hippocampus, and cerebellum.2 Although we did not perform any statistical analyses, rCBF as determined by 3DSRT could be categorized into three patterns: (i) transient increase during retrieval followed by increase after retrieval (callosomarginal and precentral ROI); (ii) transient increase during retrieval and then remaining almost constant or decreasing after retrieval (central, parietal, angular, pericallosal, and hippocampus); and (iii) remaining almost constant throughout the process or decreasing after retrieval (temporal, posterior cerebral, basal ganglia, thalamus, and cerebellum).
The continuous increase in frontal cortex rCBF after retrieval suggests that the function of this brain region might be inhibited by ‘dissociation’, which is the main pathology of psychogenic amnesia. Alternatively, an fMRI study indicated that active forgetting of unwanted memories was associated with increased prefrontal activation and reduced hippocampal activation. Therefore, the frontal rCBF findings indicating a transient increase during retrieval might reflect not only the recovery of dissociation, but also an active mental defense against unwanted memories of which the patient was not aware due to strong repression. In any case, further cases of functional imaging in psychogenic amnesia must be investigated before we can confirm or refute this speculation.