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Functional retrograde amnesia (RA) is a rare pathology and has been rarely studied in detail across different patients. We extensively examined five functional RA patients and compared their neuropsychological profile including anterograde and retrograde memory performance, executive functions, emotional processing, and formally assessed psychiatric symptoms. Across patients, neuropsychological deficits beyond RA were most consistently seen in executive functions and attention suggesting that these dysfunctions contribute to the remote memory deficit. In a majority of the patients, problems in social cognition and emotional behaviour were reflected in Theory of Mind deficits and accompanying psychiatric symptoms. Aberrances in a measure of social desirability were detected, pointing to repressive tendencies in three out of the five patients. Future studies of functional RA patients may investigate more specifically which frontal-lobe associated (dys-) functions contribute to the memory retrieval deficit. Moreover, studying more closely the interaction between social cognition, repressive personality style and memory inhibition in this disease seems worthwhile pursuing.

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JL's injury. Apart from her memory impairments, JL's cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patient's relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JL's right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JL's remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.

We report a long-term follow-up study of case JM, who demonstrated a focal retrograde amnesia (FRA) as a consequence of cerebral vasculitis. The present study showed that, several years post-onset, JM experienced considerable impairment in episodic retrograde memory, with normal anterograde autobiographical memory. Further investigations demonstrated that she showed no evidence of accelerated forgetting, unlike some other cases of FRA. Knowledge of people, pre- and post-illness, was also normal. Her ability to recall details of famous public events was good (though weaker for pre-illness events). JM's pattern of impairment is discussed in the context of other recent cases of FRA and developments in models of normal memory function.

Recent functional neuroimaging studies have suggested that different neural substrates within the frontal lobes are associated with memory encoding, retrieval and monitoring. If this is the case, then it should be possible to find frontal patients with selective deficits to these processes. However, most laboratory based memory tests (e.g. Wechsler Memory Scale) require a combination of all these processes making it hard to find clear dissociations between patients. Using tests of everyday memory, this study documents a clear dissociation between a frontal patient's (JB) impaired ability to retrieve events from the anterograde period relative to spared ability to retrieve events from the retrograde period. This is consistent with specific disruption to frontal mechanisms associated with encoding which disrupts the formation of new episodic memories. The defective mechanism may be related to more general aspects of cognitive processing (e.g. selection demands), but it is unlikely to reflect damage to working memory (as assessed by the n-back task) as there is a clear dissociation between spared performance on this task and impaired performance on a comparable episodic recognition memory task.

We report on two patients, TH and KN, with focal retrograde amnesia (FRA). Their memory loss regarding life events extended to their whole lives, whereas they could acquire and retain new information. They also showed prominent deficits in production and comprehension of common words. In addition, at least in the testing situation, they were impaired in their recognition and use of familiar objects. Although both cases of FRA followed an episode that can cause brain pathology, MRI revealed no structural abnormality in either patient. Stressful situations preceding the onset were evident in KN, but not in TH. We discuss their impairments of object knowledge from a neuropsychological perspective, and we interpret the etiology of their condition as a functional rather than a psychogenic amnesia.

After a minor closed head injury, a 33-year-old man acquired extensive retrograde amnesia (RA) covering the previous ten years and concerning autobiographical, semantic and procedural memories. The patient's learning abilities remained excellent and he recovered considerable information from his wife, the media and personal documents. This relearned information did not, however, provide a sense of personal experience in the first weeks. CT and MRI failed to show brain damage, but EEG and SPECT examination showed a marked right temporal dysfunction. After three months the patient had almost completely recovered from RA. Interestingly, a parallel recovery was observed in the second SPECT obtained at this period. There was clearly a blockade of retrieval, while the stored engrams were probably intact. The mechanisms underlying such a functional amnesia are discussed in the light of previous reports of amnesia without brain lesions.

An extensive battery of tests of anterograde amnesia and remote memory was given to ten amnesics with lesions either to the medial temporal lobes of the diencephalon. These showed that the patients had anterograde amnesia with deficits in verbal and non-verbal recall and recognition, but preservation of word stem completion and intelligence. Mild impairments on executive tests and digit span performance were largely caused by the poor performance of the Korsakoff patients. The amnesics also showed remote memory deficits for personal and public domain information, and temporal gradients were observed for some of the tests. These deficits probably arose because the patients' anterograde amnesia was more severe than their retrograde amnesia even for the recent pre-morbid past. They were more impaired in the recall of details about famous names in their ability to recognize such names. There was also a suggestion that performance on anterograde tests did not relate strongly to that on tests of retrograde amnesia of the remote pre-morbid past. However, this effect was less apparent with memory for personal information when the format and the information tapped were matched on pre- and post-morbid tests.

A 19-year-old man showed dense retrograde amnesia (RA) for autobiographical and public events covering his entire life, following a motor car accident that caused no apparent brain damage. His learning abilities remained excellent and permitted him to recover knowledge of the past, based on information gathered from other people and the media, although he never reacquired the sense of personal experience. At the onset he also showed occasional gaps in his semantic memory, e.g., he failed to recognize a few objects and was unable to provide factual information about sports he had long been playing. Eventually, his amnesia was predominantly restricted to autobiographical events or facts. After 29 months the deficit has remained unchanged. CT, MRI and PET were negative. Psychogenic amnesia was considered, but eventually ruled out for want of any evidence pointing to emotional problems, stressful situations or secondary gains. We posit that for reasons unknown a mild trauma can cause functional inhibition of the access to the engrams that are already stored, leaving intact the ability to encode and retrieve new memories.

A selective, temporally limited retrograde amnesia, confined to autobiographical memory, was the only sequela of a "minor" head trauma in two young men. The retrograde memory gap covered about one year of life before the trauma and persisted for several months, without any anterograde deficit or other cognitive disturbances. This unusual pattern of retrograde amnesia deserves close consideration and points to the dissociation of memory subsystems and mechanisms.

This study examined the memory performance of patient RK who developed substantial memory impairments due to a hypothalamic glioma but in the absence of any evidence of frontal disturbance. RK was evaluated on both tests of anterograde and retrograde memory for temporal context. In the first experiment he exhibited marked deficits on a list discrimination task even when recognition performance was well within control range. Experiment 2 confirmed this disproportionate impairment of temporal order memory and showed that RK's list discrimination deficit was as severe as that found in alcoholic Wernicke-Korsakoff Syndrome patients. Experiment 3 showed that RK's temporal discrimination deficit was not a general deficit in discrimination because he performed normally on a spatial discrimination test of comparable difficulty to the temporal task. Experiment 4 examined RK's memory for deceased famous people and his ability to indicate the half decade in which they died. RK's performance was indistinguishable from controls whereas WKS patients were extremely impaired. This study adds to the view that frontal damage is not a necessary condition for impairment on anterograde measures of temporal context memory. However, further evidence from this study indicates that temporal judgments about pre-existing memories may depend on intact frontal lobe functioning.

The condition of focal retrograde amnesia represents a new and challenging concept to our understanding of human memory disorders. Cases of both permanent and transient focal retrograde amnesia, dating from early clinical descriptions to more recent experimental reports, are critically reviewed. It is concluded that the condition of focal retrograde amnesia does represent a distinct and reliable neurological entity. Four sets of issues are discussed--methodological issues, conceptual issues, anatomical issues and therapeutic issues. Current evidence indicates an important role for temporal lobe structures in mediating focal retrograde amnesia. Both storage and retrieval deficits may contribute to the presence of focal retrograde amnesia, though available evidence points to a greater role for engram destruction/fragmentation rather than disruption of access mechanisms. In general, pharmacological and other therapies have had minimal effects in alleviating focal retrograde amnesia.

A patient with an extremely long-standing low grade glioma affecting the left temporal lobe is described. The patient was almost entirely unable to retrieve the names of current personalities, although in other respects identification was unimpaired and nominal functions were only mildly inefficient. In particular geographical features and historical figures were generally appropriately named. The problem was equally severe whether naming was to confrontation, from description or by generation. A similarly severe impairment was also found for the retrieval of new words that had come into the language in the last twenty years (eg. aids). The impairment of retrieving people's names was interpreted in terms of a long-standing inability to form new associations between meaning and phonological word-forms.

The sudden resurgence of precise information some time after the failure of its recall (memory block) suggests the intervention of unconscious processes. In normal subjects the experimental demonstration of such processes meets with methodological snags. They are avoided in patients with a pure amnesic syndrome because retrograde amnesia produces many instances of missing memories, while anterograde amnesia prevents the patient from consciously thinking about it. Three patients with a pure amnesic syndrome were submitted to 4 interviews over 12 days on 3 topics concerning places and itineraries that were very familiar before the disease, and a shocking event of their life. Retrieved memories were compared to those of normal matched subjects. The results showed a dramatic increase for memories of places and itineraries over sessions, and the absence of improvement of autobiographical memories. These findings underline the role of the activation of unconscious processes in recall and the different status of semantic and episodic memory.