Cases reported "Amnesia, Retrograde"

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1/19. Postencephalitic focal retrograde amnesia after bilateral anterior temporal lobe damage.

    BACKGROUND: Marked retrograde amnesia with no or almost no anterograde amnesia is rare. Recently, a combination of ventrolateral prefrontal and temporopolar cortical lesions has been suggested as the cause of such isolated or focal retrograde amnesia. It is also assumed that when the right-sided cortical structures are damaged, autobiographical episodic memories are affected. OBJECTIVE: To search for new anatomic substrates for focal retrograde amnesia. methods: We performed extensive neuropsychological tests and obtained detailed neuroimages on a 43-year-old woman who showed a severe, persistent retrograde amnesia but only a limited anterograde amnesia after probable herpes simplex encephalitis. RESULTS: Tests of autobiographical memory revealed that she had a memory loss extending back to her childhood for both semantics and incidents; however, the ability to recall specific episodes appeared much more severely impaired than the ability to recall factual information about her past. The patient also showed profound impairments in recalling public memories; however, her scores improved nearly to a control level on forced-choice recognition memory tasks, although the recall of memories for a decade just before her illness remained mildly impaired. MRI revealed focal pathologies in the temporal poles and the anterior parts of the inferotemporal lobes on both sides, predominantly on the left, with some extension to the anterior parts of the medial temporal lobes. There was additional damage to the left insular cortex and its surrounding structures but no evidence of frontal lobe damage on MRIs or cognitive tests. CONCLUSIONS: A profound retrograde amnesia may be produced by damage to the bilateral temporal poles and anterior inferotemporal lobes in the absence of frontal lobe pathologies, and a dense and persistent episodic old memory loss can arise even with a relatively small lesion in the right anterior temporal lobe if it is combined with extensive damage to the left.
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2/19. Long-term retrograde amnesia...the crucial role of the hippocampus.

    For patients with hippocampal pathology, disagreement exists in the literature over whether retrograde amnesia is temporally limited or very extensive depending on whether the anatomical damage is restricted to this structure or also involves additional temporal cortex. We report a comprehensive assessment of retrograde and anterograde memory functions of a severely global amnesic patient (VC). We found that he presented with a remarkably extensive and basically ungraded retrograde amnesia. This impairment profoundly affected four decades preceding the onset of his amnesia and encompassed both non personal and personal facts and events. VC also presented with a severe anterograde amnesia and a deficit in the acquisition of new semantic knowledge in the post-morbid period. Detailed MRI volumetric measurements revealed gross abnormalities in both hippocampi which were markedly shrunken. Of relevance to the debate on retrograde amnesia were the observations that the volumes of both entorhinal cortices and the remainder of both temporal lobes were normal. These data suggest that the hippocampus is critical not only for the efficient encoding and hence normal recall of new information but also for the recall of episodic information acquired before the onset of amnesia. Our results are compatible with the view that retrograde amnesia is both extensive and ungraded when the damage is limited to the hippocampus.
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3/19. Right medial thalamic lesion causes isolated retrograde amnesia.

    Pervasive retrograde amnesia without anterograde memory impairment has rarely been described as a consequence of circumscribed brain damage. We report this phenomenon in a 33 yr-old, right-handed man (JG) in association with the extension in the right thalamus of a previously small, bilateral thalamic lesion. JG presented with a dense amnesia for autobiographical material more than a few years old, with some sparing of recent memories. Furthermore, he was completely unable to recognise famous people or world events. Many other aspects of semantic knowledge were intact and there was no evidence of general intellectual impairment, executive dysfunction or loss of visual imagery. magnetic resonance imaging revealed an acute lesion in the right thalamus and two small, symmetrical, bilateral non-acute thalamic lesions. Follow-up neuropsychological assessment indicated a stable pattern of impaired retrograde and spared anterograde memory over 18 months and psychiatric assessments yielded no evidence of confabulation, malingering or other symptoms to suggest psychogenic amnesia. JG's profile indicates that the division of declarative memory into just two categories - episodic and semantic - is inadequate. Rather, his case adds to the growing body evidence to suggest that world knowledge pertaining to people and events is stored or accessed similarly to autobiographical information and differently from other types of more general factual knowledge. We hypothesize that the right mediodorsal thalamic nucleus and immediately surrounding regions comprise the central processing mechanism referred to by McClelland (Revue Neurologique, 150 (1994) 570) and Markowitsch (brain research review, 21 (1995) 117) as responsible for inducing and co-ordinating the recall of these sorts of cortically stored memory engrams.
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keywords = visual
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4/19. Selective impairment of reasoning about social exchange in a patient with bilateral limbic system damage.

    Social exchange is a pervasive feature of human social life. Models in evolutionary biology predict that for social exchange to evolve in a species, individuals must be able to detect cheaters (nonreciprocators). Previous research suggests that humans have a cognitive mechanism specialized for detecting cheaters. Here we provide neurological evidence indicating that social exchange reasoning can be selectively impaired while reasoning about other domains is left intact. The patient, R.M., had extensive bilateral limbic system damage, affecting orbitofrontal cortex, temporal pole, and amygdala. We compared his performance on two types of reasoning problem that were closely matched in form and equally difficult for control subjects: social contract rules (of the form, "If you take the benefit, then you must satisfy the requirement") and precaution rules (of the form, "If you engage in hazardous activity X, then you must take precaution Y"). R.M. performed significantly worse in social contract reasoning than in precaution reasoning, when compared both with normal controls and with other brain-damaged subjects. This dissociation in reasoning performance provides evidence that reasoning about social exchange is a specialized and separable component of human social intelligence, and is consistent with other research indicating that the brain processes information about the social world differently from other types of information.
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5/19. Long-term amnesia: a review and detailed illustrative case study.

    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.
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keywords = cortex, visual
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6/19. Item recognition is less impaired than recall and associative recognition in a patient with selective hippocampal damage.

    This article explores the recall, item recognition, and associative recognition memory of patient B.E., whose pattern of retrograde amnesia was reported by Kapur and Brooks (1999; hippocampus 9:1-8). Structural magnetic resonance imaging (MRI) has shown that B.E. has bilateral damage restricted to the hippocampus. The structural damage he had sustained was accompanied by bilateral hypoperfusion of the temporal lobe, revealed by positron emission tomography (PET), and which single photon emission computed tomography (SPECT) suggested was greater in the left than the right temporal lobe. B.E. showed a global anterograde amnesia for verbal material, but he displayed some sparing of nonverbal item recognition relative to nonverbal recall and associative recognition. His performance on an item recognition task that used the remember/know procedure and another that involved repetition of the test phase, to reduce the difference between the familiarity of the targets and foils, suggested that his relatively spared nonverbal item recognition may have been mainly supported by familiarity. This finding is consistent with the view that the anterior temporal lobe, including the perirhinal cortex, can support familiarity-based memory judgments (Brown and Bashir, 2002; Philos Trans R Soc Lond B 357:1083-1095). B.E.'s data also highlight the importance of functional as well as structural scan information for interpreting the pattern of memory deficits shown by patients with selective hippocampal structural lesions.
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7/19. The dissociation of anterograde and retrograde amnesia in a patient with herpes encephalitis.

    Establishing the precise relationship between anterograde amnesia (AA) and retrograde amnesia (RA) has implications for psychological and neuroanatomical models of memory. Many patients have been described who demonstrate AA in conjunction with RA or who demonstrate AA with little, or no apparent, RA. Intact anterograde memory in conjunction with deficits on tasks of retrograde memory is rarely encountered. In this paper, we describe a young female patient (LD) whose RA is extremely severe when contrasted with her mild to moderate deficits on tasks of verbal anterograde memory. In addition, on tests of episodic and semantic autobiographical memory, LD appeared more impaired in her recall of specific episodes than of factual information about her past. The importance of this dissociation in RA for the episodic-semantic distinction and the possible role of visual imagery in recalling remote episodic events are discussed.
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ranking = 0.0061594847276386
keywords = visual
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8/19. Acute retrograde amnesia as first presentation in terminal metastatic cancer.

    A case is presented of a 2-week onset of acute retrograde amnesia as initial presentation, caused by presumed cancer. While acute retrograde amnesia has been reported in the literature, a report linked to cancer has not previously been published. An 82-year-old Caucasian woman presented to the emergency department, with 3-day history of increasing confusion and mild frontal headaches. Until 2 weeks previously she had been living on her own and coping with her activities of daily life. She believed very firmly that she was living with her husband in the house in which they lived in over 30 years ago. A magnetic resonance imaging scan demonstrated a lesion extending from cortex anteriorly to the right basal ganglia posteriorly. Postgadolinium enhancement was consistent with a diagnosis of a primary or secondary neoplasm. In some patients, cognitive behaviour changes or amnesia is the sole presenting feature of a serious underlying pathology. A lesion in either the temporal or frontal lobe can lead to this presentation. A family conference was convened and there was decision to take a conservative approach and not to investigate further. She was discharged to the care of her daughter and died 3 months later without return of her memory.
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9/19. Primary amnesia of insidious onset with subsequent stabilisation.

    A patient had a slowly developing amnesic syndrome that remained substantially unchanged during the two and a half years of observation. Intellectual skills were excellent and there was no language, perception, praxis, or calculation deficit. The memory impairment involved verbal and visual learning, sparing spatial learning and, to a large extent, retrograde memory. magnetic resonance imaging was normal, but PET showed a hypometabolism of the left temporal mesial region and thalamus. This case extends the spectrum of monosymptomatic cognitive disorders, previously reported in the area of language, praxis, and visual recognition, to amnesia.
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ranking = 0.012318969455277
keywords = visual
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10/19. Searching for the anatomical basis of retrograde amnesia.

    The case of a patient with profound retrograde and minor anterograde amnesia is described and used to discuss the kind of brain damage which will most likely result in persistent retrograde amnesia as the principal symptom. The patient was an industrial manager who had fallen off a horse four years prior to the present neuropsychological and neuroradiological investigation. MRI examination revealed an injury to both temporal poles and to the latero-ventral portion of the right prefrontal cortex. The prefrontal and temporal cortical damage on the right side deeply invaded the white matter while the temporal cortical damage on the left side was much smaller; here, however, portions of the temporo-parietal transition zone were affected as well. The patient was of average intelligence. His attention, short-term memory, and learning ability were average or somewhat below average. His old memories were severely affected in the personal-episodic domain, and much less so in that of semantic remote memory. We conclude from this case that the necessary anatomical substrate for the retrieval of old episodic memories lies within the anterior temporal regions (including deeper situated fiber projections) and possibly involves an interaction with the prefrontal cortex, and that this damage is dissociable from the medial temporal-lobe damage leading to anterograde amnesia.
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