Cases reported "Amnesia, Retrograde"

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1/33. Persistent kluver-bucy syndrome after bilateral thalamic infarction.

    OBJECTIVE: To describe a patient who exhibited a partial kluver-bucy syndrome after small bilateral ischemic lesions in the thalami. BACKGROUND: Previously reported patients with kluver-bucy syndrome had very large, mostly bilateral lesions in the limbic system and could not provide sufficient information about its anatomo-functional correlate. METHOD: Behavioral assessments and clinical examinations, including magnetic resonance imaging and positron emission tomography, were conducted. RESULTS: The patient was severely amnestic, distractible, hyperoral, and affectively dyscontrolled, and she behaved socially inappropriately. magnetic resonance imaging showed bilateral infarctions in the territories of both thalamoperforating arteries, and positron emission tomography revealed bilaterally decreased fluorodeoxyglucose uptake in the anterior parts of the ventral thalami and, to a lesser extent, in the fronto-temporal cortices. CONCLUSIONS: This behavioral syndrome has not yet been reported with isolated diencephalic lesions, but it has been observed after bilateral temporal lobe lesions. The authors conjecture that this syndrome resulted from a disruption of the pathways connecting the dorsomedial thalami with the prefrontal cortices and with other limbic areas, systems essential for memory and the regulation of impulses and emotions.
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2/33. 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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3/33. Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis.

    We describe a patient who developed a severe but temporally limited retrograde amnesia coupled with a relatively mild anterograde amnesia following herpes simplex encephalitis. The patient showed a profound retrograde amnesia for autobiographical events extending for about 10 years prior to the disease onset. Her knowledge about public events and famous persons was also impaired for this period. An MRI and SPECT demonstrated bilateral medial temporal pathology. This case represents a further instance of a relatively focal retrograde amnesia following brain damage. We review other reported cases with focal retrograde amnesia and consider theoretical and neuroanatomical accounts for the present case. Two factors may account for her amnesic patterns: a partial disruption of the store for premorbid binding codes (i.e., information that multimodal feature representations occurred synchronously); along with a relative preservation of the encoding process required to develop new synchronous codes.
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4/33. 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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5/33. Isolated and focal retrograde amnesia: a hiatus in the past.

    Two cases of isolated retrograde amnesia were reported. Both showed the same clinical pattern in development and resolution of amnesia despite of different etiologies. Sudden insult to the brain (trauma in Case 1 and viral encephalitis in Case 2) caused concurrent antero- and retrograde amnesia. Fortunately both recovered from the anterograde amnesia completely. However, both were left with a period of postictal amnesia of a few months and retrograde amnesia of up to 14 months' duration. The analysis of their pattern of temporal evolution and dissolution of amnesia support the hypothesis that recently acquired episodic information requires a certain amount of constant activation for a certain period of time in order to be organized into a durable memory. The nature of this activation as well as its origin remains to be solved.
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6/33. 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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7/33. 'I know your name but not your face': explaining modality-based differences in access to biographical knowledge in a patient with retrograde amnesia.

    In current functional models of person recognition it is proposed that there exists a single common body of semantic information concerning people accessible from all modalities (e.g. names, faces). In this paper, we present evidence that challenges this view. Two experiments are discussed investigating residual autobiographical and public knowledge in a patient suffering from retrograde amnesia. knowledge about people was investigated in each case by asking a series of questions, ranging from the very general to the very specific. Experiment 1 examined knowledge about famous people. The results showed that the patient accessed more information about famous people when cued with names than when cued with faces. Experiment 2 examined knowledge about people known personally to the patient. Again, the same pattern of results emerged. While the patient responded accurately to all questions posed with name cues, her ability to recall the same information when prompted with face cues was clearly inferior. This modality-based difference in accessing biographical knowledge is discussed in relation to models of person recognition.
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8/33. 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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9/33. Pure retrograde amnesia following a mild head trauma: a neuropsychological and metabolic study.

    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.
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10/33. Two cases of functional focal retrograde amnesia with impairment of object use.

    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.
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