Amnesic Syndrome Research Articles

Thalamic Amnesia Following Venous Infarction: Evidence from a Single Case Study

The present paper describes the case of a right-handed Italian–English bilingual male patient suffering from amnesia following a bilateral thalamic lesion due to venous infarction. Within a few months from the onset, the lesion gradually shrank and was finally confined to the left thalamus only, in particular to the antero-medial portion and the pulvinar. The mammillary bodies and the cortical areas of both hemispheres were spared. After the regression of a series of generalized cognitive deficits implying slow psychic activity, confusion, and spatial and temporal disorientation, the patient presented a persistent amnesic syndrome with mild language disorders, both in Italian and in English. Major disorders of memory included a dissociation between verbal memory, which was severely impaired, and spatial memory, which was largely preserved.

Correlation of lesions in the hippocampal region noted on MR images with clinical features.

The purpose of our work was to compare the MR imaging findings of obvious hippocampal and/or juxtahippocampal lesions with corresponding clinical features. Magnetic resonance images of 63 patients with obvious lesions in the hippocampal and/or juxtahippocampal regions were reviewed and their findings were correlated with patients' clinical characteristics. Based on the MR and clinical findings, the patients were divided into four groups: (a) 26 patients with space occupying lesions or suspected vascular malformation frequently causing symptomatic temporal epilepsy; (b) 14 with hippocampal infarcts, which when left-sided or bilateral caused amnesia; (c) 11 with encephalitis and 5 with old temporal contusion usually accompanied by both amnesia and epilepsy; and (d) 7 with temporal atrophy and progressive dementia of subacute onset. Magnetic resonance imaging allows precise localization and evaluation of the clinical correlates of hippocampal and juxtahippocampal lesions, which frequently caused symptomatic temporal epilepsy and/or amnesic syndrome.

Co-Occurrence of Executive Impairment and Amnesic Syndrome Following Sub Arachnoid Haemorrhage: A Case Study

This case study presents a 37 year old man, P.P., who shows evidence of both profound executive impairment and diencephalic amnesia associated with two discrete lesion sites following a Sub Arachnoid Haemorrhage. The executive impairment is unusual in type and severity, amounting to a gross impairment in the initiation and organisation of action. The thalamic lesion provides a rare example of diencephalic damage resulting in an extensive retrograde amnesia of the type that is often associated with Korsakoff's syndrome, but which in this case is not associated with prolonged alcohol abuse. Some of the problems caused by the co-occurrence of two such profound and disabling impairments are discussed.

The Relationships Between Temporal Lobe and Diencephalic Structures Implicated in Anterograde Amnesia

The relationship between the anterograde amnesic syndromes associated with diencephalic and temporal lobe pathology is examined in the light of recent findings. It is proposed that a common feature of anterograde amnesia is damage to part of an “extended hippocampal system” comprising the hippocampus, the fornix, the mammillary bodies, and the anterior thalamic nuclei. Damage to this system results in deficits in the recall of episodic information, the core symptom of anterograde amnesia. In contrast, lesions in this system need not disrupt tests of recognition memory when they primarily tax familiarity judgements. It is assumed that familiarity judgements depend on other regions (e.g. the rhinal cortex in the case of temporal lobe amnesia) and that the extended hippocampal system is principally involved in those aspects of recognition that are retrieval-based rather than familiarity-based. These proposals arise from new evidence on the performance of delayed nonmatching-to-sample by animals, from a meta-analysis of the performance of amnesic subjects on a test of recognition memory, and from new research into the pattern of connections between the medial temporal lobe and the medial diencephalon in primates.

Predicting Syndromes of Amnesia from a Composite Holographic Associative Recall/ Recognition Model (CHARM)

The composite holographic associative recall/recognition model (CHARM) is used to predict the amnesia syndromes that are expected under conditions of discrete lesions to different components of the model. The components that are needed to allow recognition, recall, and rehearsal are: (1) perceptual/lexical processing and pattern identification, (2) consciousness or working memory, (3) association formation, (4) composite storage, (5) novelty monitoring and control, and (6) retrieval. Deficits in each of these components will have specific effects on memory, generating characteristic profiles of performance. Comparison of the profiles exhibited by patients to the component-based profiles predicted by the model identify the component impaired in a given patient, and connect the memory impairments to the underlying infarcted brain structures. The model, thus, relates the memory tasks to the particular memory components that allow enactment of those tasks, and shows how the dysfunction of particular components produces specific impairments.

Amnesic syndrome with a unilateral thalamic lesion: a case report

Amnesic syndrome with a unilateral thalamic lesion: a case report

Amnesia in acute herpetic and nonherpetic encephalitis.

To evaluate how often global amnesia syndrome is encountered as a sequel of herpes simplex virus type 1 encephalitis (HSVE) and in other types of acute encephalitides, and to evaluate whether there are qualitative differences in amnesia caused by different encephalitides. Forty-five consecutive patients with encephalitis (mean age, 40.8 years) studied prospectively within a 5-year period, 8 of whom had HSVE. There were 24 normal controls. Neuropsychological assessment and memory evaluation after the acute stage of encephalitis, as well as at follow-up after 27.7 +/- 18.6 months. Three patients (6%), including 1 with HSVE, had persistent anterc grade and retrograde memory defects, typical features of global amnesia. Twelve patients had anterograde amnesia in the first assessment. No statistically significant differences in the memory measures were found between the HSVE (n = 4) and the non-HSVE (n = 8) groups. Some patients had predominantly semantic difficulty, some had a "frontal-type" memory disorder, and in some patients rapid forgetting was the prominent feature. The frequency of amnesia can reliably be evaluated only in consecutive series of patients. Previous literature, mainly case reports, may give the impression that global amnesia is a common consequence of encephalitis. Our findings do not support that view. Furthermore, there are clear differences in the quality of the memory impairment between cases of acute encephalitides. Our findings suggest that amnesia as a consequence of encephalitis, even HSVE, should not be considered a uniform phenomenon.

Further analysis of the hippocampal amnesic syndrome: 14-year follow-up of HM

Further analysis of the hippocampal amnesic syndrome: 14-year follow-up of HM

Bilateral and limited amygdalohippocampal lesions causing a pure amnesic syndrome

Bilateral and limited amygdalohippocampal lesions causing a pure amnesic syndrome

Bilateral lesions of CA1 and CA2 fields of the hippocampus are sufficient to cause a severe amnesic syndrome in humans

Bilateral lesions of CA1 and CA2 fields of the hippocampus are sufficient to cause a severe amnesic syndrome in humans

Multimodal amnesic syndrome following bilateral temporal and basal forebrain damage

Multimodal amnesic syndrome following bilateral temporal and basal forebrain damage

The characterization of an amnesic syndrome following hypoxic ischaemic injury

The characterization of an amnesic syndrome following hypoxic ischaemic injury

Akinetic mutism with bithalamic infarction. Neurophysiological correlates

A 42-year-old man presented with akinetic mutism, caused by bilateral thalamic infarction, resulting in a temporary amnesic syndrome and, finally, selective downgaze palsy. Electroencephalographic recording in the initial phase showed generalized spike- and-wave discharges, similar to those found in animal studies after lesion or stimulation of specific thalamic nuclei. Analysis of magnetic resonance images (MRI) of the head showed that the centre of ischemic necrosis particularly involved the intralaminar thalamic nuclei and a small part of the rostral mesencephalon. The findings support the previously suggested involvement of cortico-thalamo-mesencephalic circuitry in the initiation of motor responses, and the association of the non-specific thalamic nuclei with the appearance of generalized epileptiform phenomena in cases of reduced vigilance.

Akinetic mutism with bithalamic infarction. Neurophysiological correlates

A 42-year-old man presented with akinetic mutism, caused by bilateral thalamic infarction, resulting in a temporary amnesic syndrome and, finally, selective downgaze palsy. Electroencephalographic recording in the initial phase showed generalized spike-and-wave discharges, similar to those found in animal studies after lesion or stimulation of specific thalamic nuclei. Analysis of magnetic resonance images (MRI) of the head showed that the centre of ischemic necrosis particularly involved the intralaminar thalamic nuclei and a small part of the rostral mesencephalon. The findings support the previously suggested involvement of cortico-thalamo-mesencephalic circuitry in the initiation of motor responses, and the association of the non-specific thalamic nuclei with the appearance of generalized epileptiform phenomena in cases of reduced vigilance.

Memory, attention, and executive function in chronic fatigue syndrome.

To examine cognitive function in chronic fatigue syndrome. Twenty patients with chronic fatigue syndrome recruited from primary care and 20 matched normal controls were given CANTAB computerised tests of visuospatial memory, attention, and executive function, and verbal tests of letter and category fluency and word association learning. Patients with chronic fatigue syndrome were impaired, predominantly in the domain of memory but their pattern of performance was unlike that of patients with amnesic syndrome or dementia. They were normal on tests of spatial pattern recognition memory, simultaneous and delayed matching to sample, and pattern-location association learning. They were impaired on tests of spatial span, spatial working memory, and a selective reminding condition of the pattern-location association learning test. An executive test of planning was normal. In an attentional test, eight subjects with chronic fatigue syndrome were unable to learn a response set; the remainder exhibited no impairment in the executive set shifting phase of the test. Patients with chronic fatigue syndrome were also impaired on verbal tests of unrelated word association learning and letter fluency. Patients with chronic fatigue syndrome have reduced attentional capacity resulting in impaired performance on effortful tasks requiring planned or self ordered generation of responses from memory.

Spared Retrograde Memory with Anterograde Amnesia and Widespread Cognitive Deficits

A case is described of a young male who suffered head injuries in a motor accident and subsequently displayed a severe anterograde amnesia in the presence of a relatively intact retrograde memory. He also demonstrated marked impairment of general intellectual ability, naming, perceptual skills and executive functioning. This case demonstrates a striking dissociation between anterograde and retrograde memory. Moreover the retention of retrograde memory in the face of such severe and global cognitive impairment accentuates the dissociation or isolability of retrograde memory. It is further argued that while frontal impairment occurred in this case it lacks any of the hallmarks of frontal amnesia. The case is further evidence for the fractionation of amnesic syndromes.

On the neuropsychology of metamemory: Contributions from the study of amnesia and dementia

Neurologic syndromes in which there is impaired deficit-awareness (termed “anosognosia”) provide useful observations for understanding the nature of metacognition and its neurobiologic correlates. Anosognosia can occur in various disorders, including stroke, head injury, particular amnesic syndromes, and various dementing illnesses (e.g., Alzheimer's disease). Research on anosognosia for memory impairment is important both for its clinical implications and for its contributions toward understanding the neural correlates of, and processes by which, persons are aware of, monitor, and develop beliefs about their own memory functioning (i.e., metamemory). Following a brief introduction to anosognosia, a review is provided of research on awareness of memory deficit in persons with neurologic amnesia or dementia syndromes. Particular emphasis is placed upon the examination of how different experimental methods shed light on specific questions about metamemory impairment.

Cognitive functioning of adult survivors of cerebral hypoxia.

What should clinical neuropsychologists look out for when asked to assess someone with hypoxic brain damage? To determine whether there are typical cognitive profiles of hypoxic patients, all referrals for a neuropsychological assessment made to the author over a period of 16 years were scanned to identify those with a primary diagnosis of cerebral hypoxia as recorded in the hospital notes. From a total sample of 567 patients, 18 (3.17%) had sustained primary cerebral hypoxia from a variety of causes including carbon monoxide poisoning, cardiac arrest, anaesthetic accident, respiratory failure following a pulmonary embolus, hanging and drowning. Not surprisingly, in view of the different degrees of brain damage, the cognitive functioning of the 18 patients was variable, with the greatest number showing deficits of memory and executive functioning (n = 6). Three presented with an amnesic syndrome; two with memory, executive and visuospatial deficits; and three with visuospatial or visuoperceptual problems without severe memory impairments. The remaining four patients were very severely impaired intellectually (VSI), with widespread cognitive deficits precluding the use of neuropsychological assessment procedures designed for adults.

Anterograde but not retrograde memory loss following combined mammillary body and medial thalamic lesions

We report the first human case of combined mammillary body and medial thalamic lesions due to focal pathology. A patient presented with a multi-lobular lesion that affected the mammillary bodies, the medial thalamus and the brain stem. On neuropsychological testing, he showed significant anterograde memory impairment, with marked impairment on delayed story recall, but normal or only mildly impaired performance on retrograde memory tasks. Our findings corroborate the results of recent non-human lesion studies and indicate that some of the well-established features of the amnesic syndrome, such as severe retrograde amnesia, may not be due to primary diencephalic pathology. Significant retrograde amnesia may result from cortical pathology or from an interaction between cortical and subcortical pathology.

A New Case of Retrograde Amnesia with Abnormal Forgetting Rate

The classic amnesic syndrome is characterised by a severe anterograde amnesia and a less important retrograde amnesia with sparing of the semantic component. We report the case of a patient who showed a global amnesic syndrome following a mild head injury. Initially, amnesia was both anterograde and retrograde, and also involved semantic knowledge. Two years later the picture had changed remarkably. The retrograde deficit for autobiographical events was still total, while semantic memory had recovered to a large extent. Learning had also greatly improved, but only if assessed after a short delay; abnormally rapid forgetting rate were found at longer intervals.This pattern of impairment does not lend itself to an easy interpretation. However, the hypothesis of a consolidation deficit may be advanced.