Amnesia following the rupture and repair of an anterior communicating artery aneurysm (original) (raw)
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Brain, 1997
Ruptured and repaired anterior communicating artery (ACoA) and provides added sensitivity by combining recall with nonrecall measures (e.g. recognition, spatial discrimination and aneurysm can result in devastating impairments involving memory, executive function, confabulation and personality spatial assembly). The major findings were: (i) immediate recall in amnesics was improved by providing an organiza-change. Importantly, traditional cerebral areas implicated in amnesia are not damaged, yet amnesia can still be manifested. tional strategy; (ii) following the organization trials, amnesics and non-amnesics retained information to a comparable While ACoA patients show normal visual-constructional skills (i.e. copy scores) on the Rey-Osterrieth complex figure extent over a 30-min delay; (iii) two subgroups of amnesics emerged, those subjects impaired in acquisition and a second test, recall is often impaired. What is unclear is whether impaired recall is attributable to problems in encoding, group with impaired retrieval; (iv) all subjects showed preserved memory on non-recall measures. These findings accelerated rates of forgetting, retrieval or some combination. To disentangle these issues, we examined 10 patients have important implications with respect to using organizational strategies in cognitive treatments and in using non-with ruptured aneurysms of the ACoA, using the Reyorganizational and extended memory procedure which uses recall measures in improving the validity and reliability of patient assessment. an organizational procedure for enhancing immediate recall
Recovery of memory and executive function following anterior communicating artery aneurysm rupture
Journal of the International Neuropsychological Society, 1996
We studied the recovery of memory and executive function in 10 patients following anterior communicating artery aneurysm (ACoA) rupture and repair. Patients were tested at 2 consecutive points in time following surgery (approximately at 2 and 3 months). At the first testing, the patients divided into 2 groups based on the severity of impairment on executive measures. Both groups had severe anterograde amnesia, but only patients with severe executive impairments had retrograde amnesia with a temporal gradient. At second testing, both groups had persistent severe anterograde amnesia. The dysexecutive group showed significant improvement in executive deficits and in retrograde amnesia, with attenuation of the temporal gradient. Patients with more severe executive impairments had more extensive bilateral frontal lesions than other patients. These results suggest that the cognitive profile following ACoA rupture changes with time. Time postonset following aneurysm rupture and lesion site...
Neuropsychology, 2008
Human anterograde amnesia can result from a variety of etiologies, including hypoxic brain injury and anterior communicating artery (ACoA) aneurysm rupture. Although each etiology can cause a similarly severe disruption in declarative memory for verbal and visual material, there may be differences in incrementally acquired, feedback-based learning, as well as generalization. Here, 6 individuals who survived hypoxic brain injury, 7 individuals who survived ACoA aneurysm rupture, and 13 matched controls were tested on 2 tasks that included a feedback-based learning phase followed by a transfer phase in which familiar information is presented in new ways. In both tasks, the ACoA group was slow on initial learning, but those patients who completed the learning phase went on to transfer as well as controls. In the hypoxic group, 1 patient failed to complete either task; the remaining hypoxic group did not differ from controls during learning of either task, but was impaired on transfer. These results highlight a difference in feedback-based learning in 2 amnesic etiologies, despite similar levels of declarative memory impairment.
Neuropsychologia, 2006
Human anterograde amnesia can develop following bilateral damage to the hippocampus and medial temporal lobes, as in hypoxic brain injury, or following damage to the basal forebrain, as following anterior communicating artery (ACoA) aneurysm rupture. In both cases, the mnestic deficit may be similar when assessed by standard neuropsychological measures. However, animal and computational models suggest that there are qualitative differences in the pattern of impaired and spared memory abilities following damage to hippocampus versus basal forebrain. Here, we show such a dissociation in human amnesia using a single two-stage task, involving conditional discrimination and reversal. Consistent with a prior study, 10 individuals with anterograde amnesia subsequent to hypoxic brain injury were spared on acquisition but impaired at reversal. However, 10 individuals with amnesia subsequent to ACoA aneurysm showed the opposite pattern of impaired acquisition but spared reversal. The differences between groups cannot be easily ascribed to severity of mnestic or cognitive deficit, since the two amnesic groups performed similarly on neuropsychological tests of memory, intelligence and attention. The results illustrate qualitative differences in memory impairments in hypoxic and ACoA amnesics and highlight the importance of considering etiology in evaluating mnemonic deficits in amnesic populations.
Progress in neurobiology, 1985
Contents 1. Introduction 2. Memory and its disturbance 191 2.1. Forms of memory and memory failures 2.1.1. Time 2.1.2. Material-specific memory failure 2.2. The (global) amnesic syndrome(s) 3. Overview of the pathology of amnesia 3.1. Vascular system 3.2. Degenerative processes 3.3. Tumorous processes 3.4. Other possible causes of amnesia 3.4.1. Traumatic lesions 3.4.2. Electroconvulsive therapy 3.4.3. Brain surgery 3.4.4. Infections 3.4.5. Metabolic deficiencies 3.4.6. Psychogenic loss of memory 4. Brain lesions and amnesia 4.1. Medial temporal lobe damage 4.1.1. General remarks on anatomy and functions of the temporal lobe 4.1.2. Case H.M. 4.1.2.1. The first years after surgery 4.1.2.2. The time period between 1970 and the present 4.1.3. Other cases of epileptics with temporal lobe resections and mnestic disturbances 4.1.4. The hippocampal formation 4.1.5. Cases with more widespread temporal lobe damage 4.1.6. Phenomena related to electrical stimulation of the temporal lobe region 4.1.7. Fornix damage 4.1.8. Relations between amnesia and medial temporal lobe damage 4.
Confabulation Following Rupture of Posterior Communicating Artery
Cortex, 1997
In this study we report a patient, MG, who following rupture of left posterior communicating artery exhibited an amnesic-confabulatory syndrome. Neuropsychological examination showed severe impairment on episodic memory tasks, which were marred by florid but plausible and semantically appropriate confabulation. Performance on tasks involving various kinds of semantic knowledge was normal or only mildly impaired.
Autobiographical amnesia following Arteriovenous Malformation, case report
2019
Aim : The aim of the current study is the description of an emblematic case of a ruptured left temporal arteriovenous malformation (AVM) causing a large intraparenchymal temporo-parietal left hematoma that resulted in a severe retrograde amnesia. Methods : The patient underwent neurosurgical evacuation of the hematoma and resection of the AVM. He was also sumbitted to several pre- and post-operative neuropsychological evaluations and to rehabilitation for different subdomains of both memory and language. Results : At the end of the rehabilitation course, a new neuropsychological assessment was performer together with a functional cortical mapping Navigated Transcranial Magnetic Stimulation (nTMS) to evaluate the focal damage to and the plastic recovery of language cortical areas. Discussion : This case report must be ecologically oriented and based on the relationship between the importance and the nature of the cognitive and type of claims of the specific environment of the indi...