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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute transient amnesia has not been previously associated with vertebral artery dissection. We describe two men with acute onset of dense anterograde amnesia and partial retrograde amnesia resulting from spontaneous vertebral artery dissection. Both amnesic syndromes completely resolved with conservative management.
Stroke 1988 Jan
PMID:Transient amnesia resulting from vertebral artery dissection. 333 8

We report a case with bilateral paramedian thalamic infarcts. The patient showed a dramatic personality change characterized by childish behavior and euphoria; which remained unchanged for 2 years after the onset. 'Vorbeireden' characterized by approximate answers was also observed. Anterograde amnesia had quite improved after 2 years, while retrograde amnesia for 1 year prior to the stroke onset and vertical gaze palsy remained unchanged. An MRI scan demonstrated bilateral medial thalamic and right midbrain infarcts without other lesions in the brain. A position emission tomography study showed that cerebral metabolic rate for glucose was markedly decreased in both thalami and in the cerebellum, and only slightly decreased in the parietal and occipital cortical regions. Cerebral metabolic rates of glucose in the frontal and temporal cortices were within normal range. The paramedian thalamic lesions per se may be responsible for the patient's personality change, 'Vorbeireden', and amnesia.
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PMID:Persisting childish behavior after bilateral thalamic infarcts. 920 63

The aim of this study was to investigate deficits of retrograde memory, semantic, autobiographical, and for famous events, associated with prefrontal, cingulate and subcortical lesions resulting from anterior communicating artery rupture. Analyses were performed during the secondary phase post-stroke in 16 patients, and performances were compared to those of an equivalent number of matched control subjects. Semantic investigations revealed a significant deficit in each task using evocation, more especially categorical and literal evocations, and the verbal subtests of the WAIS-R: vocabulary, information, comprehension, and similarities. Furthermore, the capacity to categories was preserved. The Crovitz paradigm, which evaluated the autobiographical memory showed a severe deficit in the evocation of events associated with a precise context in place and moreover in time, with a clear tendency to produce semantic responses, but without significant increase in confabulations. The questionnaire on famous events (1936-1985) did not document deficit in recognition and recall. Furthermore, the patients disorder was more severe in learning new information. Memory disorders were best explained by the severity of lesions in the medio-basal frontal and cingulate cortices, but also by the subcortical injury. Significant correlations were observed between the retrograde memory performance and "frontal" tasks, more especially the WCST; however, similar relations were also documented between learning new information and "frontal" performance. These data suggest that retrograde amnesia results from a selective impairment in accessing old memory representations, and that cognitive processes more specifically altered have tight relations with the capacity to organize the search and to shift.
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PMID:[Retrograde memory after rupture of aneurysms of the anterior communicating artery]. 968 53

A case of unilateral infarct in the territory of the left internal cerebral vein, severely disturbing cognitive processes, and more especially recall in verbal memory, is reported. This 22-year-old patient survived a left thalamic and striato-capsular infarct related to a straight sinus and left internal cerebral vein thrombosis. Motor and functional recovery was fair, despite late dystonia. At the secondary phase post-stroke, cognitive disorders were severe, including increased short-term forgetting and episodic (anterograde and retrograde) and semantic amnesia. One year later, a residual deficit of verbal recall was observed, which participated in the anterograde and retrograde amnesia. Recognition was well preserved. This case showed that: (1) internal cerebral vein thrombosis can have severe consequences on cognition and memory, and that late prognosis is not as fair as has been previously reported in selected patients, and (2) left diencephalic structures are specifically associated with recollection of verbal information from long-term memory.
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PMID:[Residual deficit of verbal recall after a left internal cerebral vein infarct]. 977 71

A 60 year old right-handed man developed severe amnesia following a left medial temporal stroke as documented by cerebral MRI, MRA and SPECT scans. Neuropsychological evaluation 13 weeks after the stroke showed a profound retrograde amnesia characterised by memory loss for public facts and events over the previous four decades. In addition, autobiographical memory showed selective loss of personal episodic memory with relative preservation of personal semantic memory. The development of this degree of amnesia with these features following a unilateral temporal lobe lesion is unusual. The possible neuroanatomical mechanisms underlying the amnesia and how they relate to current theories of memory loss are discussed.
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PMID:Severe amnesia following a unilateral temporal lobe stroke. 1246 35

Over the past two decades, there has been a growing interest in understanding the neural underpinnings of memory of the past. Numerous patients with retrograde amnesia after acute brain damage have been described, but often the causative lesions are bilateral and/or fairly diffuse and one question that has arisen is whether a unilateral lesion is sufficient to cause retrograde memory impairment. In addition, the impact of lesion side and site on the material specificity and temporal extent of retrograde memory deficits has remained unclear. We set out to investigate these issues by comparing 20 patients who had recently had a unilateral stroke that involved (but was not necessarily limited to) either the frontal or temporal lobe to a group of 10 matched normal control subjects on tests of memory of events and semantic details from the autobiographical and public domains. Results indicated that a unilateral lesion was sufficient to cause significant retrograde memory impairment, with right-sided lesions affecting recall of autobiographical events more than left-sided lesions. The memory deficits in these patients were most often relatively mild, but temporally pervasive rather than characterised by a traditional temporal gradient. Furthermore, memory of events (both autobiographical and public) was impaired in patients who had had a stroke that included the hippocampus, but not in those whose strokes spared this region. Finding that patients with mesial temporal lesions had difficulty remembering details related to public events, even when offered recognition choices, raises the possibility that part of their memory storage network (and not just their retrieval abilities) was compromised.
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PMID:Retrograde memory after unilateral stroke. 1838 46

Learning and memory deficits are typically associated with damage or dysfunction of medial temporal lobe structures; however, diencephalic lesions are another common cause of severe and persistent memory deficits. We focus specifically on the thalamus and review the pathological and neuropsychological characteristics of two common causes of such damage: Korsakoff's syndrome and stroke. We then present a patient who had sustained bilateral medial thalamic infarctions that affected the medial dorsal nucleus and internal medullary lamina. This patient demonstrated the characteristic temporally graded retrograde amnesia and a profound anterograde memory (i.e., explicit memory) deficit within the context of relatively preserved implicit memory. Implications of this explicit-implicit discrepancy are discussed within the context of cognitive rehabilitation techniques that hold promise for more severely impaired patients.
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PMID:Thalamic contributions to anterograde, retrograde, and implicit memory: a case study. 1954 81

Strategic regions correspond to associative, limbic and paralimbic structures and related circuits, that underpin cognitive/behavioral functions. Strokes in these eloquent sites produce pictures of vascular dementia with syndromic features due to specific site lesion and/or interruption of their interconnections. This study aims at analysing subcortical strategic strokes that express similar cognitive/behavioral elements, by sharing common pathways. Patients (n=6) who attended in specialized ambulatory, were submitted to neuropsychological and neuroimaging assessments through MRI (GE Signa Horizon 1.5T) and brain SPECT (Millennium MG, ECD [TC-99m]). Stroke locations and respective main symptoms were: 1. anteromedian thalamus [L]: anterograde and retrograde amnesia (ARA), expression aphasia (EA), executive dysfunction (ED), apathy, and depression; 2. anterior thalamus [R]: ARA, inattention, apathy, and aggressiveness; 3. dorsomedian thalamus [L]: inattention, ED, anosognosia, and aggressiveness; 4. central paramedian thalamus [R]: EA, visual perception deficits (VPD), ED, infantility, and personality disorder; 5. caudate nucleus (ventral-head) [L]: VPD, ED, delirium, visual hallucinations, and personality disorder; and 6. anterior capsule [L]: VPD, ED, apathy, and depression. Vascular strategic syndromes connote the predominantly impaired cognitive/behavioral symptom of each site. Temporal and frontal disconnection symptoms were produced by disrupted MTT/hippocampal and IML/amygdala circuits expressing amnesic syndrome associated with heterogeneous dysexecutive syndrome, in all the cases, by disrupting frontal-basal ganglia-thalamus-cortical net, in three different levels of their pathway.
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PMID:Cognitive disconnective syndrome by single strategic strokes in vascular dementia. 2293 18

Cortical blindness is a well described neuro-ophthalmologic complication of angiography due to neurotoxicity following contrast media exposure. A rarer association with retrograde amnesia has also been reported. Since ischemic stroke due to embolism remains the most common aetiology of neurological complications of diagnostic and therapeutic arterial catheterisation, prompt identification of the mechanism responsible for the clinical symptoms is essential for patient management. Although CT and conventional MRI findings have been reported in this condition, experience with diffusion weighted (DW) sequences is lacking especially in cases associated with memory impairment. A 65-year-old man with tinnitus underwent cerebral angiography for suspicion of a dural arteriovenous fistula. During the procedure the patient developed complete loss of vision and rapidly became confused. Brain CT showed bilateral cortical enhancement in the occipital lobes. MR with DWI was performed 3.5 hours after angiography. Early DWI showed no signal abnormalities thereby excluding an ischaemic complication. Gradual improvement of visual function occurred over the next 24 hours. After 48 hours the patient was alert and orientated but profound retrograde amnesia persisted with no memory for the events of the day of angiography. CT follow-up at one year was normal. DWI is invaluable in the evaluation of patients with cortical blindness with or without memory deficits precipitated by angiography and may advance understanding of the pathophysiology. Diffusion-weighted MRI is crucial in differentiating neuro-ophthalmologic complications precipitated by intracortical contrast leakage after angiography from an ischaemic stroke needing a prompt and often invasive treatment.
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PMID:Cortical Blindness and Retrograde Amnesia Following Cerebral Angiography Studied by Early Diffusion Weighted MR imaging. A Case Report. 2420 6

Unilateral cerebral ischemia of the hippocampus is very rare. This paper reviews the literature and presents the case of a 59-year-old woman with an amnestic syndrome due to a left hippocampal stroke. The patient suffered from retrograde amnesia which was most severe over the 2 days prior to presenting and a slight anterograde amnesia. In addition, a verbal memory disorder was confirmed 1 week after admission by neurological tests. As risk factors, arterial hypertension and a relative hyper-beta lipoproteinemia were found. This case shows that unilateral amnestic stroke, e.g. in the hippocampus region, may be the cause of an amnestic syndrome and should be included in the differential diagnostics.
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PMID:[Hippocampal stroke]. 2557 32


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