Cognitive deficits in ischemic strokes: Psychometric, electrophysiological and cranial tomographic assessment

Elwan, Osamah; Hashem, Saher; Helmy, A. A.; Tamawy, Mohamed El; Naseer, Maged Abdel; Elwan, Fadia; Madkour, Loutfy H.; Kader, Ann Ali Abdel; Tatawy, Samir El

doi:10.1016/0022-510x(94)90030-2

Cited by 18 publications

(15 citation statements)

References 32 publications

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“…In one study, 42 a linear relation between the size of the infarction and the degree of PMF was found. More circumstantial evidence for a role of stroke severity with respect to PMF comes from a study 41 that found a larger total volume of infarction among those patients who developed poststroke dementia.…”

Section: Relation Between Poststroke Memory Function and Stroke Charamentioning

confidence: 99%

“…Several studies provided a clear description of the size (volume) 26,39 -43 and the location 4,16,25,33,34,38,[42][43][44][45][46][47][48][49][50][51] of the infarction; however, the relation with PMF was only seldom investigated. In one study, 42 a linear relation between the size of the infarction and the degree of PMF was found.…”

Section: Relation Between Poststroke Memory Function and Stroke Charamentioning

confidence: 99%

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Poststroke Memory Function in Nondemented Patients

Snaphaan

Leeuw

2007

Stroke

102

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Background and Purpose-Poststroke memory dysfunction is a prerequisite for the diagnosis of poststroke dementia. This diagnosis is made within months after a stroke, apparently assuming a relatively stable course of the poststroke memory function. Clinical experience added to anecdotal evidence from the literature suggests that poststroke memory function may be reversible. The aim of the present study was to systematically review the available data on the time course of poststroke memory function in nondemented stroke survivors. In addition, we wanted to investigate the role of (pre-)stroke characteristics on poststroke memory function. Methods-We performed systematic literature search of PubMed with the following medical subject heading terms: memory and stroke. The search strategy yielded 798 articles of which 65 fulfilled our inclusion criteria and went on to the data extraction stage. Results-Five studies reported the prevalence of poststroke memory dysfunction at different poststroke intervals. The prevalence of poststroke memory dysfunction varied from 23% to 55% 3 months poststroke, which declined from 11% to 31% 1 year poststroke. Larger stroke volume, prestroke medial temporal lobe atrophy, and white matter lesions were related with decreased poststroke memory function. Conclusions-Not all patients with poststroke memory dysfunction 3 months after a stroke had memory dysfunction 1 year poststroke. Consequently, not all criteria for the dementia diagnosis were fulfilled any more. This may indicate that poststroke dementia may be reversible in a substantial proportion of patients with stroke. Preferably, standardized reassessment of cognitive function should be performed in each patient diagnosed with poststroke dementia. (Stroke.

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Section: Relation Between Poststroke Memory Function and Stroke Charamentioning

confidence: 99%

Section: Relation Between Poststroke Memory Function and Stroke Charamentioning

confidence: 99%

Poststroke Memory Function in Nondemented Patients

Snaphaan

Leeuw

2007

Stroke

102

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“…This neuronal damage can be accompanied by severe impairments in cognition. For example, human survivors of ischemic strokes typically exhibit disruptions in performance on tasks requiring attention, learning and memory (Elwan et al, 1994;Volpe et al, 1986; Address Correspondence to: Noah J. Sandstrom, Department of Psychology, Williams College, 18 Hoxsey Street, Williamstown, MA 01267, Phone: 413-597-4107, Fax: 413-597-2085, E-mail: Noah.Sandstrom@williams.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript.…”

Section: Acute Pretreatment With Estradiol Protects Against Ca1 Cell mentioning

confidence: 99%

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Sandstrom

Rowan

2007

Hormones and Behavior

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Estradiol can act to protect against hippocampal damage resulting from transient global ischemia, but little is known about the functional consequences of such neuroprotection. The present study examines whether acute estradiol administered prior to the induction of transient global ischemia protects against hippocampal cell death and deficits in performance on a spatial learning task. Ovariectomized female rats were primed with estradiol benzoate or oil vehicle 48 and 24 hrs prior to experiencing one of three durations of 4-vessel occlusion (0, 5, or 10 min). Performance on the cued and hidden platform versions of the Morris water maze was assessed one week following ischemia. On the cued platform task, neither hormone treatment nor ischemia significantly influenced acquisition. When tested on the hidden platform task, however, oil-treated rats exhibited impairments in spatial learning after either 5 or 10 min of ischemia while estradiol-treated rats showed no impairments after 5 min of ischemia and only mild impairments after 10 min of ischemia. Immediately following behavioral testing, rats were perfused and survival of CA1 pyramidal cells was assessed. Ischemia was associated with the loss of CA1 pyramidal cells but rats that received estradiol prior to ischemia showed less severe damage. Furthermore, the extent of cell loss was correlated with degree of spatial bias expressed on a probe trial following hidden platform training. These findings indicate that acute exposure to estradiol prior to ischemia is both neuroprotective and functionally protective. Keywords estrogen; ischemia; cardiac arrest; hippocampus; neuroprotection; spatial learning; water maze Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemiaTransient global ischemia leads to the dramatic loss of neurons in the CA1 region of the hippocampus in humans (Horn and Schlote, 1992;Tanabe et al., 1999;Taraszewska et al., 2002), non-human primates (Zola-Morgan et al., 1992), and rodents (Pulsinelli et al., 1982). This neuronal damage can be accompanied by severe impairments in cognition. For example, human survivors of ischemic strokes typically exhibit disruptions in performance on tasks requiring attention, learning and memory (Elwan et al., 1994;Volpe et al., 1986; Address Correspondence to: Noah J. Sandstrom, Department of Psychology, Williams College, 18 Hoxsey Street, Williamstown, MA 01267, Phone: 413-597-4107, Fax: 413-597-2085, E-mail: Noah.Sandstrom@williams.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain...

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“…These disturbances not only affect the overall wellbeing of the patient, but also confound the recovery process, so modeling poststroke emotional disturbances and emotional testing draws considerable attention. Cognitive deficits that decrease the quality of life of stroke survivors are also frequently observed after stroke (4,5). Stroke researchers who aim at exploring poststroke cognitive deficits in animal models must inevitably use behavioral tools at some point of their research.…”

Section: Introductionmentioning

confidence: 99%

Behavioral Testing in Mouse Models of Stroke

Balkaya

Endres

2010

Neuromethods

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For decades, histological assessments were the only end-point in stroke research, typically using lesion size determination to evaluate the potential therapeutic effectiveness of an agent in in vivo stroke models. While this approach is indeed valid, failures in developing effective drugs point out the fact that histological means are simply not enough to evaluate the potential of a drug or intervention and that an evaluation at the functional level is necessary. Animals subjected to stroke models develop sensory-motor, learning and memory problems and "psychological symptoms." Evaluating these symptoms via behavior is not only important in helping us to understand the pathological mechanisms, but it also gives us a powerful tool to test the therapeutic potential of interventions. This chapter will introduce some of the widely used and reliable behavior tests in stroke research. Basic tests of motor function, memory, anxiety, and depression-like behavior will be covered. Each test will be discussed in detail and widely used protocols will be introduced.

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Cognitive deficits in ischemic strokes: Psychometric, electrophysiological and cranial tomographic assessment

Cited by 18 publications

References 32 publications

Poststroke Memory Function in Nondemented Patients

Poststroke Memory Function in Nondemented Patients

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Behavioral Testing in Mouse Models of Stroke

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