Cerebral ischemia: Are the memory deficits associated with hippocampal cell loss?

Bachevalier, Jocelyne; Meunier, Martine

doi:10.1002/(sici)1098-1063(1996)6:5<553::aid-hipo8>3.0.co;2-j

Cited by 96 publications

(42 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our findings agree with the Bachevalier and Meunier study who reviewed the relationship between hippocampal cell loss and cognitive deficits due to brain ischemia (28), also Rod, Kiyota and Milani (29)(30)(31). However findings of Green and Nunn did not show any correlation between these two parameters (1,32).…”

Section: Discussionsupporting

confidence: 91%

Neuroprotective Treatment With FK506 Reduces Hippocampal Damage and Prevents Learning and Memory Deficits After Transient Global Ischemia in Rat

et al. 2013

View full text Add to dashboard Cite

Background:Behavioral studies on animals demonstrated that hippocampal damage could produce learning and memory impairments particularly spatial learning. It has been shown that ischemic damage restricted to only 50% of the CA1 cells of the hippocampus exceed the threshold for production of a behavioral impairment. Objectives: In this study we seek to evaluate the effect of FK506 (tacrolimus) on spatial learning of rats subjected to 20-min global transient ischemia/reperfusion. Material and Methods: In treatment group 2, FK506 (1mg/kg) was given intravenously (IV) 20 minutes before ischemia and in treatment group 3 rats were treated with the same dose of tacrolimus (IV) at the beginning of reperfusion. Morris water maze tests were performed 1 week after ischemia for 4 days. Brain tissue proceeded to TUNEL staining. Results: Our data showed; 1) No statistically significant differences were seen between the treatment group 2 and the control (intact) group thus, this suggests that treatment of ischemia with tacrolimus can improve spatial learning and memory. 2) Tacrolimus treatment ameliorated the increase of TUNEL-positive cells induced by cerebral ischemia indicating the neuro-protective properties of FK506. Conclusions: These results suggest that tacrolimus may reduce cognitive impairment and may be a good candidate for treatment of ischemic brain damage.

show abstract

Section: Discussionsupporting

confidence: 91%

Neuroprotective Treatment With FK506 Reduces Hippocampal Damage and Prevents Learning and Memory Deficits After Transient Global Ischemia in Rat

et al. 2013

View full text Add to dashboard Cite

show abstract

“…The question naturally arises whether the cascade of events initiated by ischemia or anoxia might produce neuronal damage sufficient to impair behavioral performance, but not sufficient to progress to cell death and to be detectable in histopathology. This possibility has been referred to as covert damage (Bachevalier and Mishkin, 1989;Bachevalier and Meunier, 1996;Squire and Zola, 1996). It is an important issue, because if covert damage commonly occurs, then ischemic or anoxic lesions apparently limited to the hippocampal region cannot be taken as evidence that only the hippocampal region is dysfunctional.…”

Section: The Hippocampal Formation and Anterograde Amnesiamentioning

confidence: 99%

Three Cases of Enduring Memory Impairment after Bilateral Damage Limited to the Hippocampal Formation

et al. 1996

View full text Add to dashboard Cite

Patient RB (Human amnesia and the medial temporal region: enduring memory impairment following a bilaterial lesion limited to field CA1 of the hippocampus, S. Zola-Morgan, L. R. Squire, and D. G. Amaral, 1986, J Neurosci 6:2950 -2967 was the first reported case of human amnesia in which detailed neuropsychological analyses and detailed postmortem neuropathological analyses demonstrated that damage limited to the hippocampal formation was sufficient to produce anterograde memory impairment. Neuropsychological and postmortem neuropathological findings are described here for three additional amnesic patients with bilateral damage limited to the hippocampal formation. Findings from these patients, taken together with the findings from patient RB and other amnesic patients, make three important points about memory. (1) Bilateral damage limited primarily to the CA1 region of the hippocampal formation is sufficient to produce moderately severe anterograde memory impairment. (2) Bilateral damage beyond the CA1 region, but still limited to the hippocampal formation, can produce more severe anterograde memory impairment. (3) Extensive, temporally graded retrograde amnesia covering 15 years or more can occur after damage limited to the hippocampal formation. Findings from studies with experimental animals are consistent with the findings from amnesic patients. The present results substantiate the idea that severity of memory impairment is dependent on locus and extent of damage within the hippocampal formation and that damage to the hippocampal formation can cause temporally graded retrograde amnesia.

show abstract

“…A review of anoxic brain injury (N 5 90) found that 44% of individuals had cortical edema or atrophy, 33% had cerebellar lesions, 22% had basal ganglia lesions, 21% had hippocampal atrophy, and 3% had thalamic lesions (Caine & Watson, 2000). & Bond, 1975), cognitive sequelae, and development of new psychiatric disorders (Bachevalier & Meunier, 1996;Caine & Watson, 2000). Neuropsychological deficits after anoxia or ischemia are heterogeneous and include agnosia (Farah, 1990), impaired memory (Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986), executive dysfunction (Hopkins et al, 1995a;Lezak, 1995), impaired visual-spatial skills (Barat et al, 1989), generalized cognitive impairments (Wilson, 1996), and motor disturbances (Lishman, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…However, brain imaging findings in near-drowning survivors are heterogeneous with abnormalities ranging from hemorrhageic infarctions to global atrophy (Fitch et al, 1985). Similarly, brain MRI findings in anoxic patients who were not near-drowning accidents include lesions in gray (e.g., basal ganglia, hippocampus, etc) and white matter, and global and focal atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986). Whereas braining imaging was normal by radiologic report in Case 1, quantitative neuroimaging was not carried out (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b).…”

Section: Near-drowning In Ice Water-introduction 657mentioning

confidence: 99%

“…Similarly, brain MRI findings in anoxic patients who were not near-drowning accidents include lesions in gray (e.g., basal ganglia, hippocampus, etc) and white matter, and global and focal atrophy (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Hopkins et al, 2004;Manns et al, 2003a;Zola-Morgan et al, 1986). Whereas braining imaging was normal by radiologic report in Case 1, quantitative neuroimaging was not carried out (Bachevalier & Meunier, 1996;Caine & Watson, 2000;Gale et al, 1999;Hopkins et al, 1995b). Nonspecific brain damage may result in general volume reduction manifested by reduced gyral volume, increased sulcal space, passive increase in ventricular volume (i.e., hydrocephalus ex vacuo), increase in whole brain cerebral spinal fluid (CSF; Graham et al, 2002), and structural atrophy (e.g.…”

Section: Near-drowning In Ice Water-introduction 657mentioning

confidence: 99%

See 1 more Smart Citation

Neurobehavioral Grand Rounds Introduction: Does near drowning in ice water prevent anoxic induced brain injury?

Hopkins

2008

J Int Neuropsychol Soc

View full text Add to dashboard Cite

Cold water near-drowning is often thought to be neuroprotective in individuals with anoxia of a longer duration than that usually required to produce irreversible neurologic damage. There is a paucity of data in adults with cold water near-drowning that assess neuropsychological outcomes. Information regarding long-term effects of near cold water near-drowning on neuropathology, neuropsychological and neurobehavioral outcomes are uncommon. This paper provides an introduction to two cases of cold water near-drowning reported in this issue of JINS by Sameulson and colleagues and provides background information for interpretation of the findings of these cases in the context of outcomes following anoxia. (JINS, 2008, 14, 656-659.)

show abstract

Cerebral ischemia: Are the memory deficits associated with hippocampal cell loss?

Cited by 96 publications

References 80 publications

Neuroprotective Treatment With FK506 Reduces Hippocampal Damage and Prevents Learning and Memory Deficits After Transient Global Ischemia in Rat

Neuroprotective Treatment With FK506 Reduces Hippocampal Damage and Prevents Learning and Memory Deficits After Transient Global Ischemia in Rat

Three Cases of Enduring Memory Impairment after Bilateral Damage Limited to the Hippocampal Formation

Neurobehavioral Grand Rounds Introduction: Does near drowning in ice water prevent anoxic induced brain injury?

Contact Info

Product

Resources

About