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"Amnesia Case studies."
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Acute hyperglycaemia leads to altered frontal lobe brain activity and reduced working memory in type 2 diabetes
How acute hyperglycaemia affects memory functions and functional brain responses in individuals with and without type 2 diabetes is unclear. Our aim was to study the association between acute hyperglycaemia and working, semantic, and episodic memory in participants with type 2 diabetes compared to a sex- and age-matched control group. We also assessed the effect of hyperglycaemia on working memory–related brain activity. A total of 36 participants with type 2 diabetes and 34 controls (mean age, 66 years) underwent hyperglycaemic clamp or placebo clamp in a blinded and randomised order. Working, episodic, and semantic memory were tested. Overall, the control group had higher working memory (mean z-score 33.15 ± 0.45) than the group with type 2 diabetes (mean z-score 31.8 ± 0.44, p = 0.042) considering both the placebo and hyperglycaemic clamps. Acute hyperglycaemia did not influence episodic, semantic, or working memory performance in either group. Twenty-two of the participants (10 cases, 12 controls, mean age 69 years) were randomly invited to undergo the same clamp procedures to challenge working memory, using 1-, 2-, and 3-back, while monitoring brain activity by blood oxygen level–dependent functional magnetic resonance imaging (fMRI). The participants with type 2 diabetes had reduced working memory during the 1- and 2-back tests. fMRI during placebo clamp revealed increased BOLD signal in the left lateral frontal cortex and the anterior cingulate cortex as a function of working memory load in both groups (3>2>1). During hyperglycaemia, controls showed a similar load-dependent fMRI response, whereas the type 2 diabetes group showed decreased BOLD response from 2- to 3-back. These results suggest that impaired glucose metabolism in the brain affects working memory, possibly by reducing activity in important frontal brain areas in persons with type 2 diabetes.
Journal Article
Neuropsychological and neuropathological observations of a long-studied case of memory impairment
We report neuropsychological and neuropathological findings for a patient (A.B.), who developed memory impairment after a cardiac arrest at age 39. A.B. was a clinical psychologist who, although unable to return to work, was an active participant in our neuropsychological studies for 24 y. He exhibited a moderately severe and circumscribed impairment in the formation of longterm, declarative memory (anterograde amnesia), together with temporally graded retrograde amnesia covering ∼5 y prior to the cardiac arrest. More remote memory for both facts and autobiographical events was intact. His neuropathology was extensive and involved the medial temporal lobe, the diencephalon, cerebral cortex, basal ganglia, and cerebellum. In the hippocampal formation, there was substantial cell loss in the CA1 and CA3 fields, the hilus of the dentate gyrus (with sparing of granule cells), and the entorhinal cortex. There was also cell loss in the CA2 field, but some remnants remained. The amygdala demonstrated substantial neuronal loss, particularly in its deep nuclei. In the thalamus, there was damage and atrophy of the anterior nuclear complex, the mediodorsal nucleus, and the pulvinar. There was also loss of cells in the medial and lateral mammillary nuclei in the hypothalamus. We suggest that the neuropathology resulted from two separate factors: the initial cardiac arrest (and respiratory distress) and the recurrent seizures that followed, which led to additional damage characteristic of temporal lobe epilepsy.
Journal Article
Hippocampal network abnormalities explain amnesia after VGKCC-Ab related autoimmune limbic encephalitis
ObjectiveLimbic encephalitis associated with antibodies to components of the voltage-gated potassium channel complex (VGKCC-Ab-LE) often leads to hippocampal atrophy and persistent memory impairment. Its long-term impact on regions beyond the hippocampus, and the relationship between brain damage and cognitive outcome, are poorly understood. We investigated the nature of structural and functional brain abnormalities following VGKCC-Ab-LE and its role in residual memory impairment.MethodA cross-sectional group study was conducted. Twenty-four VGKCC-Ab-LE patients (20 male, 4 female; mean (SD) age 63.86 (11.31) years) were recruited post-acutely along with age- and sex-matched healthy controls for neuropsychological assessment, structural MRI and resting-state functional MRI (rs-fMRI). Structural abnormalities were determined using volumetry and voxel-based morphometry; rs-fMRI data were analysed to investigate hippocampal functional connectivity (FC). Associations of memory performance with neuroimaging measures were examined.ResultsPatients showed selective memory impairment. Structural analyses revealed focal hippocampal atrophy within the medial temporal lobes, correlative atrophy in the mediodorsal thalamus, and additional volume reduction in the posteromedial cortex. There was no association between regional volumes and memory performance. Instead, patients demonstrated reduced posteromedial cortico-hippocampal and inter-hippocampal FC, which correlated with memory scores (r = 0.553; r = 0.582, respectively). The latter declined as a function of time since the acute illness (r = -0.531).ConclusionVGKCC-Ab-LE results in persistent isolated memory impairment. Patients have hippocampal atrophy with further reduced mediodorsal thalamic and posteromedial cortical volumes. Crucially, reduced FC of remaining hippocampal tissue correlates more closely with memory function than does regional atrophy.
Journal Article
Migraine in transient global amnesia: a meta-analysis of observational studies
BackgroundPurposeAlthough many studies have investigated the relationship between transient global amnesia (TGA) and migraine, to date, no meta-analysis has confirmed the existence and size of their association.MethodologyLiterature search involved MEDLINE, EMBASE, CENTRAL and PsycINFO. Observational controlled studies including TGA patients (Caplan, Hodges and Warlow) were retrieved. Quality evaluation was based on the Newcastle-Ottawa scale. The prevalence of migraine was compared in TGA patients vs. healthy controls (HC), as well as in TGA against TIA individuals. Data from case-control, cross-sectional and cohort studies were pooled separately.ResultsLiterature search yielded 1178 articles, 12 of which were included in the present meta-analysis. Results from case-control (ten), cohort (one) and cross-sectional (one) studies were compatible with an association between TGA and migraine. The nationwide inpatient cross-sectional study was of lesser value due to its inpatient orientation. The high-quality, population-based, retrospective cohort (158,301 participants per group) determined a higher relative-risk (RR) of TGA for migraine vs. non-migraine individuals [RR = 2.48, 95%confidence-interval (95% CI) = (1.32, 4.87)]. Sensitivity testing based on stricter diagnostic criteria strengthened the estimated association [RR = 3.84, 95% CI = (1.57, 9.38)]. Additionally, pooled data from eight case–control studies (700 TGA, 746 HC) yielded similar results [Odds-Ratio, OR = 2.51, 95% CI = (1.85, 3.41)], with the association mainly driven by the three high-quality studies, rather than the five articles of moderate quality. Finally, pooled findings from four case–control studies of moderate-quality revealed a higher prevalence of migraine among TGA compared to TIA patients [OR = 1.82, 95% CI = (1.22, 2.73)].ConclusionsA significant association between TGA and migraine was established. The underlying connecting mechanism remains undetermined, yet.
Journal Article
Plasma Aβ42 and Total Tau Predict Cognitive Decline in Amnestic Mild Cognitive Impairment
Levels of amyloid-β (Aβ) and tau peptides in brain have been associated with Alzheimer disease (AD). The current study investigated the abilities of plasma Aβ42 and total-tau (t-tau) levels in predicting cognitive decline in subjects with amnestic mild cognitive impairment (MCI). Plasma Aβ42 and t-tau levels were quantified in 22 participants with amnestic MCI through immunomagnetic reduction (IMR) assay at baseline. The cognitive performance of participants was measured through neuropsychological tests at baseline and annual follow-up (average follow-up period of 1.5 years). The predictive value of plasma Aβ42 and t-tau for cognitive status was evaluated. We found that higher levels of Aβ42 and t-tau are associated with lower episodic verbal memory performance at baseline and cognitive decline over the course of follow-up. While Aβ42 or t-tau alone had moderate-to-high discriminatory value in the identification of future cognitive decline, the product of Aβ42 and t-tau offered greater differential value. These preliminary results might suggest that high levels of plasma Aβ42 and t-tau in amnestic MCI are associated with later cognitive decline. A further replication with a larger sample over a longer time period to validate and determine their long-term predictive value is warranted.
Journal Article
Patients with hippocampal amnesia cannot imagine new experiences
Amnesic patients have a well established deficit in remembering their past experiences. Surprisingly, however, the question as to whether such patients can imagine new experiences has not been formally addressed to our knowledge. We tested whether a group of amnesic patients with primary damage to the hippocampus bilaterally could construct new imagined experiences in response to short verbal cues that outlined a range of simple commonplace scenarios. Our results revealed that patients were markedly impaired relative to matched control subjects at imagining new experiences. Moreover, we identified a possible source for this deficit. The patients' imagined experiences lacked spatial coherence, consisting instead of fragmented images in the absence of a holistic representation of the environmental setting. The hippocampus, therefore, may make a critical contribution to the creation of new experiences by providing the spatial context into which the disparate elements of an experience can be bound. Given how closely imagined experiences match episodic memories, the absence of this function mediated by the hippocampus, may also fundamentally affect the ability to vividly re-experience the past.
Journal Article
CA1 neurons in the human hippocampus are critical for autobiographical memory, mental time travel, and autonoetic consciousness
Autobiographical memories in our lives are critically dependent on temporal lobe structures. However, the contribution of CA1 neurons in the human hippocampus to the retrieval of episodic autobiographical memory remains elusive. In patients with a rare acute transient global amnesia, highly focal lesions confined to the CA1 field of the hippocampus can be detected on MRI. We studied the effect of these lesions on autobiographical memory using a detailed autobiographical interview including the remember/know procedure. In 14 of 16 patients, focal lesions in the CA1 sector of the hippocampal cornu ammonis were detected. Autobiographical memory was significantly affected over all time periods, including memory for remote periods. Impairment of episodic memory and autonoetic consciousness exhibited a strong temporal gradient extending 30 to 40 y into the past. These results highlight the distinct and critical role of human hippocampal CA1 neurons in autobiographical memory retrieval and for re-experiencing detailed episodic memories.
Journal Article
Manipulating the reported age in earliest memories in a Dutch community sample
Childhood amnesia in adults can be defined as the relative paucity of autobiographical memories from the first years of life. An earlier study by Wessel, Schweig and Huntjens demonstrated that 'how' we ask for an earliest memory may bias adults' estimations of when the earliest childhood memory actually happened. They suggested that snapshot memories (i.e., mental pictures) were less sensitive to an age manipulation than event memories (i.e. narratives). We aimed at replicating and extending these findings using a Dutch community sample stratified for age, gender and educational level.
Participants (N = 619) were randomized into one of three experimental conditions. Prior to recalling their earliest memory, participants in the early and late conditions were presented with examples referring to memories from age 1-2 or 5-6, respectively. The example memories in the control group did not contain any age cues. Participants reported the estimated age in their earliest memory and their strategy for arriving at this estimate. They also rated their memory's phenomenology (e.g. vividness). Independent judges rated memory type (e.g., snapshot memories).
Compared to the control group, participants in the early condition estimated the age in their memory to be significantly earlier. The difference between the late and control conditions was too small to be of interest. We did not observe a statistically significant interaction between memory type and condition. Snapshot memories were from a younger age than event memories and showed differences with respect to phenomenology (e.g., emotional intensity).
The results of this community study replicate earlier findings that instructions including age cues influence estimates of age in earliest memories. Although snapshot and event memories seem to be qualitatively different, the idea that they respond differently to an age manipulation could not be corroborated.
Journal Article