Lynette J Tippett

New Zealand Brain Research Institute, Christchurch, Canterbury Region, New Zealand

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Publications (38)127.09 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: The cellular basis of variable symptoms in Huntington's disease (HD) is unclear. One important possibility is that degeneration of the interneurons in the cerebral cortex, which play a critical role in modulating cortical output to the basal ganglia, may play a significant role in the development of variable symptomatology in HD. This study aims to examine whether symptom variability in HD is specifically associated with variable degeneration of cortical interneurons.Methods: We undertook a double-blind study using stereological cell counting methods to quantify the three major types of GABAergic interneurons (calbindin-D28k, calretinin, parvalbumin) in 13 HD cases of variable motor/mood symptomatology and 15 matched control cases in the primary motor and anterior cingulate cortices.Results: In the primary motor cortex, there was a significant loss (57% reduction) of only calbindin interneurons (p = 0.022) in HD cases dominated by motor symptoms, but no significant interneuron loss in cases with a dominant mood phenotype. By contrast, the anterior cingulate cortex showed a major significant loss in all three interneuron populations with 71% loss of calbindin (p = 0.001), 60% loss of calretinin (p = 0.001), and 80% loss of parvalbumin interneurons (p = 0.005) in HD cases with major mood disorder, while no interneuron loss was observed in cases with major motor dysfunction.Interpretation: These findings suggest that region-specific degeneration of cortical interneurons is a key component in understanding the neural basis of symptom heterogeneity in HD. ANN NEUROL 2014. © 2014 American Neurological Association
    Annals of Neurology 04/2014; · 11.19 Impact Factor
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    Andrew J Latham, Lucy L M Patston, Lynette J Tippett
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    ABSTRACT: Just how expert are "expert" video-game players? Assessing the experience and expertise of video-game players across "action" video-game genres Video-game play (particularly "action" video-games) holds exciting promise as an activity that may provide generalized enhancement to a wide range of percep-tual and cognitive abilities (for review see Latham et al., 2013a). However, in this article we make the case that to assess accurately the effects of video-game play researchers must better character-ize video-game experience and expertise. This requires a more precise and objective assessment of an individual's video-game history and skill level, and making finer distinctions between video-games that fall under the umbrella of "action" games. Failure to consider these factors may partly be responsible for mixed findings (see Boot et al., 2011).
    Frontiers in Psychology 12/2013; 4(941):1-3.
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    Andrew J Latham, Lucy L M Patston, Lynette J Tippett
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    ABSTRACT: Forty years have passed since video-games were first made widely available to the public and subsequently playing games has become a favorite past-time for many. Players continuously engage with dynamic visual displays with success contingent on the time-pressured deployment, and flexible allocation, of attention as well as precise bimanual movements. Evidence to date suggests that both brief and extensive exposure to video-game play can result in a broad range of enhancements to various cognitive faculties that generalize beyond the original context. Despite promise, video-game research is host to a number of methodological issues that require addressing before progress can be made in this area. Here an effort is made to consolidate the past 30 years of literature examining the effects of video-game play on cognitive faculties and, more recently, neural systems. Future work is required to identify the mechanism that allows the act of video-game play to generate such a broad range of generalized enhancements. Video-game play has become the past-time of choice for current generations, with entertainment software allowing individuals to engage both socially and competitively with individuals across the globe. Players engage with seamless virtual environments with success contingent on the execution of precise bimanual motor movements in response to complex visual cues. Evidence suggests that extensive video-game play may lead to the enhancement of visual attention and executive control, generalizing beyond the context of the video game, although this is still debated. Video games became publically available for the first time in 1972 with the release of the first arcade machine, and house-hold gaming console, the Magnavox Odyssey. While this new technology was quickly seized upon by the public, it was not without objection. Many saw video-game play as a mindless exercise imparting no real benefit to the player. Ball (1978) defended video-game play and suggested it offered a potential mechanism to improve a variety of cognitive skills including eye-hand coordination, decision making, following directions, and number and word recognition. Many publications that address these claims have followed. In this paper we present a comprehensive review of studies over the last 30 years that contribute both to current views concerning the effects of video-game play on specific cognitive domains and to their neural underpinnings. This review is organized primarily by cognitive functions that are argued to be influenced by video-game play. It also exam-ines the small literature addressing the neural underpinnings of superior behavioral performance in video-game players, and considers the challenges to, and limitations of, the video-game literature. Results of all the studies reviewed are summarized in Supplementary Table 1.
    Frontiers in Psychology. 09/2013; 4(629):1-10.
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    ABSTRACT: Although dystonia represents a major source of motor disability in Huntington's disease (HD), its pathophysiology remains unknown. Because recent animal studies indicate that loss of parvalbuminergic (PARV+) striatal interneurons can cause dystonia, we investigated if loss of PARV+ striatal interneurons occurs during human HD progression, and thus might contribute to dystonia in HD. We used immunolabeling to detect PARV+ interneurons in fixed sections, and corrected for disease-related striatal atrophy by expressing PARV+ interneuron counts in ratio to interneurons co-containing somatostatin and neuropeptide Y (whose numbers are unaffected in HD). At all symptomatic HD grades, PARV+ interneurons were reduced to less than 26% of normal abundance in rostral caudate. In putamen rostral to the level of globus pallidus, loss of PARV+ interneurons was more gradual, not dropping off to less than 20% of control until grade 2. Loss of PARV+ interneurons was even more gradual in motor putamen at globus pallidus levels, with no loss at grade 1, and steady grade-wise decline thereafter. A large decrease in striatal PARV+ interneurons, thus, occurs in HD with advancing disease grade, with regional variation in the loss per grade. Given the findings of animal studies and the grade-wise loss of PARV+ striatal interneurons in motor striatum in parallel with the grade-wise appearance and worsening of dystonia, our results raise the possibility that loss of PARV+ striatal interneurons is a contributor to dystonia in HD. © 2013 Movement Disorder Society.
    Movement Disorders 09/2013; · 4.56 Impact Factor
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    ABSTRACT: Increasing behavioural evidence suggests that expert video game players (VGPs) show enhanced visual attention and visuospatial abilities, but what underlies these enhancements remains unclear. We administered the Poffenberger paradigm with concurrent electroencephalogram (EEG) recording to assess occipital N1 latencies and interhemispheric transfer time (IHTT) in expert VGPs. Participants comprised 15 right-handed male expert VGPs and 16 non-VGP controls matched for age, handedness, IQ and years of education. Expert VGPs began playing before age 10, had a minimum 8 years experience, and maintained playtime of at least 20 hours per week over the last 6 months. Non-VGPs had little-to-no game play experience (maximum 1.5 years). Participants responded to checkerboard stimuli presented to the left and right visual fields while 128-channel EEG was recorded. Expert VGPs responded significantly more quickly than non-VGPs. Expert VGPs also had significantly earlier occipital N1s in direct visual pathways (the hemisphere contralateral to the visual field in which the stimulus was presented). IHTT was calculated by comparing the latencies of occipital N1 components between hemispheres. No significant between-group differences in electrophysiological estimates of IHTT were found. Shorter N1 latencies may enable expert VGPs to discriminate attended visual stimuli significantly earlier than non-VGPs and contribute to faster responding in visual tasks. As successful video-game play requires precise, time pressured, bimanual motor movements in response to complex visual stimuli, which in this sample began during early childhood, these differences may reflect the experience and training involved during the development of video-game expertise, but training studies are needed to test this prediction.
    PLOSone. 09/2013; 8(9).
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    Andrew J Latham, Lucy L M Patston, Lynette J Tippett
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    ABSTRACT: Forty years have passed since video-games were first made widely available to the public and subsequently playing games has become a favorite past-time for many. Players continuously engage with dynamic visual displays with success contingent on the time-pressured deployment, and flexible allocation, of attention as well as precise bimanual movements. Evidence to date suggests that both brief and extensive exposure to video-game play can result in a broad range of enhancements to various cognitive faculties that generalize beyond the original context. Despite promise, video-game research is host to a number of methodological issues that require addressing before progress can be made in this area. Here an effort is made to consolidate the past 30 years of literature examining the effects of video-game play on cognitive faculties and, more recently, neural systems. Future work is required to identify the mechanism that allows the act of video-game play to generate such a broad range of generalized enhancements.
    Frontiers in Psychology 01/2013; 4:629.
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    Andrew J Latham, Lucy L M Patston, Lynette J Tippett
    Frontiers in Psychology 01/2013; 4:941.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Increasing behavioural evidence suggests that expert video game players (VGPs) show enhanced visual attention and visuospatial abilities, but what underlies these enhancements remains unclear. We administered the Poffenberger paradigm with concurrent electroencephalogram (EEG) recording to assess occipital N1 latencies and interhemispheric transfer time (IHTT) in expert VGPs. Participants comprised 15 right-handed male expert VGPs and 16 non-VGP controls matched for age, handedness, IQ and years of education. Expert VGPs began playing before age 10, had a minimum 8 years experience, and maintained playtime of at least 20 hours per week over the last 6 months. Non-VGPs had little-to-no game play experience (maximum 1.5 years). Participants responded to checkerboard stimuli presented to the left and right visual fields while 128-channel EEG was recorded. Expert VGPs responded significantly more quickly than non-VGPs. Expert VGPs also had significantly earlier occipital N1s in direct visual pathways (the hemisphere contralateral to the visual field in which the stimulus was presented). IHTT was calculated by comparing the latencies of occipital N1 components between hemispheres. No significant between-group differences in electrophysiological estimates of IHTT were found. Shorter N1 latencies may enable expert VGPs to discriminate attended visual stimuli significantly earlier than non-VGPs and contribute to faster responding in visual tasks. As successful video-game play requires precise, time pressured, bimanual motor movements in response to complex visual stimuli, which in this sample began during early childhood, these differences may reflect the experience and training involved during the development of video-game expertise, but training studies are needed to test this prediction.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Increasing behavioural evidence suggests that expert video game players (VGPs) show enhanced visual attention and visuospatial abilities, but what underlies these enhancements remains unclear. We administered the Poffenberger paradigm with concurrent electroencephalogram (EEG) recording to assess occipital N1 latencies and interhemispheric transfer time (IHTT) in expert VGPs. Participants comprised 15 right-handed male expert VGPs and 16 non-VGP controls matched for age, handedness, IQ and years of education. Expert VGPs began playing before age 10, had a minimum 8 years experience, and maintained playtime of at least 20 hours per week over the last 6 months. Non-VGPs had little-to-no game play experience (maximum 1.5 years). Participants responded to checkerboard stimuli presented to the left and right visual fields while 128-channel EEG was recorded. Expert VGPs responded significantly more quickly than non-VGPs. Expert VGPs also had significantly earlier occipital N1s in direct visual pathways (the hemisphere contralateral to the visual field in which the stimulus was presented). IHTT was calculated by comparing the latencies of occipital N1 components between hemispheres. No significant between-group differences in electrophysiological estimates of IHTT were found. Shorter N1 latencies may enable expert VGPs to discriminate attended visual stimuli significantly earlier than non-VGPs and contribute to faster responding in visual tasks. As successful video-game play requires precise, time pressured, bimanual motor movements in response to complex visual stimuli, which in this sample began during early childhood, these differences may reflect the experience and training involved during the development of video-game expertise, but training studies are needed to test this prediction.
    PLoS ONE 01/2013; 8(9):e75231. · 3.73 Impact Factor
  • Sally C Prebble, Donna Rose Addis, Lynette J Tippett
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    ABSTRACT: Despite a strong intuitive and theoretical tradition linking autobiographical memory and sense of self, there are few coherent, testable models that exemplify how these constructs relate. Without any clear theoretical starting point, research efforts have been fragmented, with many different fields of psychology operating in relative isolation, using different methodological approaches and a confusing array of self-related terminology. We attempt to bridge the widening gap between theory and research by proposing a novel framework for sense of self and memory. This simple model delineates sense of self along 2 dimensions: the subjective versus objective and the present versus temporally extended aspects of sense of self. The 4 resulting components of sense of self are argued to relate to autobiographical memory in important, but very different, ways. Subjective sense of self provides a crucial precondition for episodic memory, which in turn is a prerequisite for phenomenological continuity. Autobiographical memory, and particularly its semanticized forms, are important for the formation and maintenance of a mental representation of the objective self in the present moment and across time. This model does not represent a new theoretical direction for the study of sense of self and memory; to the contrary, it is deeply grounded in the theoretical work of the past few decades. Its novelty is that it translates this theoretical groundwork into a form that is readily accessible for researchers. We review evidence for our model and suggest ways that it may provide a roadmap for future research efforts. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
    Psychological Bulletin 10/2012; · 15.58 Impact Factor
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    ABSTRACT: Huntington's disease (HD) is an autosomal dominant inherited neurodegenerative disease caused by a CAG repeat expansion in exon 1 of the Huntington gene (HD) also known as IT15. Despite the disease being caused by dysfunction ofa single gene, expressed as an expanded polyglutamine in the huntingtin protein, there is a major variability in the symptom profile of patients with Huntington's disease as well as great variability in the neuropathology. The symptoms vary throughout the course of the disease and vary greatly between cases. These symptoms present as varying degrees of involuntary movements, mood, personality changes, cognitive changes and dementia. To determine whether there is a morphological basis for this symptom variability, recent studies have investigated the cellular and neurochemical changes in the striatum and cerebral cortex in the human brain to determine whether there is a link between the pathology in these regions and the symptomatology shown by individual cases. These studies together revealed that cases showing mainly mood symptom profiles correlated with marked degeneration in the striosomal compartment of the striatum, or in the anterior cingulate gyrus of the cerebral cortex. In contrast, in cases with mainly motor symptoms neurodegeneration was especially marked in the primary motor cortex with variable degeneration in both the striosomes and matrix compartments of the striatum. These studies suggest that the variable degeneration of the striatum and cerebral cortex correlates with the variable profiles of Huntington's disease.
    Advances in experimental medicine and biology 01/2012; 769:141-52. · 1.83 Impact Factor
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    ABSTRACT: The form of the structural asymmetries across the cerebral hemispheres, that support well-established functional asymmetries, are not well understood. Although, many previous studies have investigated structural differences in areas associated with strong functional asymmetries, such as language processes, regions of the brain with less well established functional laterality have received less attention. The current study aims to address this by exploring global white matter asymmetries of the healthy human brain using diffusion tensor imaging (DTI) and tractography. DTI was conducted on twenty-nine healthy right-handed males, and pathways from the four major lobes were reconstructed using probabilistic tractography. Mean FA, parallel and perpendicular diffusion values were calculated and compared across hemispheres for each pathway generated. Significant asymmetries in the parietal (rightward asymmetry) and occipital (leftward asymmetry) pathways were found in FA measures. However, asymmetric patterns in parallel and/or perpendicular diffusion were observed in all four lobes, even in pathways with symmetrical FA. For instance, significant rightward asymmetry in parallel diffusion was found in the parietal and frontal lobes, whereas significant leftward asymmetry was found in the temporal and occipital lobes. We suggest that these different patterns of diffusion asymmetry reflect differences in microanatomy that support the known patterns of differential functional asymmetry. The different directions of anatomical asymmetry support the notion that there may be a number of different lateralising influences operating in the brain.
    Neuropsychologia 09/2011; 49(13):3599-604. · 3.48 Impact Factor
  • Sandra L Meier, Alison J Charleston, Lynette J Tippett
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    ABSTRACT: Amyotrophic lateral sclerosis, a progressive disease affecting motor neurons, may variably affect cognition and behaviour. We tested the hypothesis that functions associated with orbitomedial prefrontal cortex are affected by evaluating the behavioural and cognitive performance of 18 participants with amyotrophic lateral sclerosis without dementia and 18 healthy, matched controls. We measured Theory of Mind (Faux Pas Task), emotional prosody recognition (Aprosodia Battery), reversal of behaviour in response to changes in reward (Probabilistic Reversal Learning Task), decision making without risk (Holiday Apartment Task) and aberrant behaviour (Neuropsychiatric Inventory). We also assessed dorsolateral prefrontal function, using verbal and written fluency and planning (One-touch Stockings of Cambridge), to determine whether impairments in tasks sensitive to these two prefrontal regions co-occur. The patient group was significantly impaired at identifying social faux pas, recognizing emotions and decision-making, indicating mild, but consistent impairment on most measures sensitive to orbitomedial prefrontal cortex. Significant levels of aberrant behaviour were present in 50% of patients. Patients were also impaired on verbal fluency and planning. Individual subject analyses involved computing classical dissociations between tasks sensitive to different prefrontal regions. These revealed heterogeneous patterns of impaired and spared cognitive abilities: 33% of participants had classical dissociations involving orbitomedial prefrontal tasks, 17% had classical dissociations involving dorsolateral prefrontal tasks, 22% had classical dissociations between tasks of both regions, and 28% had no classical dissociations. These data indicate subtle changes in behaviour, emotional processing, decision-making and altered social awareness, associated with orbitomedial prefrontal cortex, may be present in a significant proportion of individuals with amyotrophic lateral sclerosis without dementia, some with no signs of dysfunction in tasks sensitive to other regions of prefrontal cortex. This demonstration of variability in cognitive integrity supports previous research indicating amyotrophic lateral sclerosis is a heterogeneous disease.
    Brain 10/2010; 133(11):3444-57. · 9.92 Impact Factor
  • Heart Lung &amp Circulation 08/2010; 19(8):489. · 1.25 Impact Factor
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    ABSTRACT: In transgenic mouse models of Huntington disease (HD) environmental enrichment significantly delays disease onset. A questionnaire-based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age-at-onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = -0.72, P < 0.001), but also with a lifestyle that included higher levels of passive activity (r = -0.38, P < 0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R(2) = 0.54, b = -0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3-7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R(2) = 0.12, b = 1.08, P < 0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. (c) 2010 Movement Disorder Society.
    Movement Disorders 07/2010; 25(10):1444-50. · 4.56 Impact Factor
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    ABSTRACT: Huntington's disease is an autosomal dominant inherited neurodegenerative disease with motor symptoms that are variably co-expressed with mood and cognitive symptoms, and in which variable neuronal degeneration is also observed in the basal ganglia and the cerebral cortex. We have recently shown that the variable symptomatology in Huntington's disease correlates with the variable compartmental pattern of GABAA receptor and cell loss in the striatum. To determine whether the phenotypic variability in Huntington's disease is also related to variable neuronal degeneration in the cerebral cortex, we undertook a double-blind study using unbiased stereological cell counting methods to determine the pattern of cell loss in the primary motor and anterior cingulate cortices in the brains of 12 cases of Huntington's disease and 15 controls, and collected detailed data on the clinical symptomatology of the patients with Huntington's disease from family members and clinical records. The results showed a significant association between: (i) pronounced motor dysfunction and cell loss in the primary motor cortex; and (ii) major mood symptomatology and cell loss in the anterior cingulate cortex. This association held for both total neuronal loss (neuronal N staining) and pyramidal cell loss (SMI32 staining), and also correlated with marked dystrophic changes in the remaining cortical neurons. There was also an association between cortical cell loss and striatal neuropathological grade, but no significant association with CAG repeat length in the Huntington's disease gene. These findings suggest that the heterogeneity in clinical symptomatology that characterizes Huntington's disease is associated with variation in the extent of cell loss in the corresponding functional regions of the cerebral cortex whereby motor dysfunction correlates with primary motor cortex cell loss and mood symptomatology is associated with cell loss in the cingulate cortex.
    Brain 04/2010; 133(Pt 4):1094-110. · 9.92 Impact Factor
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    The Annals of thoracic surgery 03/2009; 87(2):672-3; author reply 673-4. · 3.45 Impact Factor
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    ABSTRACT: Please see Platform Presentation above for abstract body.
    Neurotherapeutics. 01/2009; 6(1):209-209.
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    ABSTRACT: Transgenic HD mouse model studies have shown that raising mice in an enriched environment delays the onset of symptoms, leading us to consider whether pre-morbid lifestyle may affect age-at-onset in humans. Subjects with symptomatic HD were interviewed using a questionnaire to retrospectively ascertain pre-morbid lifestyle, including participation in a range of leisure activities and non-leisure activities (education, occupation, and domestic duties). Recorded activities were classified as physical, intellectual, or passive, and activity scores were generated under the headings leisure, non-leisure, and total lifestyle. Surveys were matched with the subject's age-at-onset and CAG repeat length. Analysis of age-at-onset data from 154 subjects in Australia and New Zealand showed a mean of 45.7 years (range 21-76), and a strong inverse correlation with CAG repeat length (r = −0.72, p < 0.001). Furthermore, a relationship between CAG repeat length and average pre-morbid lifestyle passivity was demonstrated (r = 0.34, p < 0.001), suggesting passivity to be a preclinical manifestation of disease. Upon this background, further analyses were undertaken. Multiple regression analyses that included CAG repeat length as one predictor variable showed passivity (both in leisure and non-leisure) to be a second, independent predictor of age-at-onset (b = −0.28, p = 0.04, and b = −0.27, p = 0.02, respectively), suggesting that a passive lifestyle also contributes to the early onset of symptoms. Leisure activity data covering three life stages (teens, 20s/30s, and 40s/50s) indicate that it is teenage passivity that correlates most strongly with age-at-onset (r = −0.38, p < 0.001). No relationships of significance were apparent involving age-at-onset and either intellectual or physical activity. The impact of passivity on age-at-onset is illustrated by comparing the mean age-at-onset in three groups based on lifestyle passivity score. A difference of 4.6 years (95% CI = 1.3 to 7.9) between high and low scoring groups (after adjusting for the impact of CAG repeat length) indicates a significant delay in the onset of symptoms in those who are less passive.
    Neurotherapeutics. 01/2009; 6(1):202-202.
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    ABSTRACT: Improvements in cardiac surgery mortality and morbidity have focused interest on the neurological injury such as stroke and cognitive decline that may accompany an otherwise successful operation. We aimed to investigate (1) the rate of stroke, new ischemic change on MRI, and cognitive impairment after cardiac valve surgery; and (2) the controversial relationship between perioperative cerebral ischemia and cognitive decline. Forty patients (26 men; mean [SD] age 62.1 [13.7] years) undergoing intracardiac surgery (7 also with coronary artery bypass grafting) were studied. Neurological, neuropsychological, and MRI examinations were performed 24 hours before surgery and 5 days (MRI and neurology) and 6 weeks (neuropsychology and neurology) after surgery. Cognitive decline from baseline was determined using the Reliable Change Index. Two of 40 (5%) patients had perioperative strokes and 22 of 35 (63%) tested had cognitive decline in at least one measure (range, 1 to 4). Sixteen of 37 participants (43%) with postoperative imaging had new ischemic lesions (range, 1 to 17 lesions) with appearances consistent with cerebral embolization. Cognitive decline was seen in all patients with, and 35% of those without, postoperative ischemic lesions (P<0.001), and there was an association between the number of abnormal cognitive tests and ischemic burden (P<0.001). We have provided a reliable estimate of the rate of stroke, postoperative ischemia, and cognitive impairment at 6 weeks after cardiac valve surgery. Cognitive impairment is associated with perioperative ischemia and is more severe with greater ischemic load.
    Stroke 06/2008; 39(5):1427-33. · 6.16 Impact Factor

Publication Stats

390 Citations
127.09 Total Impact Points

Institutions

  • 2014
    • New Zealand Brain Research Institute
      Christchurch, Canterbury Region, New Zealand
  • 2013
    • The University of Tennessee Health Science Center
      • Department of Anatomy and Neurobiology
      Memphis, TN, United States
  • 2003–2013
    • University of Auckland
      • • Department of Psychology
      • • Department of Anatomy with Radiology
      Окленд, Auckland, New Zealand
  • 2010
    • Auckland City Hospital
      Окленд, Auckland, New Zealand