School of Psychology - Leading psychological science, scholarship and practice


CNRG clinical research

Aging and Neurodegenerative Disorders


Aging & Alzheimer's Disease: Future Simulation (Addis)

Prof Daniel Schacter and I have recently examined how the episodic specificity of past and future events changes in healthy aging and Alzheimer's disease. Firstly, we have shown that the age-related reduction in the number of episodic details generated when remembering past events extends to imagining future experiences. However, older adults generate significantly more non-episodic details (e.g., semantic details) than young adults when describing past and future events. We have also shown that patients with Alzheimer's disease exhibit a significant reduction in both episodic and non-episodic details when describing past and future events, relative to age-matched controls. These deficits persist even when controlling for deficits in fluency.

  • Addis, D.R., Musicaro, R., Pan, L., Schacter, D.L. (2010). Episodic simulation of past and future events in older adults: Evidence from an experimental recombination task. Psychology and Aging, 25, 369–376.
  • Addis, D.R., Sacchetti, D.C., Ally, B.A., Budson, A.E., Schacter, D.L. (2009). Episodic simulation of future events is impaired in mild Alzheimer's disease. Neuropsychologia, 47, 2660–2671


Aging, Mild Cognitive Impairment & Alzheimer's Disease: Recognition Memory and LTP (Kirk/Tippett)

In this research we aim to identify an earlier marker of Alzheimer's disease (AD) that will distinguish early AD from mild cognitive impairment (MCI) and normal aging. To do this we are testing whether behavioural and neurophysiological tests (EEG and fMRI) of recognition memory and the degree to which LTP can be induced, distinguish (either alone or in combination) early AD from MCI (memory) and normal aging. With Tina Koulikova and collaborator Dr Phil Wood (North Shore Hospital), we are first testing these measures in healthy elderly samples to see if we can reliably induce LTP and generate reliable behavioural and neurophysiological correlates of recognition memory. We will then extend our research to include groups of individuals with early AD and MCI.


Alzheimer's Disease: Memory and Identity (Addis/Tippett)

Integrating methods from social psychology and neuropsychology, we have examined the impact of autobiographical memory loss on the integrity of identity (measured with the Twenty Statements Test and the Tennessee Self Concept Scale) in patients with Alzheimer's disease. This revealed that loss of late childhood/early adulthood AMs had the most significant effects on identity, such that identity became weaker (i.e., patients could not generate as much information about themselves) and more abstract in nature, even when controlling for general cognitive decline. We are also interested in how AM contributes to specific aspects of identity such as self-continuity.

  • Addis, D. R., Tippett, L.J. (2008). The contributions of autobiographical memory to the content and continuity of self: a social-cognitive neuroscience approach. In F. Sani (Ed.), Self-Continuity: Individual and Collective Perspectives (pp. 71-84). NY: Psychology Press.
  • Addis, D.R., Tippett, L.J. (2004). Memory of myself: Autobiographical memory & identity in Alzheimer's disease. Memory, 12, 56-74.


Alzheimer's Disease: Semantic Deficits (Tippett)

Impairments in semantic memory commonly occur in Alzheimer's Disease (AD) but do these occur along category-specific lines? We recently conducted a study designed to examine the effects of stimulus properties on living-nonliving category deficits. We found that a main determinant of whether or not a categorical impairment is found in AD is which stimulus properties are controlled during stimulus selection. We also concluded that AD does not generally lead to a selective category loss in semantic knowledge.  We have also examined the contribution of selection ability (i.e., selecting a response from several competing semantic representations) to semantic impairments in AD, finding that patients were disproportionately impaired in high-selection conditions requiring a response selection from competing alternatives, suggesting that impaired semantic selection abilities in AD may contribute to poor performance on some semantic tasks.

  • Tippett, LJ, Meier SL, Blackwood, K, Diaz-Asper, C. (2007). Category-specific deficits in Alzheimer's Disease:  Fact or artefact? Cortex, 43, 907-920.
  • Tippett, LJ., Gendall, A., Farah, MJ, Thompson-Schill, SJ  (2004). Selection ability in Alzheimer's Disease:  Investigation of a component of semantic processing. Neuropsychology, 18, 163-173.
  • Tippett LJ, Grossman M, Farah MJ. (1996). The semantic memory impairment of Alzheimer's disease: category-specific? Cortex, 32, 143-53.


Amyotrophic Lateral Sclerosis: Dysfunction of Orbitomedial Prefrontal Cortex (Tippett)

In collaboration with Sandra Meier and Dr Alison Charleston of Auckland City Hospital, we are investigating whether individuals with Amyotrophic Lateral Sclerosis without dementia (ALS; also known as Motor Neurone Disease) experience behavioural and neuropsychological changes associated with dysfunction of orbitomedial prefrontal cortex (OMPFC).  Dysfunction of OMPFC is associated with profound and debilitating changes in behaviour and social functioning which would place increased strain on interpersonal and familial relationships at a time when carers and family members are already experienced increased stress through having to cope with a truly debilitating illness.  In a neuropsychological study we have found that 39% of individuals with ALS without dementia showed significant impairment of tasks sensitive to dysfunction.  This can occur in conjunction with dysfunction of dorsolateral prefrontal cortex, or independently of this.  To further investigate the hypothesis that there is neural dysfunction of OMPFC, in collaboration with Dr Donna Rose Addis, we are currently conducting an fMRI study of orbitomedial function during reversal learning in healthy adults and individuals with ALS.


Huntington's Disease: Multidisciplinary Studies of Heterogeneity (Tippett)

Variable phenotype is common in neurological disorders with single-gene inheritance patterns. In Huntington's disease (HD), despite the presence of a single autosomal gene that produces the disease, there is significant clinical variability with regards to the presence and severity of mood, cognitive and motor symptoms. With the involvement of research fellow Virginia Hogg, we are undertaking a range of studies that aim to understand the clinical variability In HD and the pathological mechanisms that underlie this variability. This research requires strong links with clinical services (Dr Richard Roxburgh, Neurogenetics Clinic, Auckland City Hospital, Huntington's Disease Field Officers for Huntington's Disease), and with basic neuroscience researchers (Prof Richard Faull, Dept of Anatomy with Radiology, UoA). Studies involve both prospective studies of individuals with the disease or the HD gene (currently 65 individuals with the HD gene are enrolled), and retrospective studies, involving individuals who have died with the disease and donated their brains to the Neurological Foundation of New Zealand Human Brain Bank. In one study involving immunohistochemical analyses of donated brains of HD persons and clinical profiles derived from family members and records of individuals who had died with HD, we were able to document for the first time functional abilities associated with specific neurochemical compartments of the striatum in humans. In particular we showed a significant association between pronounced mood dysfunction in HD patients and differential loss of the GABA(A) receptor marker in striosomes of the striatum, suggesting that striatum, and that striosome-related circuits may modulate mood functioning. Our findings also suggest there may be subtypes of HD.

In another recent collaborative study our findings challenge the notion of HD as a 'basal ganglia-only' disease and suggest that clinical symptoms may be also strongly linked to the integrity of regions of cerebral cortex.  Again using brains donated to the Human Brainbank, we have found a significant relationship between cell loss in the anterior cingulate gyrus and mood disturbance, and a significant relationship between cell loss in motor cortex and movement disturbance, indicating cortical changes do contribute to the nature of clinical symptoms experienced in HD.

Environment influences may also modify the clinical expression of HD. We have been investigating the possible contribution of level of activity in age of clinical onset of symptoms in collaboration with Australian researchers at the Murdoch Children's Research Institute (lead by A/P Martin Delatyck). Data analyses that level of passive activity in leisure and non-leisure is associated with early onset on clinical symptoms, particularly in teenage years. These results been received with interest at several international meetings this year as they provide the first evidence supporting the idea that activity levels may alter the clinical onset of HD. We are currently submitting this work for publication.

  • Tippett, LJ, Waldvogel, HJ, Thomas, SJ, Hogg VM, Roon-Mom, W, Synek, BJ, Graybiel AM, Faull, RLM (2007). Striosome and mood dysfunction in Huntington's disease.  Brain, 130, 206-221).
  • Roon-Mom, WMC, Hogg, VM, Tippett, LJ, Faull, RLM (2006).  Aggregate distribution in frontal and motor cortex in Huntington's disease brain.  Neuroreport, 17, 667-670.
  • Thu DCV, Oorshot DE, Tippett, LJ, Hogg, VM, Waldvogel, HJ, Faull RLM (in preparation). Correlating pattern of cell loss in cerebral cortex with patterns of symptomatology in Huntington's Disease.  To be submitted to Journal of Neuroscience. 


Huntington's Disease: Cortical thinning in pre-symptomatic Huntington's Disease (Tippett)

Recent MRI studies have shown that cortical thinning may occur early in Huntington's Disease, suggesting that the variable clinical and neuropsychological difficulties experienced are likely to reflect cortical changes as well as the direct and indirect effects of striatal pathology. In a collaborative research project with Dr D. Diana Rosas (Athinoula A Martinos Center for Biomedical Imaging, MGH, Boston), our group (including Virginia Hogg, Sasha Moses, John Davison and Dr Richard Roxburgh of Auckland City Hospital) is conducting a longitudinal investigation of cortical and white matter changes in individuals pre-symptomatic for Huntington's Disease and its association with neuropsychological performance.  This involves measurement of cortical thinning and white matter tract integrity via DTI. We recently completed MRI image analyses of cortical thinning in 19 pre-symptomatic HD participants and 19 controls matched case-by-case and found evidence of cortical thinning predominantly in the right parieto-temporal-occipital junction in individuals within 15 years of clinical onset of the disease. The presymptomatic HD group, particularly those closer to clinical onset, also performed more poorly than controls on two of six cognitive tests subserved primarily by posterior cortical regions (Judgement of Line Orientation [JLOT] and Moneys Road Map), but not on tests subserved primarily by anterior cortical regions. These data suggest the cortical thinning measured on MRI may underlie specific functional difficulties.  We are about to undertake the second set of scans.


Multiple Sclerosis: Information processing and Quality of Life (Barker-Collo)

Information-processing speed (IPS) has been identified as an area of primary deficit in multiple sclerosis regardless of disease course. We have examined these effects using the Paced Auditory Serial Addition Test. Moreover, we have examined the significant impacts of multiple sclerosis on quality of life. Examining patient narratives has revealed that those with multiple sclerosis have concerns about the unpredictable progression of the disease, and experience both negative and positive aspects of living with a chronic illness, such as fear and anxiety in relation to the unknown, shifting roles, discrimination, re-evaluation of priorities, reinvestment in the family, and positive lifestyle changes.

  • Barker-Collo S. (2005). Within session practice effects on the PASAT in clients with Multiple Sclerosis. Archives of Clinical Neuropsychology, 20, 145-152.
  • Barker-Collo, S (2006). Quality of Life in Multiple Sclerosis: Does Information Processing Speed have an independent effect? Archives of Clinical Neuropsychology, 21, 167-174.
  • Barker-Collo, S., Cartwright, C., & Read, J. (2006). Into the Unknown: The Experiences of Individuals Living with Multiple Sclerosis.  Journal of Neuroscience Nursing, 38, 435-441.


Parkinson's Disease: Emotional Processing and Social Interactions (Tippett)

Some research findings suggest Parkinson's disease (PD) affects recognition of emotional facial expressions (especially disgust and anger), and reduces sensitivity to prosodic expressions of anger, disgust and fear, but findings are inconsistent. Sharon Buxton (in collaboration with Lorraine MacDonald of Auckland City Hospital) has investigated recognition of facial and prosodic emotional expressions (happy, sad, angry, disgust, fear, surprise) in 30 medicated-PD participants and 30 age, education and gender-matched controls. Individuals with PD had no difficulty identifying expressions on 100% emotion faces (happy, sad, angry, disgust, fear, surprise), but were impaired with morphed emotional expressions with significantly lower scores recognising disgusted, happy, sad and surprised faces but not anger or fear. PD participants were also impaired overall on emotion identification by prosody. These data suggest that PD induces subtle dysfunction of emotional processing affecting both facial and prosodic stimuli. Dopaminergic depletion interrupting basal ganglia/frontal-striatal systems is likely to underlie these findings, with orbitofrontal cortex, sensitive to judging vocal and facial emotional expressions, also implicated. We are also interested in investigating the impact of these aspects of emotional processing on the quality of social interactions experienced by individuals with PD and on levels of depression.

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Neurodevelopmental Disorders


ADHD (Waldie)

ADHD pathogenesis has been related to atypical laterality. One area of our research involves the use of EEG and fMRI to investigate the neural basis of ADHD in terms of laterality, including the neural mechanisms involved in attention. Additionally we draw upon data from longitudinal studies to track long-term outcomes of the developmental disorder.

  • Rolfe, M.H.S., Hamm. J.E., Waldie, K.E. (2008). Differences in paper-and-pencil versus computerized line bisection according to ADHD subtype and hand-use. Brain and Cognition, 66, 188-195.
  • Horrobin, S.L., McNair, N.A.,Kirk, I., Waldie, K.E. (2007). Dexamphetamine normalises electrophysiological activity in attention deficit hyperactivity disorder during the Stroop task. Neurocase, 13, 301-310.
  • Rolfe, M.H.S., Kirk, I.J., Waldie, K.E. (2007). Interhemispheric callosal transfer in adults with Attention-deficit/Hyperactivity Disorder: An event-related potential study. NeuroReport, 18, 255-259.
  • Rolfe, M.H.S., Hausmann, M., Waldie, K.E. (2006). Hemispheric functioning in children with subtypes of ADHD. Journal of Attention Disorders, 10, 20-27.


Asperger's Syndrome: Neurophysiological Responses to Faces and Emotion (Kirk)

We have used brain imaging techniques such as EEG to investigate atypical neural processing in Asperger's Syndrome. In particular, we have focussed on changes in the neural responses to faces, as well as emotional processing.

  • O'Connor K., Hamm J.P., Kirk, I.J. (2007). Neurophysiological responses to face, facial regions and objects in adults with Asperger's syndrome: An ERP investigation. International Journal of Psychophysiology, 63, 283-293.
  • O'Connor K., Hamm J.P., Kirk I.J.(2005). The Neurophysiological Correlates of Emotional Processing in Asperger's Syndrome. Brain and Cognition 59, 82-95.


Auditory Processing and Reading Disorders (Purdy)

A major focus of our research in Speech Science at present is in the area of diagnosis and intervention for school-aged children with auditory processing disorder. These projects include investigation of auditory processing (measured behaviourally and using auditory evoked potentials) in school-aged children with reading and language difficulties. We also investigate speech perception in infants with normal hearing and in hearing-impaired infants wearing hearing aids and the relationship between behavioural and auditory evoked potential measures of speech discrimination in young infants.

  • Purdy, S. C., Sharma, M., Munro, K. J. Morgan, C. L. A. (2013). Stimulus level effects on speech-evoked obligatory cortical auditory evoked potentials in infants with normal hearing. Clinical Neurophysiology, 124(3), 474-480.
  • Sharma, M., Purdy, S. C., Kelly, A. S. (2012). A randomized control trial of interventions in school-aged children with auditory processing disorders. International Journal of Audiology, 51(7):506-18.
  • Purdy, S. C., Smart, J. L., Baily, M., Sharma, M. (2009). Do children with reading delay benefit from the use of personal FM systems in the classroom? International Journal of Audiology, 48, 843-852.
  • Purdy, S. C. (2009). Hearing and speech sound disorders. In C. Bowen, Children's speech sound disorders. (pp. 350-358). Oxford: Wiley-Blackwell.
  • Sharma M, Purdy S.C, Newall P., Wheldall K., Beaman R. (2007). Refractory effects on auditory-evoked responses in children with reading disorder. Neuroreport, 18, 133-136.
  • Sharma M, Purdy S.C, Newall P., Wheldall K., Beaman R., Dillon, H. (2006). Electrophysiological and behavioral evidence of auditory processing disorders in children with reading disorder. Clinical Neurophysiology, 117, 1130-1144.


Dyslexia (Waldie)

I am interested in the neural basis and long-term outcome of dyslexia. The interhemispheric deficit theory of dyslexia postulates that reading difficulties can arise from abnormal communication between the cerebral hemispheres. Using a redundant stimuli task, we investigated interhemispheric processing and integration in children with phonological dyslexia, and results suggest there may be deficits in the transfer of information across the corpus callosum. Dyslexic children also show impairments in processing that require precise timing of sensory events. We have investigated this using a test of auditory temporal acuity (a gap-detection task) and found that children aged 6-9 years with dyslexia exhibited a significant deficit relative to age-matched controls; this deficit was not observed in reading-impaired older children or adults. These findings suggest that while auditory temporal acuity deficits may ameliorate over time, language-related perceptual problems - particularly those related to phonological processing - persist. I am currently involved in a study looking at the cognitive and neurological profiles of adults with comorbid learning disabilities: dyslexia, dyscalculia, and both.

  • Andrewes, S.G., Waldie, K.E. (2009). Developmental Dyslexia. EDUVAC: Education Weekly, 20 (792), 4-8. 
  • Badzakova-Trajkov, G., Hamm, J., Waldie, K.E. (2005). The effects of redundant stimuli on visuospatial processing in developmental dyslexia. Neuropsychologia, 43, 473-478.
  • Waldie, K.E. (2004). The role of the right hemisphere in normal and impaired reading development. In C. Rodrigues and L.M.B. Tomitch (Eds), Language and the Brain: A Multidisciplinary Perspective (pp 177-191). Brasil: Artmed Editora.
  • Hautus, M.J., Setchell, G.J., Waldie, K.E., Kirk, I.J. (2003). Age-Related Improvements in Auditory Temporal Resolution in Reading-Impaired Children. Dyslexia, 9, 37-45.
  • Waldie, K.E. (2002). Reading with the right hemisphere: From normal development to dysphonetic dyslexia. In Serge P. Shohov (Ed.) Advances in Psychology Research (Vol. 9, pp 157-184). New York: Nova Science Publishers, Inc.
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Neuropsychiatric Disorders


Schizophrenia: Interhemispheric Communication (Kirk)

We have used brain imaging techniques such as EEG to investigate atypical neural processing in schizophrenia. In particular, we have focussed on interhemsipheric transfer of information in these patients. This research is in collaboration with Dr Kylie Barnett (Trinity College, Dublin), Dr Robert Miller (Otago) & Prof Michael Corballis (UoA).

  • Barnett, K.J., Corballis, M.C., Kirk, I.J. (2005). Symmetry of callosal information transfer in schizophrenia. Schizophrenia Research, 74,171-8.
  • Barnett KJ, Kirk IJ. (2005). Lack of asymmetrical interhemispheric transfer of linguistic stimuli schizophrenia: An ERP study. Clinical Neurophysiology. 116, 1019-27.
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Neurological Disorders


Headache Disorders (Waldie)

We investigate the impact and predictors of neurological pain syndromes, such as migraine and tension-type headaches (TTH), using data from longitudinal studies. For instance, we have investigated cognitive functioning in headache disorders. We have found a relation between childhood TTH and lower scores on most cognitive measures (e.g., verbal and performance IQ). We have also found that child migraine sufferers are subtly impaired relative to those with TTH and headache-free control subjects on tests of verbal ability, which may impact later academic success.

  • Waldie, K.E., McGee, R., Reeder, T., Poulton, R. (2008). The association between frequent headaches, persistent smoking, and attempts to quit. Headache, 48, 545-552.
  • Waldie, K.E., Poulton, R. (2002). Physical and psychological correlates of primary headache in young adulthood: A 26-year longitudinal study. Journal of Neurology, Neurosurgery & Psychiatry, 72, 86-92.
  • Waldie, K.E., Hausmann, M., Milne, B.J., Poulton, R. (2002). Migraine and cognitive function: a life-course study. Neurology, 59, 904-908.
  •  Waldie, K.E. (2001). Childhood headache, stress in adolescence, and primary headache in young adulthood: A longitudinal cohort study. Headache, 41, 10-21.


Temporal Lobe Epilepsy: Lateralisation, Language and Memory Pathways using fMRI and DTI (Kirk/Tippett)

We are currently using fMRI, arterial spin labelling and DTI methods to understand the normal pathways underlying language and memory function and changes associated with temporal lobe epilepsy. The long-term aim of this work is to develop these findings for use in clinical contexts, specifically the pre-surgical assessment of language and memory for temporal lobectomy patients. This work is being conducted in collaboration with Callum Thorpe, Sarina Iwabuchi and Dr Peter Bergin (Auckland City Hospital).


Temporal Lobe Epilepsy: Neural Changes during Autobiographical Memory Retrieval (Addis)

We have examined how autobiographical memory retrieval and the associated neural network are altered by left hippocampal damage in temporal lobe epilepsy (TLE) patients and mild deficits in episodic autobiographical memory. During the retrieval of residual memories, these patients exhibited significant reductions in activation of the hippocampus, as well as other regions in the autobiographical memory network, even though memory performance was included as a covariate. Further, the effective connectivity of the autobiographical memory network was dramatically different between patients and controls, with an apparent "bypassing" of the left hippocampus.

  • Addis, D. R., Moscovitch, M. and McAndrews, M. P. (2007). Consequences of hippocampal damage across the autobiographical memory retrieval network in patients with left temporal lobe epilepsy. Brain, 130, 2327-2342.


Traumatic Brain Injury: Incidence, Outcomes and Rehabilitation (Barker-Collo)

Traumatic brain injury (TBI) impacts a significant portion of individuals, and can have lasting consequences. One of the most common and persistent difficulties experienced post-TBI is deficits in memory, which impact up to 80% of TBI survivors. Early memory rehabilitation research concentrated on the direct retraining approach. In recent years, the focus of rehabilitative efforts has shifted to teaching compensatory strategies and optimizing residual abilities.

  • Barker-Collo, S. L., Feigin, V. L. (2009) Incidence of Traumatic Brain Injury: A systematic Review. Neuroepidemiology, 31, 1 - 3
  • Barker-Collo, S. L., Feigin, V. (2008) Memory deficit after traumatic brain injury: How big is the problem in New Zealand and what management strategies are available. New Zealand Medical Journal, 121, 2903. 
  • Feigin, V. L., Barker-Collo, S. L (2008). Applied brain injury research in New Zealand: Can we do better? New Zealand Medical Journal, 121, 1258.
  • Thickpenny-Davis, K., & Barker-Collo, S. (2007) Does memory performance of adults with brain injury improve following participation in a structured memory rehabilitation group? Journal of Head Trauma rehabilitation, 22(5), 303-313.


Stroke: Incidence, Outcomes and Rehabilitation (Barker-Collo)

Stroke has an enormous physical, emotional and economic impact on the patients, families and society. Stroke care resources are scarce, and the number of stroke survivors is likely to increase with the ageing of the population. Thus, evaluating the cost, frequency and prognostic factors of long-terms stroke functional and neuropsychological outcomes is of paramount importance for evidence-based clinical decision making, including the rationale, planning, provision and allocation of health services, and the development of effective interventions.

  • Feigin VL, Lawes CM, Bennett DA, Barker-Collo SL, Parag V (2009) Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurology, 8, 355-369.
  • Feigin, V. L., Barker-Collo, S. L., McNaughton, H., Brown, P. (2008) Long term neuropsychological and functional outcomes in stroke survivors: Current evidence and perspectives for new research. International Stroke Journal, 3, 33-40.
  • Barker-Collo, S.L., Feigin, V.L., Dudley, M. D. (2007). Post stroke fatigue- Where is the evidence on which to guide practice? New Zealand Medical Journal, 120, 1-9.
  • Barker-Collo, S & Feigin, V. (2006) The Impact of Neuropsychological Deficits on Functional Stroke Outcome. Neuropsychology Review. 16, 53-64.


Stroke: Neurocognitive Decline Following Cardiac Surgery (Tippett)

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. In collaborations with Prof Barber and Mr P. Milsom (Auckland City Hospital) we are investigating (1) the rate of stroke, new ischemic change on MR assessed with diffusion-weighted imaging, and cognitive impairment after cardiac valve surgery; and (2) the controversial relationship between perioperative cerebral ischemia and cognitive decline. In a series of 40 patients who underwent pre- and post-surgical assessments, we found cognitive decline was seen in all patients with postoperative ischemic lesions, and in 35% of those without new lesions. There was an association between the number of abnormal cognitive tests and ischemic burden. These studies provide a reliable estimate of the rate of stroke, postoperative ischemia, and cognitive impairment at 6 weeks after cardiac valve surgery. Longitudinal follow-up of these patients will provide further information as to whether these associations remain beyond the 6-week period.

  • Barber PA, Tippett LJ, Merry A, Hach S, Frampton C, Milsom P. (2009). Postoperative ischemia and cognitive impairment in cardiac surgery patients. Annals of Thoracic Surgery, 87, 672-3.
  • Barber PA, Hach S, Tippett LJ, Ross, L, Merry AF, Milsom P. (2008). Cerebral ischemic lesions on diffusion-weighted imaging are associated with neurocognitive decline following cardiac surgery. Stroke, 39, 1427-1433.
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