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8 results

  • About time: neurocognitive correlates of stimulus-bound and other time setting errors in the Clock Drawing Test

  • Matan Soffer, Meryl A. Butters, Nathan Herrmann, Sandra E. Black, Sanjeev Kumar, Bradley Pugh, Tarek K. Rajji, Maria Carmela Tartaglia, David F. Tang-Wai, Morris Freedman
  • Journal:
    Journal of the International Neuropsychological Society / Volume 30 / Issue 5 / June 2024
    Published online by Cambridge University Press:
    13 December 2023, pp. 471-478
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  • Objective:

    Previous findings suggest that time setting errors (TSEs) in the Clock Drawing Test (CDT) may be related mainly to impairments in semantic and executive function. Recent attempts to dissociate the classic stimulus-bound error (setting the time to “10 to 11” instead of “10 past 11”) from other TSEs, did not support hypotheses regarding this error being primarily executive in nature or different from other time setting errors in terms of neurocognitive correlates. This study aimed to further investigate the cognitive correlates of stimulus-bound errors and other TSEs, in order to trace possible underlying cognitive deficits.

    Methods:

    We examined cognitive test performance of participants with preliminary diagnoses associated with mild cognitive impairment. Among 490 participants, we identified clocks with stimulus-bound errors (n = 78), other TSEs (n = 41), other errors not related to time settings (n = 176), or errorless clocks (n = 195).

    Results:

    No differences were found on any dependent measure between the stimulus-bound and the other TSErs groups. Group comparisons suggested TSEs in general, to be associated with lower performance on various cognitive measures, especially on semantic and working memory measures. Regression analysis further highlighted semantic and verbal working memory difficulties as being the most prominent deficits associated with these errors.

    Conclusion:

    TSEs in the CDT may indicate underlying deficits in semantic function and working memory. In addition, results support previous findings related to the diagnostic value of TSEs in detecting cognitive impairment.

  • Building the Bridge From Pediatric to Adult Neurological Care

  • Katherine M. Sawicka, Lindsey M. Vogt, Danielle M. Andrade, Hans D. Katzberg, Steven P. Miller, Mahendranath Moharir, David F. Tang-Wai, Ana Marissa Lagman-Bartolome
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 51 / Issue 5 / September 2024
    Published online by Cambridge University Press:
    27 October 2023, pp. 690-692
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  • In this brief communication, we discuss the current landscape and unmet needs of pediatric to adult transition care in neurology. Optimizing transition care is a priority for patients, families, and providers with growing discussion in neurology. We also introduce the activities of the University of Toronto Pediatric-Adult Transition Working Group – a collaborative interdivisional and inter-subspeciality group of faculty, advanced-practice providers, trainees, and patient-family advisors pursuing collaboration with patients, families, and universities from across Canada. We envision that these efforts will result in a national neurology transition strategy that will inform designation of health authority attention and funding.

  • Genetic Variation in the Ontario Neurodegenerative Disease Research Initiative

  • Part of
  • Allison A. Dilliott, Emily C. Evans, Sali M.K. Farhan, Mahdi Ghani, Christine Sato, Ming Zhang, Adam D. McIntyre, Henian Cao, Lemuel Racacho, John F. Robinson, Michael J. Strong, Mario Masellis, Dennis E. Bulman, Ekaterina Rogaeva, Sandra E. Black, Elizabeth Finger, Andrew Frank, Morris Freedman, Ayman Hassan, Anthony Lang, Christen L. Shoesmith, Richard H. Swartz, David Tang-Wai, Maria Carmela Tartaglia, John Turnbull, Lorne Zinman, the ONDRI Investigators, Robert A. Hegele
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 46 / Issue 5 / September 2019
    Published online by Cambridge University Press:
    15 August 2019, pp. 491-498
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  • Background/Objective:

    Apolipoprotein E (APOE) E4 is the main genetic risk factor for Alzheimer’s disease (AD). Due to the consistent association, there is interest as to whether E4 influences the risk of other neurodegenerative diseases. Further, there is a constant search for other genetic biomarkers contributing to these phenotypes, such as microtubule-associated protein tau (MAPT) haplotypes. Here, participants from the Ontario Neurodegenerative Disease Research Initiative were genotyped to investigate whether the APOE E4 allele or MAPT H1 haplotype are associated with five neurodegenerative diseases: (1) AD and mild cognitive impairment (MCI), (2) amyotrophic lateral sclerosis, (3) frontotemporal dementia (FTD), (4) Parkinson’s disease, and (5) vascular cognitive impairment.

    Methods:

    Genotypes were defined for their respective APOE allele and MAPT haplotype calls for each participant, and logistic regression analyses were performed to identify the associations with the presentations of neurodegenerative diseases.

    Results:

    Our work confirmed the association of the E4 allele with a dose-dependent increased presentation of AD, and an association between the E4 allele alone and MCI; however, the other four diseases were not associated with E4. Further, the APOE E2 allele was associated with decreased presentation of both AD and MCI. No associations were identified between MAPT haplotype and the neurodegenerative disease cohorts; but following subtyping of the FTD cohort, the H1 haplotype was significantly associated with progressive supranuclear palsy.

    Conclusion:

    This is the first study to concurrently analyze the association of APOE isoforms and MAPT haplotypes with five neurodegenerative diseases using consistent enrollment criteria and broad phenotypic analysis.

  • Long-Term Cognitive Outcomes in Patients with Autoimmune Encephalitis

  • Julien Hébert, Gregory S. Day, Claude Steriade, Richard A. Wennberg, David F. Tang-Wai
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 45 / Issue 5 / September 2018
    Published online by Cambridge University Press:
    25 June 2018, pp. 540-544
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  • Background: A need exists to characterise the long-term cognitive outcomes in patients who recovered from autoimmune encephalitis and to identify the modifiable factors associated with improved outcomes. Methods: We retrospectively analysed data from patients diagnosed with autoimmune encephalitis in our outpatient autoimmune encephalitis clinic over a 5-year period, where the Montreal Cognitive Assessment (MoCA) is routinely administered. Results: In total, 21 patients met the inclusion criteria, of whom 52% had persistent cognitive impairment at their latest follow-up (median delay to testing=20 months, range 13-182). Visuospatial and executive abilities, language, attention, and delayed recall were predominantly affected. Patients with status epilepticus at presentation had lower total MoCA scores at their last follow-up (median total score 21, range 15-29) compared with patients without status epilepticus at presentation (median total score 27.5, range 21-30; r2=0.366, p=0.004). Patients who experienced delays of more than 60 days from symptom onset to initiation of treatment (either immunosuppression or tumour removal) were more likely to have a MoCA score compatible with cognitive impairment at their last follow-up (r2=0.253, p=0.0239; z-score=−2.01, p=0.044). Conclusions: Our study suggests that the MoCA may be used to evaluate cognition in recovering patients with autoimmune encephalitis. Delays to treatment shorter than 60 days and absence of status epilepticus at onset were associated with better performance on the MoCA obtained more than 1 year after symptom onset, and may predict better long-term cognitive outcomes.

  • 27 - Mild cognitive impairment

  • from Part IV - Alzheimer's disease
  • M. Flint Beal, Cornell University, New York, Anthony E. Lang, University of Toronto, Albert C. Ludolph, Universität Ulm, Germany
  • Book:
    Neurodegenerative Diseases
    Published online:
    04 August 2010
    Print publication:
    02 June 2005, pp 409-415

  • Summary

    Overview

    As research in aging and dementia moves toward an earlier identification of individuals with a cognitive impairment, the concept of mild cognitive impairment (MCI) has received considerable attention. Mild cognitive impairment refers to an intermediate stage between the cognitive changes that are felt to be part of normal aging and those that represent the very earliest features of a dementia such as Alzheimer's disease. This stage of intermediate impairment is believed to be important, since several studies have indicated that these subjects are likely to progress to AD at an accelerated rate over the general population (Petersen et al., 1999). The initial literature on the concept of MCI pertained to individuals with memory impairment beyond what would be expected for normal aging (Petersen, 1995). These subjects may have a mild impairment in other cognitive domains but performance is felt to be within the range of normal. Similarly, they may have slight difficulties with activities of daily living, but these are generally felt not to be significant. More recently, the construct of MCI has been broadened to include other presentations of persons with transitional cognitive impairment and these will be discussed below. Implicit in the discussion of MCI is an understanding of the concept of normal cognitive function. While we are learning a great deal about aging and cognitive function, this still remains an area of uncertainty.

  • 28 - Alzheimer's disease: overview

  • from Part IV - Alzheimer's disease
    • By David F. Tang-Wai, Division of Neurology, University Health Network, Toronto Western Hospital, Canada, Keith A. Josephs, Division of Neurology, University Health Network, Toronto Western Hospital, Canada, Ronald C. Petersen, Division of Neurology, University Health Network, Toronto Western Hospital, Canada
  • M. Flint Beal, Cornell University, New York, Anthony E. Lang, University of Toronto, Albert C. Ludolph, Universität Ulm, Germany
  • Book:
    Neurodegenerative Diseases
    Published online:
    04 August 2010
    Print publication:
    02 June 2005, pp 416-432

  • Summary

    Dementia

    Dementia, itself, neither implies a specific disease nor implies a specific underlying pathology. It refers to a change in cognitive function that is severe enough to compromise an individual's daily function. The Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) defines dementia as an acquired impairment of cognitive function that includes a decline in memory beyond what would be expected for age and at least one other cognitive function, such as attention, visuospatial skills or language, or a decline in executive functioning such as planning, organization, sequencing, or abstracting. The decline cannot only affect emotional abilities, but must also interfere with work or social activities. The deficits should not be accompanied by an impairment of arousal (delirium) or be accounted for by another psychiatric condition, such as depression or schizophrenia. Dementia can further be defined by a possible, probable, or definite etiologic diagnosis. A degenerative dementia implies disease progression over time.

    While the DSM-IV criteria are generally useful, one problem with the criteria is that memory impairment is an essential feature. While this is common in most dementias, other dementias may present with impairment in a non-memory cognitive domain. If the initial presentation is a change in personality or behavior, rather than memory, a frontotemporal dementia may be the diagnosis. In subjects with parkinsonism, hallucinations and fluctuations in behavior, dementia with Lewy bodies may be more likely than AD.