Daniel Z Press

Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States

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Publications (43)185.99 Total impact

  • Biological psychiatry 07/2015; DOI:10.1016/j.biopsych.2015.07.027 · 10.26 Impact Factor
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    ABSTRACT: Postoperative delirium is a common complication in older people and is associated with increased mortality, morbidity, institutionalization, and caregiver burden. Although delirium is an acute confusional state characterized by global impairments in attention and cognition, it has been implicated in permanent cognitive impairment and dementia. The pathogenesis of delirium and the mechanisms leading to these disabling consequences remain unclear. The present study is the first to address the potential predisposing role of brain morphologic changes toward postoperative delirium in a large prospective cohort of patients undergoing elective surgery using state-of-the-art magnetic resonance imaging (MRI) techniques conducted before admission. We investigated the association of MRI-derived quantitative measures of white-matter damage, global brain, and hippocampal volume with the incidence and severity of delirium. Presurgical white-matter hyperintensities (WMHs), whole brain, and hippocampal volume were measured in 146 consecutively enrolled subjects, ≥70 years old, without dementia who were undergoing elective surgery. These 3 presurgical MRI indices were tested as predictors of incidence and severity of subsequent delirium. Out of 146 subjects, 32 (22%) developed delirium. We found no statistically significant differences in WMH, whole brain, or hippocampal volume between subjects with and without delirium. Both unadjusted and adjusted (age, gender, vascular comorbidity, and general cognitive performance) regression analyses demonstrated no statistically significant association between any of the MRI measures with respect to delirium incidence or severity. In persons without dementia, preexisting cerebral WMHs, general and hippocampal atrophy may not predispose to postoperative delirium or worsen its severity. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neurobiology of aging 02/2015; 36(6). DOI:10.1016/j.neurobiolaging.2015.02.024 · 5.01 Impact Factor
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    ABSTRACT: Transcranial magnetic stimulation (TMS) holds great potential in the treatment of a host of neurological conditions due to its ability to focally modulate-suppress or enhance-activity in targeted cortical brain regions and modify activity across specific brain networks. Results from early trials in a number of neurological indications are presented, including stroke rehabilitation, Parkinson's disease, tinnitus, chronic pain, migraine, and epilepsy. We emphasize both the challenges, such as the limited efficacy to date in tinnitus, as well as the opportunities, such as the use of TMS in epilepsy caused by focal/cortical lesions. However, to establish TMS as a clinically valuable neurological therapeutic intervention, a number of hurdles must be overcome, including accurate targeting of the treatment, characterization of its therapeutic benefit for specific patients/symptoms, proof of efficacy in multicenter trials that are adequately blinded and powered, proof of the durability of the effects, and assessment of potential adverse effects of cumulative dose and repeated application.
    Psychiatric Annals 06/2014; 44(6):299-304. DOI:10.3928/00485713-20140609-08 · 0.71 Impact Factor
  • Zachary A. Gray · Steven M. Greenberg · Daniel Z. Press
    Brain Stimulation 05/2014; 7(3). DOI:10.1016/j.brs.2014.02.013 · 4.40 Impact Factor
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    Sanjin Tunovic · Daniel Z Press · Edwin M Robertson
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    ABSTRACT: Different memories follow different processing pathways. For example, some motor skill memories are enhanced over wakefulness, whereas others are instead enhanced over sleep. The processing pathway that a motor skill memory follows may be determined by functional changes within motor circuits. We tested this idea using transcranial magnetic stimulation to measure corticospinal excitability at 6, 21, 36, 96, and 126 min after participants learnt tasks that either were or were not enhanced over wakefulness. There was no change in corticospinal excitability after learning a motor skill that was subsequently enhanced; whereas, there was a substantial transient decrease in corticospinal excitability after learning a motor skill that was not enhanced. In subsequent experiments, we abolished the decrease in corticospinal excitability by applying theta burst stimulation to either the dorsolateral prefrontal or primary motor cortex, and induced motor skill improvements during consolidation. The motor skill improvements in each experiment were correlated with the corticospinal excitability after learning. Together, these experiments suggest that corticospinal excitability changes act as a physiological signal, which prevents improvements from developing over wakefulness, and so when this signal is abolished improvements are induced. Our observations show that the human brain can actively prevent the processing of memories, and provides insights into the mechanisms that control the fate of memories.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 04/2014; 34(15):5302-10. DOI:10.1523/JNEUROSCI.3497-13.2014 · 6.34 Impact Factor
  • Brain Stimulation 03/2014; 7(2):e3–e4. DOI:10.1016/j.brs.2014.01.016 · 4.40 Impact Factor
  • Mark C Eldaief · Daniel Z Press · Alvaro Pascual-Leone
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    ABSTRACT: Transcranial magnetic stimulation (TMS) is a neurophysiologic technique to noninvasively induce a controlled current pulse in a prespecified cortical target. This can be used to transiently disrupt the function of the targeted cortical region and explore causal relations to behavior, assess cortical reactivity, and map out functionally relevant brain regions, for example during presurgical assessments. Particularly when applied repetitively, TMS can modify cortical excitability and the effects can propagate trans-synaptically to interconnected cortical, subcortical, and spinal cord regions. As such, TMS can be used to assess the functional integrity of neural circuits and to modulate brain activity with potential therapeutic intent.
    Neurology: Clinical Practice (Print) 12/2013; 3(6):519-526. DOI:10.1212/01.CPJ.0000436213.11132.8e
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    ABSTRACT: Those with high baseline stress levels are more likely to develop mild cognitive impairment (MCI) and Alzheimer's Disease (AD). While meditation may reduce stress and alter the hippocampus and default mode network (DMN), little is known about its impact in these populations. Our objective was to conduct a "proof of concept" trial to determine whether Mindfulness Based Stress Reduction (MBSR) would improve DMN connectivity and reduce hippocampal atrophy among adults with MCI. 14 adults with MCI were randomized to MBSR vs. usual care and underwent resting state fMRI at baseline and follow-up. Seed based functional connectivity was applied using posterior cingulate cortex as seed. Brain morphometry analyses were performed using FreeSurfer. The results showed that after the intervention, MBSR participants had increased functional connectivity between the posterior cingulate cortex and bilateral medial prefrontal cortex and left hippocampus compared to controls. In addition, MBSR participants had trends of less bilateral hippocampal volume atrophy than control participants. These preliminary results indicate that in adults with MCI, MBSR may have a positive impact on the regions of the brain most related to MCI and AD. Further research with larger sample sizes and longer-follow-up are needed to further investigate the results from this pilot study.
    Neuroscience Letters 10/2013; 556. DOI:10.1016/j.neulet.2013.10.001 · 2.03 Impact Factor
  • Alzheimer's and Dementia 07/2013; 9(4):P894. DOI:10.1016/j.jalz.2013.08.266 · 12.41 Impact Factor
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    Journal of the American Geriatrics Society 04/2013; 61(4):642-5. DOI:10.1111/jgs.12179 · 4.57 Impact Factor
  • Anli Liu · Daniel Z Press
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    ABSTRACT: Since the introduction of highly active antiretroviral therapy in 1996, the epidemiologic profile of HIV-associated neurocognitive disorder (HAND) has shifted drastically. Although HIV-associated dementia has nearly disappeared from clinical practice, presymptomatic and milder variants of HAND affect up to 50% of patients on chronic antiretroviral therapy.1,2 Furthermore, the predominant phenotype has evolved from a subcortical dementia to a mixed cortical-subcortical cognitive syndrome affecting attention, executive, and memory systems, as well as slowing processing speed.2 Yet, subtler forms of HAND often remain undetected. One Swedish HIV study found that only 27% of their patient cohort complained of cognitive dysfunction, but 67% actually demonstrated objective deficits on cognitive testing.3.
    Neurology 02/2013; 80(13). DOI:10.1212/WNL.0b013e3182887970 · 8.29 Impact Factor
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    ABSTRACT: Dementia is an important consequence of Parkinson's disease (PD), with few known modifiable risk factors. Cumulative exposure to lead, at levels experienced in the community, may exacerbate PD-related neural dysfunction, resulting in impaired cognition. Among 101 persons with PD ("cases") and, separately, 50 persons without PD ("controls"), we evaluated cumulative lead exposure, gauged by tibia and patella bone lead concentrations, in relation to cognitive function, assessed using a telephone battery developed and validated in a separate sample of PD patients. We also assessed the interaction between lead and case-control status. After multivariable adjustment, higher tibia bone lead concentration among PD cases was associated with worse performance on all of the individual telephone tests. In particular, tibia lead levels corresponded to significantly worse performance on a telephone analog of the Mini-Mental State Examination and tests of working memory and attention. Moreover, higher tibia bone lead concentration was associated with significantly worse global composite score encompassing all the cognitive tests (P = 0.04). The magnitude of association per standard deviation increment in tibia bone lead level was equivalent to the difference in global scores among controls in our study, who were approximately 7 years apart in age. The tibia lead-cognition association was notably stronger within cases than within controls (P(difference) = 0.06). Patella bone lead concentration was not consistently associated with performance on the tests. These data provide evidence suggesting that cumulative exposure to lead may result in worsened cognition among persons with PD. © 2012 Movement Disorder Society.
    Movement Disorders 02/2013; 28(2). DOI:10.1002/mds.25247 · 5.68 Impact Factor
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    Jordan B Brayanov · Daniel Z Press · Maurice A Smith
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    ABSTRACT: Actions can be planned in either an intrinsic (body-based) reference frame or an extrinsic (world-based) frame, and understanding how the internal representations associated with these frames contribute to the learning of motor actions is a key issue in motor control. We studied the internal representation of this learning in human subjects by analyzing generalization patterns across an array of different movement directions and workspaces after training a visuomotor rotation in a single movement direction in one workspace. This provided a dense sampling of the generalization function across intrinsic and extrinsic reference frames, which allowed us to dissociate intrinsic and extrinsic representations and determine the manner in which they contributed to the motor memory for a trained action. A first experiment showed that the generalization pattern reflected a memory that was intermediate between intrinsic and extrinsic representations. A second experiment showed that this intermediate representation could not arise from separate intrinsic and extrinsic learning. Instead, we find that the representation of learning is based on a gain-field combination of local representations in intrinsic and extrinsic coordinates. This gain-field representation generalizes between actions by effectively computing similarity based on the (Mahalanobis) distance across intrinsic and extrinsic coordinates and is in line with neural recordings showing mixed intrinsic-extrinsic representations in motor and parietal cortices.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 10/2012; 32(43):14951-65. DOI:10.1523/JNEUROSCI.1928-12.2012 · 6.34 Impact Factor
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    R Wells · G Yeh · C Kerr · J Wolkin · R Davis · Y Tan · R Wall · J Walsh · T Kaptchuk · D Press · R Phillips · J Kong
    BMC Complementary and Alternative Medicine 06/2012; 12(1). DOI:10.1186/1472-6882-12-S1-P202 · 2.02 Impact Factor
  • 10/2011; 1(5):409-412. DOI:10.2217/npy.11.52
  • Tamara G. Fong · Daniel Z. Press
    The Handbook of Alzheimer's Disease and Other Dementias, 09/2011: pages 131 - 144; , ISBN: 9781444344110
  • The journal of ECT 06/2011; 27(2):176-7. DOI:10.1097/YCT.0b013e3181e6336e · 1.39 Impact Factor
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    ABSTRACT: Dementia with Lewy bodies (DLB) is often associated with occipital hypometabolism or hypoperfusion, as well as deficits in cholinergic neurotransmission. In this study, 11 mild DLB, 16 mild AD and 16 age-matched controls underwent arterial spin-labeled perfusion MRI (ASL-pMRI) and neuropsychological testing. Patterns of cerebral blood flow (CBF) and cognitive performance were compared. In addition, combined ASL-pMRI and ChEI drug challenge (pharmacologic MRI) was tested as a probe of cholinergic function in 4 of the DLB participants. Frontal and parieto-occipital hypoperfusion was observed in both DLB and AD but was more pronounced in DLB. Following ChEI treatment, perfusion increased in temporal and parieto-occipital cortex, and cognitive performance improved on a verbal fluency task. If confirmed in a larger study, these results provide further evidence for brain cholinergic dysfunction in DLB pathophysiology, and use of pharmacologic MRI as an in vivo measure of cholinergic function.
    Brain Imaging and Behavior 10/2010; 5(1):25-35. DOI:10.1007/s11682-010-9108-x · 4.60 Impact Factor

Publication Stats

2k Citations
185.99 Total Impact Points


  • 2002–2015
    • Beth Israel Deaconess Medical Center
      • • Department of Neurology
      • • Department of Radiology
      • • Laboratory for Magnetic Brain Stimulation
      Boston, Massachusetts, United States
  • 2007–2014
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1999–2014
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 2004–2006
    • Boston University
      • Department of Biomedical Engineering
      Boston, Massachusetts, United States