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The Feinstein Institute for Medical Research

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Bruce T. Volpe, MD

Investigator, Laboratory of Biomedical Science, The Feinstein Institute for Medical Research

Professor, Department of Molecular Medicine, Hofstra North Shore-LIJ School of Medicine

Phone: (516) 562-3384
Email: bvolpe1@nshs.edu

About the Investigator

Dr. Bruce Volpe graduated with a BS from Yale University and an MD from Yale Medical School. He completed a residency in internal medicine at the University of Chicago Medical Center and at Columbia Presbyterian Medical Center and received further clinical training in neurology at Cornell-New York Hospital Medical Center.

Dr. Volpe has headed brain trauma and stroke recovery units at Cornell affiliated hospitals, and directed the neurorehabilitation fellowship training for neurologists also at the Cornell-Burke Program. He worked with the first interactive robotic devices in the dawn of the modern age of neuro-recovery, testing whether these devices were effective. Now at The Feinstein Institute for Medical Research, he is attempting to extend the reach of restoration after neurological injury with non-invasive technology and with novel pharmacology. His laboratory at The Feinstein Institute also applies techniques of quantitative histopathology in collaborative projects that study the effect of autoantibodies on the brain and the toxic delayed effects of severe sepsis on the brain.

He is a member of the Departments of Neurology and Physical Medicine and Rehabilitation at the North Shore-LIJ Hospital Center, and he mentors residents from those departments in performing clinical research projects.

Research Focus

Non-Invasive Stroke Recovery Lab

Clinical research in stroke recovery has demonstrated that many stroke survivors can relearn skills that are lost when part of the brain is damaged. Rehabilitation efforts focus on teaching new ways of performing tasks to circumvent or compensate for residual disabilities. This approach leaves aside training for the affected limbs. Now, robotic devices can be used to re-train weakened upper limbs. This novel technology moves a patient’s paralyzed or paretic limb and senses when a patient is moving so that it can get out of the way and let the patient execute the movement. Interactive robot training has progressed so that a patient’s movement behaviors can be shaped and guided. These training techniques have demonstrated significant advantages in movement outcomes when compared to standard techniques. These robotic tools are used by therapists to focus training on an impaired limb, deliver reproducible, high-intensity training that will deliver the “just-right” amount of challenge to maintain motivation and attention.

The robots also provide a series of objective measures of movement behavior outcome. Recent tests that use robot measured kinematics have captured motor outcome as well as standard clinical scales and when suitably scaled and combined by an artificial neural network, the robotic measures demonstrated greater sensitivity in measuring the recovery of patients. If robotic measures were biomarkers in a stroke treatment or recovery study this improved sensitivity would decrease the required sample size.

The lab uses four different robotic devices in several different training protocols and training programs: a wrist device, shoulder-elbow device, a hand device, and an anti-gravity shoulder device. There is a fifth device in early development stage that interacts with the patients weakened leg by moving the foot and ankle. We are gaining experience with this device to test new approaches to improving gait after stroke.

The lab is also testing whether robotic training can be complemented and enhanced by transcranial direct current stimulation (tDCS), and eventually by repetitive trans-cranial magnetic stimulation (rTMS).

Quantitative Neuropathological Analysis

The lab has identified neurotoxic events that follow innate and adaptive immunological stress in animal experiments that mimic aspects of human disease. For example, after severe sepsis in the clinic, the predominant morbidity in survivors is characterized by neurological deficits. The lab has demonstrated that after severe sepsis in mice, the ultra-structural analysis of dendritic arbors and spine density of neurons in the hippocampus is altered. Animals with this structural alteration have impaired memory performance, and altered hippocampal electrophysiology. The structural changes after sepsis in mice evolve over days and weeks and so investigation into the neurotoxic mechanism may reveal new therapeutic opportunities.

In autoimmune diseases like systemic lupus erythematosus (SLE), there are B cells that make antibodies not only to DNA but also to the NMDA receptor. The lab has demonstrated in animal experiments that this abnormal adaptive response leads to neuron death and an altered phenotype. The neuropathological details of neuron dysfunction and damage in animal experiments will aid in understanding a mechanism for the neurological impairments in the patients with SLE in the clinic, and may lead to new treatments.

Lab Members

Johanna Z. Chang
Clinical Research Coordinator
Robotics and Non-invasive Stroke Recovery Lab

Phone: (516) 562-3646
Email: jchang13@nshs.edu

Roseann Berlin
Senior Research Associate
Director, Histopathology Laboratory

Phone: (516) 562-1465
Email: rberlin@nshs.edu

Education

Yale College, New Haven, CT
Degree: BS
1969
Field of Study: Molecular Biophysics

Yale Medical School, New Haven, CT
Degree: MD
1973
Field of Study: Medicine

University of Chicago Medical Center, Chicago, IL
Degree: Resident
1975
Field of Study: Medicine

Columbia Presbyterian Medical Center, NY
Degree: Resident
1976
Field of Study: Medicine

Cornell-New York Hospital, NY, NY
Degree: Neurology Resident
1979
Field of Study: Neurology

Publications
  1. Vo A, Volpe BT, Tang CC, Schiffer WK, Kowal C, Huerta PT, Uluğ AM, Dewey SL, Eidelberg D, Diamond B. “Regional brain metabolism in a murine systemic lupus erythematosus model.” J Cereb Blood Flow Metab. 2014 May 14. doi: 10.1038/jcbfm.2014.85. [Epub ahead of print] PubMed PMID: 24824914.
  2.  Krebs HI, Krams M, Agrafiotis DK, Dibernardo A, Chavez JC, Littman GS, Yang E, Byttebier G, Dipietro L, Rykman A, McArthur K, Hajjar K, Lees KR, Volpe BT. “Robotic Measurement of Arm Movements After Stroke Establishes Biomarkers of Motor Recovery.” Stroke. 2014 Jan;45(1):200-4. doi: 10.1161/STROKEAHA.113.002296. Epub 2013 Dec 12. PubMed PMID: 24335224.
  3. Edwards DJ, Cortes M, Thickbroom GW, Rykman A, Pascual-Leone A, Volpe BT. “Preserved corticospinal conduction without voluntary movement after spinal cord injury.” Spinal Cord. 2013 Jul 30. doi: 10.1038/sc.2013.74. [Epub ahead of print]  PubMed PMID: 23896664.
  4. Diamond B, Honig G, Mader S, Brimberg L, Volpe BT. “Brain-reactive antibodies and disease. Annu Rev Immunol.” 2013 Mar 21;31:345-85. doi:10.1146/annurev-immunol-020711-075041. PubMed PMID: 23516983
  5. Diamond B, Volpe BT. “A model for lupus brain disease.” Immunol Rev. 2012 Jul;248(1):56-67. doi: 10.1111/j.1600-065X.2012.01137.x. Review. PubMed PMID: 22725954.
  6. Chavan SS, Huerta PT, Robbiati S, Valdes-Ferrer SI, Ochani M, Dancho M, Frankfurt M, Volpe BT, Tracey KJ, Diamond B. “HMGB1 mediates cognitive impairment in sepsis survivors.” Mol Med. 2012 Sep 7;18:930-7. doi:10.2119/molmed.2012.00195. PubMed PMID: 22634723; PubMed Central PMCID:PMC3459473.
  7. Wang L, Zhou D, Lee J, Niu H, Faust TW, Frattini S, Kowal C, Huerta PT, Volpe BT, Diamond B. “Female mouse fetal loss mediated by maternal autoantibody.” J ExpMed. 2012 Jun 4;209(6):1083-9. Epub 2012 May 7. PubMed PMID: 22565825.
  8. Mackay M, Bussa MP, Aranow C, Uluğ AM, Volpe BT, Huerta PT, Argyelan M, Mandel A, Hirsch J, Diamond B, Eidelberg D. “Differences in regional brain activation patterns assessed by functional magnetic resonance imaging in patients with Systemic Lupus Erythematosus stratified by disease duration.” Mol Med. 2011 Sep 21. doi: 10.2119/molmed.2011.00185. [Epub ahead of print] PubMed PMID: 21953419.
  9. Giacobbe V, Volpe BT, Thickbroom GW, Fregni F, Pascual-Leone A, Krebs HI, Edwards DJ. “Reversal of TMS-induced motor twitch by training is associated with a reduction in excitability of the antagonist muscle.” J Neuroeng Rehabil. 2011 Aug 24;8:46. PubMed PMID: 21861922; PubMed Central PMCID: PMC3179941.
  10. Lo AC, Guarino P, Richards LG, Haselkorn JK, Wittenberg GF, Federman DG, Ringer RJ, Wagner TH, Krebs HI, Volpe BT, Bever CT, Bravata DM, Duncan PW, Corn BH, Maffucci AD, Nadeau SE, Conroy SS, Powell JM, Huang GD, Peduzzi P. “Robot assisted therapy for long-term upper-limb impairment after stroke.” N Engl J Med. 2010 May 13;362(19):1772-83. Epub 2010 Apr 16.PMID: 20400552.

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