Bruce T. Volpe, MD

Professor, The Center for Biomedical Science,
The Feinstein Institute for Medical Research

Professor, Department of Molecular Medicine,
Donald and Barbara Zucker School of Medicine at Hofstra/Northwell

Phone: (516) 562-3384

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 Northwell Health 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

Roseann Berlin
Senior Research Associate
Director, Histopathology Laboratory

Phone: (516) 562-1465


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

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

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

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

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

  1. Huerta PT, Robbiati S, Huerta TS, Sabharwal A, Berlin RA, Frankfurt M, Volpe BT. “Preclinical models of overwhelming sepsis implicate the neural system that encodes contextual fear memory.” Mol Med. 2016 Nov 17;22. doi:10.2119/molmed.2015.00201. [Epub ahead of print] PubMed PMID: 27878209; PubMedCentral PMCID: PMC5193462.
  2. Son M, Porat A, He M, Suurmond J, Santiago-Schwarz F, Andersson U, Coleman TR, Volpe BT, Tracey KJ, Al-Abed Y, Diamond B. “C1q and HMGB1 reciprocally regulate human macrophage polarization.” Blood. 2016 Nov 3;128(18):2218-2228. PubMed PMID: 27683415; PubMed Central PMCID: PMC5095756.
  3. VanPatten S, Sun S, He M, Cheng KF, Altiti A, Papatheodorou A, Kowal C, Jeganathan V, Crawford JM, Bloom O, Volpe BT, Grant C, Meurice N, Coleman TR,Diamond B, Al-Abed Y. “Amending HIV Drugs: A Novel Small-Molecule Approach To Target Lupus Anti-DNA Antibodies.” J Med Chem. 2016 Oct 13;59(19):8859-8867. PubMed PMID: 27603688.
  4. Brimberg L, Mader S, Jeganathan V, Berlin R, Coleman TR, Gregersen PK, Huerta PT, Volpe BT, Diamond B. “Caspr2-reactive antibody cloned from a mother of an ASD child mediates an ASD-like phenotype in mice.” Mol Psychiatry. 2016 Dec;21(12):1663-1671. doi: 10.1038/mp.2016.165. PubMed PMID: 27698429.
  5. Thickbroom G, Cortes M, Rykman A, Volpe BT, Fregni F, Krebs HI, Pascual-Leone A, Edwards D. “Stroke subtype and motor impairment influence contralesional excitability.” Neurology. 2015 Aug 11;85(6):517-20. doi:10.1212/WNL.0000000000001828. Epub 2015 Jul 17. PubMed PMID: 26187228; PubMed Central PMCID: PMC4540249.
  6. Chang EH, Volpe BT, Mackay M, Aranow C, Watson P, Kowal C, Storbeck J, Mattis P, Berlin RA, Chen H, Mader S, Huerta TS, Huerta PT, “Diamond Selective impairment of spatial cognition caused by autoantibodies to the n-methyl-d-aspartate receptor.” EBioMedicine. 2015 May 30;2(7):755-64. doi:10.1016/j.ebiom.2015.05.027. eCollection 2015 Jul. PubMed PMID: 26286205; PubMed Central PMCID: PMC4534689.
  7. Braniste V, Al-Asmakh M, Kowal C, Anuar F, Abbaspour A, Tóth M, Korecka A, Bakocevic N, Guan NL, Kundu P, Gulyás B, Halldin C, Hultenby K, Nilsson H, Hebert H, Volpe BT, Diamond B, Pettersson S. “The gut microbiota influences blood-brain barrier permeability in mice.” Science Transl Med. 2014 Nov 19;6(263):263ra158. doi: 0.1126/scitranslmed.3009759.
  8. Edwards DJ, Cortes M, Thickbroom GW, Rykman A, Pascual-Leone A, Volpe BT. “Evidence against volume conduction to explain normal MEPs in muscle with low motor power in SCI. Spinal Cord.” Advance online publication, 22 July 2014; doi:10.1038/sc.2014.117.
  9. Brimberg L, Mader S, Fujieda Y, Arinuma Y, Kowal C, Volpe BT, Diamond B. “Antibodies as mediators of brain disease.” Trends in immunology. 2015. doi: 10.1016/ PubMed PMID: 26494046.
  10. Volpe BT. “Pathogenesis of tissue injury in the brain in patients with SLE.” In, Tsokos G, (ed) Systemic Lupus Erythematosus, Elsevier Academic Press, 2016.

View more at PubMed

Dr. Volpe's research uses smart robots to rehabilitate stroke patients quickly and in a fun and effective way.

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