Joachim Scholz, MD Assistant Professor of Anesthesia Neural Plasticity Research Group Department of Anesthesia & Critical Care Massachusetts General Hospital & Harvard Medical School 149 13th Street, Room 4307 Charlestown, Massachusetts 02129 TEL: 617-724-3623 FAX: 617-724-3632 E-mail: scholz.joachim@mgh.harvard.edu

Background

Dr. Scholz studied human medicine at the Universities of Bochum and Essen, Germany. He completed his residency training in neurology and one year of residency training in psychiatry at the Medical University of Lübeck, Germany. Dr. Scholz joined the Neural Plasticity Research Group in 2000, supported by a Feodor Lynen Research Fellowship of the Alexander von Humboldt Foundation.

Research Interests

The major goal of my research is to identify neurobiological mechanisms responsible for the development of persistent pain after a lesion or disease affecting the sensory nervous system (neuropathic pain).

Nerve injury-induced irreversible loss of spinal cord interneurons offers one explanation for chronic pain, because these interneurons normally inhibit nociceptive input. We are studying the impact of afferent activity on the survival of interneurons in the dorsal horn of the spinal cord, which constitutes the first major relay station for sensory input. We explore if neuroprotective modulation of synaptic transmission provides a novel disease-modifying approach to pain management.

Nerve lesions provoke a marked and well organized response from peripheral immune cells and glia. We examine routes of communication between neurons and spinal glia and signaling pathways between different types of glial cells to define their role in the induction of neuropathic pain.

It is currently not possible to determine the activity of pain mechanisms in patients. However, their contribution to a patient’s pain is reflected in the symptoms and signs that represent the clinical pain phenotype. We have developed a standardized assessment tool that allows characterizing distinct subtypes of pain independent of the underlying disease. We are testing the utility of this tool in genetic research, as a method to validate patient-specific cellular pain models and for the development of personalized analgesic treatment strategies.

Selected Publications

Scholz J, Woolf CJ. Can we conquer pain? Nature Neuroscience (2002) 5 (Supplement): 1062–1067

Scholz J, Broom DC, Youn DH, Mills CD, Kohno T, Suter MR, Moore KA, Decosterd I, Coggeshall RE, Woolf CJ. Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of spinal inhibition following peripheral nerve injury. Journal of Neuroscience (2005) 25:7317–7323

Tegeder I, Costigan M, Griffin RS, Abele A, Belfer I, Schmidt H, Ehnert C, Nejim J, Marian C, Scholz J, Wu T, Allchorne A, Diatchenko L, Binshtok A, Goldman D, Adolph J, Sama S, Atlas SJ, Carlezon WA, Parsegian A, Lötsch J, Fillingim RB, Maixner W, Geisslinger G, Max MB, Woolf CJ. GTP-cyclohydrolase, the rate-limiting enzyme in tetrahydrobiopterin biosynthesis, regulates pain sensitivity and persistence. Nature Medicine (2006) 12:1269–1277

Bennett MI, Attal N, Backonja MM, Bouhassira D, Freynhagen R, Scholz J, Tölle TR, Wittchen HU, Jensen TS. Using screening tools to identify neuropathic pain. Pain (2007) 127:199–203.

Scholz J, Woolf CJ. The neuropathic pain triad: neurons, immune cells, and glia. Nature Neuroscience (2007) 10:1361–1368.

Scholz J, Mannion RJ, Hord ED, Griffin RS, Rawal B, Zheng H, Scoffings D, Phillips A, Guo J, Laing RJC, Abdi S, Decosterd I, Woolf CJ. A Novel tool for the assessment of pain: validation in low back pain. PLoS Medicine (2009) 6:e1000047.