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REVIEW : The Pathology of Pain

Departments of Anesthesiology and Neurology Massachusetts General Hospital Harvard Medical School Boston, Massachusetts

It has recently become recognized that neuropathic forms of chronic pain represent true neurologic disease. Current investigations are largely molecular, yet knowledge of the anatomy and cell biology of pain is also important for the development of more effective medications. Although acute pain is beneficial, neuropathic pain is pathological and creates devastating disability. It occurs when an abnormal somatosensory system chronically transmits pain signals despite the absence of acute injury. Any type of lesion anywhere in the peripheral or central spinothalamic pathway can cause it. The most common scenario involves interruption of peripheral sensory axons with distal Wallerian degeneration. Regenerating peripheral sensory axons can develop ongoing spontaneous action potentials or ectopic mechano- and chemosensitivity that contribute to pain. Axotomy also induces morphological and functional alterations proximally that can contribute to pain. Central axon terminals can degenerate or sprout aberrantly within the dorsal horn. Higher order sensory neurons within the CNS can experience trans-synaptic damage. Lesions wholly within the CNS, such as stroke and multiple sclerosis, can also produce neuropathic pain. This review of a nascent field is presented in hopes of stimulating further investigation into this common, under-recognized medical problem. NEURO SCIENTIST 5:302-310, 1999

Key Words: KEY WORDS Pain/physiopathology • Nociceptors • Human • Ganglia • Spinal • Nerve degeneration/physiology • Spinal cord/pathology • Dis ease models • Animal • Sciatic nerve/injuries • Nerve compression syndromes/physiopathology

The Neuroscientist, Vol. 5, No. 5, 302-310 (1999)
DOI: 10.1177/107385849900500516


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