This article discusses whether diaschisis is an epiphenomenon or whether it truly has any clinical relevance. Because of my interest in diaschisis for the past 30 years, and because this laboratory has studied the phenomenon both clinically and experimentally, I will once again review the subject (1,2). Von Monakow (3), a Russian neurologist who was active at the turn of the 19th and 20th centuries, was the first to describe his clinical observations of depressed brain function that occurred at distances remote from localized injuries to the central nervous system (CNS). He was the first to propose the term diasch isis, by which he described a splitting apart of the brain to describe the phenomenon. Von Monakow postulated that diaschisis was caused by severance of afferent CNS connections via white matter fiber tracts. Since then, technical advances in neuroimaging including regional measurements of cerebral blood flow and metabolism have proven Von Monakow's concept to be correct, so that the term diaschisis is now used to cover all remote effects of localized CNS injury, including not only depressed function but the associated decreases in perfusion and metabolism. It has long been clinically obvious to neurologists, physiatrists, and neurophysiologists caring for patients with acute trauma to the cord that spinal shock results. This is characterized by widespread areflexia, hypotonia, and flaccid paralysis of the limbs extending beyond the level of the lesion and including loss of control of bowel and bladder with eventual partial or complete recovery within weeks or months, depending on the severity of the cord lesion. Controlled collaborative clinical trials have recently established that functional recovery following acute traumatic cord paralysis is hastened and im-