Pathogenesis of Neurotrauma

The disease initiated by neurotrauma; the spinal cord injury (SCI) and the traumatic brain injury (TBI) has been recently elucidated by Dr. Kwiecien in his systematic studies on the rat model of the SCI.  A trauma to the spinal cord initiates a severe, destructive and extraordinarily protracted inflammation confined to a cavity of injury (COI) but continually damaging the surrounding spinal cord for a long time, >16 weeks.  The white matter injury in the SCI result in large quantity of damaged myelin, a very immunogenic, pro-inflammatory material targeted by phagocytic macrophages and contributing to a mechanism of the vicious cycle producing such protracted disease with destructive severity.  Inflammatory damage to blood vessels in the surrounding spinal cord causes a chronic vasogenic edema persisting along the active inflammation, >16 weeks.  Neurologic deficits are related to:

  1. Destruction of the spinal cord at the time of neurotrauma

  2. Destruction of the spinal cord by the severe inflammation after neurotrauma

  3. Persistence of the vasogenic edema


Every year, the SCI occurs in 500-700 thousand people around the world; primarily young male adults, victims of automobile accidents, battle and also falls in elderly.  These considerable numbers have tendency to increase and the medical and social costs related to treating, hospitalization and care for the SCI patients are very high.

Although stroke is not initiated by a traumatic event but rather by an occlusive vascular accident in the brain, it does result in necrosis of a defined area in the brain, very often involving the white matter.  This initiates a severe, destructive inflammation of the same pathogenesis as that in the SCI and in the TBI.  There are 2-2.5 million cases of the TBI and 12-15 million cases of stroke with the survival every year.


There are no effective treatments for neurotrauma and stroke, constituting a very large un-met market.

Treatment of Acute Neurotrauma and Stroke

The newly elucidated and understood pathogenesis of neurotrauma and stroke indicates that anti-inflammatory agents able to cross the blood-brain barrier (BBB) or blood-spinal cord barrier (BSCB) will constitute the first and necessary treatment designed to inhibit and eliminate severe inflammation to arrest the enlargement of the lesion and provide neuroprotection.  Studies on anti-inflammatory agents in the rat model of the SCI allowed Dr. Kwiecien to develop novel clinical tests and a quantitative histologic test to measure neuroprotective effects and determine uniquely favorable, therapeutic qualities of xanthohumol.  Oral administration of this flavonoid chalcone isolated from hops resulted in inhibition of inflammation in the COI and its elimination therein within 8 weeks with corresponding accelerated improvement of neurologic deficits.