Pharmacologic Modulation of Recovery After Brain Injury: A Reconsideration of DiaschisisDepartment of Psychology, University of New Mexico, Albuquerque, NM 8713 USA Pharmacologic interventions promoting recovery after cortical injury, particularly the beneficial effects on hemiplegia of drugs that increase noradrenergic activity, are interpreted as alleviations of the depressed neuronic activity in morphologically intact brain areas. This is related to the theory that diaschisis, and von Monakow's conception is discussed as one stage in the continuing evolution of a hypothesis regarding the sequelae of brain injury. Data bearing upon recent theoretical revisions are reviewed and a hypothesis proposed to account for such neuronal dysfunctions. It is suggested that some reversible symptoms result from depressed neural activity due to excessive sublethal, excitatory synaptic input originating in a remote brain lesion. Studies of cerebral metabolism indicate that amelioration of postinjury neuronal depression in intact brain regions is the basis of some pharmacological treatments for stroke and cerebral trauma. Data supporting this hypothesis are discussed in detail for one promising treatment regimen developed from laboratory investigations of an animal model of hemiplegia. Even when given days after injury, drugs that increase noradrenergic activity, when combined with symptom-relevent experience, i.e., physical therapy, hasten recovery and normalize reduced glycolytic and oxidative metabolism. Such dysfunctional neuronal states are considered important therapeutic targets after brain damage, and a more descriptive concept, Remote Functional Depression, is suggested as a current conception to replace the theory of diaschisis.
Neurorehabilitation and Neural Repair, Vol. 5, No. 1-2,
113-128 (1991) |
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