HE pathogenesis of cerebral concussion has long been debated. The present experiments were undertaken to clarify the nature of acute cerebral disorders resulting from head injury. Concussion was defined by Denny-Brown as a "transitory and reversible nervous reaction with immediate onset following physical stress of sufficient violence and brevity, and characterized by progressive recovery thereafter. ''~ There are two main theories concerning the pathogenesis of concussion: the excitation theory of Walker, et al., 4a and the paralytic theory of Denny-Brown and Russell2 These two theories, which postulate opposite mechanisms, will be reviewed. Walker and his associates 43 observed the appearance of fast activity in the electroencephalogram (EEG) with little change in amplitude immediately after a compressive impact applied to the exposed dura and brain in experimental animals. This was followed by '"extinction." The EEG changes were frequently accompanied by tonic extension movements of the extremities. They suggested that this type of concussion resulted from excitation of the central nervous system. An opposite view was proposed by Denny-Brown and Russell. Based on experimental observations of concussion produced by a pendulum striking the freely moving head (acceleration concussion), they concluded that this type of concussion was due to temporary paralysis of nervous function. In man, concussion is characterized by transient loss of neural function, accompa
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