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Cerebral Hemodynamics and Metabolism Following Experimental Head Injury

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TLDR
The present experiments were undertaken to clarify the nature of acute cerebral disorders resulting from head injury and based on experimental observations of concussion produced by a pendulum striking the freely moving head, it was concluded that this type of concussion was due to temporary paralysis of nervous function.
Abstract
T 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, e t 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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Experimental head injury in the rat. Part 3: Cerebral blood flow and oxygen consumption after concussive impact acceleration.

TL;DR: The combined data, including cerebrospinal fluid pressure measurements, indicated primary cerebrovascular effects of the concussive trauma may induce critical cerebral ischemia and thus profoundly influence posttraumatic cerebral function, and cause irreversible damage.
Journal ArticleDOI

Experimental head injury in the rat Part 1: Mechanics, pathophysiology, and morphology in an impact acceleration trauma model

TL;DR: The model appeared well standardized for further studies of concussion pathophysiology, expressed in terms of cerebral energy metabolism and blood flow, and the concept of concussion as primarily a neuronal, functional disturbance was confirmed.
Journal ArticleDOI

The effects of hypovolemic hypotension on high-energy phosphate metabolism of traumatized brain in rats.

TL;DR: After traumatic injury, the brain is extremely vulnerable to hypovolemic hypotension, as reflected in the loss of high-energy phosphates in brain, and decreases in intracellular pH were greater in rats with impact injury and hypotension.
Journal Article

Central neurogenic control of cerebral blood flow.

TL;DR: The experiments reported herein were designed to determine whether there are central mechanisms which increase CBF following stimulation of the brainstem and diencephalon which are independent of EEG.
Journal ArticleDOI

Cerebral blood flow in normal and abnormal sleep and dreaming

TL;DR: In REM sleep and dreaming CBF values greatly increased, particularly in right temporo-parietal regions in subjects experiencing both visual and auditory dreaming.
References
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Journal ArticleDOI

Brain stem reticular formation and activation of the EEG

TL;DR: In this paper, it was shown that reticular activation is associated with the activation of the reticular formation of the brain stem, and that reticulus activation can be induced by low frequency stimulation of the diffuse thalamic projection system, rather than intra-cortical spread following the arrival of afferent impulses at the sensory receiving areas of the cortex.
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Relationships of pyruvate and lactate during anaerobic metabolism. I. Effects of infusion of pyruvate or glucose and of hyperventilation.

TL;DR: In shock state associated with a reduced or maintained blood flow, an important proportion of muscle lactate release is regulated by a "2 receptor stimulation and not secondary to a reduced oxygen availability", demonstrating that lactate production during shock states is related, at least in part, to increased NaK-ATPase activity under "2 stimulation.
Journal ArticleDOI

Experimental cerebral concussion

D. Denny-Brown, +1 more
- 01 Sep 1941 - 
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