Brain Stem Reticular Formation And Activation Of The Eeg Pdf

brain stem reticular formation and activation of the eeg pdf

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The Reticular Formation

John Wilson born Specialist in neurology and clinical neurophysiology with a special interest in neurophysiological mechanisms and EEG in connection with sleeping disorders, epilepsy and coma. Email: johwil ous-hf. Helge J. The author has completed the ICMJE form and reports the following conflicts of interest: He has had assignments for lawyers, insurance companies and courts of law in personal injury compensation cases and has received fees for holding lectures in continuing professional education courses for lawyers and doctors. Coma is a dynamic condition that may have various causes. Important changes may take place rapidly, often with implications for treatment.

Reticular formation

Metrics details. The brainstem conveys sensory and motor inputs between the spinal cord and the brain, and contains nuclei of the cranial nerves. It controls the sleep-wake cycle and vital functions via the ascending reticular activating system and the autonomic nuclei, respectively. Brainstem dysfunction may lead to sensory and motor deficits, cranial nerve palsies, impairment of consciousness, dysautonomia, and respiratory failure. The brainstem is prone to various primary and secondary insults, resulting in acute or chronic dysfunction. Of particular importance for characterizing brainstem dysfunction and identifying the underlying etiology are a detailed clinical examination, MRI, neurophysiologic tests such as brainstem auditory evoked potentials, and an analysis of the cerebrospinal fluid. Detection of brainstem dysfunction is challenging but of utmost importance in comatose and deeply sedated patients both to guide therapy and to support outcome prediction.

After the evidence of anesthetic lipophilicity was presented by Meyer 1 and Overton, 2 it was widely assumed that all these actions were accomplished at some unitary site. As has been pointed out by Rampil, 5 the variability among anesthetics of the ratios of concentrations needed to suppress consciousness, to block memory, and to achieve surgical immobility further invalidate the unitary hypothesis. A comprehensive explanation of the mechanism by which anesthetics cause loss of consciousness LOC has not yet been developed. Campagna et al. They document research indicating that subtle differences in the clinical actions of inhaled anesthetics may be attributed to distinct actions on a number of critical molecular targets. Although this evidence makes it clear that neuronal actions and interactions at many different levels and in many different brain tissues are altered or disrupted by anesthetic drugs, it does not explain why these different more or less discrete effects have the common global effect of causing LOC, which we define as suppression of awareness. This article attempts to provide such an explanation in terms of the alteration of neurophysiologic processes that are essential for the mediation of consciousness.

Motivation pp Cite as. Experiments by Moruzzi and Magoun , Green and Arduini , and many subsequent investigators French, ; Green, ; Jasper, ; Rossi and Zanchetti, indicated the existence of diffuse ascending pathways from the brainstem reticular formation which were responsible for producing generalized activation of the neocortex and hippocampus. During nonactivated periods both types of cortex generated irregular wave patterns of large amplitude and low frequency. Unable to display preview. Download preview PDF.


Stimulation of the reticular formation of the brain stem evokes changes in the EEG, consisting of abolition of synchronized discharge and introduction of low voltage fast activity in its place, which are not mediated by any of the known ascending or descending paths that traverse the brain stem.


Brainstem dysfunction in critically ill patients

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Abbie , A. Motor mechanisms of the anuran brain. Adey , W.

EEG in connection with coma

The ascending reticular activating system ARAS is known to play an essential role in maintaining arousal and consciousness.

Introduction: the concept of brainstem dysfunction

Разные лаборатории приводят разные цифры. ГЛАВА 127 Собравшиеся на подиуме тотчас замолчали, словно наблюдая за солнечным затмением или извержением вулкана - событиями, над которыми у них не было ни малейшей власти. Время, казалось, замедлило свой бег. - Мы терпим бедствие! - крикнул техник.  - Все линии устремились к центру. С левого экрана в камеру неотрывно смотрели Дэвид и агенты Смит и Колиандер.

Беккер с трудом сдержал крик ужаса. Меган сидела на унитазе с закатившимися вверх глазами.

Она повернулась к монитору и показала на работающего Следопыта. - Я никуда не спешу. Стратмор сокрушенно вздохнул и начал мерить шагами комнату. - Очевидно, когда Танкадо умер, рядом находились свидетели. Согласно словам офицера, который отвел Дэвида в морг, некий канадский турист сегодня утром в панике позвонил в полицию и сказал, что у одного японца в парке случился сердечный приступ.

Он был принят сегодня утром. Его карточка должна лежать где-то сверху. Беккер еще больше усилил акцент, но так, чтобы собеседница могла понять, что ему нужно, и говорил слегка сбивчиво, подчеркивая свою крайнюю озабоченность.

Опустив руки, он незаметными быстрыми движениями соединял кончики пальцев. Перед его глазами появилось сообщение, которое он должен был отправить. ТЕМА СООБЩЕНИЯ: П.

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