Bateman2007 (2)

Bateman2007(2) - J Neurol Neurosurg Psychiatry 2001;71(suppl I:i13i17 NEUROLOGICAL ASSESSMENT OF COMA David E Bateman i13 he neurologist is often

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NEUROLOGICAL ASSESSMENT OF COMA David E Bateman T he neurologist is often required to evaluate the unconscious patient from both the diagnostic and prognostic perspective. Knowledge of the anatomical basis of coma is essential for competent evaluation but must be combined with an understanding of the many, often multi-factorial, medical conditions that result in impaired consciousness. Consciousness is a state of awareness of self and the environment. This state is determined by two separate functions: c awareness (content of consciousness) c arousal (level of consciousness ). These are dependant upon separate physiological and anatomical systems. Coma is caused by disordered arousal rather than impairment of the content of consciousness, this being the sum of cognitive and a V ective mental function, dependent on an intact cerebral cortex. The absence of all content of consciousness is the basis for the vegetative state. Arousal depends on an intact ascending reticular activating system and connections with dien- cephalic structures. Like awareness, arousal is not an all or nothing concept and gradations in awareness have been described in the past as inattentiveness, stupor, and obtundation. Such terms lack precision and coma can be more objectively assessed using measures such as the Glasgow coma scale (GCS) (table 1). This analyses three markers of consciousness—eye opening, and motor and verbal responses—bringing a degree of accuracy to evaluation. The GCS arbitrarily defines coma as a failure to open eyes in response to verbal command (E2), perform no better than weak flexion (M4), and utter only unrecognisable sounds in response to pain (V2). The GCS is of no diagnostic value, but is a reliable way of objectively monitoring the clinical course of the patient with an acute cranial insult without elucidating cause. c NEUROANATOMICAL BASIS OF COMA Clinicopathological correlation and neurophysiological experimentation has shown that coma is caused by di V use bilateral hemisphere damage, failure of the ascending reticular activating system, or both. The reticular activating system is a core of grey matter continuous caudally with the reticular intermediate grey lamina of the spinal cord and rostrally with the subthalamus, hypothalamus, and thalamic nuclei. It runs in the dorsal part of the brain stem in the paramedian tegmental zone. A unilateral hemisphere lesion will not result in coma unless there is secondary brain stem compression, caused by herniation, compromising the ascending reticular activating system. Extensive bilateral damage or disturbance of the hemisphere function is required to produce coma. Bilateral thalamic and hypothalamic lesions also cause coma by interrupting activation of the cortex mediated through these structures. In hypothalamic lesions, phenomena associated with sleep, such as yawning, stretching, and sighing, are prominent. The speed of onset, site, and size of a brainstem
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This note was uploaded on 10/14/2010 for the course ZOO 4125 taught by Professor Flanigan during the Fall '10 term at Wyoming.

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Bateman2007(2) - J Neurol Neurosurg Psychiatry 2001;71(suppl I:i13i17 NEUROLOGICAL ASSESSMENT OF COMA David E Bateman i13 he neurologist is often

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