NEUROLOGICAL ASSESSMENT OF COMA

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: 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 affective 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 diencephalic 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. View this table: Table 1  Glasgow coma scale. Adapted from Teasdale et al1 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. Clinicopathological correlation and neurophysiological experimentation has shown that coma is caused by diffuse bilateral hemisphere damage, failure of the ascending …