The degree of impairment of consciousness is correlated with the extent of the causative lesion. The severity and prognosis of coma are judged from the patient's response to stimuli. There is no universally accepted grading system for coma. Proper documentation involves an exact description of the stimuli given and the responses elicited, rather than isolated items of information such as "somnolent" or "GCS 10." Coma scales (e. g., the Glasgow Coma Scale) are useful for the standardization of data for statistical purposes but do not replace a detailed documentation of the state of consciousness. Spontaneous movement. Assessment of motor function yields clues to the site of the lesion (p. 44 ff) and the etiology of coma. The examiner should note the pattern of breathing, any utterances, yawning, swallowing, coughing, and movements of the limbs (twitching of the face or hands may indicate epileptic activity; there may be myoclonus or flexion/extension movements).
Stimuli. Lesions of the mid brain or lower dien-cephalon produce the decerebration syndrome (arm/leg extension with adduction and internal rotation of the arms, pronation and flexion of the hands), while extensive bilateral lesions at higher levels produce the decortication syndrome (arm/hand flexion, arm supination, leg extension) (p. 47). These pathological flexion and extension movements occur spontaneously or in response to external stimuli (verbal stimu lation, tickling around the nose, pressure on the knuckles or other bones) whether the cause of coma is structural or metabolic. Withdrawal of the limb from the stimulus usually means that the pyramidal pathway for the affected limb is intact. Stereotyped flexion or extension movements are usually seen in patients with severe damage to the pyramidal tract. Brain stem reflexes (p. 26). Structural lesions of the brain stem usually impair the function of the internal and external eye muscles (p. 70 ff), while supratentorial lesions generally do not, unless they secondarily affect the brain stem. Coma in a patient with intact brain stem reflexes is likely to be due to severe bihemispheric dysfunction (if no further objective deficit is found, coma may be psychogenic or factitious; see p. 120). Physicians should be aware that coma due to intoxication or drug overdose (p. 92) may be difficult to distinguish from that due to structural damage by clinical examination alone. Preservation of the vestibulo-ocular reflex (VOR) and of the doll's eyes reflex is compatible with either a bihemispheric lesion or a toxic or metabolic disorder. The VOR induces conjugate eye movement only if its brain stem pathway is intact (from the cervical spinal cord to the oculomotor nucleus). Nonetheless, the VOR may be absent in some cases of toxic coma (due to, e. g., alcohol, barbiturates, phenytoin, pancuronium, or tricyclic antidepressants). Abnormalities of the respiratory pattern (p. 151) are of limited localizing value. Cheyne-Stokes respiration is characterized by regular waxing and waning of the tidal volume, punctuated by apneic pauses. It has a number of causes, including bihemispheric lesions and metabolic disorders. Slow, shallow respiration usually reflects a metabolic or toxic disorder. Rapid, deep respiration (Kussmaul's respiration) usually reflects a pontine or mid brain lesion, or metabolic acido-sis. Medullary lesions and extensive supraten-torial damage produce ataxic, cluster, or gasping respiration.
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