An abnormal posture of some consequence is decerebrate rigidity, which in its fully developed form consists of opisthotonos, clenching of the jaws, and stiff extension of the limbs, with internal rotation of the arms and plantar flexion of the feet (see Chap. 3). It is most often manifest as brief tonic extension of the limbs. This postural pattern was first described by Sherrington, who produced it in cats and monkeys by transecting the brainstem at the intercollicular level. Decerebrate posture was noted in animals to be ipsilateral to a one-sided lesion, hence not a result of involvement of the corticospinal tracts; the opposite is true in humans. A precise anatomic correlation between posturing and the level of the lesion is rarely possible in patients who develop stereotyped extensor posturing as it arises in a variety of settings—with midbrain compression caused by a hemispheral mass; with cerebellar or other posterior fossa lesions; in certain metabolic disorders such as anoxia and hypoglycemia; and, rarely, with hepatic coma and profound drug or alcohol intoxication. Patients with an acute lesion of one cerebral hemisphere may show a similar type of extensor posturing of the contralateral and sometimes ipsilateral limbs, and this may coexist with the ability to make purposeful movements of the same limb. Extensor postures, unilateral or bilateral, occur spontaneously, but more often they are in response to manipulation of the limbs or a tactile or noxious stimulus. Another related pattern consists of extensor posturing of an arm and leg on one side, and flexion and abduction of the opposite arm.
In some patients with the extensor postural changes the lesion is clearly in the cerebral white matter or basal ganglia, which is difficult to reconcile with the classic physiologic explanation for decerebrate posturing. Decerebrate posturing, either in experimental preparations or in humans, is usually not a persistent state. Hence, the term decerebrate state, as suggested by Feldman and Sahrmann, is preferable to decerebrate rigidity, which implies a fixed, tonic extensor attitude.
Decorticate posturing, usually, with arm or arms in flexion and adduction and leg(s) extended, signifies lesions at a more rostral level of the nervous system—in the cerebral white matter or internal capsule and thalamus. Bilateral decorticate rigidity is essentially a bilateral spastic hemiplegia. Diagonal postures, for example, flexion of one arm and extension of the opposite arm and leg, usually indicate a supratentorial lesion. Forceful extensor postures of the arms and weak flexor responses of the legs are usually seen with lesions at about the level of the vestibular nuclei. Lesions below this level lead to flaccidity and abolition of all postures and movements. If preceded by decorticate or decerebrate postures, the coma is profound and usually progresses to brain death.
Only in the most advanced forms of intoxication and metabolic coma, as might occur with anoxic necrosis of neurons throughout the entire brain, are coughing, swallowing, hiccoughing, and spontaneous respiration all abolished. Further, the tendon and plantar reflexes may give little indication of what is happening. Tendon reflexes are preserved until the late stages of coma that is due to metabolic disturbances and intoxications. In coma caused by a large cerebral infarct or hemorrhage, the tendon reflexes may be normal or only reduced on the hemiplegic side and the plantar reflexes may initially be absent before becoming extensor. Plantar flexor responses, succeeding extensor responses, signify either a return to normalcy or, in the context of deepening coma, a transition to brain death.
Patterns of Breathing