Decerebration

By I. Dvavvudovsviy · Neurology, Physiology, Pathology

Also known as: Decerebrate Rigidity, Decerebrate Posturing, Decerebrate Syndrome, Decerebrate Posturing, Decerebrate Rigidity

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

This article from the 1928–1936 Soviet medical encyclopedia details the phenomenon of decerebration rigidity, a state of increased muscle tone observed after brainstem transection in animals. It explores the neurological mechanisms, the roles of specific brain centers like the red nucleus and cerebellum, and the influence of peripheral stimuli. The text also discusses the clinical attempts to identify a similar syndrome in humans.

Encyclopedia article (1928–1936)

DECEREBRATION, DECEREBRATION RIGIDITY

The red nucleus, known as Forel's crossing (Magnus and Rademaker), is located in the midbrain. Obviously, the normal distribution of tone depends on the red nuclei. Their removal causes rigidity. However, rigidity developing after cutting only the rubro-spinal tract is not as strong as after cutting the entire brainstem. It is certain that the rupture of pyramidal and other descending pathways plays an essential role in the origin of rigidity. The cerebellum also undoubtedly plays a role in the genesis of rigidity, since rigidity develops if the superior cerebellar peduncles are cut (Bremer). Obviously, some nervous centers come into a state of heightened activity in connection with the cutting of the brainstem behind the red nuclei. If the cut is made at the lower boundary of the medulla oblongata, decerebration rigidity is completely absent. With cuts through the anterior part of the medulla oblongata, decerebration rigidity develops, and the stronger the higher the cut is made. Hence it follows that the development of decerebration rigidity depends on the centers of the medulla oblongata (Magnus). Removal of the cerebellum does not influence the development of rigidity (Beritov). Peripheral irritations, both exteroceptive and proprioceptive, strengthen rigidity. After cutting the posterior roots of a limb or the injection of novocaine into the muscles of a limb, extensor rigidity weakens (Magnus, de Klein, Sherrington). If extensor tone has completely disappeared, it can be restored by peripheral irritation (Bazett, Penfield). However, if the limb is beforehand deprived of peripheral sensitivity by cutting the posterior roots, significant rigidity in connection with D. occurs on this leg as well (Magnus and de Klein). Theory. Powerful centers regulating the distribution of muscular tone through tonic reflexes caused by irritation of the static organ of the ear lie in the medulla oblongata. Centers of cervical tonic reflexes lie in the cervical part of the brain (Magnus). But tonic centers also exist in other parts of the spinal cord. Thus, in the lumbar part of the brain, centers of standing of the hind limbs are located (Beritov). Under the influence of cutting the rubro-spinal and pyramidal, as well as other pathways, all these tonic centers come into an active state, which lasts a long time after the operation due to continuing chemical and mechanical irritation, as well as regeneration of the cut nerve pathways. Apparently, the irritating action of nerve pathways originating from the red nuclei to the spinal and medulla oblongata is much stronger than the action of cortical pathways. As long as this irritating action lasts, all tonic and other centers of the medulla oblongata and spinal cord work intensively, and since the action of reciprocal innervation of extensor tonic centers on these animals is much stronger than that of flexor tonic centers, the peripheral effect has an extensor character. In this case, the subsequent change of extensor rigidity with flexor rigidity should represent nothing other than the consequence of the weakening of the activity of extensor tonic centers and the predominant activity of flexor tonic centers (Beritov). Any external or internal irritation favors the existing state of rigidity, since it acts by irradiation of the excitation it causes on those same tonic centers, the excitability of which is most increased by irritation of the cut conducting pathways (Beritov). I. Beritov. Decerebration rigidity in man. Under the name of D. rigidity in man, attempts have been made in recent years (Wilson, Lhermitte, Walshe and others) to distinguish a clinical symptom complex reproducing the phenomena established in the experiments described above on animals. However, different authors denote by this name different states. Some call this name the presence of extensor-pronator postures observed, for example, in torsion dystonia (as well as in many other pathological states); others, taking into account the degree of development of postural reflexes, find an analogy between decerebration rigidity and extrapyramidal hypertonia in tremor paralysis or in parkinsonism; thirdly, noting the presence of Magnus and de Klein's cervical reflexes, which are easiest to find in pyramidal spastic paralyses, consider these last ones as decerebration rigidity of man; finally, in relation to the speed of development of hypertonia, its subsequent regression, and its obviously reflex origin, known analogies can be established with early contracture of hemiplegics (see also Hysteria). In recent times, the theory of Rademaker has become widespread, according to which hypertonia in damage to the central nervous system in man depends on the disease of the same parts whose destruction in animals leads to the appearance of decerebration rigidity, namely the red nucleus and its descending connections. From the point of view of this theory, one should expect that paralyzes in damage to only the pyramidal pathways, contrary to the generally accepted view, should proceed in man with low muscle tone. Clinical data, however, contradict such a generalization. Furthermore, the central nervous system of man and higher animals is arranged in relation to different components of the motor apparatus so differently that it is hardly possible to count on finding in human pathology a complete reproduction of the regularities discovered in physiological experiment. Thus, the question of the clinical syndrome of decerebration rigidity in man remains OPEN.

S. Davidenkov.

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Cite this page

“Decerebration.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/decerebration-2/