Clinical Evaluation of Traumatic Decerebration.
- Author:
Dong Hyun PARK
1
;
Suk Hong HAN
Author Information
1. Department of Neurosurgery, College of Medicine, Chosun University, Korea.
- Publication Type:Original Article
- MeSH:
Adrenal Cortex Hormones;
Adult;
Animals;
Brain;
Brain Stem;
Cerebral Angiography;
Craniocerebral Trauma;
Decerebrate State;
Gravitation;
Hematoma;
Hematoma, Subdural;
Humans;
Mortality;
Muscles;
Posture;
Spasm;
Survivors;
Vestibular Nuclei;
Young Adult
- From:Journal of Korean Neurosurgical Society
1977;6(1):47-54
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Decerebrate rigidity, in which there is an exaggereted posture with continuous spasm of muscles, especially the extensors, was first produced in 1898 by Sherrington in animals by transection of the brain at a prepontine level. Since it was shown that intact vestibular nuclei were necessary for decerebrate ridigity to persist, the disorder was believed to be caused by release of vestibular nuclei from higher extrapyramidal control. We have experienced 42 cases of the presence of decerebrate ridigity following head injury who were admitted to the Chosun University Hospital from March 1972 to February 1976. Although no one doubts the prognostic gravity of the decerebrate state following cranial trauma, a surpring number of patients in this study survived in a reasonably functional state. The particular factors we have evaluated are the duration of decerebration, the presence or absence of an intracranial hematoma of surgical proportions, the time of surgical intervention in relation to onset of decerebration and the use of corticosteroids. 42 consecutive parients with traumatic decerebration were studied to determine factors that influence the recovery from the decerebrate state. All these cases were diagnosed by clinical findings and cerebral angiography and assessed the prognostic factors on the result of treatment. Although the data did not lend themselves to precise statistical analysis, it is our option that the following conclusions be inferred ; 1. Intracranial hematoma was found in 25 patients (about 60%) from 42 patients who were presence of decerebrate rigidity, among these the sites of intracranial hematoma were as follows ; a) Epidural hematoma was found in 8 patients(32%). b) Subdural hematoma was found in 13 patients(52%). c) Intracerebral hematoma was found in 4 patients(16%). 2. The mortality of decerebrate patients(65%) with direct damage to the brain stem was greater than that of those supratentorial hematoma(52%). However the quality of survival was better in the latter group, indicating the likehood that brain stem compression is often reversible after evacuation of the hematoma even though with residual neurological deflicit. 3. The mortality and morbidity were greater with traumatic intracerebral and subdural hematoma than with epidural hematoma. This correlation was probably related to the amount of associated diffuse brain damage. 4. A progressive increase in the mortality rate in the surgical group could be correlated with the duration of decerebrate rigidity prior to surgical intervention. 5. Patients who recovered from the decerebrate state usually survived even though with residual sequelae. 6. There was an increase in the mortality rate when decerebration persisted for more than on weeks, but there was one survivor after even 35 days of decerebrate state. 7. The mortality rate was highest over 40 years old and was on the contrary under 20 years old. 8. There was no specific effectiveness in the patients with the presence of decerebrate state with the use of parenteral corticosteroid therapy.
