Decerebrate posture [Decerebrate rigidity, abnormal extensor reflex]
Decerebrate posture is characterized by adduction (internal rotation) and extension of the arms, with the wrists pronated and the fingers flexed. The legs are stiffly extended, with forced plantar flexion of the feet. In severe cases, the back is acutely arched (opisthotonos). This sign indicates upper brain stem damage, which may result from primary lesions, such as infarction, hemorrhage, or tumor; metabolic encephalopathy; head injury; or brain stem compression associated with increased intracranial pressure (ICP).
Decerebrate posture may be elicited by noxious stimuli or may occur spontaneously. It may be unilateral or bilateral. With concurrent brain stem and cerebral damage, decerebrate posture may affect only the arms, with the legs remaining flaccid. Or, decerebrate posture may affect one side of the body and decorticate posture the other. The two postures may also alternate as the patient’s neurologic status fluctuates. Generally, the duration of each posturing episode correlates with the severity of brain stem damage. (See Comparing decerebrate and decorticate postures, page 224.)
Emergency interventions
Your first priority is to ensure a patent airway. Insert an artificial airway and institute measures to prevent aspiration. (Don’t disrupt spinal alignment if you suspect spinal cord injury.) Suction the patient as necessary.
Next, examine spontaneous respirations. Give supplemental oxygen, and ventilate the patient with a handheld resuscitation bag if necessary. Intubation and mechanical ventilation may be indicated. Keep emergency resuscitation equipment handy, but be sure to check the patient’s chart for a do-not-resuscitate order.
History and physical examination
After taking vital signs, determine the patient’s level of consciousness (LOC). Use the Glasgow Coma Scale (GCS) as a reference. Decerebrate posturing indicates the second-lowest measure of motor response, according to the GCS. Patients exhibiting this abnormal posturing have a decreased LOC and may be in a comatose state. Evaluate the pupils for size, equality, and response to light. Test deep tendon reflexes (DTRs) and cranial nerve reflexes, and check for doll’s eye sign.
Next, explore the history of the patient’s coma. If you’re unable to obtain this information, look for clues to the causative disorder, such as hepatomegaly, cyanosis, diabetic skin changes, needle tracks, or obvious trauma. If a family member is available, find out when the patient’s LOC began deteriorating. Did it occur abruptly? What did the patient complain of before he lost consciousness? Does he have a history of diabetes, liver disease, cancer, blood clots, or aneurysm? Ask about any accident or traumatic injury responsible for the coma.
Medical causes
Brain stem infarction
Decerebrate posture may be elicited when this primary lesion produces a coma. Associated signs and symptoms vary with the severity of the infarct and may include cranial nerve palsies, bilateral cerebellar ataxia, and sensory loss. In a deep coma, all normal reflexes are usually lost, resulting in absence of doll’s eye sign, a positive Babinski’s reflex, and flaccidity.
Brain stem tumor
In a brain stem tumor, decerebrate posture is a late sign that accompanies a coma. Early findings commonly include hemiparesis or quadriparesis, cranial nerve palsies, vertigo, dizziness, ataxia, and vomiting.
Cerebral lesion
Whether the cause is trauma, tumor, abscess, or infarction, any cerebral lesion that increases ICP may also produce decerebrate posture, which is typically a late sign. Associated findings vary with the lesion’s site and extent but commonly include a coma, abnormal pupil size and response to light, and the classic triad of increased ICP—bradycardia, increasing systolic blood pressure, and widening pulse pressure.
Hepatic encephalopathy
A late sign in this disorder, decerebrate posture occurs with a coma resulting from increased ICP and ammonia toxicity. Associated signs include fetor hepaticus (foul-smelling breath), a positive Babinski’s reflex, and hyperactive DTRs.
Hypoglycemic encephalopathy
Characterized by extremely low blood glucose levels, this disorder may produce decerebrate posture and a coma. It also causes dilated pupils, bradypnea, and bradycardia. Muscle spasms, twitching, and seizures eventually progress to flaccidity.
Hypoxic encephalopathy
Severe hypoxia may produce decerebrate posture—the result of brain stem compression associated with anaerobic metabolism and increased ICP. Other findings include a coma, a positive Babinski’s reflex, absence of doll’s eye sign, hypoactive DTRs, and possibly fixed pupils and respiratory arrest.
Pontine hemorrhage
Typically, this life-threatening disorder rapidly leads to decerebrate posture with a coma. Accompanying signs include total paralysis, absence of doll’s eye sign, a positive Babinski’s reflex, and small, reactive pupils.
Posterior fossa hemorrhage
This subtentorial lesion causes decerebrate posture. Its early signs and symptoms include vomiting, headache, vertigo, ataxia, stiff neck, drowsiness, papilledema, and cranial nerve palsies. The patient eventually slips into a coma and may experience respiratory arrest.
Other causes
Diagnostic tests
Removal of spinal fluid during a lumbar puncture to relieve high ICP may precipitate cerebral compression of the brain stem and cause decerebrate posture and a coma.
Special considerations
Help prepare the patient for diagnostic tests that will determine the cause of his decerebrate posture. These include skull X-rays, computed tomography scan, magnetic resonance imaging, cerebral angiography, digital subtraction angiography, EEG, brain scan, and ICP monitoring.
Monitor the patient’s neurologic status and vital signs every 30 minutes or as indicated. Also, be alert for signs of increased ICP (bradycardia, increasing systolic blood pressure, and widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature).
Inform the patient’s family that decerebrate posture is a reflex response—not a voluntary response to pain or a sign of recovery. Offer emotional support.
Pediatric pointers
Children younger than age 2 may not display decerebrate posture because the nervous system is still immature. However, if this posture occurs, it’s usually the more severe opisthotonos. In fact, opisthotonos is more common in infants and young children than in adults and is usually a terminal sign. In children, the most common cause of decerebrate posture is head injury. It also occurs in Reye’s syndrome—the result of increased ICP causing brain stem compression.
Pictures
![Decerebrate posture [Decerebrate rigidity, abnormal extensor reflex] - 2543.png](/bookimages/8/2543.png)
Book Source Details
- Book Title: Professional Guide to Signs & Symptoms (Fifth Edition)
- Author(s): Springhouse
- Year of Publication: 2006
- Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2006 Lippincott Williams & Wilkins.
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Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2008 Williams & Wilkins.
More About Causes of Posture symptoms
» Next page:
Decorticate posture [Decorticate rigidity, abnormal flexor response] (Professional Guide to Signs & Symptoms (Fifth Edition))
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