Porth's Essentials of Pathophysiology, 4e

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Nervous System

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FIGURE 37-6. Mechanism of brain injury (A) acceleration–deceleration and (B) acceleration–decelerations with rotational motion of the cerebral hemispheres around the fixed-in-place brainstem that affects neurons in reticular activating system (RAS), which extends through the central core of the brainstem. (Adapted from Hickey JV. The Clinical Practice of Neurological and Neurosurgical Nursing. 6th ed. Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams &Wilkins; 2009:372.)

Midbrain

A

B

Front and back injury

Rotational injury

Because the brain floats freely in the CSF within the rigid confines of the skull, blunt force to the head causes the brain to accelerate within the skull, and then decelerate abruptly upon hitting the inner skull surfaces. 7,10–12 As the brain strikes the rough surface of the cranial vault, brain tissue, blood vessels, nerve tracts, and other structures are bruised and torn, resulting in contusions and hematomas (Fig. 37-6). A special type of acceleration-deceleration motion is angular rotation. 7,12 It involves the rotational motion of the cerebral hemispheres in the anterior-posterior plane around the fixed-in-place brain stem, caus- ing disruption of electrical and subcellular activities of neurons in the reticular activating system (RAS), which extends through the central core of the brain stem (Fig. 37-6). There are two main stages in the development of brain damage after brain injury: primary and second- ary. Primary injuries, which represent the immediate response to the initial injury, include focal lesions (con- tusions and hemorrhage) and diffuse injuries (concus- sion and diffuse axonal injuries). 1,4 Secondary injures involve complicating processes resulting from the ini- tial injury, including brain swelling, and infection. 7,9–12 Ischemia is considered the most common cause of sec- ondary brain injury. It can result from the hypoxia and hypotension that occur during the resuscitation process or from the impairment of regulatory mechanisms that control cerebrovascular responses that maintain blood flow and oxygen supply. Contusions Contusions represent a bruising on the brain surface or a lacerations or tearing of brain tissue. 1,4 Contusions can result from direct force, a depressed skull frac- ture, or a closed acceleration-deceleration injury. Closed injury contusions are often distributed along the rough, irregular inner surface of the brain and are more likely to occur in the frontal or temporal lobes,

resulting in cognitive and motor deficits. The clinical effects of a contusion depend on its size and related cerebral edema. Small, unilateral, frontal lesions may be asymptomatic; whereas larger lesions may result in neurological defects. They can cause secondary mass effects from edema resulting in an increased ICF, and possible herniation syndromes. Persons suffering from cerebral contusions are usually managed medi- cally with emphasis toward prevention of secondary injuries. Hematomas Hematomas result from vascular injury and bleeding. Depending on the anatomic position of the ruptured vessel, bleeding can occur in any of several compart- ments, including the epidural, subdural, and sub- arachnoid spaces, or into the brain itself (intracerebral hematoma). Epidural Hematoma. An epidural hematoma is one that develops between the inner side of the skull and the dura 1,4,7 (Fig. 37-7). It usually results from a tear in an artery, most often the middle meningeal, usu- ally in association with a head injury in which the skull is fractured. 1,5,17 Because bleeding is arterial in origin, rapid expansion of the hematoma compresses the brain. Epidural hematoma is more common in a young person because the dura is less firmly attached to the skull surface than in an older person; as a con- sequence, the dura can be easily separated from the inner surface of the skull, allowing the hematoma to grow. Typically, a person with an epidural hematoma pres- ents with a history of head injury and a brief period of unconsciousness followed by a lucid period in which consciousness is regained. There is then a rapid pro- gression to unconsciousness. The lucid interval does not always occur, but when it does, it is of great diag- nostic value. With rapidly developing unconsciousness,