Porth's Essentials of Pathophysiology, 4e

929

Disorders of Brain Function

C h a p t e r 3 7

SUMMARY CONCEPTS

■■ Many of the agents that cause brain damage do so through common and often interrelated pathways, including hypoxia or ischemia, accumulation of excitatory amino-acid neurotransmitters, and cerebral edema. ■■ Deprivation of oxygen (i.e., hypoxia) or blood flow (i.e., ischemia) can have deleterious effects on the brain structures. Ischemia can be focal, as in stroke, or global as occurs during cardiac arrest when blood flow is inadequate to meet the metabolic needs of the entire brain. ■■ Excitotoxicity is a final common pathway for neuronal cell injury and death. It is associated with excessive activity of excitatory amino-acid neurotransmitters, particularly glutamate. ■■ Cerebral edema represents an increase in brain volume secondary to abnormal fluid accumulation. Vasogenic edema occurs when integrity of the blood–brain is disrupted allowing intravasular fluid to move into the extracellular fluid surround brain cells; whereas, cytotoxic edema involves swelling of brain cells due to the movement of the extracellular fluid into the brain cells. ■■ The intracranial pressure (ICP) is the pressure exerted by the essentially incompressible tissue and fluid volumes of the three compartments contained within the rigid confines of the skull— brain tissue, blood, and cerebral spinal fluid (CSF). Excessive ICP can obstruct cerebral blood flow, destroy brain cells, displace brain tissue as in herniation, and otherwise damage delicate brain structures. ■■ Hydrocephalus represents enlargement of the CSF compartment owing to an abnormal CSF volume. It can result from impaired reabsorption from the arachnoid villi into the venous system (communicating hydrocephalus) or from obstruction of the ventricular system (noncommunicating hydrocephalus), which prevents the CSF from reaching the arachnoid villi. ■■ The term traumatic brain injury refers to injuries to the skull, brain, or both.The brain injuries can be primary, because of direct impact, or secondary, resulting from complicating processes that were initiated at the time of injury.They can be focal, as occurs with contusions and hematoma formation; or diffuse, as in concussion or diffuse axonal injury.

A

B

Decorticate (flexion) posturing is characterized by the arms being held tightly to the sides, with flexion of the arms, wrists, and fingers; and extension and internal rotation of the legs with plantar flexion of the feet (see Fig. 37-4A). Decorticate posturing results from lesions of the cerebral hemisphere or internal capsule. Decerebrate (extensor) posturing results from increased muscle excitability (see Fig. 37-4B). It is char- acterized by rigidity of the arms with the wrists and fin- gers flexed and turned away from the body and with stiffly extended legs and plantar flexion of the feet. This response occurs with rostral-to-caudal deterioration, when lesions of the diencephalon extend to involve the midbrain and upper brain stem. Respiratory Responses. Early respiratory changes include yawning and sighing, with progression to Cheyne- Stokes breathing, in which there is waxing and waning of respirations with variable periods of apnea. When the progression of injury continues to the midbrain, respi- rations change to neurogenic hyperventilation, in which the frequency of respirations may exceed 40 breaths per minute because of uninhibited stimulation of inspiratory and expiratory centers. With medullary involvement, res- pirations become ataxic (i.e., totally uncoordinated and irregular). Apnea may occur because of a lack of respon- siveness to carbon dioxide stimulation. Complete venti- latory assistance is often required at this point. FIGURE 37-11. The doll’s-head eye response demonstrates the always-present vestibular static reflexes without forebrain interference or suppression. Severe damage to the forebrain or to the brain stem rostral to the pons often results in loss of rostral control of these static vestibular reflexes. If the person’s head is moved from side to side or up and down, the eyes will move in conjugate gaze to the opposite side (A) , much like those of a doll with counterweighted eyes. If the doll’s-head phenomenon is observed, brain stem function at the level of the pons is considered intact (in a comatose person). In the unconscious person without intact brain stem function and vestibular static reflexes, the eyes stay in midposition (fixed) or turn in the same direction (B) as the head is turned.

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