Porth's Essentials of Pathophysiology, 4e

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Nervous System

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evaluate decision-making ability, reaction time, attention, memory, and cognitive processing speed in an objective fashion. CT or MRI imaging is usually reserved for cases in which intracranial bleeding is suspected. Treatment, which is largely supportive, includes both physical and mental rest. Once symptoms have resolved, the person may begin shortened work days with decreased work demands. Students may benefit from short periods of reading and studying with frequent breaks. Athletes are advised to follow a slow stepwise return to play. The complications of concussion, although rare, are potentially serious. Currently, the clinical and neuro- pathic consequences of repeated mild head injury are known as chronic traumatic encephalopathy . The dis- orders often manifests years or decades after the incit- ing head injuries with effects on behavior, cognition, and movement. Cognitive changes may occur early in the disease course and include loss of executive func- tion and poor memory. A widely feared complication of concussion is the second-impact syndrome . It is thought to occur when someone who is still recovering from a recent concussion suffers a second head trauma. Significant morbidity and even death can result from edema caused by cerebral congestion that occurs. Diffuse Axonal Injury Diffuse axonal injury is caused by shearing of fragile axons by acceleration-deceleration forces at the time of trauma. 1,4,7 The difference in acceleration–deceleration gradient on certain areas of the brain, permits generation of rotational forces that cause axonal shearing injury. It is characterized by distinct and microscopic findings, including axonal swelling, that are widely distributed in the cerebral hemispheric white matter, corpus callosum, and upper brain stem. Diffuse axonal injury is characterized clinically by functional cerebral impairment, which may range from confusion to coma and death. The clinical diagnosis of diffuse axonal injury is based on immediate onset of unconsciousness in a person with significant cerebral trauma and no intracranial lesion noted on CT scan. Current treatment modalities focus on supportive care, especially for the unconscious person. Studies indicate that axonal injury evolves over a period of hours or days, suggesting that there may be an opportunity to arrest its progression and preserve axonal integrity. Diffuse (global) brain injury, whether due to head trauma or other pathologic processes, is manifested by alterations in sensory, motor, and cognitive function and by changes in the level of consciousness. In contrast to a localized injury, which causes focal neurologic defi- cits without altered consciousness, global injury nearly always results in altered levels of consciousness, rang- ing from inattention to stupor or coma. Severe injury that seriously compromises brain function may result in brain death. Manifestations of Diffuse Brain Injury

Epidural hematoma

Cerebral contusions

Subarachnoid hemorrhages

FIGURE 37-9. Computed tomography scan of brain in traumatic brain injury, showing hemorrhagic cerebral contusions in right temporal and bifrontal lobes, subarachnoid hemorrhages, and epidural hematoma.

The signs and symptoms produced by an intracere- bral hematoma depend on its size and location in the brain. Signs of increased ICP can be manifested if the hematoma is large and encroaching on vital structures. A hematoma in the temporal lobe can be dangerous because of the potential for lateral herniation. Concussions A cerebral concussion can be defined as a transient neu- rogenic dysfunction caused by mechanical force to the brain. 7,10–12 Acceleration–deceleration is the mechanism of injury, usually due to a nonpenetrating force such as a sudden blow to the head. There may be a momen- tary loss of consciousness without demonstrable symp- toms, except for residual amnesia. Microscopic changes can often be detected in neurons and neuroglia within hours of injury, but brain imaging is usually negative. Although recovery usually takes place within 24 hours, mild symptoms, such as headache, irritability, insomnia, and poor concentration and memory, may persist for months. This is known as the postconcussion syndrome. The amnesia or memory loss usually includes an interval of time preceding the injury (retrograde amnesia) and following the injury (anterograde amnesia). The dura- tion of retrograde amnesia correlates with the severity of the brain injury. Traditionally, the diagnosis and management of con- cussion has relied heavily on the person’s self-reporting of symptoms. Because symptom resolution often pre- cedes cognitive recovery and because many persons don’t report symptoms in an effort to return to their normal activities, additional neurophysiologic testing and moni- toring can be useful. Neurophysiologic tests commonly