Porth's Essentials of Pathophysiology, 4e

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Disorders of Brain Function

C h a p t e r 3 7

the amount of volume increase, the time frame for accommodation, and the size of the intracranial com- partments. For example, small volume increments over long periods of time can be better accommodated than a comparable increase introduced over a short period of time. The cerebral perfusion pressure (CPP), which rep- resents the difference between the mean arterial blood pressure (MABP) and the ICP (CPP = MABP − ICP), is the pressure perfusing the brain. 7,8 CPP (normally 70 to 100 mm Hg) is determined by the pressure gradient between the internal carotid artery and the subarach- noid veins. The MABP and ICP are monitored fre- quently in persons with brain conditions that increase ICP and impair brain perfusion. When the pressure in the cranial cavity approaches or exceeds the MABP, tissue perfusion becomes inadequate, cellular hypoxia results, and neuronal death may occur. The highly spe- cialized cortical neurons are the most sensitive to oxy- gen deficit; a decrease in the level of consciousness is one of the earliest and most reliable signs of increased ICP. Continued cellular hypoxia leads to general neurologic deterioration, with the level of consciousness deteriorat- ing from alertness to confusion, lethargy, obtundation, stupor, and coma. Brain Herniation The brain is protected by the nonexpandable skull and two supporting septa, the falx cerebri and the tentorium cerebelli, which divide the intracranial cavity into com- partments that normally protect against excessive move- ment (Fig. 37-3A). 1,4,7 The falx cerebri is a sickle-shaped septum that divides the supratentorial space into right and left hemispheres. The tentorium cerebelli (so named because it is shaped like a tent) is a double fold of dura mater that forms a sloping partition between the cerebrum and cerebellum. In the center of the tentorium is a large semicircular opening called the incisura or tentorial notch (Fig. 37-3B). The brain stem, blood vessels ( anterior cere- bral, internal carotid, posterior communicating, and pos- terior and superior cerebellar arteries), and oculomotor nerve (cranial nerve [CN] III) pass through the inciscura. Brain herniation represents a displacement of brain tissue under the falx cerebri or through the tentorial notch of the tentorium cerebelli. It occurs when an ele- vated ICP in one brain compartment causes displace- ment of the cerebral tissue toward an area of lower pressure. The different types of herniation syndromes are based on the area of the brain that has herniated and the structure under which it has been pushed. They commonly are divided into two broad categories, supra- tentorial and infratentorial , based on whether they are located above or below the tentorium. Supratentorial Herniation. Progressive supratento- rial lesions develop sequential signs and symptoms of ocular, motor, and respiratory function. This pattern follows the predictable continuum of rostal-to-caudal (head to tail) failure that proceeds from the diencepha- lon to the midbrain (ocular), followed by pons (motor), ( text continues on page 921 )

rupture, allowing the escape of intracellular contents into the surrounding extracellular fluid. This leads to damage of neighboring cells. Major changes in cerebral function, such as stupor and coma, occur with cytotoxic edema. The edema associated with ischemia may be severe enough to produce cerebral infarction with necrosis of brain tissue. Increased Intracranial Pressure, Herniation, and Hydrocephalus Intracranial pressure is, literally, the pressure inside the cranium. Its increase can cause herniations or hydro- cephalus. Neurons can be injured when excessive pres- sure is exerted upon brain tissue, whether that pressure builds up gradually, such as from increasing CSF levels, or occurs suddenly, as from trauma. The cranial cavity contains blood (approximately 10%), brain tissue (approximately 80%), and CSF (approximately 10%) in the rigid confines of a nonex- pandable skull. 7,8 Each of these three intracranial volumes contributes to the intracranial pressure, which normally is maintained within a range of 0 to 15 mm Hg when measured in the lateral ventricles. Increased intracranial pressure (ICP) is a common pathway for brain injury from different types of insults and agents. The volumes of each of three intracranial compo- nents can vary slightly without causing marked changes in ICP. This is because small increases in the volume of one component can be compensated for by a decrease in the volume of one or both of the other two components. This association is called the Monro-Kellie hypothe- sis. 4,7,8 Reciprocal compensation occurs among the three intracranial compartments. Of the three intracranial compartments, the CSF and blood volume are best able to compensate for changes in ICP, with the tissue vol- ume being relatively restricted in its ability to change. Initial increases in ICP are buffered by a translocation of CSF to the spinal subarachnoid space and increased reabsorption of CSF. The compensatory ability of the blood compartment is limited by the small amount of blood that is in the cerebral circulation, most of which is contained in the low-pressure venous system. As the volume-buffering capacity of this compartment becomes exhausted, venous pressure increases, and cerebral blood volume and ICP rise. Also, cerebral blood flow is highly controlled by autoregulatory mechanisms, which affect its compensatory capacity. For example, conditions such as ischemia and an elevated partial pressure of carbon dioxide (PCO 2 ) in the blood produce a compensatory vasodilation of the cerebral blood vessels. A decrease in PCO 2 has the opposite effect. For this reason, hyper- ventilation, which results in a decrease in PCO 2 levels, is sometimes used in the treatment of ICP. The impact of increases in blood, brain tissue, or CSF volumes on ICP varies among individuals and depends on the amount of increase, effectiveness of compensa- tory mechanisms, and compliance or “distensibility” of brain tissue. 7 An increase in intracranial volume will have little or no effect on ICP as long as the compli- ance is high. Factors that influence compliance include

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