If brain volume increases, both blood and CSF are displaced until the intracranial pressure (ICP) increases. The consequent pression of the brain against the inelastic dura mater (Fig. 4.2) and the skull can lead to a lethal series of complications in clinical neurology. The following remarks are based largely on Ironside and Pickard (2002).
Brain volume depends on the following factors:
1. Water content (cerebral hydration). The brain has a normal water content of about 75%. A disturbance of the blood-brain barrier (BBB) can lead to an increase in the fluid content, with a consequent increase in brain volume.
2. Intracranial blood volume (Hirai et al. 1986). This can be driven upward by a number of factors: arterial hypertension (Marshall et al. 1969); enhanced cerebral blood flow secondary to elevated cerebral perfusion pressure (Artru et al. 1976); a decline in the cerebrovascular resistance of arterioles, capillaries, and postcapillary vessels (Langfitt et al. 1965) due to hypercapnia, hypoxemia associated with severe elevation of arterial pressure (Marmarou et al. 1997), or due to obstruction of the venous outflow of the brain. Elevated cerebral blood volume, also known as "brain swelling," is a congestive process.
3. Cerebrospinal fluid (CSF) pressure. The central nervous system (CNS) of the average adult contains a CSF volume of approximately 120-140 ml. Among the causes of a rise in CSF pressure is acute obstructive high pressure hydrocephalus (see pp. 54 f).
A number of additional factors may also influence brain volume. The congested brain expands particularly rapidly under high arterial pressure (Leech and Miller 1974). Nawashiro et al. (1995) used experimental closed brain injury in rats to demonstrate a rapid and widespread increase in regional cerebral blood flow and impaired cerebral autoregulation. In humans a variety of factors act in concert after the incidence of severe brain injury. Cerebral computed tomography (CCT) and magnetic resonance imaging (MRI) studies have shown that brain edema is the major fluid component of brain swelling (Marmarou et al. 1997, 2000). A reactive hyperemia is an additional factor and may be the mechanism underlying mechanical/ischemic brain injury (Seida et al. 1989). Moreover, regional cerebral ischemia additionally is
attributed to a compromised, leaky microvasculature rather than to vasospasm of larger vessels (Schroder et al. 1998).
The conclusion that brain swelling is due primarily to edema and not congestion of blood appears to be valid also for children (see Chap. 20, pp. 415 f). Cerebral blood flow in children with severe head injuries is not substantially increased over that in uninjured children (Zwienenberg and Muizelaar 1999). This has also been demonstrated following experimental generation of brain trauma in newborn and juvenile pigs (Armstead and Kurth 1994). The experimental findings of Biagas and coworkers (1996), in contrast, demonstrated a delayed rise in cerebral blood flow following experimental contusion in young and adult, but not in elderly, rats.
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