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I n the process of better understanding Lundberg's Plateau and B wave phenomena, a general model evolved that could be used to predict the appearance and behavior of many intracranial pressure (ICP) events and that provided a theoretical basis for the management of ICP problems in general. 58, 61 We have termed this model the “complex vasodilatory/vasoconstriction cascade” 29, 57, 60 ( Figs. 1 – 3 ). By stabilizing cerebral perfusion pressure (CPP) at higher levels, we found that ICP could be better controlled without cerebral ischemia. Fig. 1. The

E levation of the head of the bed has been standard neurosurgical practice for management of intracranial pressure (ICP). 1, 2, 4 Yet, such elevation has been shown to be capable of elevating ICP and even inducing pressure waves. 1, 3 More recently, we have provided laboratory and clinical evidence linking pressure waves to cerebral perfusion pressure (CPP) decrements. 9–11 These latter observations have led us in the present study to examine CPP as a function of head elevation. In our recent descriptions of the “vasodilatory cascade,” we have pointed out

P revious studies of the relationship of cerebral perfusion pressure (CPP) changes to “brain stiffness, ” whether measured by compliance, elastance, volume pressure response, or pressure-volume index (PVI), have suggested that at normal levels of intracranial pressure (ICP), “brain stiffness” does not change significantly when CPP is changed within the 50- to 160-mm Hg range. 1, 10, 18 Recent work by us in cats has shown that deep barbiturate anesthesia nearly obliterates the relationship between PVI and CPP, but under light anesthesia cats showed a

relatively constant despite changes in cerebral perfusion pressure (CPP) over the 60- to 170-mm Hg range. 8, 9, 14, 18, 20, 32, 41 Autoregulation of CBF is accomplished by changes in the cerebrovascular resistance (CVR) achieved by alterations in the caliber of the vessels. 10, 11, 20, 26, 32 A consequence of constant flow and changing vessel size is a change in the cerebral blood volume (CBV); 36 however, CBF is influenced by other factors, including PaCO 2 , 15, 35, 43 blood viscosity, 16, 19, 30 and many anesthetic agents. 12 The PVI for a normal neuraxis has

A lthough many factors may affect outcome in the patient with head injury, an increase in intracranial pressure (ICP) and a reduction in arterial blood pressure (ABP) are both independently predictive of poor outcome. 11 Both systemic hypotension and intracranial hypertension lead to a reduction in cerebral perfusion pressure (CPP) and a potential decrease in cerebral blood flow (CBF), causing secondary ischemic insults. 3, 8, 9, 12, 19 Therefore, the goal of intensive care of head-injured patients is to optimize CPP, a targeted therapy that shows promise as

management of severe traumatic brain injury . J Neurotrauma 17 : 451 – 553 , 2000 3 Chesnut RM : Avoidance of hypotension: conditio sine qua non of successful head injury management . J Trauma 42 : 5 Suppl S4 – S9 , 1997 10.1097/00005373-199705001-00002 4 Daley M , Pourcyrous M , Timmons S , Leffler CH : Assessment of cerebrovascular autoregulation: changes of highest modal frequency of cerebrovascular pressure transmission with cerebral perfusion pressure . Stroke 35 : 1952 – 1956 , 2004 10.1161/01.STR.0000133690.94288.c9 5 Downard C

these injuries. 11 Controlled hyperventilation, osmotherapy, and barbiturates are standard therapy for intracranial hypertension; however, these treatments are not consistently successful. On the basis of preliminary clinical reports about the effectiveness of indomethacin, a prostaglandin inhibitor, in lowering ICP, 3, 10 we decided to evaluate its influence on ICP and cerebral perfusion pressure (CPP) in a group of patients who exhibited poor response to standard therapy. Clinical Material and Methods Patient Population Our study focused on 11 patients

F rom clinical studies it is well known that mean arterial blood pressure (MABP), intracranial pressure (ICP), and the resulting cerebral perfusion pressure (CPP) significantly influence neurological outcome after severe head injury. 8, 21, 24, 26, 31 The optimum range of CPP, however, has been the subject of debate during recent years. In the “Lund therapy protocol” of posttraumatic edema, a relatively low CPP is preferred. 14 This therapy is based on the concept that intracranial hypertension following traumatic brain injury is caused more by the vasogenic

I schemic brain damage is found in the majority of head-injured patients who die. 6 For this reason, management of severe head injuries has often attempted to improve cerebral blood flow (CBF), for example by increasing the cerebral perfusion pressure (CPP). Nevertheless, there have been few clinical reports of changes in CBF in response to such maneuvers, 13 particularly with reference to different types of injury. Mannitol is used widely, in varying regimens, in the management of severe head injury, 1, 11, 14, 15 and there is a large body of evidence