Fall In Intracranial Pressure Research Articles

An equiosmolar study on early intracranial physiology and long term outcome in severe traumatic brain injury comparing mannitol and hypertonic saline

The impact of hypertonic saline (HTS) on long term control of intracranial hypertension (ICH) is yet to be established. The current prospective randomized controlled study was carried out in 38 patients with severe traumatic brain injury (TBI). Over 450 episodes of refractory ICH were treated with equiosmolar boluses of 20% mannitol in 20 patients and 3.0% HTS in 18 subjects. Intracranial pressure (ICP) was monitored for 6days. ICP and cerebral perfusion pressure (CPP) were comparable between the groups. The mannitol group had a progressive increase in the ICP over the study period (p=0.01). A similar increase was not seen in the HTS group (p=0.1). The percentage time for which the ICP remained below a threshold of 20 mmHg on day6 was higher in the HTS group (63% versus 49%; p=0.3). The duration of inotrope requirement in the HTS group was less compared to the mannitol group (p=0.06). The slope of fall in ICP in response to a bolus dose at a given baseline value of ICP was higher with HTS compared to mannitol (p=0.0001). In-hospital mortality tended to be lower in the HTS group (3 versus 10; p=0.07) while mortality at 6 months was not different between the groups (6 versus 10; p=0.41). Dichotomized Glasgow Outcome Scale scores at 6months were comparable between the groups (p=0.21). To conclude, immediate physiological advantages seen with HTS over mannitol did not translate into long term benefit on ICP/CPP control or mortality of patients with TBI.

Coupling of Central Venous Pressure and Intracranial Pressure in a 6-Year-Old Patient With Fontan Circulation and Intracranial Hemorrhage

A sharp rise in intracranial pressure (ICP) was noted in a 6-year-old girl with Fontan circulation after surgical removal of a hematoma associated with intracranial hemorrhage. Inhalation of nitric oxide resulted in reduction of central venous pressure (CVP) and precipitous fall in ICP, which was otherwise resistant to conventional therapy. Specifically, the rate of fall of ICP (9 mm Hg) exceeded that of the CVP (3 mm Hg), indicating disproportionate CVP-ICP coupling. The present case provides not only a novel insight into cardio-cerebral interaction in Fontan physiology but also useful information regarding the treatment of Fontan patients in the setting of increased ICP.

Randomized Controlled Trial Comparing the Effect of 8.4% Sodium Bicarbonate and 5% Sodium Chloride on Raised Intracranial Pressure after Traumatic Brain Injury

Hypertonic sodium chloride solutions are routinely used to control raised intracranial pressure (ICP) after traumatic brain injury but have the potential to cause a hyperchloremic metabolic acidosis. Sodium bicarbonate 8.4% has previously been shown to reduce ICP and we have therefore conducted a randomized controlled trial to compare these two solutions. Patients with severe traumatic brain injury were randomly allocated to receive an equiosmolar dose of either 100 ml of sodium chloride 5% or 85 ml of sodium bicarbonate 8.4% for each episode of intracranial hypertension. ICP and blood pressure were measured continuously. Arterial pCO(2), sodium, chloride, osmolality, and pH were measured at intervals. We studied 20 episodes of intracranial hypertension in 11 patients. Treatments with 8.4% sodium bicarbonate and 5% sodium chloride reduced raised ICP effectively with a significant fall in ICP from baseline at all time points (P < 0.001). There was no significant difference in ICP with time between those episodes treated with 5% sodium chloride or 8.4% sodium bicarbonate, P = 0.504. Arterial pH was raised after treatment with 8.4% sodium bicarbonate. An equiosmolar infusion of 8.4% sodium bicarbonate is as effective as 5% sodium chloride for reduction of raised ICP after traumatic brain injury when infused over 30 min.

A Bolus of Conivaptan Lowers Intracranial Pressure in a Patient with Hyponatremia after Traumatic Brain Injury

Hyponatremia may complicate brain injury and exacerbate cerebral edema and intracranial pressure (ICP). Vasopressin-receptor antagonists (such as conivaptan) are promising novel agents to treat hyponatremia that act by inducing aquaresis. It is unclear whether raising serum sodium in this way could also confer an acute osmotic benefit, reducing brain water and thereby ICP. We evaluated the effect of a bolus of conivaptan on ICP in a patient with hyponatremia after traumatic brain injury (TBI). A 22-year-old suffered severe TBI with occlusive left carotid dissection. Her course was complicated by left hemispheric infarcts with cerebral edema and intermittently elevated ICP. Conivaptan 20-mg IV was given as a bolus when serum sodium rapidly dropped to 128 mEq/l. This dose resulted in significant aquaresis, with over 1 l per hour of dilute urine peaking at 3-5 h after the dose. By 8 h, sodium had risen to 146 mEq/l. ICP had been stable at 11-15 mmHg for several hours prior to the dose, remained in this range for 2 h after, but then fell to 2 mmHg at 4 h, and remained reduced out to 8 h. Cerebral perfusion pressure, initially stable at 60-80 mmHg, rose to over 90 mmHg at 4 h. In this preliminary case report, a single dose of conivaptan not only resulted in rapid correction of acute hyponatremia, but also a significant fall in ICP temporally associated with peak aquaresis. Vasopressin-receptor antagonists, by reversing osmotic shifts, may be novel agents to control ICP and cerebral edema, especially in the setting of falling sodium.

Cervical MRI Findings in Intracranial Hypotension

Intracranial hypotension is characterised by a fall in intracranial pressure presenting clinically with postural headache and cervical pain. The syndrome may arise after lumbar puncture, surgery, trauma, severe dehydration or spontaneously. We studied two patients with intracranial hypotension presenting hallmark intracranial MR features of the syndrome with different involvement of the cervical spine in terms of MR features and clinical presentation and course. MR imaging of the cervical and dorsal spine in both patients was carried out using T1, T2 and T2-FLAIR weighted sagittal spin echo sequences and T2 weighted axial turbo spin echo (TSE) sequences. In the first patient, MR disclosed an area of altered signal intensity within the cerebral canal in an extradural, anterior and lateral location both right and left, symmetrical with craniocaudal extension from C1 to D2. The area was strongly hyperintense in T2-FLAIR sequences compressing the anterolateral surface of the dura mater and was ascribed to an enlargement of the anterior vertebral venous plexus. MR examination four days later showed an almost complete resolution of the previous picture. In the second patient, MR imaging showed a fluid collection in the subdural space in the cervicodorsal spine in sagittal FLAIR and axial TSE images wth a hyperintense signal consistent with hygroma. Follow-up disclosed slow gradual resolution of the previous changes. The dilated epidural venous plexuses in the first patient could compensate the loss of CSF, as occurs intracranially where CSF volume is balanced with blood volume (Monro-Kellie's theory). The spinal hygroma evident in the second patient may have been a transudate secondary to meningeal hyperaemia. This hypothesis is supported by the raised proteins and cells found in the CSF and the meningeal enhancement after contrast administration. Intracranial hypotension is characterized not only by well-known changes in intracranial MR signal, but also by specific MR findings in the cervicodorsal spine. Knowledge of these MR features allows prompt recognition and adoption of the most suitable MR sequence with due assessment of the morphology of areas of altered signal intensity to disclose the pathogenesis.

Effect of hypertonic saline on cerebral blood flow in poor-grade patients with subarachnoid hemorrhage.

The goal of this study was to examine the effects of hypertonic saline on cerebral blood flow (CBF) in poor-grade patients with subarachnoid hemorrhage. We administered 23.5% hypertonic saline (2 mL/kg IV) 1 time to 10 patients, 2 times to 7 patients, and 3 times to 1 patient. All patients had transcranial Doppler (TCD), intracranial pressure (ICP) monitoring, and analysis of serum sodium and osmolality; 6 had xenon CT (XeCT). Data were used to characterize the changes in CBF, cerebral vascular resistance (CVR), ICP, cerebral perfusion pressure (CPP), and potential rheological mechanisms of action. In the first treatment episode, CPP increased 26.8% (P=0.0003, at 28.3 minutes) from a rise in mean arterial blood pressure (ABP) of 10.5% (P=0.02, at 22.2 minutes) and a fall in ICP (-74.7%, P=0.002, at 60.0 minutes). Flow velocity (FV) of the middle cerebral artery increased 70.8% (P=0.00005, at 20.0 minutes), resulting in a corresponding fall in estimated CVR (-26.6%, P=0.01, at 16.3 minutes). The half-lives of effects on ABP, CPP, ICP, FV, and estimated CVR were 20.0, 53.6, 139.1, 42.7, and 27.1 minutes, respectively. In the second treatment episode, all these parameters had the same response except estimated CVR, which did not reach statistical significance. XeCT confirmed the increase in CBF (22.9%, P=0.02) without regional differences. A fall in CBF after hypertonic saline was identified in only a single region of interest in a patient in whom baseline flow was low but not infarcted. Serum sodium rose by 11.4 and 8.8 mmol/L, and osmolality rose by 26.7 and 16.3 mosm/L in the first and second treatment episodes, respectively. Hemoglobin decreased by 0.7 and 0.6 g/L and hematocrit decreased by 1.9% and 2.4% in the first and second treatment episodes, respectively. We found that 23.5% hypertonic saline increases CBF in poor-grade patients with subarachnoid hemorrhage. These effects are associated with improved indexes of blood rheology. Potential therapeutic benefits are discussed.

Arterial hypertension increases intracranial pressure in cat after opening of the blood-brain barrier.

Increased permeability for small solutes in brain capillaries means that a change in hydrostatic capillary pressure may influence transcapillary fluid exchange according to the Starling fluid equilibrium, and a high arterial pressure may cause transcapillary fluid filtration and raised intracranial pressure. This could be of clinical relevance in states of disrupted blood-brain barrier such as meningitis and after a severe head injury, especially since these patients quite often are spontaneously hypertensive, and hypertensive therapy is sometimes used to increase cerebral perfusion pressure. This study on cat investigated the long-term relation between arterial pressure and intracranial pressure in a state of disrupted blood-brain barrier. Endotoxin was given intrathecally to open the blood-brain barrier and depress cerebral autoregulation. Arterial pressure was increased by about 30 mm Hg during 5 hours by dopamine and angiotensin II infusion. The immediate fall in intracranial pressure after normalization of blood pressure reflects the blood volume component of an intracranial pressure increase. Increased arterial pressure had no effect on intracranial pressure before endotoxin. Endotoxin infusion increased intracranial pressure from the normal value of 10 to 12 mm Hg. and at steady state by almost 10 mm Hg. Intracranial pressure increased further after the arterial pressure increase. At steady state (achieved within 5 hours), this increase was almost as great as the arterial pressure increase, and about 80% persisted when measured directly after normalization of the arterial pressure. Increased arterial pressure in a state of disrupted blood-brain barrier increases intracranial pressure, mainly because of brain edema. This stresses that arterial hypertension may be deleterious in conditions such as meningitis or after a brain trauma.

Postural Changes in Intracranial Pressure in Chronically Shunted Patients

A subset of hydrocephalic patients with indwelling shunts become symptomatic when they are upright and active. Intracranial pressure (ICP) measurements in these patients have shown a significant drop in pressure when the patient is upright with return to normal levels when the patient is supine. In 20 chronically shunted hydrocephalic patients who previously had no siphon protection devices, ICP changes in supine and upright position were studied at the time when the patient had external ventriculostomy for treatment of shunt infection. Our hypothesis was that these patients might display rapid changes in ICP from fluid shifts occurring in non-CSF compartments. To minimize the effects of hysteresis, drift and zero-point error, measurements were made using a fluid manometer rather than a strain gauge pressure transducer. The pressure-volume index was estimated using the standard technique of bolus injection. Intracranial CSF volume was estimated on CT scans. The fluid shift was calculated using a mathematical model of the CSF compartment that incorporates negative pressure and volume components that permits simulation of siphoning. Sixteen patients had small, slit ventricles; 3 patients had moderate-sized ventricles and in 1 patient the ventricular size was normal. The average intracranial CSF volume estimated on CT scan was 12 cm³. There was a mean drop in ICP in the upright position of 159 mm H₂O. The mean PVI of 42 ml suggested a volume displacement out of proportion to the available intracranial CSF volume. Based on these findings, we conclude that even in the absence of drainage through the shunt, chronically shunted patients still display a fall in ICP when assuming the upright position. This raises the possibility of fluid shifts other than of CSF through nonshunt pathways. Possible mechanisms involving altered CSF-venous system interaction are discussed.

Determining cerebral perfusion pressure thresholds in severe head trauma.

Laboratory studies suggest the pulsatile component of the transcranial doppler (TCD) waveform may be useful in determining lower autoregulatory threshold. This study aimed to assess the effect of increasing CPP on jugular bulb oximetry (SjO2) and middle cerebral artery (MCA) TCD flow velocities in the early management of severe head injury. 16 severely head injured patients (GCS < or = 8), had intracranial pressure (ICP), mean arterial pressure, SjO2 and MCA Doppler velocity monitored continuously. CPP was increased by intravenous fluids (right atrial pressure approximately equal to 10) and supplemented with adrenaline infusion until TCD pulsatility (Gosling pulsatility index [PI] reached a plateau. The mean CPP at which SjO2 surpassed 55% was 62 +/- 6.2 mm Hg. TCD PI did not plateau until a significantly higher mean CPP of 74 +/- 5.1 mm Hg was achieved (p < 0.01). In 8 cases, increased CPP was associated with a fall in ICP, ranging from 1 to 8 mm Hg. We conclude that a critically low level of SjO2 is a late indicator of failed autoregulation. CPP values associated with intact autoregulation identified by TCD assessment of MCA flow are significantly higher than those indicated by SjO2 monitoring. MCA Doppler flow assessment may be useful in determining the level of CPP at which therapy should be aimed in the early resuscitation of head trauma.

Hyperventilation therapy for acute traumatic brain injury.

Because hyperventilation is often associated with a rapid fall in intracranial pressure, it has been assumed to be effective in the treatment of severe head injury. Hyperventilation reduces raised intracranial pressure by causing cerebral vasoconstriction and a reduction in cerebral blood flow. Whether reduced cerebral blood flow improves neurological outcome however, is unclear. To quantify the effect of hyperventilation on death and neurological disability following head injury. The search strategy drew on that of the Injuries Group as a whole. The reference lists of all relevant articles identified were checked and the first author of reports was contacted to ask for assistance in identifying any further trials. Most recent search was done in September 1999. All randomised trials of hyperventilation, in which study participants had a clinically defined acute traumatic head injury of any severity. There were no language restrictions. We collected data on the participants, the timing and duration of the intervention, duration of follow up, neurological disability and death. Relative risks (RR) and 95% confidence intervals were calculated for each trial on an intention to treat basis. Timing, degree and duration of hyperventilation were identified a-priori as potential sources of heterogeneity between trials. One trial of 113 participants was identified. Hyperventilation alone, as well as in conjunction with the buffer THAM showed a beneficial effect on mortality at one year after injury, although the effect measure was imprecise (RR=0.73; 95% CI 0.36;1.49 and RR=0.89; 95% CI 0.47;1.72 respectively). This improvement in outcome was not supported by an improvement in neurological recovery. For hyperventilation alone, the RR for death or severe disability was 1. 14 (95% CI 0.82;1.58). The RR for death or severe disability in the hyperventilation plus THAM group, was 0.87 (95% CI 0.58;1.28). The data available are inadequate to assess any potential benefit or harm that might result from hyperventilation in severe head injury. Randomised controlled trials to assess the effectiveness of hyperventilation therapy following severe head injury are needed.

Early effects of mannitol in patients with head injuries assessed using bedside multimodality monitoring.

We have employed bedside multimodality methods to assess the influence of a slow (20 min) bolus of hypertonic mannitol on cerebral hemodynamics in comatose patients with head injuries. Middle cerebral artery flow velocities (FV) and cortical microcirculatory flows were measured in comatose patients with head injuries after the administration of 200 ml of 20% mannitol. A comparison was made with the effects of an identical bolus of isotonic saline. Fourteen patients with diffuse head injuries and with raised intracranial pressure were selected, and mannitol infusion studies were conducted when clinically indicated (n = 23). Using transcranial doppler and laser doppler flowmetry (LDF), indices of estimated cerebrovascular resistance (eCVR) were calculated for the macro- (eCVR-FV) and micro- (eCVR-LDF) circulation. During mannitol infusion, a significant rise in cerebral perfusion pressure was detected (+10%, P = 0.03) as a result of a fall in intracranial pressure (-21%, P = 0.001). Increases in both FV (+13%, P < 0.001) and LDF (+14%, P = 0.002) occurred only after the administration of mannitol and persisted beyond completion of infusion. The effect on FV and LDF decayed exponentially, with a time constant of 34.0 and 38.0 minutes, respectively, and was independent of the pressure autoregulatory status. There was a tendency for eCVR-FV and eCVR-LDF to decrease. No significant effects resulted from the administration of saline. Bedside multimodality monitoring may provide a useful means for assessing the effects of therapy in the comatose patient. The mechanisms by which mannitol reduces intracranial pressure in patients with head injuries are discussed.

Is there a reasonable differential indication for different hydrocephalus shunt systems?

We tested various shunt systems for pressure/flow characteristics and long-term reliability. In addition, we used a model to simulate activities of daily life postural changes, blood and airway pressure changes and their impact on CSF pressure and flow through various ventriculo-peritoneal shunt systems. In the recumbent position, the changes in flow rate and CSF pressure depended on the valve resistance. Various valves showed deviations from the pressure/flow characteristics claimed for them and proved to be unreliable during long-term perfusion. The flow rate increased in the head-up position. Negative intracranial CSF pressure was due to the continued flow through the shunt system afforded by the siphon effect. The siphon effect was so marked in the upright position that valves of various kinds and with various resistances did not make any significant difference in the resulting intracranial pressure (ICP). The shunt systems, however, differed in the maximum flow rate in the upright position, leading to a different steep fall in ICP following elevation of the body. Ball-and-spring valves had the highest flow rates (> 500 ml/h), leading to negative ICP within seconds. Diaphragm valves, and especially the self-adjusting diaphragm valve, demonstrated a slower drop in ICP, taking several minutes to reach negative ICP. ASD and SCD, however, did prevent any siphoning effects, leading to an ICP within the corresponding valve opening/closing pressure range. Our results demonstrate that in most patients there is no significant difference in various different shunting systems as long as the patient is mobile.(ABSTRACT TRUNCATED AT 250 WORDS)

Falling Intracranial Pressure: An Important Element in the Genesis of Intracranial Hemorrhage in the Beagle Puppy

To study the role of extravascular intracranial pressure (ICP) in the genesis of intracranial hemorrhage in the beagle puppy, we measured ICP in animals on the day of birth, untreated 3-day-old controls, and 3-day-old animals treated from birth with prolactin. Baseline ICP varied substantially in all 3 groups. Only 8% of this variability was attributable to variability in mean arterial pressure and central venous pressure. ICP was lower in the 3-day-old controls, animals at high risk for intracranial hemorrhage after a hypovolemic/hypotensive insult followed by rapid volume expansion, than in the other groups which are at lower risk. Administration of a hyperosmolar insult, intraperitoneal glycerol, to animals whose ICP was relatively high promptly lowered ICP. After this treatment, the risk of intracranial hemorrhage was markedly increased in these previously low-risk groups. We conclude that the normal neonatal decrease in brain water content and the consequent fall in ICP substantially increase the risk of intracranial hemorrhage in the beagle puppy, a model which appears similar in pathophysiology to hemorrhage in the preterm human infant.

Continuous EEG and ICP monitoring as a guide to the administration of althesin sedation in severe head injury.

The effects of 142 intravenous boluses of althesin (0.05 ml/kg) on cerebral perfusion pressure (CPP) were studied in twelve head injured comatose patients. The data were divided into those where the mean pre-bolus intracranial pressure (ICP) was above or below 20 mmHg and then subdivided into those where the minimum pre-bolus voltage of the cerebral function monitor (CFM) was above or below 5 microV (representing marked reduction in cortical electrical activity). The pre-bolus ICP influenced the extent of the fall in ICP and thus the direction of the resulting change in CPP. A mean reduction in CPP was observed in both groups in which ICP was below 20 mmHg irrespective of the CFM voltage. In the subgroups with high ICP, CPP increased when CFM was not depressed and fell when CFM was below 5 microV. The effects of individual boluses varied within and between the subgroups and, occasionally, severe and unpredictable hypotension occurred. If althesin administration had been restricted to the high CFM and high ICP group, 90% of the episodes of reduced CPP would have been avoided. In fact, when cortical electrical activity is already severely depressed, further administration of hypnotic anaesthetic agents produces only small reductions in ICP and usually a fall in CPP. These findings suggest that the minimum voltage of the CFM trace is a clinically useful guide to the administration of intravenous anaesthetic agents and offers a relevant prediction of their effects on CPP.

Medical management of raised intracranial pressure after severe birth asphyxia.

The effects of dexamethasone and 20% mannitol infusion in reducing raised intracranial pressure were assessed in severely asphyxiated newborn infants. Intracranial pressure was measured continuously by a percutaneously placed subarachnoid catheter, and cerebral perfusion pressure was calculated from this and blood pressure data. Dexamethasone treatment, assessed in seven infants, produced an overall fall in intracranial pressure which was sustained for at least six hours, but this was coincident with a simultaneous reduction in systemic blood pressure with no change in the cerebral perfusion pressure. Mannitol, studied on nine occasions, produced a fall in intracranial pressure in each case, together with an overall rise in cerebral perfusion pressure 60 minutes after starting the infusion; this was sustained for a further four hours. We can find little to support the routine use of dexamethasone in severe perinatal asphyxia but mannitol infusion seems of value in treating raised intracranial pressure associated with cerebral oedema.

Mechanism of the fall in intracranial pressure due to the action of furosemide

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Alterations in intracranial pressure following ketamine anesthesia in hydrocephalic children.

Intracranial pressure was measured in 12 hydrocephalic children during ketamine anesthesia. Of the four who received no premedication, intracranial pressure increased in three and decreased in one patient. Seven out of eight children who received premedication with trimeperazine tartrate (3 mg/kg) orally showed a decrease in pressure. One patient who had a high initial pressure showed a steep rise necessitating termination of the study. Second dose of ketamine (1 mg/kg iv) produced a fall in all patients, being more prominent in those who had an elevation after the first dose. It is possible that the premedicants alter the response of cerebral vasculature to ketamine leading to a fall in intracranial pressure. Another possibility is that the standard intravenous dose of ketamine (2 mg/kg) is not uniformly effective in all patients of hydrocephalus.

Evidence of prolactin receptors in the choroid plexus and a possible role in water balance in neonatal brain.

Tissue dehydration, including that of the brain, is a natural part of maturation. In the newborn it is accompanied by an acute salt water diuresis which is particularly pronounced in the premature infant. The decrease in cranial volume and fall in intracranial pressure to subatmospheric levels observed in premature infants after birth suggests that the brain shares in this process. Since fluid homeostasis is normally under hormonal control, the inordinate loss of fluid in the prematurely born may be attributable to a hormonal imbalance. The possibility that prolactin, a proven osmoregulatory hormone in submammalian species but not in mammals and primates, may have an important role in this process is suggested by recent evidence that prolactin regulates tissue water in fetal and newborn animals. If this hormone assists in the regulation of water and electrolyte content of the brain during the perinatal period then prolactin receptors might be expected at blood-brain and blood-CSF barriers. Our study with preterm, term and adult rabbits indicates that prolactin receptors are present and in much higher concentrations in the choroid plexus than in other tissues examined. Specific binding of prolactin to receptors on tissues normally is observed to increase with age. Since binding to the choroid plexus decreased with age it would suggest that the effect of prolactin on choroid plexus function may be more important during the perinatal than later stages of development.

Effect of mannitol and furosemide on blood-brain osmotic gradient and intracranial pressure

The effect of mannitol (1.0 gm/kg) and furosemide (0.7 mg/kg), alone and in combination, on the blood-brain extracellular fluid and cerebrospinal fluid (CSF) osmotic gradient, elevated intracranial pressure (ICP), CSF and serum osmolality, and urine output was studied in 26 mongrel dogs. Mannitol and furosemide, when used together, produced a greater (62.4% versus 56.6%) and more sustained (5 hours versus 2 hours) fall in ICP than mannitol alone. This correlated with a prolongation of the reversal of the blood-brain osmotic gradient (-3.4 to + 38.5 mOsm/kg) and a rate of urine formation 15 times control values. There was a transient but not significant fall in serum Na+ with the combined treatment, but the arterial pressure did not vary from pretreatment levels. The results from this present study suggest that the distal loop diuretics in a dose of less than 1.0 mg/kg act synergistically with mannitol by causing preferential excretion of water over solute in the renal distal tubule, and thereby sustaining the osmotic gradient initially established by the mannitol infusion. It is possible, but unlikely in the doses used, that the additive effect of furosemide on reducing ICP in the presence of mannitol is due to interference with CSF formation or Na+ and H2O movement across the blood-brain barrier.

Analysis of the cerebrospinal fluid pulse wave in intracranial pressure.

The configuration of the intracranial pressure (ICP) pulse wave represents a complex sum of various components. Amplitude variations of an isolated component might reflect changes in a specific intracranial structure. Fifteen awake patients suffering from hydrocephalus, benign intracranial hypertension, or head injury underwent ICP monitoring through a ventricular catheter and were subjected to three standardized maneuvers to alter the intracranial dynamics: head elevation, voluntary hyperventilation, and cerebrospinal fluid (CSF) withdrawal. A 12 degrees head elevation and fractionated CSF withdrawal caused a mild ICP drop and a proportionate amplitude reduction of all the wave components. Voluntary hyperventilation caused a comparable fall in ICP, and a disproportionate reduction in the amplitude of the wave components, especially the P2 component. It is postulated that the decrease in amplitude of the P2 component reflects the reduction of the cerebral bulk caused by hyperventilation. Head elevation and CSF withdrawal caused a decrease of global ICP but no specific changes in any intracranial structure, and consequently the configuration of the pulse wave remained unchanged. The establishment of relationships between anatomical substrate and particular wave components is promising since potentially it could be useful for monitoring conditions such as vasoparalysis, impaired cerebrovascular reactivity, and cerebral edema.