Tissue resonance analysis: a novel method for noninvasive monitoring of intracranial pressure

2002 ◽  
Vol 96 (6) ◽  
pp. 1132-1137 ◽  
Author(s):  
David Michaeli ◽  
Z. Harry Rappaport
Keyword(s):  
Intracranial Pressure ◽  
Brain Tissue ◽  
Noninvasive Monitoring ◽  
The Body ◽  
Mechanical Resonance ◽  
Content Type ◽  
Resonance Analysis ◽  
Arterial Blood ◽  
Significant Difference ◽  
Fine Print

✓ A number of noninvasive methods used to measure intracranial pressure (ICP) have been proposed in the literature. For a variety of reasons, however, none of these have displayed significant practical applicability. The authors describe their development of a new, computerized, portable device based on tissue resonance analysis (TRA) technology for the noninvasive monitoring and measurement of ICP. In response to the heart beat, the soft tissue and fluid compartments of the brain each exhibit characteristic vibration and mechanical resonant responses that radiate through the organs and tissues of the body. Patterns of vibration and mechanical resonance of various body organs and tissues are different and provide the possibility of extracting new and specific information in a noninvasive fashion. According to the TRA approach, ICP is dependent on the value of the dominant secondary (mechanical) resonance level of brain tissue. By digitally processing a reflected ultrasound signal (by using a concave ultrasonography probe with a carrier frequency of 1 MHz) from the third ventricle, the authors obtained a digital high-resolution echopulsogram, which visually is equivalent to ICP waves that are obtained invasively. The fast Fourier relationship of electrocardiogram and echopulsogram waves allowed the derivation of the secondary mechanical resonance levels. The authors developed a formula for a quantitative, noninvasive measurement of ICP, which uses information regarding multiple components of the intracranial space—both mechanical (secondary resonance) and physiological (time required for transfer of arterial blood to venous blood through brain tissue)—and the relationship between these components. A comparison of invasive and noninvasive ICP measurements was made during blinded trials in 40 patients with various diseases of the central nervous system, and ranges of ICP were measured from 1 to 66 mm Hg. The ICP values obtained using the two methods were highly correlated (r = 0.99), without a statistically significant difference between simultaneously obtained readings (p = 1). By using an integrative approach that reflects all components of the intracranial compartment, TRA allows for accurate noninvasive recordings of ICP. This method has significant advantages over other noninvasive technologies reported to date.

Evaluation of a method for noninvasive intracranial pressure assessment during infusion studies in patients with hydrocephalus

2000 ◽  
Vol 92 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Bernhard Schmidt ◽  
Marek Czosnyka ◽  
Jens Jürgen Schwarze ◽  
Dirk Sander ◽  
Werner Gerstner ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Time Course ◽  
Cerebral Blood Flow Velocity ◽  
Absolute Error ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Clinical Benefit ◽  
The Mean ◽  
Fine Print

Object. A mathematical model previously introduced by the authors allowed noninvasive intracranial pressure (nICP) assessment. In the present study the authors investigated this model as an aid in predicting the time course of raised ICP during infusion tests in patients with hydrocephalus and its suitability for estimating the resistance to outflow of cerebrospinal fluid (Rcsf).Methods. Twenty-one patients with hydrocephalus were studied. The nICP was calculated from the arterial blood pressure (ABP) waveform by using a linear signal transformation, which was dynamically modified by the relationship between ABP and cerebral blood flow velocity. This model was verified by comparison of nICP with “real” ICP measured during lumbar infusion tests. In all simulations, parallel increases in real ICP and nICP were evident. The simulated Rcsf was computed using nICP and then compared with Rcsf computed from real ICP. The mean absolute error between real and simulated Rcsf was 4.1 ± 2.2 mm Hg minute/ml. By the construction of simulations specific to different subtypes of hydrocephalus arising from various causes, the mean error decreased to 2.7 ± 1.7 mm Hg minute/ml, whereas the correlation between real and simulated Rcsf increased from R = 0.73 to R = 0.89 (p < 0.001).Conclusions. The validity of the mathematical model was confirmed in this study. The creation of type-specific simulations resulted in substantial improvements in the accuracy of ICP assessment. Improvement strategies could be important because of a potential clinical benefit from this method.

Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs

1986 ◽  
Vol 64 (6) ◽  
pp. 924-931 ◽  
Author(s):  
Alan A. Artru ◽  
Kim Wright ◽  
Peter S. Colley
Keyword(s):  
Sodium Nitroprusside ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Energy Charge ◽  
Metabolic Disturbances ◽  
Induced Hypotension ◽  
Content Type ◽  
Arterial Blood ◽  
Cerebral Metabolites ◽  
Fine Print

✓ This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the α and β2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG α and β2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.

Association between elevated brain tissue glycerol levels and poor outcome following severe traumatic brain injury

2005 ◽  
Vol 103 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Tobias Clausen ◽  
Oscar Luis Alves ◽  
Michael Reinert ◽  
Egon Doppenberg ◽  
Alois Zauner ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Time Course ◽  
Glycerol Concentration ◽  
Significant Information ◽  
Content Type ◽  
Significant Difference ◽  
Fine Print

Object. Glycerol is considered to be a marker of cell membrane degradation and thus cellular lysis. Recently, it has become feasible to measure via microdialysis cerebral extracellular fluid (ECF) glycerol concentrations at the patient's bedside. Therefore the aim of this study was to investigate the ECF concentration and time course of glycerol after severe traumatic brain injury (TBI) and its relationship to patient outcome and other monitoring parameters. Methods. As soon as possible after injury for up to 4 days, 76 severely head-injured patients were monitored using a microdialysis probe (cerebral glycerol) and a Neurotrend sensor (brain tissue PO2) in uninjured brain tissue confirmed by computerized tomography scanning. The mean brain tissue glycerol concentration in all monitored patients decreased significantly from 206 ± 31 µmol/L on Day 1 to 9 ± 3 µmol/L on Day 4 after injury (p < 0.0001). Note, however, that there was no significant difference in the time course between patients with a favorable outcome (Glasgow Outcome Scale [GOS] Scores 4 and 5) and those with an unfavorable outcome (GOS Scores 1–3). Significantly increased glycerol concentrations were observed when brain tissue PO2 was less than 10 mm Hg or when cerebral perfusion pressure was less than 70 mm Hg. Conclusions. Based on results in the present study one can infer that microdialysate glycerol is a marker of severe tissue damage, as seen immediately after brain injury or during profound tissue hypoxia. Given that brain tissue glycerol levels do not yet add new clinically significant information, however, routine monitoring of this parameter following traumatic brain injury needs further validation.

Relative importance of hypertension compared with hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage

2005 ◽  
Vol 103 (6) ◽  
pp. 974-981 ◽  
Author(s):  
Andreas Raabe ◽  
Jügen Beck ◽  
Mike Keller ◽  
Hartmuth Vatter ◽  
Michael Zimmermann ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Vasospasm ◽  
Moderate Hypertension ◽  
Cerebral Oxygenation ◽  
Brain Oxygenation ◽  
Content Type ◽  
Arterial Blood ◽  
Hypertension Therapy ◽  
Fine Print

Object. Hypervolemia and hypertension therapy is routinely used for prophylaxis and treatment of symptomatic cerebral vasospasm at many institutions. Nevertheless, there is an ongoing debate about the preferred modality (hypervolemia, hypertension, or both), the degree of therapy (moderate or aggressive), and the risk or benefit of hypervolemia, moderate hypertension, and aggressive hypertension in patients following subarachnoid hemorrhage. Methods. Monitoring data and patient charts for 45 patients were retrospectively searched to identify periods of hypervolemia, moderate hypertension, or aggressive hypertension. Measurements of central venous pressure, fluid input, urine output, arterial blood pressure, intracranial pressure, and oxygen partial pressure (PO2) in the brain tissue were extracted from periods ranging from 1 hour to 24 hours. For these periods, the change in brain tissue PO2 and the incidence of complications were analyzed. During the 55 periods of moderate hypertension, an increase in brain tissue PO2 was found in 50 cases (90%), with complications occurring in three patients (8%). During the 25 periods of hypervolemia, an increase in brain oxygenation was found during three intervals (12%), with complications occurring in nine patients (53%). During the 10 periods of aggressive hypervolemic hypertension, an increase in brain oxygenation was found during six of the intervals (60%), with complications in five patients (50%). Conclusions. When hypervolemia treatment is applied as in this study, it may be associated with increased risks. Note, however, that further studies are needed to determine the role of this therapeutic modality in the care of patients with cerebral vasospasm. In poor-grade patients, moderate hypertension (cerebral perfusion pressure 80–120 mm Hg) in a normovolemic, hemodiluted patient is an effective method of improving cerebral oxygenation and is associated with a lower complication rate compared with hypervolemia or aggressive hypertension therapy.

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004 ◽  
Vol 101 (4) ◽  
pp. 594-599 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
John M. Abrahams ◽  
Stephanie Bloom ◽  
Michelle J. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Oxygenation ◽  
Content Type ◽  
Poor Grade ◽  
Physiological Variables ◽  
Arterial Blood ◽  
End Tidal ◽  
Fine Print

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

Cerebral perfusion pressure, intracranial pressure, and head elevation

1986 ◽  
Vol 65 (5) ◽  
pp. 636-641 ◽  
Author(s):  
Michael J. Rosner ◽  
Irene B. Coley
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Pressure Waves ◽  
Content Type ◽  
Arterial Blood ◽  
Head Elevation ◽  
Adequate Hydration ◽  
Fine Print

✓ Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20° to 30°, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10° of head elevation from 0° to 50°. For every 10° of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 ± 3.4 mm Hg (mean ± standard error of the mean)) always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0° head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.

Glomus jugulare tumor presenting with increased intracranial pressure

1979 ◽  
Vol 50 (6) ◽  
pp. 823-825 ◽  
Author(s):  
David W. Beck ◽  
Neal F. Kassell ◽  
Charles G. Drake
Keyword(s):  
Intracranial Pressure ◽  
Visual Loss ◽  
Intracranial Extension ◽  
Increased Intracranial Pressure ◽  
Content Type ◽  
Glomus Jugulare Tumor ◽  
Glomus Jugulare ◽  
Venous Sinuses ◽  
Arterial Blood ◽  
Fine Print

✓ The authors report a case of glomus jugulare tumor presenting with papilledema and visual loss. The tumor was extremely vascular with significant shunting of arterial blood into venous sinuses. There was no intracranial extension of tumor, and papilledema resolved after removal of the lesion.

Use of microfibrillar collagen as a topical hemostatic agent in brain tissue

1977 ◽  
Vol 46 (4) ◽  
pp. 501-505 ◽  
Author(s):  
John D. Rybock ◽  
Don M. Long
Keyword(s):  
Brain Tissue ◽  
Tissue Reaction ◽  
Hemostatic Agent ◽  
Histological Evaluation ◽  
Content Type ◽  
Two Agents ◽  
Significant Difference ◽  
Fine Print

✓ Microfibrillar collagen, a recently introduced topical hemostatic agent, was used to obtain hemostasis in suction-evacuation lesions of canine cortex. Gelatin foam was used as a control in identical lesions on the opposite side. Microfibrillar collagen was found to be faster acting and more effective than gelatin foam. Histological evaluation of the lesions at 2, 4, and 6 months postoperatively showed no significant difference in the amount or type of tissue reaction to the two agents.

Intracranial pressure changes induced during papaverine infusion for treatment of vasospasm

1995 ◽  
Vol 83 (3) ◽  
pp. 430-434 ◽  
Author(s):  
William McAuliffe ◽  
Murphy Townsend ◽  
Joseph M. Eskridge ◽  
David W. Newell ◽  
M. Sean Grady ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Carotid Artery ◽  
Pulse Rate ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Signs ◽  
Average Dose ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ The authors reviewed the cases of 21 patients who received intraarterial infusions of papaverine to determine the drug's effects on intracranial pressure (ICP), mean arterial blood pressure, pulse rate, and cerebral perfusion pressure (CPP). The study focused on patients with aneurysmal subarachnoid hemorrhage who developed clinical signs and symptoms of vasospasm, which was documented by cerebral angiography. In 18 patients, an average dose of 300 mg papaverine was administered over 20 to 35 minutes using a No. 5 French catheter inserted into the high cervical internal carotid artery or vertebral artery. Two other patients received superselective infusions via a microcatheter placed in the anterior cerebral artery. Sixteen patients (76%) experienced good angiographic results, and 11 (52%) obtained objective clinical improvement within 48 hours. Significant elevations in ICP, blood pressure, and pulse rate were noted during papaverine infusion. In contrast, no statistically significant sustained change in CPP was observed, although it tended to decrease during papaverine infusion. In one elderly patient, infusion of the common carotid artery resulted in profound bradycardia and hypotension with a subsequent significant increase in ICP and a marked decrease in CPP. The increase in ICP in these patients correlates well with changes seen in animal models and is probably related to increased cerebral blood flow. A careful, titrated infusion of papaverine, with constant reference to the patient's ICP, blood pressure, and pulse rate, minimizes the transient increase in ICP while maintaining adequate blood pressure and CPP. Failure to monitor these parameters during the infusion, with appropriate modification of the rate of titration, could potentially produce an uncontrolled change in ICP or CPP.

Age, intracranial pressure, autoregulation, and outcome after brain trauma

2005 ◽  
Vol 102 (3) ◽  
pp. 450-454 ◽  
Author(s):  
Marek Czosnyka ◽  
Marcella Balestreri ◽  
Luzius Steiner ◽  
Piotr Smielewski ◽  
Peter J. Hutchinson ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Older Patients ◽  
Brain Trauma ◽  
Reactivity Index ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Arterial Blood ◽  
Pressure Reactivity ◽  
Age Related ◽  
Fine Print

Object. The object of this study was to investigate whether a failure of cerebrovascular autoregulation contributes to the relationship between age and outcome in patients following head injury. Methods. Data obtained from continuous bedside monitoring of intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP = ABP — ICP) in 358 patients with head injuries and intermittent monitoring of transcranial Doppler blood flow velocity (FV) in the middle cerebral artery in 237 patients were analyzed retrospectively. Indices used to describe cerebral autoregulation and pressure reactivity were calculated as correlation coefficients between slow waves of systolic FV and CPP (autoregulation index [ARI]) and between ABP and ICP (pressure reactivity index [PRI]). Older patients had worse outcomes after brain trauma than younger patients (p = 0.00001), despite the fact that the older patients had higher initial Glasgow Coma Scale scores (p = 0.006). When age was considered as an independent variable, it appeared that ICP decreased with age (p = 0.005), resulting in an increasing mean CPP (p = 0.0005). Blood FV was not dependent on age (p = 0.58). Indices of autoregulation and pressure reactivity demonstrated a deterioration in cerebrovascular control with advancing age (PRI: p = 0.003; ARI: p = 0.007). Conclusions. An age-related decline in cerebrovascular autoregulation was associated with a relative deterioration in outcome in elderly patients following head trauma.

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