Acetazolamide vasoreactivity evaluated by transcranial power harmonic imaging and Doppler sonography.

BACKGROUND: Cerebral vasoreactivity (CVR) in the major cerebral arteries evaluated by transcranial Doppler sonography has shown some correlation with CVR in the brain tissue measured by other neuroradiological modalities. To clarify vasoreactive differences in the brain tissue and the major cerebral arteries, we have evaluated the relationship of acetazolamide (ACZ) CVR between transcranial ultrasonic power harmonic imaging (PHI) and color Doppler sonography (CDS), in cases ofparenchymal pathology with and without occlusive vascular lesions. MATERIALS AND METHODS: The subjects were 31 stroke patients with intraparenchymal pathologies, 15 with (occlusive group) and 16 without (non-occlusive group) occlusive carotid and/or middle cerebral artery lesions. CVR based on values before/after ACZ (angle-collected CDS velocity in the middle and posterior cerebral arteries, PHI contrast area size, peak intensity, time to peak intensity), and correlation of CVR between PHI and CDS were compared between the side with and without lesions in both groups. FINDINGS: (a) PHI CVR tended to be more disturbed than CDS CVR. CVR side differences were not significant. (b) CVR correlations between PHI and CDS were always lower in the pathological sides. CONCLUSIONS: CVR in brain tissue evaluated by PHI is susceptible to disturbance in comparison with CDS, due to both parenchymal and vascular occlusive pathologies.

Quantitative evaluation of cerebrovascular reactivity in brain tissue by a refill kinetic method of transcranial ultrasonic perfusion imaging: a comparison with Doppler sonography.

UNLABELLED: To confirm the reliability of a refill kinetic method of ultrasonic harmonic perfusion imaging (HPI) capable of quantifying separate parameters of microvascular blood flow velocity and volume in brain tissue, we evaluated acetazolamide (ACZ) cerebrovascular reactivity by transcranial HPI in comparison with Doppler sonography (TCD). Methods. HPI during continuous Levovist infusion with changing pulsing intervals (t) and TCD time-averaged maximum velocity (TAMX) in the middle and posterior cerebral arteries were evaluated before and after ACZ administration in 12 patients, 8 without and 4 with a temporal skull defect. Plateau value (A) and rise rate (beta) of intensity (I) represented by HPI time-intensity curves of I(t) = A(1 - e(-beta*t)) were analyzed on the axial diencephalic plane. RESULTS: 1) A significantly decreased in proportion to the region of interest location depth only in the intact skull cases. 2) Despite inter- and intra-individual data scattering, in correspondence with TAMX increases after ACZ, significant beta increases were more frequently identified than increases of A. CONCLUSIONS: Cerebral vasoreactivity analysis utilizing refill kinetics of transcranial HPI can potentially provide separate quantification based on microvascular blood velocity and volume (capillary patency) with consideration of depth-dependant ultrasound attenuation. This should be suitable for bedside evaluation of neurointensive care patients.

Acetazolamide vasoreactivity in persistent vegetative state and vascular dementia evaluated by transcranial harmonic perfusion imaging and Doppler sonography.

UNLABELLED: To clarify the pathophysiological differences of the cerebrovascular reserve capacity in relation to cerebral cognitive impairments between persistent vegetative state (PVS) and vascular dementia (VD), we evaluated acetazolamide (ACZ) vasoreactivity testing by transcranial harmonic perfusion imaging (HPI) and Doppler sonography (TCD). METHODS: The subjects were 11 adult patients with severe cognitive impairments (4 PVS, 7 VD). TCD mean velocity (Vm) in the middle and posterior cerebral artery (MCA, PCA) and peak intensity (PI), area under curve (AUC), and mean transit time (MTT) analyzed by HPI time-intensity curves in the bilateral temporal lobe (TL), basal ganglia (BG), and thalamus (Th) were evaluated before and after ACZ administration. Resting values and relative changes (%delta) of TCD and HPI parameters were compared between PVS and VD. RESULTS: a) Resting values: There were no significant differences between the two groups. b) Vasoreactivity: 1) PVS: %delta Vm decreased in the left PCA and MCA. %delta PI/AUC/MTT decreased in the left TL and bilateral BG. 2) VD: %delta PI/AUC decreased in the right TL. %delta MTT tended to decrease in the right side. CONCLUSION: ACZ vasoreactivity tests by transcranial HPI and TCD allowed bedside, non-invasive, quantitative evaluation of the pathophysiology of cognitive function impairment and treatments, in relation to cerebrovascular reserve capacity in PVS and VD.

Acetazolamide vasoreactivity evaluated by transcranial harmonic perfusion imaging: relationship with transcranial Doppler sonography and dynamic CT.

UNLABELLED: To establish the reliability and clinical significance of transcranial ultrasonic harmonic perfusion imaging (HPI), we evaluated HPI's relationships with transcranial Doppler (TCD) and with dynamic CT (DCT), during acetazolamide (ACZ) vasoreactivity tests. METHODS: The subjects were 12 neurological patients. Time-averaged maximum velocity (TAVMX) in the middle (MCA) and posterior cerebral arteries was measured by TCD. Time-intensity (-density) curves of HPI (DCT) after bolus intravenous contrast injections were created in 3 regions of interest (ROI) on the axial plane involving the temporal lobe, basal ganglia, and thalamus on both sides. Assessments of vasoreactivity were based on comparisons conducted before and after ACZ administration in terms of: a) relative changes (%delta) of the TCD TAVMX, b) HPI contrast area enlargement, c) %delta of calculated cerebral blood volume and flow of the HPI and DCT. RESULTS: 1) TCD vasoreactivity decrease in the left MCA tended to correlate with lower frequency of HPI contrast area enlargement on the left side. 2) HPI and DCT vasoreactivity tended to be disturbed in the same side ROIs. CONCLUSIONS: Transcranial HPI achieves repeatable non-invasive bedside evaluation of cerebrovascular reserve capacity through qualitative and quantitative measurements of brain tissue perfusion, and will have clinical value in pathophysiological follow-up and therapeutic effectiveness determination of neurointensive care patients.

Acetazolamide vasoreactivity in vascular dementia and persistent vegetative state evaluated by transcranial harmonic perfusion imaging and Doppler sonography.

To clarify the pathophysiological differences of the cerebrovascular reserve capacity in relation to cerebral cognitive impairments between vascular dementia (VaD) and persistent vegetative state (PVS), we evaluated acetazolamide (ACZ) vasoreactivity testing by transcranial harmonic perfusion imaging (HPI) and Doppler sonography (TCD). Sixteen patients (age: 29-85 years; mean: 62) were divided into three groups: 7 VaD, 4 PVS, and 5 nondementia patients. Mean velocity (Vm) in the middle and posterior cerebral artery (MCA, PCA) was measured, and time-intensity curves of the HPI were evaluated at three regions of interest-the bilateral temporal lobe (TL), basal ganglia (BG), and thalamus (Th). TCD and HPI were evaluated before (resting state) and after ACZ administration, and vasoreactivity was compared among the three groups in terms of resting values and relative changes (%Delta) of Vm, peak intensity (PI), area under curve (AUC), and mean transit time (MTT). Results of the resting state: Decreased Vm, PI, and AUC of the VaD and PVS groups were more obvious in the right side. Results of vasoreactivity: In the PVS group, %DeltaVm decreased in the left PCA and MCA; %DeltaPI and %DeltaAUC decreased in the left TL and bilateral BG. In the VaD group, %DeltaPI and %DeltaAUC decreased in the right TL; %DeltaMTT tended to increase in the left side. ACZ vasoreactivity tests by transcranial HPI and TCD allowed bedside, noninvasive quantitative evaluation of the pathophysiology of cognitive function impairment in relation to cerebrovascular reserve capacity in VaD and PVS.

Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.

INTRODUCTION: Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. PATIENTS AND METHODS: Continuous monitoring of cerebrospinal fluid (CSF) pH, PCO2, HCO3-, base excess (BE), PO2, SO2, temperature, lactate and pyruvate (La and Py) measurements were conducted in 8 patients with severe head injury. Temperature-corrected CSF parameters were correlated with those in the jugular blood including oxygen saturation (SjO2), regional oxygen saturation (rSO2), intracranial pressure (ICP) and cerebral perfusion pressure (CPP), jugular blood temperature (Tjb), and endtidal PCO2 (PetCO2). Therapeutic significance of hyperventilation and hypothermia was evaluated. RESULTS: 1) CSF acidosis was observed in all cases (minimum pH 6.59-7.17) due to increased CSF PCO2 and/or decreased CSF HCO3- and tended to associate with abnormal ICP and/or CPP or ischemic episodes indicated by CSF PO2 and SO2, rSO2, and/or SjO2 during monitoring. 2) It was more obvious in CSF than in jugular blood that increased PCO2, La and Py, and/or decreased HCO3- resulted in decreased BE and pH. 3) Decreased CSF PO2 and SO2 only correlated with severe CSF acidosis. 4) Hyperventilation: Decreased PetCO2 did not always closely correlate with CSF PCO2 decrease and CSFpH increase. 5) Hypothermia: There were negative correlations of Tjb with CSF pH and SO2 in all cases, though correlation coefficients were not always high. CONCLUSIONS: CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. Hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.

Comparative effects of hypothermia, barbiturate, and osmotherapy for cerebral oxygen metabolism, intracranial pressure, and cerebral perfusion pressure in patients with severe head injury.

UNLABELLED: In order to select the optimal neurointensive treatment for patients with severe head injury and intracranial hypertension, the effects of hypothermia (HT), barbiturates (BT), and osmotic agents (OT) on focal and diffuse cerebral oxygen metabolism were evaluated by means of continuous monitoring of bifrontal regional oxygen saturation (rSO2), jugular bulb oxygen saturation (SjO2), jugular bulb temperature (Tjb), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). PATIENTS AND METHODS: Cerebral oxygen metabolism in SjO2 and rSO2, ICP, CPP, and Tjb were continuously monitored in severe head injury patients with Glasgow Coma Scale < 8, ages 10-62: 13 with focal and 10 with diffuse injuries. The effects of BT (n = 6), HT (n = 9), and OT (n = 8) on these parameters (ICP/CPP, SjO2, and rSO2) were compared. Evaluations were performed in terms of: a) Percentage of abnormal values based on normal control values; ICP < 20 mm Hg, CPP > 60 mm Hg, SjO2 55-75%, and rSO2 60-80% were calculated, b) Effects of pentobarbital dose (mg/kg/h) for the parameters compared among < 1.0, 1.1-2.0, 2.1-3.0, and > 3.1. c) Effects of Tjb (degree C) on parameters compared among hyperthermia (> 38 degrees C), normothermia (36-37.9 degrees C), mild hypothermia (34-35.9 degrees C) and moderate hypothermia (< 33.9 degrees C). RESULTS: a) Abnormal data differed significantly among the three treatment groups. rSO2 showing ischemia on the affected side was more marked in BT than in HT or OT. b) ICP decreases and CPP increases correlated significantly with the pentobarbital dose. c) ICP decreases and CPP increases correlated significantly with decreased Tjb. CONCLUSION: The therapeutic effects of hypothermia, barbiturates, and osmotherapy on cerebral oxygen metabolism and ICP/CPP are different according to the underlying pathological lesions of patients with severe head injury.

Morphological and hemodynamic evaluations by means of transcranial power Doppler imaging in patients with severe head injury.

The following conditions of 17 patients with severe head injury (ages 9-76; mean 37:12 focal and 5 diffuse injuries) were evaluated during acute phase (1-14 days after injury, mean 5) by transcranial power Doppler imaging (PDI), a new color Doppler ultrasound technique: a) morphological changes via temporal window, b) hemodynamic changes in major intracranial/cervical arteries based on measured angle-corrected time-averaged mean (TAM)/ peak velocities and vessel diameter (Va), and calculated pulsatility indices (PI), vessel area (Va), and flow volume (Vf = TAM x Va). a) 1) Major trunks of intracranial vessels and circle of Willis and pathological changes in frontal/temporal lobes and midbrain were finely visualized. 2) Contusional hemorrhage and cerebral contusion demonstrated irregular hyper- and hypo-echoic lesions, respectively. 3) Delayed epidural hematoma showed a hyper-echoic band. b) 1) Decreased velocities, significant PI increase, and Va increase tendency were observed in intracranial arteries. 2) Increased velocities with Vf increase but no Va decrease indicated hyperemia rather than vasospasm. 3) Va in the intracranial vessels, however, tended to increase PDI appears useful in evaluating real-time and simultaneous morphological and hemodynamic information in pathogenesis and neurointensive care of patients with severe head injury.

Consensus opinion on diagnosis of cerebral circulatory arrest using Doppler-sonography: Task Force Group on cerebral death of the Neurosonology Research Group of the World Federation of Neurology.

BACKGROUND AND PURPOSE: Oscillating flow or systolic spikes are typical Doppler-sonographic flow signals found in the presence of cerebral circulatory arrest, which if irreversible, results in brain death. The Neurosonology Research Group (NSRG) of the World Federation of Neurology (WFN) created a Task Force Group in order to evaluate the role of Doppler-sonography as a confirmatory test for determining brain death. METHODS: The available evidence from the literature has been reviewed and discussed by a group of experts, the members of the Task Force Group on cerebral death of the NSRG. RESULTS AND CONCLUSIONS: Extra- and intracranial Doppler-sonography is a useful confirmatory test to establish irreversibility of cerebral circulatory arrest as optional part of a brain death protocol. Doppler-sonography is of special value when the therapeutic use of sedative drugs renders electroencephalography unreliable. Doppler-sonographic criteria are defined and guidelines for the use of Doppler-sonography in this setting are presented.

Correlation between intracranial pressure (ICP) and changes in CT images of cerebral hemorrhage.

The relationship between intracranial pressure and CT images was investigated in 80 cases of cerebral hemorrhage that occurred between 1984 and 1990. In traumatic intracerebral hematoma, positive correlation was found between intracranial pressure and both shift of midline structures and volume of hematoma except in the occipital lobe or at the base of the frontal lobe. In nontraumatic intracerebral hematoma, increased intracranial pressure was found to correlate with changes in the configuration of the lateral ventricles, intraventricular hemorrhage, and compression of the basal cisterns and cortical sulci. No correlation between intracranial pressure and hematoma volume was observed, most likely due to the number of elderly patients in the subject population. In nontraumatic subarachnoid hemorrhage, positive correlation existed between increased intracranial pressure and intraventricular hemorrhage as well as Evans' ratio calculated using repeat CT images that were obtained due to disturbances in cerebrospinal fluid circulation. These results suggest that the degree by which intracranial pressure increases in patients with cerebral hemorrhage can be estimated by the changes in CT images.

[Relationship between cerebral circulatory arrest and loss of brain functions--analysis of patients in a state of impending brain death].

To clarify the temporal discrepancies between cerebral circulatory arrest and loss of brain functions in relation to neuroradiological differences of brain damage, we analyzed 100 cases of impending brain death evaluated by neurological findings and continuous, simultaneous neuromonitoring of somatosensory and brainstem auditory evoked potentials (SEP, BAEP), compressed spectral arrays (CSA), and transcranial Doppler sonography (TCD). A) Cases of supratentorial lesions: 1) Loss of brain functions after supratentorial circulatory arrest (TCD) were advanced rostrocaudally -(SEP N20 > CSA) > (BAEP III-V > SEP P13/14). 2) All patients demonstrated supratentorial circulatory arrest (TCD) after both neurological and cerebral (CSA) functions had been lost for more than 6 hours or after loss of neurological, cerebral (CSA), and brainstem (BAEP, SEP) functions. B) Cases of diffuse or infratentorial lesions: Supratentorial circulation persisted in a few cases after loss of all brain functions. C) The interval from supratentorial circulatory arrest to brainstem function loss was longer than that to cerebral function loss. Both intervals were less than 24 hours in almost all cases. In applying ancillary studies to the diagnosis of brain death, consideration should be given to the time lag between cerebral circulatory arrest and loss of brain functions caused by pathophysiological differences in brain damage.

Transcranial Doppler monitoring in severe brain damage: relationships between intracranial haemodynamics, brain dysfunction and outcome.

Transcranial Doppler (TCD) monitoring in the middle cerebral (MCA) and common carotid arteries (CCA) was studied in 105 comatose patients with severe brain damage. TCD-measured velocity waveforms in the MCA were evaluated in relation to loss of cerebral function as assessed by EEG and compressed spectral arrays, loss of brain stem function as measured by somatosensory and auditory evoked potentials, loss of all brain function and the clinical outcome. The velocity waveforms exhibited six patterns: continuous forward flow (FF); diastolic no flow (NF); diastolic reverse flow with (RF) or without (DRF) diastolic FF; brief systolic FF (SFF); and undetectable (U). In the 58 fatal cases, the appearance of RF/DRF or SFF in the MCA more often preceded loss of brain stem function than loss of cerebral function. A U pattern in the MCA, which was confirmed by loss of FF in the CCA, was correlated with loss of brain stem function. Only one of the 47 survivors showed DRF in the MCA. No patients in whom SFF or U was observed in the MCA survived. Therefore the presence of these patterns is reliably predictive of brain death. Intracranial diastolic reverse flow (DRF), however, indicates imminent loss of brain function and the need for prompt resuscitative measures.

[Brain metastasis from primary pericardial mesothelioma. Case report].

A 50-year-old female was admitted because of nausea, vomiting, and cerebellar ataxia. Computed tomography scan revealed an enhanced mass accompanied with a cyst in the right cerebellar hemisphere. The mass situated in the subcortical region was removed. Histologically, highly vascular tumor cells lined the cavities. Postoperative radio- and chemotherapy were administered and the clinical symptoms improved gradually. Two months later, the patient complained of dyspnea. Chest X-ray on second admission demonstrated cardiomegaly. Hemorrhagic pericardial effusion amounting to 1000 ml was aspirated by pericardial puncture. Papillary clusters of tumor cells were demonstrated in the pericardial effusion. The patient died of cardiac failure. At necropsy solid tumors were located in the heart, lung, left inguinal region, and cerebellum. Histological diagnosis was mesothelioma arising from the heart. Primary pericardial mesotheliomas are rare; approximately 106 cases have been reported. Pericardial mesothelioma frequently spreads to the adjacent pleura and mediastinum, but distant metastases are extremely rare because patients with pericardial mesothelioma tend to die early due to cardiac failure or cardiac tamponade.

[Evaluation of electrophysiological neuromonitoring in the diagnosis of brain death: Part III. Compressed spectral arrays].

Electrophysiological neuromonitoring of compressed spectral array (CSA) EEG, brainstem auditory evoked potentials (BAEP) and short-latency somatosensory evoked potentials (SEP) can provide precise and immediate information concerning functional integrity of severe brain damage. We applied this neuromonitoring system in 185 cases of severe brain damage in order to evaluate its reliability in the diagnosis of brain death. This report considers the relationships between CSA and neurological, conventional EEG (CEEG), BAEP and SEP findings, and the significance of CSA in the assessment of brain death. CSA monitoring of 59 patients (37 brain-dead in group A and 22 non brain-dead in group B) was performed and analysed. Brain damage was caused by cerebrovascular insult in 31 cases, head injury in 25, meningitis in 2, dan anoxia in 1. Mean patient age was 49 (ages 5-84). There were no significant differences in causes and age distribution between the two groups. CSA monitoring, using 5 or 7 microV/mm, of two channels (Cz-A1 and Cz-A2) of EEG activity was performed. Power spectral analysis (0-16 Hz) was carried out at 10 to 120 second epochs. Automatic BAEP (54 patients) and/or SEP (33 patients) monitoring was performed simultaneously 10 to 30 minutes. CSA was classified into three patterns: 1) "Electrocerebral silence; ECS" revealed bilateral absence of the CSA power spectra for periods longer than 40 seconds. 2) "Biological activity; BA" showed continuous peaks of activity. 3) "Equivocal; EQ" pattern showed intermittent peaks of activity, and unilateral loss of power spectra or bilateral loss within 30 seconds. CSA findings indicated the loss of CSA "BA" pattern (LCBP) in 36 group A patients (17 "ECS" and 19 "EQ"). All but two revealing LCBP had satisfied the neurological criteria of brain death (deep coma, absent brainstem reflexes and apnea) during CSA monitoring. "BA" was always present in 22 group B and one group A patients had not fulfilled neurological criteria of brain death. The CEEG results of all group A patients demonstrating "ECS" of CSA were of the classification Hockaday grade Va or Vb. Four patients classified as grade IV b demonstrated "EQ" An examination of CSA and neurological brainstem function of 28 group A patients revealed LCBP preceded the loss of brainstem reflexes and apnea in 15 patients or was coincided with them in 13.(ABSTRACT TRUNCATED AT 400 WORDS)

[Evaluation of electrophysiological neuromonitoring in the diagnosis of brain death: Part I. Brainstem auditory evoked potentials].

Electrophysiological neuromonitoring of brainstem auditory evoked potentials (BAEP), short-latency somatosensory evoked potentials (SSEP) and compressed spectral array (CSA) EEG can provide precise and immediate information concerning functional integrity of the brain, brainstem and upper spinal cord of severely brain-damaged patients. We applied this neuromonitoring system in the cases of 154 severely brain-damaged patients in order to evaluate its reliability in the diagnosis of brain death. In particular, this study considers the relationships between BAEP and neurological findings, conventional EEG findings and factors affecting final BAEP findings. As a result, we evaluated the significance of BAEP in the diagnosis of brain death. A total of 109 brain-dead patients were divided into two groups: group A with 48 patients determined brain dead neurologically and by EEG prior to BAEP monitoring, and group B with 61 patients who had undergone automatic BAEP monitoring every 10 to 30 minutes before and/or after determination of clinical brain death. A third group, C, included 45 non brain-dead patients subjected to neuromonitoring, and served as a comparative group. Brain damage was caused by subarachnoid hemorrhage in 50 patients, intracerebral hemorrhage in 36, cerebral infarction in 8, head injury in 47, meningitis in 3, brain tumor in 3 and anoxia in 7. There were no significant differences in causes among the three groups (chi 2 = 20.3). The mean ages in the three groups were 50 (ages 10-91) in group A, 51 (14-86) in group B, and 50 (5-87) in group C. There were no significant differences in age distribution among the three group (chi = 25.0). The last BAEP findings of the 109 brain-dead patients indicated loss of all waves in 99 (91%), the presence of wave I in 9 (8%), and the presence of waves I and II in one patient (1%) (Table 1). Only three of the 45 group C non brain-dead patients indicated loss of all BAEP waves within one month after onset (Table 1). The one demonstrated loss of all BAEP waves 17 days after her accident, with recovery of waves I to V three months later. The temporal relationships in group B patients of the course of BAEP findings and the time of neurological brain death diagnosis are shown in Table 2 and Fig. 1. All but two of the 61 patients were followed up until final loss of BAEP waves (Fig. 1).(ABSTRACT TRUNCATED AT 400 WORDS)

Necessity for ICP monitoring to supplement GCS in head trauma cases.

The necessity for ICP monitoring together with GCS findings to detect deterioration in head trauma cases and determine the treatment required was studied. There were 18 subjects (14 males, 4 females) aged from 11 to 61. Cases of primary brain stem damage were excluded. Eight cases had GCS of 6-10, and 10 cases scores of 11-15. Initial CTs of these cases indicated the following conditions: thin acute extradural haematoma (A-EDH), thin acute subdural haematoma (A-SDH), brain contusion, and single or multiple intracerebral haematoma (ICH). However, in no case was any mass effect clearly shown. Medical decompression (osmotherapy, barbiturate, steroid and mechanical hyperventilation) was carried out with simultaneous ICP monitoring. Based upon our cases which showed a GCS score of 10 or less, ICP monitoring should accompany medical decompression. Where the ICP cannot be maintained below 20 mm Hg, there is a high risk (about 60%) of haematoma enlargement, delayed haematoma, or increasing brain oedema. ICP monitoring in these cases should be maintained for at least one week. Timely surgical decompression is necessary when the ICP stays above 20 mm Hg, the GCS score drops below 10, and repeat CT scan indicates progress of the mass effect.