Morphometry and morphological analysis of carotico-clinoid foramen: an anatomical study with clinical implications.

BACKGROUND: The dural fold between anterior and middle clinoid processes on mineralisation leads to the formation of caroticoclinoid foramen (CCF). Different morphology of this foramen presents with different clinical features. The present study reports the frequency of CCF in the population of Bihar, while providing an account of assimilated information from previous literature regarding the association of caroticoclinoid ligament ossification with age and human genetics. MATERIALS AND METHODS: The study was conducted on 100 adult dry human skulls of unknown age and sex, and 50 lateral view radiographs of the head. RESULTS: Of the 100 dry skull bones, 9 presented with different forms of CCF. Bilateral complete foramina were noticed in 2 (2%) skull bones, while the incomplete foramina were observed bilaterally in 3 (3%) and unilaterally in 4 (4%) skulls. The lateral view radiograph data (n = 50) presented with a bilateral foramen in one subject and unilateral complete CCF in two different subjects. On measurements of the diameters of the complete CCF the mean values observed were 4.06 mm and 4.51 mm on the right side, while that on the left side were 5.15 mm and 4.14 mm. For the incomplete foramina, the mean values for the vertical diameter were 4.48 mm on the right and 4.19 mm on the left side, respectively. CONCLUSIONS: The frequency of CCF in the present study population of Bihar was much lesser than that of previously studied populations. However, the variation in frequency of different morphological types of CCF was observed to be the same across populations. The variations in CCF's metric data could help in predicting the morphological changes it causes to the clinoidal segment of the internal carotid artery, as well as in distinguishing its varieties.

Adrenal Myelolipoma Mimics Ectopic Adrenal or Renal Tissue: An Incidental Finding During Cadaveric Dissection.

CONTEXT: On naked eye examination adrenal myelolipoma (AML) tissue appears to be an ectopic adrenal or renal tissue, based on the similarity to their external texture. This necessitates a histo-pathological study for confirming the origin of the tissue. OBJECTIVE: To establish the origin and histological features of the incidental AML tissue found during cadaveric dissection and review the literature for similar findings with clinical picture and treatment description. SUBJECTS AND METHODS: Unilateral adrenal gland obtained from cadaveric dissection was subjected to histological study by H & E staining of the slides prepared. The literature review was done from articles published in PubMed indexed journals. CASE REPORT: A case of an incidental finding of AML during cadaveric dissection is presented which on naked eye examination was appearing to be an ectopic adrenal or renal tissue, based on the similarity to their external texture. On histological examination, a thin rim of adrenocortical tissue, surrounding the mature adipose tissue, and attenuated by islets of myeloid, erythroid and megakaryocytic cell lines in varying proportions, resembling the mature bone marrow morphology, was observed. The literature review on PubMed explains similar incidental post-mortem autopsy findings due to the asymptomatic nature of the tumor. The incidence of AML varied between 0.08% and 0.2% in the last decade of the 20th century, which increased up to 10 - 15% of incidental adrenal masses due to the widespread use of non-invasive imaging modalities leading to an increase in the diagnosis of the pathology. CONCLUSIONS: Before considering the ectopic incidence of tissue during cadaveric dissection, a histo-pathological examination is mandatory for confirmation. Adreno-myelolipoma is an asymptomatic post-mortem finding in 10-15% of cases of adrenal tissue which mimics ectopic adrenal gland or renal tissue due to its external texture.

Evolution of the fabric of cardiovascular science: Saga of an enduring process of refinement.

BACKGROUND: The core elements of cardiovascular science have been established by scholarly pursuits of numerous scientists across centuries. In this article, we have tried to trace the evolutionary journey of cardiovascular science from a rudimentary form in ancient period to a robust scientific discipline in modern times. METHODS: A literature search of relevant, peer-reviewed, published articles was undertaken from indexed databases (Medline & Pubmed, Scopus, Embase, CINAHL Plus, Web of Science and Google Scholar). RESULTS: Cardiovascular science has its roots in antiquity, when Greek scholars mostly relied on philosophical thoughts and ancient texts. This was followed by addition of few structural details to the theory of circulation by Galen based on animal dissection. Arab scholar Ibn al-Nafis provided new insights regarding circulation pathway in humans. Nevertheless, an erroneous concept prevailed into the onset of European Renaissance. Even with legalization of human dissection, little headway could be made till sixteenth century due to persistent reliance of anatomists on ancient Galenic principles. During seventeenth century, the circulatory pathway (as we know it today) was established due to significant contributions from scholars like Harvey and Malpighi. Their efforts were based on findings from experiments and logical conclusions. Eighteenth century witnessed the emergence of autopsy based methods which led to valuable contributions from Vieussens, Thebesius, Morgagni and Hunter regarding normal and pathologic anatomy of cardiovascular system. With structural details mostly established, researchers during nineteenth century focussed on innovations in diagnostic methods based on human experiments. Further development of advanced human experiment models during twentieth century led to emergence of contemporary treatment methods for various cardiac conditions. In the twenty-first century, cardiovascular science is undergoing comprehensive progress at an exponential rate due to technological advances. CONCLUSION: The evolutionary journey of cardiovascular science as a discipline across centuries has been intriguing and eventful.

Variations in the morphology of stylomastoid foramen: a possible solution to the conundrum of unexplained cases of Bell's palsy.

BACKGROUND: Stylomastoid foramen is the terminal part of facial canal and is the exit gateway for facial nerve from skull base. We hypothesized that anatomical variations of this foramen could be a risk factor for the injury of facial nerve resulting in unilateral facial nerve paralysis or Bell's palsy. Hence the present study was conducted to study the variations in size and shape of stylomastoid foramen in dry adult human skulls. MATERIALS AND METHODS: The study was conducted on 37 dry adult human skulls of unknown age and sex. High resolution images of the skulls under study were processed by ImageJ software and observations were undertaken. RESULTS: Total eight variations of stylomastoid foramen were observed in terms of shape. The common variants were round, oval and square (present in 83.79% skulls on right side and 81.07% skulls on left side), whereas the rare variants were triangular, rectangular, serrated, bean-shaped and irregular. It was noted that stylomastoid foramen were associated with extensions (45.95% skulls) and also adjacent foramen (18.92% skulls). Exclusively unilateral observations included bifurcation of foramen (16.22% skulls), foramen situated deep inside skull groove (5.41% skulls) and foramen interrupted by bony spur (2.7% skulls). No significant differences were observed between the mean diameters (antero-posterior and transverse) of the stylomastoid foramen. CONCLUSIONS: The unilateral variations along with rare variations in terms of shape such as serrated, bean-shaped and irregular foramen (which were also unilateral findings) could be potential risk factors towards injury of facial nerve at the point of exit from skull base leading to Bell's palsy.

Ossification around intercavernous sinus: An osteological finding that can complicate trans - sphenoidal surgery.

The aim of the study was to document an anatomical variation around the sella turcica which was unique and lacked any reference in the literature. A low lying osseous bar connecting the right middle clinoid process to the midpoint of the right lateral border of the dorsum sella was observed in a human skull specimen. The osseous bar was forming a foramen close to the floor of the sella, and the structure in association with this part of sella is the inferior intercavernous sinus. Measurements of the sella turcica bridge (STB), carotico-clinoid foramen (CCF), interclinoid foramen (ICF) on both sides and that of the ossified bar and foramen formed by itself were taken with the help of ImageJ software. The values observed for the measurements of different parameters of STB and its components, for CCF and ICF were bilaterally different. While the values for the osseous bar and foramen formed by it cannot be compared because of its unilateral occurrence. The presence of foramen around the inferior intercavernous sinus may lead to difficulty in performing procedures like transsphenoidal surgery (TSS) or extended TSS (eTSS) while extracting intradural lesions, thus increasing the chances of haemorrhage.

Anatomy of nervous system and emergence of neuroscience: A chronological journey across centuries.

Scholars began exploring anatomy of nervous system from ancient times; however, considerable progress could only be made during the European Renaissance from the 14th century onwards. The present study aimed to document significant discoveries in this context in chronological order to establish the cascading pattern of advancement in knowledge. The findings of Leonardo da Vinci (15th century), Vesalius (16th century) and their contemporaries, which were based on macroscopic dissection, helped to break the shackles of misconceptions in hypotheses prevalent from the time of Galen. However, very little headway could be achieved beyond superficial descriptions. Willis (17th century), through his experimental studies, provided the much-needed impetus and his discoveries put the study of brain and nervous system on their modern footing. In the following years, prominent researchers through their observations based on the use of microscopy and advanced histological techniques (prevalent after invention of microtome) contributed towards significant discoveries related to the morphological details of different components of nervous system. Such scientific activities culminated in remarkable advancements by the middle of 19th century. The advent of Golgi's staining technique and subsequent histological exploits of Cajal (late 19th century) established the neuron theory, which is central to comprehending the functioning of nervous system. Availability of Golgi's staining technique remarkably contributed in detailing the anatomical structure of nervous system at microscopic level. Access to structural details pertaining to living anatomy (late 20th century) and focus on findings at the molecular level by turn of 21st century have firmly established neuroscience as a sovereign academic discipline.

Anatomical variations of testicular artery: a review.

The testicular arteries (TAs) also known as internal spermatic arteries are long and slender arteries usually arising from the anterolateral aspect of the abdominal aorta, 2.5 cm to 5 cm caudal to the renal arteries. The variation in TAs may be found with respect to their origin, number or course. They can originate from the abdominal aorta itself at an abnormal level. If not arising from abdominal aorta the TA variants may arise from renal artery, suprarenal artery or any one of the lumbar arteries. Rarely it can arise from common or internal iliac artery, or from the superior epigastric artery. The most common variation with respect to origin of TA was found in association with renal vessels. In regard to their number, double TA was found to be most common and with respect to course most common variation was arched TA over ipsilateral renal vein. The arched TA at times on right side had a retrocaval course. Occurrence of TA variants is explained with embryology and the knowledge of its clinical significance is essential for future surgeons for designing vascular surgeries. Four studies had attempted to classify TA variants regarding their origin, number and course but they could not accommodate recently found TA variants. This led to our new proposed classification.

Osteomyelitis of the skull in early-acquired syphilis: evaluation by MR imaging and CT.

We present an unusual case of acquired secondary syphilis manifesting as osteomyelitis of the skull in a patient with a history of human immunodeficiency virus infection, evaluated by CT, volumetric CT reconstructions, and MR imaging.

The relationship of psychopathology and hyperhidrosis.

BACKGROUND: Hyperhidrosis is a common yet poorly understood disease that is often exacerbated by emotional stress. While a psychiatric explanation of causality is frequently offered, there is little evidence to support or reject the view that the condition is primarily an anxiety-based disorder. OBJECTIVES: To quantify objectively the degree of psychopathology in patients with hyperhidrosis. METHODS: Forty-two patients diagnosed as having hyperhidrosis were examined prior to endoscopic sympathectomies. All patients took the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) and State-Trait Anxiety Inventory (STAI) before surgery. Results were compared with established norms. RESULTS: The group scored well within established norms on both psychometric measures. On scales measuring anxiety, depression and conversion phenomena, 88% of the MMPI-2 profiles lacked elevations, and 86% of the patients lacked elevations on the STAI State and Trait Anxiety scales. Personality variables were not associated with postsurgical outcome. CONCLUSIONS: Most individuals suffering from essential hyperhidrosis lack overt psychopathology. While some patients subjectively describe symptoms of anxiety, mild depression and social isolation, these complaints appear often to be in reaction to or superimposed upon an organic disease process and not the primary cause of their condition.

Prolonged cyclooxygenase-2 induction in neurons and glia following traumatic brain injury in the rat.

Cyclooxygenase-2 (COX2) is a primary inflammatory mediator that converts arachidonic acid into precursors of vasoactive prostaglandins, producing reactive oxygen species in the process. Under normal conditions COX2 is not detectable, except at low abundance in the brain. This study demonstrates a distinctive pattern of COX2 increases in the brain over time following traumatic brain injury (TBI). Quantitative lysate ribonuclease protection assays indicate acute and sustained increases in COX2 mRNA in two rat models of TBI. In the lateral fluid percussion model, COX2 mRNA is significantly elevated (>twofold, p < 0.05, Dunnett) at 1 day postinjury in the injured cortex and bilaterally in the hippocampus, compared to sham-injured controls. In the lateral cortical impact model (LCI), COX2 mRNA peaks around 6 h postinjury in the ipsilateral cerebral cortex (fivefold induction, p < 0.05, Dunnett) and in the ipsilateral and contralateral hippocampus (two- and six-fold induction, respectively, p < 0.05, Dunnett). Increases are sustained out to 3 days postinjury in the injured cortex in both models. Further analyses use the LCI model to evaluate COX2 induction. Immunoblot analyses confirm increased levels of COX2 protein in the cortex and hippocampus. Profound increases in COX2 protein are observed in the cortex at 1-3 days, that return to sham levels by 7 days postinjury (p < 0.05, Dunnett). The cellular pattern of COX2 induction following TBI has been characterized using immunohistochemistry. COX2-immunoreactivity (-ir) rises acutely (cell numbers and intensity) and remains elevated for several days following TBI. Increases in COX2-ir colocalize with neurons (MAP2-ir) and glia (GFAP-ir). Increases in COX2-ir are observed in cerebral cortex and hippocampus, ipsilateral and contralateral to injury as early as 2 h postinjury. Neurons in the ipsilateral parietal, perirhinal and piriform cortex become intensely COX2-ir from 2 h to at least 3 days postinjury. In agreement with the mRNA and immunoblot results, COX2-ir appears greatest in the contralateral hippocampus. Hippocampal COX2-ir progresses from the pyramidal cell layer of the CA1 and CA2 region at 2 h, to the CA3 pyramidal cells and dentate polymorphic and granule cell layers by 24 h postinjury. These increases are distinct from those observed following inflammatory challenge, and correspond to brain areas previously identified with the neurological and cognitive deficits associated with TBI. While COX2 induction following TBI may result in selective beneficial responses, chronic COX2 production may contribute to free radical mediated cellular damage, vascular dysfunction, and alterations in cellular metabolism. These may cause secondary injuries to the brain that promote neuropathology and worsen behavioral outcome.

The early assessment and intensive care unit management of patients with severe traumatic brain and spinal cord injuries.

The assessment and management of neurotrauma have progressed significantly over the past several years. Improved understanding of the physiology of injured neural tissue and advances in technology have refined the approach to the care of patients suffering neurologic injury. Evidence-based clinical management guidelines, such as those developed by the Brain Trauma Foundation and the American Association of Neurological Surgeons, for the management of traumatic brain injury have been introduced to standardize certain aspects of care. The ongoing evolution of critical care also has had a significant impact on the care of patients suffering from neurotrauma. This article reviews some current issues related to the diagnosis and management of traumatic brain injury and spinal cord injury as we head into the next millennium.

Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial.

OBJECT: Sedation regimens for head-injured patients are quite variable. The short-acting sedative-anesthetic agent propofol is being increasingly used in such patients, yet little is known regarding its safety and efficacy. In this multicenter double-blind trial, a titratable infusion of 2% propofol accompanied by low-dose morphine for analgesia was compared with a regimen of morphine sulfate in intubated head-injured patients. In both groups, other standard measures of controlling intracranial pressure (ICP) were also used. METHODS: Forty-two patients from 11 centers were evaluated to assess both the safety and efficacy of propofol: 23 patients in the propofol group (mean time of propofol usage 95+/-87 hours) and 19 patients in the morphine group (mean time of morphine usage 70+/-54 hours). There was a higher incidence of poor prognostic indicators in the propofol group than in the morphine group: patient age older than 55 years (30.4% compared with 10.5%, p < 0.05), initial Glasgow Coma Scale scores of 3 to 5 (39.1% compared with 15.8%, p < 0.05), compressed or absent cisterns on initial computerized tomography scanning (78.3% compared with 57.9%, p < 0.05), early hypotension and/or hypoxia (26.1% compared with 10.5%, p = 0.07). During treatment there was a trend toward greater use of vasopressors in the propofol group. However, the mean daily ICP and cerebral perfusion pressure were generally similar between groups and, on therapy Day 3, ICP was lower in the propofol group compared with the morphine group (p < 0.05). Additionally, there was less use of neuromuscular blocking agents, benzodiazepines, pentobarbital, and cerebrospinal fluid drainage in the propofol group (p < 0.05). At 6 months postinjury, a favorable outcome (good recovery or moderate disability) was observed in 52.1% of patients receiving propofol and in 47.4% receiving morphine; the mortality rates were 17.4% and 21.1%, respectively. Patients who received the highest doses of propofol for the longest duration tended to have the best outcomes. There were no significant differences between groups in terms of adverse events. CONCLUSIONS: Despite a higher incidence of poor prognostic indicators in the propofol group, ICP therapy was less intensive, ICP was lower on therapy Day 3, and long-term outcome was similar to that of the morphine group. These results suggest that a propofol-based sedation and an ICP control regimen is a safe, acceptable, and, possibly, desirable alternative to an opiate-based sedation regimen in intubated head-injured patients.

In vitro inhibition of human malignant brain tumour cell line proliferation by anti-urokinase-type plasminogen activator monoclonal antibodies.

A brain tumour-associated marker, urokinase (UK), was investigated using rabbit anti-UK polyclonal and murine anti-UK monoclonal antibodies, which were prepared by immunization with low molecular weight UK (LMW-UK) and high molecular weight urokinase (HMW-UK) synthetic peptide respectively. The polyclonal antibody cross-reacted with both LMW-UK and HMW-UK, whereas the murine MAbs were specific for HMW-UK. These immunological probes were used to study urokinase in glioma extracts, tissues, sera and cell lines that had been prepared from primary cultures of freshly dissected gliomas. Radioimmunoassays showed that glioma extracts had much higher level (5- to 44-fold) of UK than normal human brain extracts. This result was confirmed by immunoblotting of electrophoresis gels of glioma and human brain extracts. Immunohistochemical study using anti-UK MAb demonstrated much higher levels of UK in glioma tissue than normal brain tissue. Immunohistochemical study using anti-UK MAbs localized UK on the cell surface of glioma cells. Anti-UK MAbs inhibited the proliferation of AA cell lines and GB cell lines (50% to > 90%) and exerted minor effects (< or = 20%) on normal human liver, intestine and lymphocyte cell lines. Taken together, these results suggest that anti-UK MAbs may have therapeutic potential for human gliomas and cancer metastasis.

Anti-urokinase-type plasminogen activator monoclonal antibodies inhibit the proliferation of human breast cancer cell lines in vitro.

The levels of several tumor-associated proteases, including plasminogen activators (PA), are elevated in many malignant tumors compared to their benign tumor counterparts. Extracellular matrix degradation mediated by PA may facilitate tumor cell invasion and metastasis. In this study, the anti-proliferative activities of anti-urokinase-type plasminogen activator monoclonal antibodies (anti-UK MAbs) against human breast cancer cell lines were tested. Immunofluorescence studies localized urokinase (UK) on the surfaces of breast cancer cells. Inhibition studies showed that anti-UK MAb concentrations exerted 50% inhibition of 3H-thymidine uptake by human breast cancer cell lines; CRL-1500 and CRL-1504 were 5.6 x 10(-9)-1.82 x 10(-13) and 3.16 x 10(-10)-3.54 x 10(-12) M, respectively. Anti-UK MAbs exhibited little effect (10-20%) on normal human lymphocyte and liver cell lines. Dye exclusion indicated that anti-UK MAbs had a potent cytolytic effect on human breast cancer cells. Taken together, these results demonstrated the potential of anti-UK MAbs to be a valuable reagent for cancer immunotherapy and anti-metastatic therapy.

Human glioma associated intermediate filament proteins: over-expression, co-localization and cross-reactivity.

The identification of human brain tumor-associated markers could facilitate the development of new diagnostic and therapeutic strategies for these malignancies. The type III intermediate filament proteins (IFPs): vimentin, desmin and glial fibrillary acidic protein (GFAP) were studied in human glioma tissue extracts, in sera from glioma patients and in low passage glioma cell lines prepared from primary cultures of freshly dissected tumors. Radioimmunoassay (RIA) studies, using anti-GFAP, anti-desmin and anti-vimentin mAbs, showed high levels of these proteins in glioma extracts. Binding studies with authentic IFPs indicated the absence of circulating antibodies against these proteins in the sera of glioma patients. On the other hand, these sera showed high levels of vimentin. Binding studies with these antibodies using RIAs and western immunoblotting, showed that while anti-GFAF mAbs were specific to GFAP, anti-desmin mAb cross-reacted completely with GFAP, anti-vimentin mAb cross-reacted substantially with desmin and GFAP. Immunofluorescence staining of frozen sections revealed high levels of neurofilaments in gliomas and strikingly low levels in normal brain tissue. Double immunofluorescence staining showed co-occurrence of all three IFPs in the same filaments. This suggests either co-expression or cross-reactivity of these proteins due to their high degree of homology. Thus, caution should be exercised in the use and interpretation of immunohistochemical data using antibodies to IFs.

Secondary insults to the injured brain.

While reversing established central nervous system damage is clearly a difficult task, preventing or limiting ongoing destructive processes in the brain may be a more achievable goal. The monitoring technology required to detect clinically significant adverse secondary events has evolved considerably in the past few years. As a result it has become evident that such adverse events are common in the head injured patient and that they can have a dramatic effect on outcome. Furthermore, it is also becoming clear that these secondary insults are, to a significant degree, preventable. It is likely that simple physiological maneuvers, such as maintaining the cerebral perfusion pressure, as well as newer pharmacological agents, will be useful for this purpose. The pathophysiology of brain swelling remains unclear and deserves continued study. This review describes the factors responsible for secondary brain injury, some practical ways of identifying and managing them, and certain newer pharmacological agents that may be valuable in the clinical setting.

In vitro efficacy of anti-glial fibrillary acidic protein monoclonal antibodies against human malignant glioma cell lines.

Our studies have confirmed the presence of large concentrations of various intermediate filament proteins (IFPs) in glioma tissue compared to normal brain. This avenue of research was extended to assess the anti-proliferative activity of anti-intermediate filament protein monoclonal antibodies (anti-IFP mAbs) against human glioma cells. In this study, anti-proliferative activity of glial fibrillary acidic protein monoclonal antibodies (anti-GFAP mAbs) has been tested in vitro, using glioma cell lines prepared and established from freshly resected brain tumors. One anaplastic astrocytoma (AA), two glioblastoma multiforme (GB1 and GB2) cell lines and three anti-GFAP mAbs (B12C4, B12B4 and B6C6, all IgG1, kappa) were used. Immunofluorescence study indicated the ability of anti-GFAP mAbs to recognize the cell surface of glioma cells and the inhibition study showed that mAb B12B4 inhibited the proliferation of GB1 (96%), GB2 (85%) and AA (93%) at a concentration of 3.2 x 10(-10) M. mAb B12C4 inhibited the proliferation of GB1 (95%), GB2 (86%) and AA (94%) at a concentration of 3.26 x 10(-10) M and mAb B6C6 inhibited the proliferation of GB1 (75%), GB2 (75%) and AA (91%) at a concentration of 2.074 x 10(-10) M. Thymidine release assay demonstrated the cytolytic activities of anti-GFAP mAbs towards these glioma cell lines, and this observation was confirmed by dye exclusion, which indicated the lysis of glioma cells after anti-GFAP mAbs treatment. Anti-GFAP mAbs had little effect (< or = 20%) on normal human lymphocyte, liver and intestine cell lines. These results look promising for radioimaging and immunotherapy of human gliomas.

Evaluation of a regional oxygen saturation catheter for monitoring SjvO2 in head injured patients.

OBJECTIVES: Monitoring jugular venous oxygen saturation (SjvO2) has been useful for the early identification and treatment of cerebral ischemia in patients with severe head injury. However, the catheters that have been used for this purpose have not performed optimally. The purpose of this study was to evaluate the performance of a new regional oxygen saturation catheter for monitoring SjvO2. METHODS: Eighteen regional oxygen saturation catheters, 4-Fr in diameter (Baxter Healthcare Corporation, Edward Critical Care), were used in this study. Each catheter was inserted percutaneously into the dominant jugular vein and the catheter's tip position in the jugular bulb was verified by radiograph. The catheter was calibrated in vitro prior to insertion using the optic calibrator provided by the manufacturer. The catheter was recalibrated every 8 to 12 hours by comparing the oxygen saturation value from the catheter with that measured by a co-oximeter in a blood sample drawn through the catheter. RESULTS: In vitro calibration using the optic calibrator was not always successful. Five catheters could not be calibrated. The remaining 13 catheters could all be calibrated, but only 9 provided a value that was within 4% of the oxygen saturation derived from the blood sample. After the first in vivo calibration, the correlation between the catheter and the blood sample values was improved. A total of 196 comparisons were made. The median, 25th, and 75th quartile differences between the catheter and the blood sample measurement of SjvO2 were 0.00, -1.15, and 1.25%, respectively. Using longitudinal data regression, the overall slope of the regression between the catheter and blood values was 0.997 (p = 0.001). CONCLUSIONS: The new regional oxygen saturation catheter provided reliable measurement of SjvO2 83% of the time when the signal quality index was < or = 3, and may be useful for continuous monitoring of SjvO2.