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Biomedical subjects

R K Narayan

Publications and source records attributed to R K Narayan.

At least 19 recordsLinked to original sources
PubMed2002

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.

Adolescent↗
PubMed2000

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.

Brain Injuries↗
PubMed2000

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.

Animals↗
PubMed1999

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.

Adult↗
PubMed1998

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.

Antibodies, Monoclonal↗
PubMed1998

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.

Antibodies, Monoclonal↗
PubMed1997

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.

Antibodies, Monoclonal↗
PubMed1996

Lactic acid and amino acid fluctuations measured using microdialysis reflect physiological derangements in head injury.

We examined the extracellular neurochemical milieu in 34 head injured patients using microdialysis while simultaneously monitoring intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Derangements of anaerobic metabolism reflected by increased lactate and lactate/pyruvate ratios, and release of amino acids were seen at the same time as physiological deterioration in the majority of instances. Clinical microdialysis may provide insights into the neurochemistry of head injury, and such information may lead to new methods of monitoring and treating head injured patients.

Adult↗
PubMed1996

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.

Blood Gas Analysis↗
PubMed1995

Intracranial pressure waveform indices in transient and refractory intracranial hypertension.

Analysis of data obtained by continuous computerized monitoring of intracranial pressure (ICP) in 109 adult patients with severe head trauma was performed to examine the pattern of change in indices of the ICP waveform. Indices derived from direct measurement of the ICP wave and obtained from a Fast Fourier Transform (FFT) were examined. Concurrent physiologic measurements were made. Two types of intracranial hypertension (ICH) were defined for comparison. 'Transient intracranial hypertension' occurred when an abrupt rise in ICP was followed by a return to below 25 mm Hg (n = 63). Increases in ICP that were progressive and led to neurologic deterioration and death were termed 'refractory intracranial hypertension' (n = 18). During transient ICH heart rate, arterial pressure, end-tidal carbon dioxide and jugular venous oxygen saturation all increased, while these measures either were unchanged or decreased during refractory ICH. The pulse amplitude of the ICP wave increased in both types of ICHtn. Other changes in the waveform indices were consistent with this change in pulse amplitude. HFC responded differently to the two types of changes, with an increase during the transient changes and a decrease during the refractory changes. The differences in changes in physiologic measurements as ICH occurred in the 2 groups suggest that in refractory ICH cerebral blood flow is maintained against the mounting ICP, while in transient ICH the hypertension is caused by an increase in cerebral blood flow. The waveform indices do not discriminate between the two types of changes.

Adult↗
PubMed1995

SjvO2 monitoring in head-injured patients.

Jugular venous oxygen saturation (SjvO2) measures the balance between cerebral oxygen delivery and cerebral oxygen consumption. Abnormalities that increase oxygen consumption (e.g., fever or seizures) or that decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia, hypocapnia, or anemia) can decrease SjvO2. Measuring SjvO2 continuously in the ICU in 177 patients with severe head injury, jugular venous desaturation (SjvO2 < 50%) was identified at least once in 39% of the patients. Approximately half of the episodes of desaturation were due to intracranial hypertension and half were due to systemic causes. The occurrence of one or more episodes of desaturation was strongly associated with a poor outcome, suggesting that the reduction in oxygen delivery identified with the SjvO2 monitoring contributed to the neurological injury. In the operating room, jugular venous desaturation was identified in 6 of 8 patients who were monitored during emergency evacuation of a traumatic intracranial hematoma. The lowest SjvO2 observed was 28%. In all 8 cases, the SjvO2 increased, from 47 +/- 10% to 63 +/- 5% after evacuation of the hematoma. Additional data supporting the hypothesis that these secondary insults identified with the SjvO2 monitoring contribute to the patient's neurological injury come from measurement of the extracellular concentrations of lactate and excitatory amino acids in the brain using microdialysis. Lactate concentration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mumol/L and glutamate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mumol/L during 8 episodes of jugular venous desaturation in 7 of 22 patients monitored with microdialysis. SjvO2 identifies global reductions in cerebral oxygenation due to a variety of causes, and is useful as a monitor for secondary insults in patients with severe head injury.

Adult↗
PubMed1995

Development of guidelines for the management of severe head injury.

Organized neurosurgery has taken a major step forward in developing guidelines for the management of severe head injury. This represents the first area in which neurosurgeons have tackled this difficult but important undertaking. The head injury guidelines, which are to be published soon, are evidenced-based, i.e., they are based upon published data rather than on expert opinion. The quality of data has been carefully analyzed and graded. The level of the recommendations, i.e., standard, guideline, or option, is based upon the strength of the data available. An attempt is made to provide a summary of the terminology and methodology used to develop guidelines. Arguments for and against practice guidelines are also summarized.

Craniocerebral Trauma↗
PubMed1995

Survey of critical care management of comatose, head-injured patients in the United States.

OBJECTIVE: This survey was designed to study current practices in the monitoring and treatment of patients with severe head injury in the United States. DATA SOURCES: The collected data represent answers to telephone interviews of nurse managers, clinical specialists, and staff nurses specializing in neurotrauma care at 277 randomly selected hospitals from a total pool of 624 trauma centers. Overall, 261 (94%) centers participated in the survey. Of the participating centers, 219 (84%) were providers of care for severely head-injured patients. In order to assess reliability and account for differences among respondents, personnel from 40 (15%) centers were resurveyed 6 months later and a different nursing professional was interviewed, although the questions remained the same. DATA EXTRACTION: The largest group of respondents came from level I centers (49%), followed by level II (32%) and level III (2%). Thirty-four percent of the surveyed hospitals had a designated neurologic/neurosurgical intensive care unit, and 24% of all units surveyed were under the direction of either a neurosurgeon or a neurologist. Twenty-eight percent of the centers routinely performed intracranial pressure monitoring, while 7% of the centers reported never using this technique. The use of ventriculostomy catheters for intracranial pressure monitoring was employed in 72% of the centers, but cerebrospinal fluid drainage was utilized by only 44% of the hospitals. The percentage of patients who had their intracranial pressure monitored was significantly higher in level I trauma centers and at hospitals that treated larger numbers of severely head-injured patients (15 to 30 patients per month, which represented 15% of the hospitals surveyed). Hyperventilation and osmotic diuretics were used in 83% of centers to reduce intracranial hypertension. The administration of barbiturates was reported in 33% of the units as a treatment for intracranial hypertension. Corticosteroids were used more than half of the time in 64% of trauma centers. Twenty-nine percent of the centers reported aiming for PaCO2 values of < 25 torr (< 3.3 kPa). CONCLUSIONS: The survey data indicate that there is a considerable variation in the management of patients with severe head injury in the United States. The establishment of guidelines for the management of head injury based on available scientific data and moderated by practical and financial considerations may lead to improvement in the standard of care.

Adrenal Cortex Hormones↗
PubMed1995

Clinical evaluation of a miniature strain-gauge transducer for monitoring intracranial pressure.

In 25 patients, we evaluated the accuracy of a new miniature strain-gauge transducer developed for the measurement of intracranial pressure (ICP). The ICP in each patient was measured with the intraventricular, miniature strain-gauge transducer, and that value was compared with the ICP measured with a ventriculostomy catheter coupled to an external strain-gauge transducer. From the two monitors, 2218 simultaneous measurements of ICP were obtained. The average ICP measured with the miniature strain-gauge transducer was 15.9 +/- 10.0 mm Hg (range, -3 to 104 mm Hg). The ICP measured with the ventriculostomy-catheter transducer averaged 15.4 +/- 10.1 mm Hg (range, -9 to 104 mm Hg). A highly significant correlation was found over the wide range of pressures observed (n = 2218, r = 0.97, P < 0.001). The average difference between the two measurements of the ICP was 0.5 +/- 2.6 mm Hg, and the differences were equally positive and negative, demonstrating no consistent bias. The two values for the ICP were within 2 mm Hg of each other on 63% of the measurements and within 4 mm Hg of each other on 89% of the measurements. The average zero drift of the miniature strain-gauge transducer, measured at ambient pressure after removal of the catheter, was 0.2 +/- 0.5 mm Hg. The results indicate that this miniature strain-gauge transducer is highly accurate and stable and that it is a reliable alternative to a ventriculostomy for monitoring the ICP.

Adult↗
PubMed1995

Early detection of delayed traumatic intracranial hematomas using near-infrared spectroscopy.

Delayed intracranial hematomas are an important treatable cause of secondary brain injury in patients with head trauma. Early identification and treatment of these lesions, which appear or enlarge after the initial computerized tomography (CT) scan, may improve neurological outcome. Serial examinations using near-infrared spectroscopy (NIRS) to detect the development of delayed hematomas were performed in 167 patients. The difference in absorbance of light (delta OD) at 760 nm between the normal and the hematoma side was measured serially during the first 3 days after injury. Twenty-seven (16%) of the patients developed a type of late hematoma: intracerebral hematoma in eight, extracerebral hematoma in six, and postoperative hematoma in 13 patients. Eighteen of the delayed hematomas caused significant mass effect and required surgical evacuation. The hematomas appeared between 2 and 72 hours after admission. In 24 of the 27 patients, a significant increase (> 0.3) in the delta OD occurred prior to an increase in intracranial pressure, a change in the neurological examination, or a change on CT scan. A favorable outcome occurred in 67% of the patients with delayed hematomas, which suggests that early diagnosis using NIRS may allow early treatment and reduce secondary injury caused by delayed hematomas.

Adolescent↗