Search PubMed⌕ Search

Biomedical subjects

J C Goodman

Publications and source records attributed to J C Goodman.

At least 19 recordsLinked to original sources
PubMed2002

Microdialysate nitrate/nitrite levels following severe head injury.

Nitric oxide (NO) has important regulatory functions within the central nervous system. The purpose of this study was to measure the concentration of nitric oxide in the brain after severe traumatic brain injury. NO is oxidized in vivo to nitrate and nitrite. Measurement of these products gives an index of NO production. Laboratory studies have shown a good correlation between NO measured directly with an electrode, and indirectly by microdialysis nitrate/nitrite. Using chemiluminescence method we measured nitrate/nitrite levels in 2024 microdialysate samples obtained from 24 patients during the first five days following severe head injury. We used CMA 70 probe (AB Microdialysis, Sweden) perfused by normal saline at a rate of 2 microliters/min. The median values of nitrate/nitrite for the whole group were highest on day 1 and gradually decreased over the 5 day monitoring period (day 1-19.2 mumol/l, day 5-12.7 mumol/l). Average values were lowest in the patients that died of their injury (14.3 mumol/l), and highest in patients who recovered by 3 months after injury with a moderate or severe disability (25.8 mumol/l or 31.9 mumol/l). In addition, there was a strong interaction between the severity of neurological injury and the change in dialysate nitrate/nitrite over time. The results suggest that nitric oxide may have a role in secondary injury mechanisms, but that this role is complex and varies as the injury evolves over time.

Biomarkers↗
PubMed2002

Measurement of the nitric oxide metabolites nitrate and nitrite in the human brain by microdialysis.

To examine the feasibility of measuring the nitric oxide (NO) metabolites nitrate and nitrite in microdialysate samples from the human brain, microdialysis probes were placed in normal appearing cerebral cortex of severely head injured patients in the Neurosurgical Intensive Care Unit at Ben Taub General Hospital. Nitrate/nitrite analysis was performed using NO chemiluminescence. Low micromolar levels of NO metabolites were consistently and easily detected. These levels seen are comparable to levels reported in CSF but tissue tortuosity and probe recovery considerations suggest that the absolute concentrations at the probe site are probably ten fold higher. Microdialysis with measurement of nitric oxide metabolites is technically feasible and may provide valuable insights into both normal neurochemistry and neurochemical derangements in disease.

Biomarkers↗
PubMed2002

Comparison of microdialysate arginine and glutamate levels in severely head-injured patient.

L-arginine concentrations in the brain are of interest following TBI because L-arginine is the immediate precursor of nitric oxide (NO). In addition, in vitro studies suggest that glutamate, which is a mediator of secondary injury after TBI, may stimulate release of arginine from glial cells. This study examines arginine concentrations in brain tissue using the microdialysis technique after human TBI. From 78 TBI patients, a total of 1739 microdialysate samples were collected using a CMA-70 probe perfused with normal saline at 2 microliters/min and concentrations of amino acids in microdialysate were determined. Amino acid concentrations for each patient were averaged for 8-hour periods during the first 3 days after injury, and daily for postinjury days 4 and 5. Following an initial rapid decrease in arginine, the dialysate arginine concentrations were low on days 1-3 and then increased over the days 4-5 after injury. In contrast, the microdialysate glutamate levels decreased slowly over the first 48 hours after TBI and thereafter remained low. Thirty-five episodes of jugular venous desaturation (SjvO2 < 50%) occurred during monitoring. Arginine and glutamate levels simultaneously doubled during desaturation and decreased as the clinical episode resolved. The low concentrations of arginine during the first 3 days after TBI may indicate that substrate unavailability could contribute to the decreased NO concentrations that have been observed after TBI. The simultaneous increase in glutamate and arginine during ischemic events is consistent with experimental data which has observed that glutamate induces release of arginine.

Arginine↗
PubMed2001

Interstitial brain adenosine and xanthine increase during jugular venous oxygen desaturations in humans after traumatic brain injury.

OBJECTIVE: Adenosine decreases the cerebral metabolic rate for oxygen and increases cerebral blood flow, and it may play an important role in cerebrometabolic and cerebrovascular responses to hypoperfusion after traumatic brain injury. Jugular venous oxygen saturation is monitored after traumatic brain injury to assess brain oxygen extraction, and desaturations may reflect secondary brain insults. We hypothesized that brain interstitial adenosine and related purine metabolites would be increased during jugular venous oxygen saturation desaturations (<50%) and determined associations between the purines, lactate, and glucose to assess the role of adenosine during secondary insults in humans. DESIGN: Study of critically ill adults with severe traumatic brain injury. SETTING: Adult neurointensive care unit. PATIENTS: We prospectively defined periods of normal saturation and desaturation in six patients after severe traumatic brain injury. INTERVENTIONS: During these periods, cerebral microdialysis samples of brain interstitial fluid were collected, and adenosine and purine metabolites were measured by high-pressure liquid chromatography. MEASUREMENTS AND MAIN RESULTS: Adenosine increased 3.1-fold and xanthine increased 2.5-fold during desaturation periods (both p <.05 vs. normal saturation period, signed rank). Adenosine, xanthine, hypoxanthine, and cyclic-adenosine monophosphate correlated with lactate over both study periods (r(2) =.32,.14,.31,.07, and.26, respectively, all p <.05, Pearson product moment correlation). CONCLUSION: The marked increases in interstitial brain adenosine that occur during jugular venous oxygen desaturations suggest that adenosine may play an important role during periods of secondary insults after traumatic brain injury. The correlation of these metabolites with lactate further suggests that adenosine is increased during periods of enhanced glycolytic metabolism.

Adenosine↗
PubMed2000

Phase I study of adenoviral delivery of the HSV-tk gene and ganciclovir administration in patients with current malignant brain tumors.

Between December 1996 and September 1998, 13 patients with advanced recurrent malignant brain tumors (9 with glioblastoma multiforme, 1 with gliosarcoma, and 3 with anaplastic astrocytoma) were treated with a single intratumoral injection of 2 x 10(9), 2 x 10(10), 2 x 10(11), or 2 x 10(12) vector particles (VP) of a replication-defective adenoviral vector bearing the herpes simplex virus thymidine kinase gene driven by the Rous sarcoma virus promoter (Adv.RSVtk), followed by ganciclovir (GCV) treatment. The VP to infectious unit ratio was 20:1. Our primary objective was to determine the safety of this treatment. Injection of Adv.RSVtk in doses <==2 x 10(11) VP, followed by GCV, was safely tolerated. Patients treated with the highest dose, 2 x 10(12) VP, exhibited central nervous system toxicity with confusion, hyponatremia, and seizures. One patient is living and stable 29.2 months after treatment. Two patients survived >25 months before succumbing to tumor progression. Ten patients died within 10 months of treatment, 9 from tumor progression and 1 with sepsis and endocarditis. Neuropathologic examination of postmortem tissue demonstrated cavitation at the injection site, intratumoral foci of coagulative necrosis, and variable infiltration of the residual tumor with macrophages and lymphocytes.

Adenoviridae↗
PubMed2000

Extracellular glutamate and aspartate in head injured patients.

Eighty-six patients in coma from a severe head injury underwent monitoring of extracellular concentrations of glutamate and aspartate by a microdialysis technique during the first few days after injury. The median value for glutamate was 7.4 microM (interquartile range 3.6-18.8 microM). The median value for aspartate was 2.4 microM (interquartile range 1.1-5.0 microM). Average values for the dialysate concentrations of glutamate and aspartate, were closely related to outcome (p < .001 and p = .002, respectively). Patients who died of their head injury had significantly higher dialysate glutamate and aspartate concentrations compared to patients who recovered to a Glasgow Outcome Score of good recovery or moderate disability. Dialysate glutamate and aspartate levels were also significantly related to type of injury (p = .008 and p = .004, respectively). The highest values were found in patients with gunshot wounds, followed by patients with evacuated and unevacuated mass lesions. Patients with diffuse injuries had the lowest values of glutamate and aspartate. These results suggest that excitatory amino acids may play a role in the evolution of injury to the brain after trauma.

Adolescent↗
PubMed2000

Neuro-ophthalmologic manifestations of neuroendocrine carcinoma.

The neuro-ophthalmologic findings of parasellar neuroendocrine carcinoma are reported. Two patients with parasellar neuroendocrine carcinoma had headache, ptosis, and ophthalmoplegia. In both patients, neuroimaging revealed a parasellar mass with extension into the cavernous sinus. The tumors initially were believed to be pituitary adenomas, but histopathology confirmed neuroendocrine carcinoma. Clinicians should be aware of neuroendocrine carcinoma in the differential diagnosis of sellar/parasellar lesions causing ophthalmoplegia.

Adult↗
PubMed2000

Brain nitric oxide changes after controlled cortical impact injury in rats.

Nitric oxide (NO) and the NO end products, nitrate and nitrite, were measured at the impact site after a 5-m/s, 3-mm deformation controlled cortical impact injury in rats. Immediately after the impact injury and the NO and microdialysis probes could be replaced, there was an increase from baseline in NO concentration of 83 +/- 16 (SE) nM, compared with 0.5 +/- 4 nM in the sham injured animals (P < 0.001). This marked increase in NO occurred at the time of the initial rise in blood pressure (BP) and intracranial pressure (ICP) in response to the injury. After the initial increase in BP and ICP, the BP decreased and stabilized at a value which was approximately 20 mmHg below the preinjury values, and ICP plateaued at an average value of 20 mmHg, compared with 8 mmHg in the sham-injured animals. This provided an average cerebral perfusion pressure of 40-50 mmHg, compared with 65-75 mmHg for the sham-injured animals. These values were relatively constant for the remainder of the 3-h monitoring period. The NO values also stabilized during this time period. By 1 h after the impact injury the NO concentration measured directly using the NO electrode had decreased from baseline values by an average value of 25 +/- 6 nM. NO concentration remained significantly lower than baseline values throughout the remainder of the 3-h monitoring period. The concentration of nitrate/nitrite in the dialysate fluid also decreased by an average value of 341 +/- 283 nM 20-40 min after the injury. Dialysate nitrite/nitrate concentrations remained less than the preinjury baseline values throughout the remainder of the 3-h monitoring period. Preinjury treatment with L-nitro-arginine methyl ester (L-NAME) blunted the injury-induced increase in NO and resulted in more severe immediate intracranial hypertension and more severe systemic hypotension at one hour after injury. Mortality was also 67% with L-NAME pretreatment, compared with 1% in untreated animals.

Animals↗
PubMed1999

Simultaneous measurement of cortical potassium, calcium, and magnesium levels measured in head injured patients using microdialysis with ion chromatography.

Potassium, calcium and magnesium were measured in 3717 microdialysate samples in 43 patients with head injury experiencing refractory increased ICP, episodes of jugular venous oxygen desaturation and brain death. Cation analysis was performed with 'ion chromatography'. Potassium levels remained stable until severe physiological deterioration occurred, whereupon they increased 100-400%, usually associated with release of amino-acids including glutamate, aspartate, and taurine into the extracellular space. The magnesium and calcium levels remained unchanged, regardless of the severity of physiological deterioration.

Brain Injuries↗
PubMed1999

Validation of a controlled cortical impact model of head injury in mice.

A controlled cortical impact model of head injury was validated with mice. Mice were randomly assigned to moderate head injury, mild head injury, and sham injury groups. Beam balancing, open field activity, slant board inclination, grasp strength, and motor coordination were assessed prior to the injury and on days 1-5 postinjury. Morris water maze performance was evaluated on days 11-15 postinjury. Moderately head-injured mice took a significantly longer time to complete the motor coordination task and to find the hidden platform on the Morris water maze and had significantly fewer successful trials on both tasks than the mildly head-injured and sham-injured mice. Mildly head-injured and sham-injured mice performed similarly on both tasks. Contusion volume at the site of impact varied with severity of injury. Moderately head-injured mice had significantly larger contusions than mice with a mild head injury, and these mice in turn had significantly larger contusions than the sham-injured mice. Both moderately and mildly head injured mice had significantly fewer surviving cells in CA1 than the sham-injured mice but did not differ from each other in this regard. Although there was a group effect, only the mildly head-injured mice had significantly fewer surviving cells in CA3.

Animals↗
PubMed1999

Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis.

OBJECTIVE: To study cerebral glucose and lactate metabolism in head-injured patients using microdialysis. DESIGN: Prospective, nonrandomized, clinical study. SETTING: Neurosurgical intensive care unit in a university-affiliated county hospital. PATIENTS: One hundred twenty-six head-injured patients. INTERVENTIONS: Cerebral cortical neurochemical monitoring using microdialysis coupled with systemic hemodynamic and oxygenation monitoring, measurement of cerebral perfusion pressure and intracranial pressure, and measurement of global cerebral oxygenation using jugular venous oxygen saturation in all 126 patients. In selected cases, cerebral blood flow was also measured using cortical thermodilution probes in 33 patients, and regional cerebral oxygenation was measured using PO2 probes in 65 patients. MEASUREMENTS AND MAIN RESULTS: Elevated extracellular lactate, reduced glucose, and an elevated lactate/glucose ratio were observed with cerebral hypoxia and ischemia. Elevated lactate and an increased lactate/glucose ratio strongly correlated with death. Other more subtle alterations of lactate and glucose were seen early after injury that may reflect compensatory alterations in cerebral metabolism. CONCLUSIONS: Clinical neurochemical monitoring of glucose and lactate levels in the extracellular space of the cerebral cortex is technically feasible and provides insight into the bioenergetic status of the brain. Increased lactate and decreased glucose, indicating accelerated glycolysis, commonly occurred with cerebral ischemia or hypoxia, and increased anaerobic glycolysis in this setting is associated with a poor outcome.

Adult↗
PubMed1999

Cerebral hemodynamic effects of phenylephrine and L-arginine after cortical impact injury.

OBJECTIVE: To determine the effects of a pressor agent (phenylephrine and L-arginine) on the abnormal cerebral hemodynamics and on neurologic outcome after a severe cortical impact injury in rats. DESIGN: Prospective, randomized study. SETTING: University laboratory. SUBJECTS: Male Long-Evans rats, weighing 300 to 400 g, fasted overnight. INTERVENTIONS: The animals were anesthetized with isoflurane, and a severe cortical impact injury (velocity, 5 m/sec; deformation, 3 mm) was produced in the right parietal cortex. Five minutes after impact injury, one of the following three treatments were infused: 1 mL saline intravenously for 10 mins, 300 mg/kg L-arginine in 1 mL saline intravenously for 10 mins, or 0.3 microg/kg/min phenylephrine intravenously for 3 hrs. Mean arterial pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flow (LDF) at the impact site and in the contralateral parietal cortex were monitored for 3 hrs after the impact injury. Histologic examination of the brain was performed at 2 wks after injury in a separate group of L-arginine- and saline-treated animals. MEASUREMENTS AND MAIN RESULTS: The immediate response to the impact injury was an increase in ICP, and a decrease in mean arterial pressure, CPP, and LDF. In the saline-treated animals, LDF decreased to <25% of the baseline values at the impact site and stayed at that level for the entire 3-hr monitoring period. On the contralateral side, LDF decreased initially and recovered gradually to approximately 50% of the preimpact baseline value. Infusion of both phenylephrine and L-arginine increased LDF back to near-baseline levels. However, phenylephrine increased ICP significantly, whereas ICP with L-arginine did not change. L-arginine treatment reduced the contusion volume from a median value of 5.28 mm3 to 0.63 mm3. CONCLUSIONS: Phenylephrine increased cerebral blood flow (CBF) by increasing CPP. L-arginine, however, increased CBF without changing CPP. The improvement in CBF was accompanied by a decrease in neurologic injury. Although the pressor agents are used currently to increase CBF after traumatic brain injury, other strategies may also increase CBF without the potential adverse effects of induced hypertension.

Animals↗
PubMed1998

Metabolic changes in the brain during transient ischemia measured with microdialysis.

Forty-four patients with severe head injury were monitored for episodes of cerebral ischemia using jugular venous oxygen saturation (sjvO2), brain tissue pO2 (ti-pO2), and a microdialysis probe. The concentration of lactate and glucose were measured in the microdialysate. A total of 10 episodes of global ischemia were observed. The characteristic pattern of a simultaneous decrease in sjvO2 and brain ti-pO2 with an increase in the concentration of lactate occurred in all 10 patients. In addition, 3 episodes of regional ischemia were observed. Although brain ti-pO2 decreased to very low values and the concentration of lactate increased in the microdialysate, sjvO2 remained unchanged. Brain ti-pO2 adds another dimension to our cerebral monitoring by allowing the detection of regional cerebral ischemia.

Adult↗
PubMed1998

Effect of glucose administration on contusion volume after moderate cortical impact injury in rats.

Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.

Animals↗
PubMed1998

Hyperglycemia increases neurological damage and behavioral deficits from post-traumatic secondary ischemic insults.

The effects of post-traumatic administration of glucose 2.0 g/kg was compared to saline infusion with and without control of brain temperature at 37 degrees C on behavioral and histological measures of brain injury after controlled cortical impact injury complicated by a secondary ischemic insult. The glucose infusion increased blood glucose concentration from 114 +/- 4 to 341 +/- 76 mg/dl prior to the secondary ischemic insult. The resulting outcome measures were significantly worse in the glucose infusion group than in either control group. Mortality rate was significantly increased by the glucose administration, from 0% to 55% (p < 0.001). The median contusion volume was increased from 7.9 to 64.2 by glucose administration (p < 0.001) and the neuronal loss in the CA1 and CA3 areas of the hippocampus were greater in the glucose infusion group. In the animals that survived for the 2 weeks of behavioral studies, the duration of beam balance was shorter; the percent of animals that could balance on the beam for at least 60 s was less, the percent of animals that could perform the beam-walking task was less, and the length of time required to find the platform in the Morris water maze task was longer in the glucose infusion group. These studies demonstrate that the infusion of glucose after the cortical impact injury significantly increases the damage caused by post-traumatic ischemic insults. The adverse effect on neurological outcome could not be explained by the temperature effects of glucose infusion.

Animals↗
PubMed1998

Comparison of brain tissue oxygen tension to microdialysis-based measures of cerebral ischemia in fatally head-injured humans.

This study investigated the relationship between brain tissue oxygen tension (PbtO2) and cerebral microdialysate concentrations of several compounds in five patients with refractory intracranial hypertension after severe head injury. The following substances were assayed: lactate and glucose; the excitatory amino acids glutamate and aspartate; and the cations potassium, calcium, and magnesium. Glucose concentrations did not correlate with PbtO2, but lactate increased as PbtO2 decreased. The lactate/glucose ratio exhibited a close relationship to PbtO2, increasing sharply only when oxygen tension reached zero. Although glucose and oxygen eventually reached very low levels and zero, respectively, in these fatally head-injured patients, the terminal decrease in PbtO2 slightly preceded that of glucose in four of the five patients. This time lag is the cause of the poor correlation between glucose and PbtO2. Glutamate and aspartate concentrations both demonstrated a close relationship to PbtO2, with sharp increases not occurring until PbtO2 was zero. Concentrations of these amino acids exhibited a similar pattern in response to decreasing glucose concentrations. Potassium concentrations began increasing at a PbtO2 of 35 mm Hg, which is not generally considered indicative of hypoxia. Sharper increases began occurring once PbtO2 dropped below 15 mm Hg, with a slight rise in the minimum potassium concentrations recorded at these low PbtO2 values. Calcium and magnesium concentrations did not vary in response to PbtO2. In summary, the most robust biochemical indicators of cerebral anoxia were elevations in the lactate/glucose ratio and in the concentrations of lactate and of the excitatory amino acids glutamate and aspartate. Furthermore, the fact that glucose concentrations continue to decrease for a short period after oxygen levels reach zero suggests that cells continue to utilize glucose anaerobically for such functions as maintenance of cellular integrity, with collapse of the cell membrane as evidenced by increases of extracellular glutamate and aspartate not occurring until both oxygen and glucose concentrations reach zero.

Adult↗
PubMed1998

Parafalcine and bilateral convexity neurosarcoidosis mimicking meningioma: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Sarcoidosis is a granulomatous disorder of unknown origin that may rarely present solely as an intracranial tumor. Neurosarcoidosis can mimic more common disease processes, such as meningioma, glioma, or metastases. It is important to keep neurosarcoidosis in mind, both preoperatively and intraoperatively, to guide appropriate treatment. We present a case of neurosarcoidosis mimicking a parafalcine and bilateral convexity meningioma. CLINICAL PRESENTATION: A 44-year-old African-American woman was referred to our institution with a diagnosis of meningioma based on a 4-month history of headaches, decreased memory, personality changes, and decreased coordination and on the results of axial computed tomography, which revealed a parafalcine and bilateral convexity mass. INTERVENTION: Cerebral arteriography and magnetic resonance imaging were performed to better characterize the lesion for anticipated surgery. Despite corticosteroid therapy, the patient continued to have progressive symptoms and underwent surgery. Intraoperative frozen sections were consistent with neurosarcoidosis. The mass was then significantly debulked unilaterally. CONCLUSION: Laboratory studies and follow-up examinations revealed no evidence of systemic sarcoidosis. The patient received corticosteroid therapy and subsequently improved. Serial magnetic resonance imaging examinations during several months revealed decreasing tumor size.

Adult↗