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Biomedical subjects

R G Grossman

Publications and source records attributed to R G Grossman.

At least 73 records · Page 4Linked to original sources
PubMed1992

Continuous monitoring of jugular venous oxygen saturation in head-injured patients.

The continuous measurement of jugular venous oxygen saturation (SjvO2) with a fiberoptic catheter is evaluated as a method of detecting cerebral ischemia after head injury. Forty-five patients admitted to the hospital in coma after severe head injury had continuous and simultaneous monitoring of SjvO2, intracranial pressure, arterial oxygen saturation, and end-tidal CO2. Cerebral blood flow, cerebral metabolic rates of oxygen and lactate, arterial and jugular venous blood gas levels, and hemoglobin concentration were measured every 8 hours for 1 to 11 days. Whenever SjvO2 dropped to less than 50%, a standardized protocol was followed to confirm the validity of the desaturation and to establish its cause. Correlation of SjvO2 values obtained by catheter and with direct measurement of O2 saturation by a co-oximeter on venous blood withdrawn through the catheter was excellent after in vivo calibration when there was adequate light intensity at the catheter tip (176 measurements: r = 0.87, p less than 0.01). A total of 60 episodes of jugular venous oxygen desaturation occurred in 45 patients. In 20 patients the desaturation value was confirmed by the co-oximeter. There were 33 episodes of desaturation in these 20 patients, due to the following causes: intracranial hypertension in 12 episodes, hypocarbia in 10, arterial hypoxia in six, combinations of the above in three, systemic hypotension in one, and cerebral vasospasm in one. The incidence of jugular venous oxygen desaturations found in this study suggests that continuous monitoring of SjvO2 may be of clinical value in patients with head injury.

Adult↗
PubMed1992

Cerebral blood flow, AVDO2, and neurologic outcome in head-injured patients.

A reduced cerebral blood flow (CBF) and a widened arteriovenous oxygen difference (AVDO2) almost always have been associated with a poor neurologic outcome. The literature on this relationship is reviewed. A logistic regression analysis model of the effect of CBF on neurologic outcome was developed, which was adjusted for various confounding factors. CBF remained significantly associated with neurologic outcome-despite these adjustments.

Adult↗
PubMed1992

Blood flow and metabolic therapy in CNS injury.

A hypermetabolic state, consisting of increased resting energy expenditure, excessive protein wasting, and hyperglycemia, occurs in patients with a severe head injury. The hypermetabolism can affect survival by rapidly resulting in protein-calorie malnutrition (increased energy expenditure and protein wasting) and may adversely affect neurological recovery by altering the microenvironment of the injured brain (hyperglycemia).

Animals↗
PubMed1991

Evaluation of the Leeds prognostic score for severe head injury.

According to the Leeds scale for identifying severely head injured patients, death can be predicted with certainty within 12 hours of admission if a patient has a score higher than 13. The withdrawal of treatment from such patients has considerable moral and legal implications. Therefore, to test the reliability of the Leeds scale, it was applied to two patient populations with severe head injuries (479 retrospectively, 131 prospectively). In both groups the scale failed to predict mortality with 100% accuracy: in the first group, 16 of 23 (69.6%) of the patients with a score of more than 13 (and therefore predicted to die) died, and 380 (83.3%) of 456 patients with scores of 13 or less survived; the data for the second group are 6/10 (60%) and 98/121 (81%), respectively. The findings suggest that the Leeds prediction model is not infallible and should be applied cautiously when making decisions about the early termination of care in severely head injured patients.

Adolescent↗
PubMed1991

United Parkinson Foundation Neurotransplantation Registry on adrenal medullary transplants: presurgical, and 1- and 2-year follow-up.

Thirteen centers participated in a multicenter database with systematic evaluation of US and Canadian patients who had adrenal medullary transplantation for Parkinson's disease. This voluntary registry collected demographic, safety, and efficacy data using the same scoring measures over a 2-year follow-up period. Baseline data on 61 patients and 2-year follow-up data on 56 patients were compared. Eighteen percent died during the study period, and one-half of these deaths were related or questionably related to the surgery. Of the remaining 45 patients with data, global improvement, defined as an improved summed score of the "on" and "off" motor and activities of daily living functions from the Unified Parkinson's Disease Rating Scale, occurred in 32% of the patients at 2 years after surgery. At follow-up, significant group improvement persisted in the amount of daily "on" time and the quality of "off" function, but other measures were no better than baseline. When the global improvement calculation was based on the total sample and included deaths and patients lost to follow-up as "not improved," only 19% were improved 2 years after surgery. Twenty-two percent of survivors had persistent psychiatric morbidity not present prior to surgery. These data document a modest group improvement in "off" function after neurotransplantation, but a serious level of mortality and morbidity.

Adrenal Medulla↗
PubMed1991

The effect of glucose administration on carbohydrate metabolism after head injury.

The role of intravenous infusion of glucose in limiting ketogenesis and the effect of glucose on cerebral metabolism following severe head injury were studied in 21 comatose patients. The patients were randomly assigned to alimentation with or without glucose. Systemic protein wasting, arterial concentrations of energy substrates, and cerebral metabolism of these energy substrates were monitored for 5 days postinjury. Both groups were in negative nitrogen balance, and had wasting of systemic proteins despite substantial protein intake. Blood and cerebrospinal fluid (CSF) glucose concentrations were highest on Day 1, but remained higher than normal fasting levels on all days of study, even in the patients who received no exogenous glucose. Although there were no differences in blood or CSF glucose concentrations in the two groups of patients, the glucose group had higher plasma insulin levels, with a mean +/- standard deviation of 14.8 +/- 7.3 microU/ml compared to 10.3 +/- 4.2 microU/ml in the saline group. The blood concentrations of beta-hydroxybutyrate, acetoacetate, pyruvate, glycerol, and the free fatty acids were higher in the saline group than in the glucose group. Cerebral oxygen consumption was similar in the two groups, while the cerebral metabolism of glucose and of the ketone bodies was dependent on whether glucose was administered. In the glucose group, glucose was the only energy substrate utilized by the brain. In the saline group, the ketone bodies beta-hydroxybutyrate and acetoacetate replaced glucose to the extent of 16% of the brain's total energy production. Cerebral lactate production and CSF lactate concentration were lower in the saline group. These studies suggest that administration of glucose during the early recovery period of severe head injury is a major cause of suppressed ketogenesis, and may increase production of lactic acid by the traumatized brain by limiting the availability of nonglycolytic energy substrates.

3-Hydroxybutyric Acid↗
PubMed1990

Tyrosine hydroxylase-immunoreactive neurons in the temporal lobe in complex partial seizures.

The anterior mesial portion of the temporal lobe removed from 16 patients who underwent surgery for the treatment of complex partial seizures was found to contain tyrosine hydroxylase-immunoreactive neurons. The distribution of these neurons was correlated with the underlying neuropathological features. Ammon's horn sclerosis was present in 8 patients; a ganglioglioma, in 7 patients; and an infarction in the distribution of the middle cerebral artery, in 1 patient. Tyrosine hydroxylase-immunoreactive neurons were found in Ammon's horn of 6 of the 8 patients with Ammon's horn sclerosis, and in the subiculum and entorhinal cortex of all 8 patients with the same pathology. None of these neurons were found in Ammon's horn of the 7 patients with a ganglioglioma, but were found in the subiculum of 5 of the 7 patients and in entorhinal cortex of all 7 patients. Tyrosine hydroxylase immunoreactivity was also studied in 13 control autopsy specimens. No tyrosine hydroxylase-immunoreactive neurons were found in Ammon's horn or the subiculum of any of the control specimens, but were found in the entorhinal cortex of 6 of the 13 specimens. The tyrosine hydroxylase-immunoreactive neurons in the mesial portion of the temporal lobe of patients with complex partial seizures may contribute to the increased levels of tyrosine hydroxylase found in neurochemical studies of specimens taken at temporal lobectomy.

Adolescent↗
PubMed1990

Elevation of tumor necrosis factor in head injury.

Tumor necrosis factor (TNF) is a cytokine which mediates protein wasting in pathological states by promoting the catabolism of visceral tissues and skeletal muscle. The role that TNF plays in nitrogen wasting following head injury was studied by measuring TNF in the serum of 21 patients with severe head injury. Parallel measurements of TNF and urinary nitrogen excretion were performed on days 1, 3, and 5 after head injury. TNF values after head injury ranged from 65 pg/ml to 7500 pg/ml, with a mean of 1147 pg/ml, compared to control values of serum TNF of less than 38 pg/ml. The mean daily urinary nitrogen loss was 13 g/day with a range of 2.8 to 27.6 g/day, and the mean nitrogen balance was -5.8 g with a range of +4.6 to -19.1 g. While both serum TNF levels and nitrogen loss were increased after head injury, the elevation of TNF did not correlate strongly with nitrogen wasting.

Adult↗
PubMed1990

Reduction in spinal cord postischemic lactic acidosis and functional improvement with dichloroacetate.

Pyruvate dehydrogenase complex (PDHC) is a major enzyme of glucose metabolism. Dichloroacetate (DCA) is a noncompetitive inhibitor of PDHC kinase, an enzyme that inactivates PDHC. We examined the effects of DCA on extracellular lactate and pyruvate concentration changes and spinal somatosensory evoked potentials (SSEP) in ischemic rabbit spinal cords. In the first group of 26 animals, the aorta was occluded until postsynaptic SSEP waves were completely suppressed for 10 min, a period of ischemia that causes neurologic deficits in 50% of untreated animals. DCA (25 mg/kg) was given to 13 of these animals before ischemia. In the second group of 24 animals, the aorta was occluded until the postsynaptic SSEP waves were absent for 20 min, a period of ischemia that produces paraplegia in 100% of untreated animals. DCA (25 mg/kg) was given to 16 of these animals just before the aortic occlusion was released. After occlusion, extracellular spinal lactate concentrations increased abruptly while pyruvate concentrations fell. Both lactate and pyruvate concentrations reached a plateau during the ischemic period but increased when the aortic balloon was deflated. DCA-treated animals had lower lactate and pyruvate peak concentrations during reperfusion, as well as more rapid and greater recovery of SSEP at 2 h after reperfusion. DCA did not alter spinal metabolism during the ischemia but appeared to produce a more rapid shift to glucose metabolism on reperfusion. Thus, DCA treatment resulted in better electrophysiological recovery after both moderate and severe ischemia, either by reducing lactic acidosis or by increasing the recovery rate of aerobic energy production.

Acetates↗
PubMed1989

Cardiovascular and metabolic responses to severe head injury.

The cardiovascular and metabolic responses to severe head injury were studied in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. The cardiovascular response to head injury was studied by measurement of cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases and arterial and mixed venous epinephrine and norepinephrine serially in 15 patients during the first three days after injury. A hyperdynamic state was found characterized by increased cardiac output and cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting and increased oxygen delivery and utilisation. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Score, or findings on CT scan. The metabolic response to head injury was studied by measurement of resting metabolic expenditure (RME) in 14 comatose head-injured patients in the first nine days after injury. During this period patients were fed with a continuous parenteral infusion of a formula containing 2 Kcal/cc and 10 mg nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated, nonparalyzed patients was 138 +/- 37% of that expected for a non-injured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 109 patient-days. The mean excretion was 20.2 +/- 6.4 mg/day. The mean protein caloric contribution was 23.9 +/- 6.7% and was greater than 25% for six patients, compared to normal values of 10-15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with the parenterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20-40% of the body surface.

Adolescent↗
PubMed1989

Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients.

The hypothesis that cerebral arteriovenous difference of oxygen content (AVDO2) can be used to predict cerebral blood flow (CBF) was tested in patients who were comatose due to head injury, subarachnoid hemorrhage, or cerebrovascular disease. In 51 patients CBF was measured daily for 3 to 5 days, and in 49 patients CBF was measured every 8 hours for 5 to 10 days after injury. In the latter group of patients, when a low CBF (less than or equal to 0.2 ml/gm/min) or an increased level of cerebral lactate production (CMRL) (less than or equal to -0.06 mumol/gm/min) was encountered, therapy was instituted to increase CBF, and measurements of CBF, AVDO2, and arteriovenous difference of lactate content (AVDL) were repeated. When data from all patients were analyzed, including those with cerebral ischemia and those without, AVDO2 had only a modest correlation with CBF (r = -0.24 in 578 measurements, p less than 0.01). When patients with ischemia, indicated by an increased CMRL, were excluded from the analysis, CBF and AVDO2 had a much improved correlation (r = -0.74 in 313 measurements, p less than 0.01). Most patients with a very low CBF would have been misclassified as having a normal or increased CBF based on the AVDO2 alone. However, when measurements of AVDO2 were supplemented with AVDL, four distinct CBF patterns could be distinguished. Patients with an ischemia/infarction pattern typically had a lactate-oxygen index (LOI = -AVDL/AVDO2) of 0.08 or greater and a variable AVDO2. The three nonischemic CBF patterns had an LOI of less than 0.08, and could be classified according to the AVDO2. Patients with a normal CBF (mean 0.42 +/- 0.12 ml/gm/min) had an AVDO2 between 1.3 and 3.0 mumol/ml. A CBF pattern of hyperemia (mean 0.53 +/- 0.18 ml/gm/min) was characterized by an AVDO2 of less than 1.3 mumol/ml. A compensated hypoperfusion CBF pattern (mean 0.23 +/- 0.07 ml/gm/min) was identified by an AVDO2 of more than 3.0 mumol/min. These studies suggest that reliable estimates of CBF may be made from AVDO2 and AVDL measurements, which can be easily obtained in the intensive care unit.

Arteries↗
PubMed1989

Electrophysiological connections between the hippocampus and entorhinal cortex in patients with complex partial seizures.

The electrophysiological properties of the neural pathways between the hippocampus and the entorhinal cortex were studied intraoperatively in 31 patients undergoing anterior temporal lobectomy for medically intractable complex partial seizures. The hippocampus, removed en bloc, was studied histologically and the pathology was correlated with the electrophysiological findings. In 29 of the patients, entorhinal stimulation evoked a characteristic positive-negative potential in the hippocampus. The entorhinal-evoked hippocampal response closely resembled, or was identical to, the spontaneously occurring hippocampal interictal spike discharge. In patients with Ammon's horn sclerosis in whom there was a major loss of neurons in the hippocampal subfields CA1, CA3, and CA4, the evoked responses were of simple morphology and long latency (mean 21.9 msec to the peak of the first potential). In patients with a ganglioglioma in whom the hippocampus was histologically normal, the evoked responses were of greater complexity and shorter latency (mean 11.8 msec). Stimulation at a single entorhinal site evoked similar waveforms at different hippocampal recording sites. Conversely, stimulation at different entorhinal sites evoked similar responses at a single hippocampal recording site. Stimulation of the hippocampus evoked a potential in the entorhinal cortex and, in some instances, in the amygdala, insula, and lateral temporal cortex. These connections may produce a positive feedback loop that favors seizure generation.

Amygdala↗
PubMed1989

Clinical experience with a continuous monitor of intracranial compliance.

Intracranial compliance, as estimated from a computerized frequency analysis of the intracranial pressure (ICP) waveform, was continuously monitored during the acute postinjury phase in 55 head-injured patients. In previous studies, the high-frequency centroid (HFC), which was defined as the power-weighted average frequency within the 4- to 15-Hz band of the ICP power density spectrum, was found to inversely correlate with the pressure-volume index (PVI). An HFC of 6.5 to 7.0 Hz was normal, while an increase in the HFC to 9.0 Hz coincided with a reduction in the PVI to 13 ml and indicated exhaustion of intracranial volume-buffering capacity. The mean HFC for individual patients in the present study ranged from 6.8 to 9.0 Hz, and the length of time that the HFC was greater than 9.0 Hz ranged from 0 to 104.8 hours. The mortality rate increased concomitantly with the mean HFC, from 7% when the mean HFC was less than 7.5 Hz to 46% when the mean HFC was 8.5 Hz or greater. The length of time that the HFC was 9.0 Hz or greater was also associated with an increased mortality rate, which ranged from 16% if the HFC was never above 9.0 Hz to 60% if the HFC was 9.0 Hz or greater for more than 12 hours. In 12 patients who developed uncontrollable intracranial hypertension or clinical signs of tentorial herniation during the monitoring period, 75% were observed to have had an increase in the HFC to 9.0 Hz or more 1 to 36 hours prior to the clinical decompensation. The more rapid the increase in the HFC, the more likely the deterioration was to be caused by an intracranial hematoma. Continuous monitoring of intracranial compliance by computerized analysis of the ICP waveform may provide an earlier warning of neurological decompensation than ICP per se and, unlike PVI, does not require volumetric manipulation of intracranial volume.

Adaptation, Physiological↗
PubMed1988

Alterations in cerebral availability of metabolic substrates after severe head injury.

Cerebral and systemic metabolism of oxygen, glucose, lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, and amino acids were studied in 27 comatose patients during the first 7 days after a head injury. Systemic oxygen consumption was elevated initially and gradually returned toward normal over the week of study. In contrast, cerebral oxygen consumption was depressed and decreased further over the week of study. Cardiac output and cerebral blood flow were increased with respect to systemic and cerebral metabolic requirements, and remained elevated for the entire week of study. Systemic hyperglycemia and lactic acidosis were present. The injured brain often made a sizeable contribution to the lactic acidosis. The arterial concentrations of pyruvate, beta-hydroxybutyrate and acetoacetate were low. The early postinjury arterial amino acid profile was typically an increased level of alanine, taurine, glutamic acid, and a reduced concentration of valine, leucine, isoleucine, threonine, serine, ornithine, and arginine. At 3-4 days postinjury, as the early abnormalities were returning toward normal, glutamine, lysine, phenylalanine, tyrosine, and methionine became elevated. These late increases in amino acids occurred at the time of the peak in plasma catecholamine concentrations. The net cerebral flux of amino acids followed the same general pattern of evolution over time as did the arterial concentration of amino acids. On days when the availability of the individual amino acid was increased, the net cerebral flux tended to be positive; when the availability was decreased, the net cerebral flux was zero or there was a net efflux of the amino acid. There was a significant linear relationship between the arterial concentration and the net flux of 13 of the 17 amino acids studied. Unlike the fasting state in normal man, in which beta-hydroxybutyrate and acetoacetate are important metabolic substrates, cerebral metabolism after head injury is almost totally dependent upon the aerobic and anaerobic metabolism of glucose. This is at least in part due to injury-induced limitations in the variety of substrates that are available for the brain to extract.

Adolescent↗