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Biomedical subjects

D F Hanley

Publications and source records attributed to D F Hanley.

At least 127 records · Page 7Linked to original sources

Plasma atrial natriuretic factor and subarachnoid hemorrhage.

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.

Atrial Natriuretic Factor↗

Influence of chemoreceptors on neurohypophyseal blood flow during hypoxic hypoxia.

Neurohypophyseal blood flow was studied using radiolabelled microspheres in 13 dogs. Hypoxic hypoxia and carbon monoxide hypoxia with similar arterial oxygen contents (CaO2, approximately 8 vol %) were produced. Under conditions of hypoxic hypoxia, 100-200% increases in blood flow in caudate nucleus, white matter, neurohypophysis, and all other brain regions occurred. Similar blood flow responses were observed with carbon monoxide hypoxia in all brain regions except the neurohypophysis. The role of carotid and aortic chemoreceptors in mediating this blood flow response was studied in 6 additional dogs. Similar degrees of hypoxic hypoxia were produced in chemoreceptor-intact and completely denervated animals (CaO2 approximately 8 vol %, PaO2 approximately 33 mm Hg). Hypoxic hypoxia produced a 250% increase in neurohypophyseal blood flow and a concurrent rise in plasma arginine vasopressin from 8 +/- 3 to 52 +/- 8 pg/ml. Chemoreceptor denervation completely inhibited the increase in neurohypophyseal blood flow associated with hypoxic hypoxia. Arginine vasopressin was not increased by hypoxic hypoxia under conditions of complete denervation. A unique role for peripheral chemoreceptors in regulating neurohypophyseal blood flow is postulated.

Animals↗

Effect of hypoxia and hypercapnia on neurohypophyseal blood flow.

Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.

Animals↗

Eye movements induced by head rotation in unresponsive patients.

Eye movements induced by head rotation were studied in 6 patients in acute coma, 4 patients in a persistent vegetative state, and 6 healthy, alert control subjects. Results from control subjects suggest that the oculocephalic response in the supine position is principally a vestibulo-ocular reflex. A position-step rotation of the head produced an initial oppositely directed eye movement, followed by a drift of the eyes back toward midline with a negative exponential time course. The time constant of this drift was greater than or equal to 10 seconds in control subjects but less than or equal to 1.5 seconds in unconscious patients and less than or equal to 0.5 seconds in vegetative patients. The rapid drift back of the eyes in unresponsive patients implies dysfunction of reticular and, possibly, cerebellar connections; the rate of this drift may indicate the severity and extent of brain injury. Sinusoidal head rotation produced slow and quick phases of nystagmus in normal subjects. Quick phases were absent in patients in acute coma; although present in vegetative patients, the quick phases did not keep the eyes close to primary position, as was the case in control subjects.

Adult↗

Correlation of transient neurological deficit and somatosensory evoked potentials after intracranial aneurysm surgery. Case report.

A patient is reported in whom intraoperative somatosensory evoked potential (SEP) changes occurred in response to temporary clipping of the right middle cerebral artery. A period of 10 minutes elapsed before changes in SEP's in response to contralateral nerve stimulation were noted and, during the following 2 minutes, the waves decreased in amplitude and then were unrecordable. Waves of SEP, with amplitude similar to those recorded before clipping but with abnormal latency, returned within 45 seconds of removal of the clip, and the latency abnormalities persisted until the end of the operation. The patient awakened promptly at the end of the procedure with a dense left hemiparesis which resolved over 24 hours. At the end of 24 hours, the SEP's in response to median nerve stimulation were symmetrical in both latency and amplitude. This report demonstrates the accuracy of intraoperative evoked potential monitoring in demonstrating alterations of cerebral perfusion during aneurysm surgery. It also suggests that a prolonged period of observation may be necessary to assess the effects of temporary vessel occlusion during surgery on aneurysms or arteriovenous malformations.

Brain↗

Prevention of a first stroke: a review of guidelines and a multidisciplinary consensus statement from the National Stroke Association.

OBJECTIVE: To establish, in a single resource, up-to-date recommendations for primary care physicians regarding prevention strategies for a first stroke. PARTICIPANTS: Members of the National Stroke Association's (NSA's) Stroke Prevention Advisory Board and Cedars-Sinai Health System Department of Health Services Research convened on April 9, 1998, in an open meeting. The conference attendees, selected to participate by the NSA, were recognized experts in neurology (9), cardiology (2), family practice (1), nursing (1), physician assistant practices (1), and health services research (2). EVIDENCE: A literature review was carried out by the Department of Health Services Research, Cedars-Sinai Health System, Los Angeles, Calif, using the MEDLINE database search for 1990 through April 1998 and updated in November 1998. English-language guidelines, statements, meta-analyses, and overviews on prevention of a first stroke were reviewed. CONSENSUS PROCESS: At the meeting, members of the advisory board identified 6 important stroke risk factors (hypertension, myocardial infarction [MI], atrial fibrillation, diabetes mellitus, blood lipids, asymptomatic carotid artery stenosis), and 4 lifestyle factors (cigarette smoking, alcohol use, physical activity, diet). CONCLUSIONS: Several interventions that modify well-documented and treatable cardiovascular and cerebrovascular risk factors can reduce the risk of a first stroke. Good evidence for direct stroke reduction exists for hypertension treatment; using warfarin for patients after MI who have atrial fibrillation, decreased left ventricular ejection fraction, or left ventricular thrombus; using 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors for patients after MI; using warfarin for patients with atrial fibrillation and specific risk factors; and performing carotid endarterectomy for patients with stenosis of at least 60%. Observational studies support the role of modifying lifestyle-related risk factors (eg, smoking, alcohol use, physical activity, diet) in stroke prevention. Measures to help patients improve adherence are an important component of a stroke prevention plan.

Alcohol Drinking↗

Adaptive Fourier series modeling of time-varying evoked potentials: study of human somatosensory evoked response to etomidate anesthetic.

Evoked potentials (EPs) have traditionally been analyzed in time domain, with amplitude and latency of various signal components used in clinical interpretation. A new approach, called adaptive Fourier series modeling (FSM), is presented here. Dynamic changes in magnitudes of Fourier coefficients are analyzed for diagnostic purposes. In order to estimate the time-varying changes in the Fourier coefficients of noisy signals, a least mean-square filtering algorithm is applied. Results of computer simulations as well as experimental data are presented. Time-varying trends are presented in a new compressed evoked spectrum format. These techniques are applied to the study of alterations in human somatosensory EPs caused by the intravenous administration of etomidate during neurosurgical procedures. Amplitude increases of the order of 200-500% occurring within a time span of about 100 sec were captured. Due to its superior convergence properties, the adaptive FSM technique estimates more rapid changes in amplitude and latency than exponentially weighted averaging or moving window averaging schemes.

Computer Simulation↗

Use of midazolam in the treatment of refractory status epilepticus.

Status epilepticus is an epileptic seizure that lasts at least 30 minutes or is repeated at sufficiently brief intervals to produce a continued epileptic condition lasting a total of 30 minutes without the patient fully regaining consciousness. Various combinations of anticonvulsant agents, including benzodiazepines, phenytoin, and phenobarbital, have been used to manage this condition. However, at least 9% of patients with generalized convulsive status epilepticus do not respond to conventional first-line agents, and additional intervention is required. Refractory status epilepticus refers to sustained seizures that do not respond to initial drug therapy and persist longer than 60 minutes. Reports on the response to first- and second-line agents suggest that the incidence of refractory status epilepticus is between 2000 and 6000 cases per year in the United States. Refractory status epilepticus is a major medical and neurologic emergency that requires immediate treatment to avoid significant morbidity and mortality. The anticonvulsive agent midazolam has proved to be effective, well tolerated, and fast acting when used to treat refractory status epilepticus in both adults and children. Its pharmacodynamic effects can be seen within 1 to 5 minutes of administration, and its anticonvulsive effects are apparent as early as 5 to 15 minutes after administration. This article reviews the pharmacology of midazolam and recent clinical reports on the drug's tolerability and effectiveness in the treatment of patients with refractory status epilepticus.

Animals↗

Computed tomography of dural sinus thrombosis.

The four patients presented here demonstrate the value of contrast enhanced CT in the diagnosis and serial evaluation of dural sinus thrombosis. Two patients were young women using oral contraceptives; another patient had lateral sinus thrombosis complicating mastoiditis; a fourth patient developed superior sagittal sinus thrombosis following hip surgery. Improvements in CT diagnosis, including the use of thin sections for evaluation of the deep venous structures and lateral sinuses complemented by multiplanar reconstruction or direct coronal scanning, are discussed. Sequential scans for following the progress of two patients treated by barbiturate coma added to the understanding of dural sinus occlusive disease.

Adult↗

Hypermetabolism and hypercatabolism in Guillain-Barré syndrome.

We studied 21 patients with Guillain-Barré syndrome who demonstrated multiple nutritional risk factors upon admission to an intensive care unit: ventilator dependence (71.4%), adynamic ileus (23.8%), significant weight loss in the 2 weeks before admission (53.0%), antecedent viral illness with gastrointestinal sequelae (43.0%), cranial nerve deficits impairing oral intake and gastrointestinal motility (60%), and depressed serum transferrin (85.7%). Patients are hypermetabolic and hypercatabolic because of endocrine, infectious, and inflammatory components of the disease. High-energy (40 to 45 nonprotein kcal/kg), high-protein (2.0 to 2.5 g/kg) nutrition support appears to exert a favorable effect on visceral protein repletion, nitrogen balance, and resistance to pulmonary infection. Immediate attainment of positive energy balance in these hypermetabolic patients, ideally assessed by indirect calorimetry and followed by high-energy, high-protein feedings, may promote positive nitrogen balance early and attenuate muscle wasting in Guillain-Barré syndrome.

Adolescent↗

Treatment of status epilepticus with midazolam in the critical care setting.

Status epilepticus (SE) is a potentially life-threatening condition that requires prompt and aggressive treatment. Prolonged status seizures are associated with significant physiological sequelae and neurological deficits. Although systemic events such as hyperthermia and anoxia contribute to neuronal damage, SE in and of itself can induce cell death. In general, the sooner it is brought under control, the more favourable is the prognosis. Benzodiazepines, as a group, are the most frequently used anticonvulsants in the management of status seizures. Midazolam, a water-soluble benzodiazepine, is a potent anticonvulsant that offers many advantages over typical benzodiazepines. Because of its stability in aqueous media, midazolam dissolves in common diluents such as normal saline or dextrose water. Consequently, midazolam both intravenously (i.v.) and intramuscularly (i.m.) is well tolerated locally and is associated with less venoirritation than benzodiazepines or antiepileptics that require organic solvents. The water solubility of midazolam also allows rapid and reliable absorption of the drug from the i.m. injection site. Because it is rapidly metabolised and its metabolites are pharmacologically inactive, midazolam has a short duration of action. Most patients regain full conscious state and can be evaluated soon after the cessation of treatment. Midazolam by continuous i.v. infusion and by the i.m. route has been successfully used in the treatment of SE. Although some respiratory and haemodynamic side-effects have been associated with midazolam, no clinically significant side-effects were observed with its use for the indication of SE. It is suggested that midazolam is a safe and rapidly effective treatment option in the management of SE in the critical care setting.

Barbiturates↗