PubMed Health⌕ Search

Biomedical subjects

V Zelman

Publications and source records attributed to V Zelman.

At least 19 recordsLinked to original sources
PubMed2001

The antinociceptive effect of the combination of spinal morphine with systemic morphine or buprenorphine.

UNLABELLED: We sought to analyze the mode of interaction of spinal morphine with systemic morphine or buprenorphine, administered in a wide range of antinociceptive doses. The study was performed on Sprague-Dawley rats by using a plantar stimulation test and isobolographic and fractional analyses of drug interaction. The isobolographic and fractional analyses demonstrated that intrathecal morphine interacted with subcutaneous morphine in a synergistic manner while producing a 50% or 75% antinociceptive effect. The sum of D(75) fractions was more than that for 50% antinociception, suggesting a less dramatic interaction. The combination with a maximal relative dose of systemic morphine (0.66:1) showed a maximal degree of supraadditivity. The interaction between spinal morphine and systemic buprenorphine was similar to that of morphine/morphine, although the supra-additivity was not as pronounced. For the doses that produced a 50% antinociceptive effect, a synergistic interaction was observed only for the combination with a morphine/buprenorphine ratio of 1.33:1. When the relative amount of intrathecal morphine was decreased or increased, the effect became additive. At the doses that produced 75% antinociception, both combinations of morphine and buprenorphine demonstrated supraadditive interaction. IMPLICATIONS: Spinal morphine interacts with systemic morphine or buprenorphine in asupraadditive manner. This mode of interaction most probably results from the simultaneous activation of spinal and supraspinal antinociceptive systems. Supraspinal structures played a more important role in the antinociceptive effect of experimental combinations than structures of the spinal cord.

Algorithms↗
PubMed2000

A tribute to Dr. Fedor A. Serbinenko, founder of endovascular neurosurgery.

From humble beginnings in the former Soviet Union, Fedor A. Serbinenko, M.D., Ph.D., became a leading figure at Moscow's famed Burdenko Neurosurgery Institute. While there, he invented and perfected the technique of balloon embolization, which was destined to change the practice of neurovascular surgery forever. We present the life and achievements of the father of endovascular neurosurgery.

Angioscopy↗
PubMed1999

Gamma knife radiosurgery for metastatic melanoma: an analysis of survival, outcome, and complications.

OBJECTIVE: Although the mainstays for treatment of metastatic brain disease have been surgery and/or external beam radiation therapy, an increasing number of patients are being referred for stereotactic radiosurgery as the primary intervention for their intracranial pathological abnormalities. The lack of efficacy and cognitive and behavioral consequences of whole brain irradiation have prompted clinicians to select patients for alternative therapies. This study analyzes the effectiveness of Leksell gamma unit therapy for metastatic melanoma to the brain. METHODS: We present our experience with 59 Leksell gamma unit treatment sessions in 45 consecutive patients who presented with metastatic melanoma to the brain. Five of these procedures were performed as salvage therapy for patients who needed second radiosurgical treatment for new lesions that were remote from the previous targets and were not included in the overall analyses. RESULTS: The population included 78% male patients. The mean patient age was 53 years (age range, 24-80 yr). The mean time from diagnosis of primary melanoma to discovery of brain metastasis was 43 months (median, 27.5 mo; range, 1-180 mo). At the time of diagnosis of brain disease, 35.5% of the patients (16 of 45 patients) had neurological symptoms, 77.7% (35 of 45 patients) had known visceral metastases, and 11.1% (5 of 45 patients) had seizure disorders. Eighty-six percent of the lesions (80 of 93 lesions) were cortical, 12% (11 of 93 lesions) were cerebellar, 1% (1 of 93 lesions) were pontine, and 1% (1 of 93 lesions) were thalamic. Fifty-seven percent of the sessions (31 of 54 sessions) were performed for a single lesion, 24.1% (13 of 54 sessions) for two lesions, 9.2% (5 of 54 sessions) for three lesions, 7.4% (4 of 54 sessions) for four lesions, and 1.8% (1 of 54 sessions) for five lesions. The mean treatment volume was 5.6 cc, with a mean prescription of 21.6 Gy to the 56.0% mean isodose line. The median survival time of the patients in our population, using Kaplan-Meier curves, was 43 months from the time of diagnosis of primary melanoma (range, 3-180 mo) and 8 months (range, 1-20 mo) from the time of gamma knife treatment. Complications included seizures within 24 hours of the procedure in four patients, with transient nausea and vomiting in three patients, transient worsening of preprocedure paresis responsive to steroids in three patients, and increased confusion in one patient. All 45 patients were located for follow-up (mean follow-up duration, 1 yr). After gamma knife treatment, 78% of the patients (35 of 45 patients) experienced either improved or stable neurological symptomatology before death or at the time of the latest follow-up examination. There were 26 deaths (58%). The cause of death was determined to be neurological in only 2 of 45 patients (7.7%). Follow-up magnetic resonance images revealed a 97% local tumor control rate of gamma knife-treated lesions, with 28% radiographic disappearance (9 of 32 cases). Six patients developed new lesions remote from radiosurgical targets and underwent second procedures. CONCLUSION: Although metastatic melanoma to the brain continues to have a foreboding prognosis for long-term survival, gamma knife radiosurgery seems to be a relatively safe, noninvasive, palliative therapy, halting or reversing neurological progression in 77.8% of treated patients (35 of 45 patients). The survival rate matches or exceeds those previously reported for surgery and other forms of radiotherapy. Only 7.7% of the patients in our study population who died as a result of metastatic melanoma (2 of 26 patients) died as a result of neurological disease. The routine use of therapeutic level antiseizure medication is emphasized, considering the findings of our review.

Adult↗
PubMed1997

Spinal artery syndrome masked by postoperative epidural analgesia.

PURPOSE: We report a case of a patient who developed a postoperative anterior spinal artery syndrome that was masked by the use of epidural analgesia. We wish to alert other anaesthetists that the use of epidural anaesthesia in this setting may mask the symptoms and delay the diagnosis of this rare complication. CLINICAL FEATURES: The patient was a 22-yr-old obese man with metastatic testicular carcinoma who underwent a left-sided thoracoabdominal retroperitoneal tumour resection. A lumbar epidural catheter was placed preoperatively for pain management. Postoperatively, the patient developed bilateral lower extremity weakness, which was at first attributed to epidural administration of local anaesthetics. Despite discontinuation of the local anaesthetics, the symptoms persisted. Further work-up led to the diagnosis of anterior spinal artery syndrome. The patient was sent to a rehabilitation hospital and had a partial recovery. CONCLUSION: Anterior spinal artery syndrome can occur following retroperitoneal surgery. It is important to recognize the potential for this complication when postoperative epidural analgesia is contemplated, especially following a left-sided surgical dissection. The use of epidural local anaesthetics immediately after surgery delays the diagnosis of a postoperative neurological deficit. Moreover, when the deficit is recognized the epidural itself may be falsely blamed for postoperative paraplegia. If epidural analgesia is used, opioids may be preferred over local anaesthetics in the immediate postoperative period to prevent masking of an anterior spinal artery syndrome.

Adult↗
PubMed1997

Systemic physostigmine increases the antinociceptive effect of spinal morphine.

In this study we evaluated the antinociceptive effect of concurrent intrathecal (i.t.) and subcutaneous (s.c.) administration of morphine and physostigmine, respectively. The experiments were performed on male Wistar rats. Intrathecal administration of morphine was performed through a catheter implanted in the subarachnoid space. The 'tail-immersion' test was used to measure animals' responses to evoked nociceptive stimuli. Interaction of drugs was analyzed using a dose addition model. Both i.t. (1-5 microg) administration of morphine and s.c. (50-250 microg/kg) administration of physostigmine increased the latencies of nociceptive responses in a dose-dependent manner. Two micrograms of i.t. morphine and 100 microg/kg of s.c. physostigmine demonstrated 31.6 +/- 10.6 and 34.2 +/- 11.4 percentage of maximal possible effect (%MPE), respectively. Simultaneous administration of 1 microg of i.t. morphine and 50 microg/kg of s.c. physostigmine produced a %MPE equal to 84.8 +/- 16.9. Thus, combined administration of 1 microg i.t. morphine and 50 microg/kg s.c. physostigmine resulted in a strong, highly significant antinociceptive effect. This effect was much higher than the effect expected if both drugs acted in an additive manner. Supra-additive interaction observed in this study might be a result of simultaneous activation of different neurotransmitter systems involved in nociceptive processing at the spinal as well as at the supraspinal level of the CNS.

Analgesics, Opioid↗
PubMed1997

Rapid reversal of endothelin-1-induced cerebral vasoconstriction by intrathecal administration of nitric oxide donors.

OBJECTIVE: To determine the capability of donors of nitric oxide (NO) (sodium nitroprusside, nitroglycerine) to reverse endothelin-1 (ET-1)-induced cerebral vasoconstriction in vivo, when administered through the cerebrospinal fluid (CSF) to the adventitial side of the constricted blood vessel. METHODS: The rabbit basilar artery was exposed through a transcervical, transclival approach and subsequently subjected to pharmacological manipulations and direct observation of effects by videomicroscopy. Specific manipulations were suffusion of ET-1 (100 nmol/L, 1 ml/min) in synthetic CSF (sCSF) to provoke vasoconstriction and then either suffusion of an NO donor in sCSF (2 mg/ml/min), or sCSF alone. The second suffusion was always made separately and begun during the period of stable maximal vasoconstriction, which occurred between 20 and 30 minutes after beginning the first suffusion. Measurements of the diameter of the artery were made using an inline video caliper. RESULTS: Sodium nitroprusside and nitroglycerine, both donors of NO, rapidly and completely reversed ET-1-induced vasoconstriction without causing hypotension. The average value for maximal vasoconstriction by ET-1/sCSF was 50.4% of baseline arterial diameter and occurred between 20 and 30 minutes. The rate of vasodilatory response was 100% of significantly constricted arteries. The response was complete in less than 6 minutes in all preparations, as compared to the 60 minutes required for spontaneous relaxation (sCSF suffusion alone). CONCLUSION: NO donors are effective in reversing cerebral vasoconstriction when administered intrathecally, cause no significant hemodynamic change when so administered, and may represent an important therapeutic intervention for cerebral vasospasm.

Animals↗
PubMed1997

Attenuation of brain injury and reduction of neuron-specific enolase by nicardipine in systemic circulation following focal ischemia and reperfusion in a rat model.

A reversible middle cerebral artery occlusion was performed in rats to determine whether nicardipine, a dihydropyridine voltage-sensitive Ca++ channel (VSCC) antagonist, exerts neuroprotective effects when administered 10 minutes following an ischemic insult, and if it does, whether this is due to its vasodilatory action and effect on cerebral blood flow (CBF) or to direct blockade of Ca++ entry into ischemic brain cells. An increase in the intracellular calcium, [Ca++]i, plays a major role in neuronal injury during cerebral ischemia. Although a large amount of Ca++ enters neurons through the VSCC during ischemia, inconsistent neuroprotective effects have been reported with the antagonists of the VSCC. An intraperitoneal injection of nicardipine (1.2 mg/kg) was administered to rats 10 minutes after the onset of ischemia, and 8, 16, and 24 hours after occlusion. Cortical CBF was determined by laser-Doppler flowmetry. Neurological and neuropathological examinations were performed after 72 hours. Neuron-specific enolase, a specific marker for the incidence of neuronal injury, was measured in plasma. The CBF and other physiological parameters were not affected by nicardipine during occlusion or reperfusion. However, nicardipine treatment significantly improved motor neurological outcome by 29%, and the infarction and edema volume in the pallium as well as the edema volume in the striatum were significantly reduced by 27%, 37%, and 52%, respectively. Nicardipine also reduced the neuron-specific enolase plasma levels by 50%, 42%, and 59% at 24, 48, and 72 hours after the occlusion, respectively. It is concluded that nicardipine may attenuate focal ischemic brain injury by exerting direct neuroprotective and antiedematous effects that do not depend on CBF.

Animals↗
PubMed1996

Vagus nerve stimulation activates central nervous system structures in epileptic patients during PET H2(15)O blood flow imaging.

OBJECTIVE: To determine the central areas of activation by vagal nerve stimulation (VNS) in epilepsy. VNS is a promising neurosurgical method for treating patients with partial and secondary generalized epilepsy. The anti-epileptic mechanism of action from VNS is not well understood. METHODS: We performed H2(15)O PET blood flow functional imaging on three patients with epilepsy in a vagal nerve stimulation study (E04 Protocol with Cyberonics). The three patients included two that had previous epilepsy surgery but continued to have frequent seizures. Seizure onset was frontal in two patients and bitemporal in the third patient. Twelve PET scans per subject were acquired every 10 minutes with a Siemens 953/A scanner. In 6 stimulus scans, VNS was activated for 60 seconds (2 mA, 30 Hz) commensurate with isotope injection. In 6 control scans no VNS was administered. No clinical seizures were present during any scan. Three way ANOVA with linear contrasts subject, task, repetition) of coregistered images identified significant treatment effects. RESULTS: The difference between PET with VNS and without revealed that left VNS activated right thalamus (P < 0.0006), right posterior temporal cortex (P < 0.0003), left putamen (P < 0.0002), and left inferior cerebellum (P < 0.0009). CONCLUSIONS: VNS causes activation of several central areas including contralateral thalamus. Localization to the thalamus suggests a possible mechanism to explain the therapeutic benefit, consistent with the role of the thalamus as a generator and modulator of cerebral activity.

Adult↗
PubMed1996

Mechanical malfunction of the Leksell Gamma knife during patient treatment.

During the course of a patient treatment with a North American U-type gamma unit, the remote hydraulic valve controlling the direction of couch motion failed to change state. The couch, helmet and patient remained in treatment position after the expiration of treatment time for one of the target shots. No unusual equipment warning indications had been observed prior to the malfunction. The gamma unit was new, having been used to treat approximately 20 patients since it had begun to be used clinically 11 weeks previously. This specific situation was not addressed in our posted Emergency Procedures, which dealt explicitly with loss of electrical power, and loss of hydraulic pressure. In the present case, the hydraulic gauges indicated full pressure. After attempts to disengage the patient remotely proved unsuccessful, personnel entered the room. The table clutch at the foot of the couch was operated to disengage the couch/helmet assembly from its docked position. While this was not mentioned in our emergency procedures, the act had the effect of causing the cobalt-60 sources to be misaligned with the collimator apertures, thereby immediately terminating the patient treatment. This also had the unanticipated effect of substantially reducing radiation leakage exposure rate next to the couch near the tunnel opening. The patient was released from the helmet trunnions using a manufacturer-supplied long-handled special Allen key. The key was used conventionally, to release the trunnion locking mechanism, and also unconventionally to force a separation of a trunnion from the docking slot on the patient head frame. The patient was then removed from the tunnel by sliding out the pad on which she was lying. Anesthesiology personnel accompanied the patient out of the room. The unit functioned properly upon the replacement of the valve by manufacturer service personnel the next day. The patient returned for completion of treatment 1 week later. There were only minor changes to the overall patient dosimetry as a result of the malfunction. Personnel exposures were very low. The malfunction was reported to State authorities, who conducted an investigation, that was in turn followed up by an investigation by the Nuclear Regulatory Commission.

Dose-Response Relationship, Radiation↗
PubMed1996

Gamma unit facility: concept genesis, architectural design and practical realization.

The physical creation of a gamma unit facility requires the development of a broad-perspective multidisciplinary plan. The primary goal is radiosurgical treatment of intracranial lesions in a functional environment. The practical realization of a facility optimally designed for patient treatment is dependent on factors which include the facility setting, architectural goals, radiation safety requirements, and patient and medical team needs. This necessitates combined intellectual resources from neurosurgery, radiation oncology and physics, anesthesia, radiology, nursing, administration, and architectural and engineering teams. We undertook the development of a gamma unit facility which optimized the ergonomics and efficiency of patient evaluation, care and treatment, given the instrument requirements. This general plan based on our experience can be used for the development of other gamma unit facilities.

Clinical Protocols↗
PubMed1996

Intraoperative maintenance of tissue perfusion prevents ARDS. Adult Respiratory Distress Syndrome.

Patients undergoing prolonged, complex oncological surgery are at increased risk of developing the adult respiratory distress syndrome (ARDS) and other organ failures. Our hypothesis is that maintaining adequate tissue perfusion and oxygenation may prevent tissue hypoxia and acidosis in pulmonary, peripheral, and splanchnic microcirculations. Experimental evidence suggests that the hypoxic, acidotic endothelium stimulates the release of cytokines, kinins, and other mediators. We developed and tested an intraoperative protocol for surgical patients likely to develop ARDS and organ dysfunction; the protocol focuses on the intraoperative period but is not limited to this time. Nitroglycerin and fluids were used to maintain tissue perfusion and prevent tissue hypoxia as reflected by transcutaneous oxygen tension values. In 155 high-risk patients, none developed ARDS. We conclude that maintenance of tissue perfusion and oxygenation in high-risk surgical patients decreases the incidence of ARDS.

Adult↗
PubMed1995

Propylene glycol toxicity following continuous etomidate infusion for the control of refractory cerebral edema.

Continued elevations in Intracranial Pressure (ICP) following traumatic or ischemic compromise are known to cause markedly increased morbidity and mortality. Because of the side effects of barbiturates including hypotension and prolonged recovery time, the use of shorter-acting anesthetic agents to control ICP has been considered. Etomidate, when administered by continuous infusion, has been shown to decrease cerebral metabolism resulting in a secondary decrease in cerebral blood flow with minimal changes in cerebral perfusion pressure. We initially intended to randomize 20 patients prospectively into a study protocol that would assess the effects of either pentobarbital or the cardioprotective agent etomidate on ICP and cardiac performance. Given the sequelae of the therapy, we were only able to randomize seven patients with cerebral edema refractory to medical management to receive either etomidate or pentobarbital in a blinded fashion. Three patients who received etomidate developed renal compromise (mean low creatinine clearance 41 ml/min, range 37-44 ml/min) which was initially noted at 24 hours. We believed that this represented an adverse effect that was probably related to the study drug and the study was stopped. Each patient received a 0.30 mg/kg IV induction of etomidate and then 0.02 mg/kg/min continuous infusion for 24-72 hours titrated burst suppression. All patients also received dexamethasone 2 mg IV every six hours to prevent the adrenocortical insufficiency that might occur as a consequence of etomidate-induced suppression of cortisol synthesis. Intracranial pressure decreased (mean = 12mmHg) following the initiation of etomidate. Cardiac parameters remained unchanged (cardiac output 4.8 +/- .6 liters/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1994

Cardiac performance enhancement and hypervolemic therapy.

This article discusses guidelines the authors have established in managing patients with ruptured intracranial aneurysms and associated vasospasm. These guidelines represent methods of improving cardiac output or the ideal cardiac indices, to improve or maximize cerebral blood flow and potentially improve outcome. The guidelines for hypervolemic therapy for the volume and timing of intravenous fluid administration and the target cardiac performance parameters also are discussed.

Adolescent↗
PubMed1993

Cardiac performance enhancement from dobutamine in patients refractory to hypervolemic therapy for cerebral vasospasm.

The use of the beta-agonist dobutamine in combination with hypervolemic preload enhancement of cardiac performance was analyzed in 23 patients who failed to respond to traditional preload enhancement following aneurysmal subarachnoid hemorrhage. The patients ranged in age from 13 to 82 years, and three had a history of cardiac disease. Each patient underwent placement of a flow-directed balloon-tipped catheter and the following measurements were obtained during hyperdynamic therapy: pulmonary artery wedge pressure, central venous pressure, cardiac index, stroke volume index, total peripheral resistance, and left ventricular stroke work index (LVSWI). Mean baseline cardiac function was found to be within normal limits (LVSWI = 47.6 +/- 4.2 gm/min/sq m and cardiac index = 3.30 +/- 0.22 liter/min/sq m). After baseline measurements were recorded, 5% albumin was infused at 300 cc/hr and dobutamine was initiated at a rate of 5 to 10 micrograms/kg/hr. This hyperdynamic therapy with dobutamine in the presence of volume loading resulted in a 52% increase in cardiac index, a 15% increase in LVSWI, and a 21% decrease in total peripheral resistance. The clinical reversal of ischemic symptoms due to subarachnoid hemorrhage was evident in 18 (78%) of the 23 patients.

Adolescent↗