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Biomedical subjects

L I Malis

Publications and source records attributed to L I Malis.

At least 19 recordsLinked to original sources
PubMed1991

Brain-stem auditory evoked responses in 56 patients with acoustic neurinoma.

The brain-stem auditory evoked responses (BAER's) recorded from 56 patients with acoustic neurinomas were analyzed. Ten of the patients had intracanalicular tumors and 46 had extracanalicular tumors. It was possible to obtain BAER's following stimulation of the affected side in 28 patients and after stimulation of the unaffected side in all 56. Five patients (11%) had normal BAER's following stimulation of both sides; three of these patients had intracanalicular tumors. Among BAER's obtained following stimulation of the affected ear, the mean interpeak latency (IPL) for peaks I to III associated with extracanalicular tumors was significantly prolonged relative to controls (p less than 0.001), and linear regression analysis revealed a significant positive correlation between tumor size and IPL of peaks I to III (p less than 0.05). Analysis of the 56 BAER's recorded after stimulation of the unaffected side revealed a significant positive correlation between the IPL's of peaks III to V and tumor size (p less than 0.001). This correlation was not strengthened when accounting for the degree of brain-stem compression. Finally, evidence of preserved function within the auditory pathway, even in the presence of partial hearing loss, is presented. This finding suggests that more patients might benefit from surgical procedures that spare the eighth cranial nerve.

Cranial Nerve Neoplasms↗
PubMed1991

Lumbar stenosis.

Lumbar stenosis continues to be inadequately appreciated as a major cause of sciatica, neurogenic claudication, and cauda equina syndrome. Review of the nineteenth-century medical literature reveals articles on narrow canal syndrome in achondroplastic dwarfs; connection to the clinical presentation of developmental spinal stenosis awaited the middle decades of the twentieth century. Appropriate neurosurgical intervention has evolved with a better understanding of the pathophysiologic changes that take place with this disorder and the introduction of myelography, computerized tomography, and magnetic resonance imaging.

Humans↗
PubMed1989

Titanium mesh and acrylic cranioplasty.

Since June 1985 100 cranioplasties have been carried out using titanium mesh and acrylic. There have been no complications and no infections. Titanium mesh is virtually radiolucent. Titanium is nonmagnetic and is the most biocompatible metal known.

Acrylic Resins↗
PubMed1989

Systemic biodistribution of radioiodinated interleukin-2 in the rat.

Interleukin-2 (IL-2) is a lymphokine capable of modulating a variety of immune functions. In vitro and in vivo studies have shown promising cytotoxic potential. Despite numerous ongoing clinical trials, however, little is known about the biodistribution of this lymphokine after in vivo administration. In this study using a rat model, the fate of radioiodinated human recombinant IL-2 (RIL-2) was analyzed by camera imaging, autoradiography, and well counting experiments. Camera imaging demonstrated the liver and kidney to be the organs of greatest radioactivity accumulation with peak liver uptake noted at approximately 10 min from onset of infusion, and peak kidney uptake at approximately 20 min. Autoradiographic assessment of selected organs (kidney, adrenal, liver, lung, and brain) revealed marked heterogeneity of uptake in the kidney and adrenal gland with preponderance of RIL-2 in the cortex of these organs. A more homogeneous distribution of RIL-2 uptake was noted in liver, lung, and brain parenchyma. Well counting confirmed the liver and kidney as the organs of greatest RIL-2 accumulation. Knowledge of the biodistribution of IL-2 may be of benefit both in studying mechanisms of toxicity and in designing novel therapeutic approaches.

Animals↗
PubMed1988

Effects of etoposide-induced blood-brain barrier disruption on brain water, intracranial pressure, and cerebral vasomotor tone.

This study investigated the effects of hypertension and water loading on etoposide-induced, reversible blood-brain barrier disruption in a rat model. Twenty-nine animals were divided into four groups: group 1--intracarotid (i.c.) injection of saline followed in 1 h by 5 ml i.c. water; group 2--i.c. etoposide followed by i.c. water; group 3--i.c. saline followed by i.v. metaraminol to increase systemic blood pressure; group 4--i.c. etoposide followed by i.v. metaraminol. Systemic blood pressure and intracranial pressure were monitored continuously. Evans blue staining of the brain was used as a monitor of blood-brain barrier disruption. Animals were killed 1 h after either aramine or water infusion, and the brains removed and inspected for the degree of disruption. After dehydration, brain water was calculated for each hemisphere. Two-thirds of the animals infused with etoposide had evidence of barrier disruption, whereas none of the control animals infused with saline were disrupted. Neither control groups 1 or 3 showed significant change in intracranial pressure after water loading or augmentation of systemic blood pressure, respectively. Group 4 animals failed to demonstrate any significant change in intracranial pressure despite marked barrier disruption and acute hypertension (within the limits of normal autoregulation). A small but statistically significant increase in intracranial pressure was noted in group 2 animals with the greatest degree of barrier disruption. A significant increase in brain water was observed ipsilateral to etoposide infusion in only those animals with the most marked barrier disruption. These results indicate that etoposide-induced blood-brain barrier disruption caused significant increases in brain water without significant alteration of cerebral vasomotor tone or increases in intracranial pressure after water loading except in the most severe disruption. The classic untoward consequences of vasogenic edema were not encountered in the present model.

Animals↗
PubMed1988

Noncortical origins of the spinal motor evoked potential in rats.

Motor evoked potentials (MEPs) were recorded from the spinal cord, sciatic nerve, or both during transcortical electrical stimulation in the rat. Four peaks could be consistently identified in the spinal MEP. The latency and amplitude of the peaks varied differentially with intensity and polarity of stimulation. Conduction velocity for Peak 1 of the MEP was 43 m/sec. Bilateral sciatic nerve MEPs were present after unilateral cortical stimulation. The spinal MEP was elicited by stimulation of areas outside the motor cortex, and the response persisted during subcortical stimulation and after motor cortex ablation. We present evidence suggesting that components of the spinal MEP in rats arise from pathways outside the motor cortex.

Action Potentials↗
PubMed1986

The protective effect of experimental subarachnoid haemorrhage on sodium dehydrocholate-induced blood-brain barrier disruption.

The potential interactive effects between subarachnoid hemorrhage (SAH) and blood brain barrier (BBB) disruption were studied in a rat model. Experimental subarachnoid hemorrhage was produced in twenty rats (experimental group) by the intracisternal injection of blood. In ten additional rats (control group), saline was administered in place of blood. Analysis of mean blood pressure (MBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) demonstrated an increase in ICP and MBP and a drop in CPP in all animals following intracisternal injection. Subsequent infusion of the left internal carotid artery with sodium dehydrocholate resulted in blood-brain barrier (BBB) disruption in both groups as evidenced by Evans blue staining of the infused cortex. The extent of BBB disruption was significantly greater in the control group than the experimental group. Analysis of the experimental group demonstrated that animals with the lowest pre-SAH MBP and the lowest CPP during the maximum blood pressure response to SAH demonstrated the greatest resistance to experimental BBB disruption. The possibility of ischemia as a contributing factor in BBB protection subsequent to SAH is discussed.

Animals↗
PubMed1986

Ruptured intracranial aneurysms as a cause of subdural haematoma. Potential diagnostic pitfalls and the surgical management of the acute patient.

Seven cases of aneurysms that ruptured into the subdural space and were treated surgically are reviewed. Six out of the seven presented with signs of uncal herniation, three of them for at least for four hours or more. They all died in spite of urgent decompression and drainage. Three others suffered from uncal herniation for less than four hours and they all did well. The seventh patient had a small subdural haematoma with no signs of compression of the underlying neural structures. This last patient also had a good outcome. The authors point out that the aneurysm causing the haematoma might be overlooked should one utilize CT (computerized tomography) scan alone without contrast. However, in most instances the history gives the aneurysm diagnosis despite the CT scan of haematoma only. Intravenous contrast CT scan may occasionally demonstrate the aneurysm, provided modern CT equipment is adequately utilised. Severe neurological deficit and uncal herniation might still be reversible provided decompression can be carried out in less than four hours. If accessible the aneurysm should also be clipped at the same time.

Adult↗
PubMed1986

Physiological and electrophysiological consequences of etoposide-induced blood-brain barrier disruption.

The present study investigates the effects of etoposide-induced blood-brain barrier (BBB) disruption on systemic blood pressure (SBP), intracranial pressure (ICP), and electroencephalographic (EEG) activity. A total of 29 rats were divided into two groups. In Group 1, 8 control animals received intracarotid normal saline; in Group 2, 21 animals received intracarotid etoposide. SBP, ICP, and EEG were monitored continuously under general anesthesia and controlled ventilation after tracheostomy. Intravenous Evans blue dye was used for determination of BBB disruption. Although none of the Group 1 animals showed BBB disruption, 57% of the animals in Group 2 showed marked BBB disruption (3+). A slight but statistically significant increase in ICP was noted in the Group 2 animals with 3+ BBB disruption, although lesser degrees of barrier disruption (1+ or 2+) resulted in no significant alteration in ICP. The amplitude and frequency of the EEG decreased significantly ipsilateral to the side of intracarotid infusion in all animals with 3+ barrier disruption with a tendency to return toward normal within 2 hours. The degree of transient EEG change observed correlates well with the degree of barrier disruption, potentially allowing clinical determination of BBB disruption by this method.

Animals↗
PubMed1986

Neurological deterioration after lumbar puncture below complete spinal subarachnoid block.

The risk of neurological deterioration after removal of cerebrospinal fluid below the level of a complete spinal subarachnoid block is generally accepted. The actual incidence of deterioration after lumbar puncture in the presence of a complete block remains unknown. The present retrospective case analysis includes a review of 100 patients found to have complete block on myelography: 50 cases with a lumbar puncture and 50 cases with a C1-2 puncture. Each group consisted of a similar age range, neurological status prior to myelography, level of block, and nature of disease. Seven patients (14%) had significant neurological deterioration after lumbar puncture, while no deterioration was seen after a C1-2 puncture. A summary of those cases in which deterioration followed lumbar puncture is presented and the possible pathophysiology is discussed. From this analysis, the estimated risk of downward spinal coning after lumbar puncture below a complete spinal subarachnoid block caused by a mass lesion is at least 14%.

Abscess↗
PubMed1986

Etoposide induced blood-brain barrier disruption in rats: duration of opening and histological sequelae.

The intracarotid infusion of the antineoplastic compound etoposide enhances blood-brain barrier (BBB) permeability. In a rat model system, the functional reversibility and anatomic sequelae of etoposide induced BBB disruption were investigated. Etoposide, in a dose range from 3.0 to 22.5 mg/kg, was infused into the left internal carotid artery of Sprague-Dawley rats. BBB disruption was evaluated by the appearance in the infused hemisphere of systemically administered Evans blue dye and quantitatively by the ratio of counts of the technetium labeled chelate of diethylenetriaminepentaacetic acid in the infused to the noninfused hemisphere. Functional reversibility of altered BBB permeability was investigated at three dose levels of etoposide (3.0, 15.0, and 22.5 mg/kg) by the administration of Evans blue dye at the time of etoposide infusion and the administration of the technetium labeled chelate of diethylenetriamine-pentaacetic acid at varying time intervals after etoposide infusion. Fourteen groups of 12 rats each were studied to define the time course of altered BBB permeability at these three doses. The anatomic sequelae of etoposide induced BBB disruption were investigated at varying time intervals (up to 3 weeks) after intracarotid etoposide infusion. Nineteen rats were examined after sacrifice by intracardiac fixation perfusion with 10% formalin. Each brain was sectioned coronally and examined under light microscopy after hematoxylin and eosin staining. Evidence of BBB disruption was seen at all dose levels of etoposide. The degree of BBB disruption increased with increasing doses of etoposide. The duration of altered BBB permeability increased from less than 1 day at 3.0 mg/kg to between 3 and 4 days at 22.5 mg/kg. Histological studies revealed no evidence of parenchymal damage, although at 4 days postdisruption, a mild perivascular lymphocytic infiltration was noted in the infused hemisphere. Etoposide infusion and subsequent BBB disruption were well tolerated by all test animals. In a rat model system the intracarotid infusion of etoposide is capable of producing prolonged reversible BBB disruption.

Animals↗
PubMed1985

Electroencephalographic consequences of sodium dehydrocholate-induced blood-brain barrier disruption: Part 1. Acute and chronic effects of intracarotid sodium dehydrocholate.

Prior work has shown that the intracarotid infusion of sodium dehydrocholate can produce prolonged reversible blood-brain barrier (BBB) disruption. Associated with barrier disruption is the occasional presence of behavioral seizure activity. Electroencephalographic changes were monitored in 32 rats after BBB disruption by the left internal carotid artery infusion of sodium dehydrocholate. The electroencephalogram (EEG) was monitored for 3 hours after disruption in 20 animals, and the remaining 12 animals were followed for 24 hours. The EEG was also monitored in 8 additional control animals: 4 had undergone carotid artery infusion with normal saline, and 4 had received sodium dehydrocholate intravenously. The 20 rats monitored for up to 3 hours postinfusion were found to have varying grades of BBB disruption as measured by the presence of Evans blue staining of the brain. EEG alterations in this group included decreased amplitude and slowing as well as the presence of spike activity over the disrupted and the nondisrupted hemispheres. The more extensive the disruption, the more severe the EEG changes. In animals with minimal to moderate disruption, the EEG usually returned to base line levels within 3 hours after infusion. Animals with marked disruption usually had bilaterally flat EEGs before the end of the observation period. The remaining 12 animals were followed for 24 hours postinfusion. Of 9 animals surviving 24 hours, 1 animal had a decrease in amplitude over the disrupted hemisphere; in the remaining 8 animals, the spontaneous EEG was unchanged from predisruption levels except for occasional spikes in 2 animals. Animals infused with intracarotid saline or intravenous sodium dehydrocholate demonstrated no EEG changes or Evans blue staining.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Electroencephalographic consequences of sodium dehydrocholate-induced blood-brain barrier disruption: Part 2. Generation and propagation of spike activity after the topical application of sodium dehydrocholate.

Sodium dehydrocholate was applied topically to the right hemispheric cortex of eight rats and the electrocorticogram was monitored from both the treated cortex and the homotopic cortex of the contralateral hemisphere. All animals developed blood-brain barrier (BBB) disruption in the treated cortex as evidenced by cortical staining with systemically administered Evans blue dye. Spike activity developed in three of eight animals after the topical application of dehydrocholate. The subsequent intravenous injection of sodium dehydrocholate provoked spike activity in both hemispheres in all eight animals. Dependent and independent spike activity was recorded in the nondisrupted hemisphere. The intravenous administration of gamma-aminobutyric acid (GABA) resulted in alterations in spike activity in four of five animals because of penetration of the GABA through the altered BBB. These findings demonstrate that sodium dehydrocholate can result in increased BBB permeability when applied directly to the cortical surface. Spike activity subsequent to the topical application of dehydrocholate can be enhanced by systemic loading with dehydrocholate. Spike activity occurring over the nontreated cortex (secondary focus) represents interhemispheric propagation of spike activity from the disrupted hemisphere (primary focus). The lack of Evans blue staining in the actively discharging secondary focus suggests that spike activity does not account for the increases in BBB permeability observed with dehydrocholate treatment.

Administration, Topical↗
PubMed1985

Changes in contralateral brain-stem auditory evoked responses to cerebellopontine angle compression in rats.

Eleven rats were subjected to graded compression of the brain stem at the cerebellopontine angle (CPA) following craniectomy and cerebellectomy. Clicks were delivered to the ear contralateral to the compression site, and brain-stem auditory evoked responses (BAER's) were collected before and during compression. With increasing compression, there was an increase in the latency and a decrease in the amplitude of the peaks of the BAER. The later peaks of the BAER (V and VI) demonstrated changes with minimal compression that progressed as compression increased, while changes in the amplitude and latency of the earlier peaks (II, III, and IV) occurred at the higher grades of compression. Following decompression of the brain stem, there was a decrease in the latencies of most of the BAER peaks. Peak amplitude remained depressed following brain-stem decompression. These experimental findings corroborate clinical reports of abnormal BAER's elicited from stimulation of the ear contralateral to a CPA tumor. The relative sensitivity of the later peaks of the BAER to even minimal brain-stem compression explains the prolonged III to V interpeak latency reported in the literature in patients with brain-stem compression from a CPA lesion. The possible mechanisms for the BAER changes that were observed contralateral to compression are discussed.

Animals↗