Occupational exposure to organic solvents and long-term nervous system damage detectable by brain imaging, neurophysiology or histopathology.

The purpose of the present review is to assess the evidence published in scientific literature that industrial organic solvents as a generic group have the ability to induce long-term nervous system damage in workers that can be detected by techniques other than neuropsychological testing. The main body of evidence considered in this review was 40 studies involving the use of brain imaging, neurophysiological testing, gross autopsy or histopathology in groups of workers with long-term solvent exposure. Case reports involving both solvent abuse and occupational exposure, and experimental animal data have also been reviewed as supporting data. A number of the studies in groups of workers provide evidence of the presence of marginal atrophic abnormalities in the brain or deficits in nerve conduction velocity in solvent-exposed workers. However, there are limitations in the design of many of these studies, the strength of association between exposure and effect is not consistently strong, no dose-response relationship can be detected, the reported changes lack specificity and there is no coherence between the human and experimental animal data. Overall, it is not possible to draw reliable conclusions with respect to the presence or absence of nervous system damage related to the common properties of organic solvents.

A national survey of attitudes towards the use of MRI in patients known to have intracranial aneurysm clips.

The objective of this study was to determine the attitudes and practice of neuroradiology centres across the UK regarding the use of MRI in patients known to have intracranial aneurysm clips. A postal survey comprising three questions and a comments section was sent to 35 neuroradiology centres across the UK. There were 32 (91%) respondents to the single questionnaire. 16 (50%) respondents said that they would not consider performing MRI on a patient with an intracranial aneurysm clip. Of the remaining 50%, all said that identification of the clip type and assurance of its safety would be needed prior to scanning the patient. The magnetic strength of the system did not appear to affect the decision regarding whether or not to perform MRI on such patients. There was a variation in attitude towards the use of MRI in such patients between different regions. Neuroradiology centres are equally divided in their attitude and practice about whether it is safe to use MR to image a patient known to have an intracranial aneurysm clip. This is most probably due to the conflicting literature, as well as uncertainty about the identification and ferromagnetic properties of individual clips.

Carotico-cavernous fistula following septorhinoplasty.

Septorhinoplasty is a very common operation in otolaryngological practice. We report the second case of a carotico-cavernous fistula following septorhinoplasty. This case presented with very severe epistaxis before the appearance of the typical pulsating exophthalmos, ophthalmoplegia, headache and engorged veins on the right side of the face. Our case was treated by endovascular thrombosis with electrolytically detachable coils.

Variability in measurement of extracranial internal carotid artery stenosis as displayed by both digital subtraction and magnetic resonance angiography: an assessment of three caliper techniques and visual impression of stenosis.

BACKGROUND AND PURPOSE: The degree of stenosis in the extracranial internal carotid artery helps predict the risk of an individual suffering subsequent cerebrovascular ischemic events. Different techniques have evolved to measure stenosis from angiograms, leading to some confusion and a call for the adoption of a single technique. To help choose the most reliable technique, this study assessed observer variability in reporting carotid stenosis for four different techniques, from both digital subtraction (DSA) and MR angiograms (MRA). Three of the techniques used caliper measurements; the fourth was the visual impression of stenosis. METHODS: From a total of 137 angiograms, caliper measurements were possible on 105 DSAs and 74 MRAs. Measurements from these angiograms were made by two independent observers on two separate occasions to assess interobserver and intraobserver variation in reporting. RESULTS: For DSA, the variability in reporting and the number of clinically significant differences arising as a result were similar for each of the four techniques. While the typical measurement errors for each of the techniques studied were on the order of +/- 5%, each technique produced some sizable individual differences for the same angiogram, with resultant wide 95% limits of agreement. Observer variability for reporting MRA was generally a little greater than for DSA. Compared with the caliper techniques, the visual impression of stenosis technique performed well, particularly for MRA. CONCLUSIONS: Although observer variability in reporting can be considerable, no important differences were found among the different techniques widely used for measuring carotid stenosis.

Demonstration of neurovascular compression in trigeminal neuralgia with magnetic resonance imaging. Comparison with surgical findings in 52 consecutive operative cases.

Until recently, the inability to demonstrate neurovascular compression of the trigeminal nerve preoperatively resulted in surgery being offered only in cases of severe trigeminal neuralgia (TGN), frequently after a prolonged trial of medical treatment and following less invasive procedures, despite the fact that posterior fossa microvascular decompression gives long-term pain relief in 80% to 90% of cases. To assess whether vascular compression of the nerve could be demonstrated preoperatively, high definition magnetic resonance tomographic angiography (MRTA) was performed in 50 consecutive patients, five of whom had bilateral TGN, prior to posterior fossa surgery. The imaging results were compared with the operative findings in all patients, including two patients who underwent bilateral exploration. Vascular compression of the trigeminal nerve was identified in 42 of 45 patients with unilateral symptoms and on both sides in four patients with bilateral TGN. In the last patient with bilateral TGN, neurovascular compression was identified on one side, and on the other side the compressing superior cerebellar artery was separated from the nerve by a sponge placed during previous surgery. There was full agreement regarding the presence or absence of neurovascular compression demonstrated by MRTA in 50 of 52 explorations, but MRTA misclassified four vessels compressing the trigeminal nerve as arteries rather than veins. In two cases, there was disagreement between the surgical and MRTA findings. In the first of these cases, surgery revealed distortion of the nerve at the pons by a vein that MRTA had predicted to lie 6 mm remote from this point. In the second patient, venous compression was missed; however, this patient was investigated early in the series and did not have gadolinium-enhanced imaging. In nine cases, MRTA correctly identified neurovascular compression of the trigeminal nerve by two arteries. Moreover, MRTA successfully guided surgical reexploration in one patient in whom a compressing vessel was missed during earlier surgery and also prompted exploration of the posterior fossa in two patients with multiple sclerosis and one patient with Charcot-Marie-Tooth syndrome, in whom neurovascular compression was identified preoperatively. It is concluded that MRTA is an extremely sensitive and specific method for demonstrating vascular compression in TGN. As a result, open surgical procedures can be recommended with confidence, and microvascular decompression is now the treatment of choice for TGN at the authors' unit. They propose MRTA as the definitive investigation in such patients in whom surgery is contemplated.

Traumatic aneurysm of the maxillary artery: the role of interventional radiology. A report of two cases.

Two cases of post-traumatic aneurysm of the maxillary artery are described. The first patient was a 20-year-old man who sustained a Le Fort III type fracture in a road traffic accident. He experienced two episodes of significant maxillofacial haemorrhage, the first following admission and the second 5 days after initial reduction and fixation of his midfacial fractures. The second patient was a 23-year-old man with a bilateral cleft palate and extreme midfacial hypoplasia who underwent Le Fort I osteotomy. Significant bleeding commenced 3 h postoperatively and was not completely controlled by anterior and posterior nasal packing. Both the aneurysms were diagnosed on selective carotid angiography and successfully treated by embolization.

Changes in muscle mechanics during chronic conditioning for cardiomyoplasty.

Chronic repetitive stimulation of skeletal muscle causes significant changes in contractile mechanics and makes the muscle fatigue resistant. The purpose of this study was to quantify the magnitude and time course of these changes. One latissimus dorsi muscle from each of 28 mongrel dogs was stimulated in situ at 1 Hz for 0, 3, 7, 14, 21, 42, or 70 days. Changes in isometric and isotonic mechanical performance were measured as a function of conditioning time. Isotonic force and velocity data were fitted to the Hill equation to obtain Vmax. The most striking early change was a 30 and 26% decline in muscle mass and cross-sectional area, respectively. Coincident with this was an approximate 40% decline in tetanic and twitch tension. There was a similar decline in the rates of rise and fall of twitch and tetanus tensions (+dT/dt and -dT/dt). The decline in tetanus +dT/dt and -dT/dt followed a similar time course, suggesting that these muscle functions were under similar influences. Calculation of the isometric force data per unit of cross-sectional area minimized the effect of stimulation on isometrically measured muscle function but did not eliminate it. Fusion frequency declined 52% with conditioning. The increases in time-to-peak twitch tension and half-relaxation time were independent of cross-sectional area. Time-to-peak twitch tension and half-relaxation time increased after 7 days of stimulation and became maximal after 42 or 70 days, respectively. Time-to-peak tetanus tension was unchanged by muscle conditioning. Changes in the force-velocity relationship began after 3 days of stimulation, changed very little between 3 and 21 days of stimulation, and showed another change after 42 and 70 days of stimulation. It may be possible to better modify the muscle for dynamic cardiomyoplasty by pharmacological or stimulation regimens once the mechanism of fiber switching is better understood.

Transcriptional regulation of phospholamban gene and translational regulation of SERCA2 gene produces coordinate expression of these two sarcoplasmic reticulum proteins during skeletal muscle phenotype switching.

Chronic 1 Hz stimulation of the canine latissimus dorsi muscle produced a time-dependent switch from the fast-twitch to the slow-twitch phenotype. This included changes in the proteins of the sarcoplasmic reticulum. After 3 days of muscle stimulation, there was down-regulation of fast-twitch Ca-ATPase (SERCA1a) mRNA and induction of slow-twitch Ca-ATPase (SERCA2a) mRNA; most changes in both mRNAs were nearly complete after 14 days of stimulation. Although the induction of phospholamban mRNA began after 3 days of muscle stimulation, its up-regulation was not completed until the muscle had been stimulated for 42 days. The time course of expression of SERCA2a protein was very different from that of SERCA2a mRNA, suggesting that SERCA2 gene expression is regulated at the translational as well as the transcriptional level. The time course of expression of phospholamban protein closely followed that of phospholamban mRNA, suggesting that this gene is under transcriptional control. Thus coordinated expression of SERCA2a and phospholamban proteins is achieved via translational control of the SERCA2 gene and transcriptional control of the phospholamban gene.

Vascular contact with the fifth cranial nerve at the pons in patients with trigeminal neuralgia: detection with 3D FISP imaging.

OBJECTIVE: Vascular contact with the trigeminal nerve at the pons is known to cause trigeminal neuralgia; however, this finding also is present in some asymptomatic subjects. We evaluated the usefulness of high-resolution MR imaging and MR angiography of the posterior fossa to determine the presence or absence of vascular contact with the fifth cranial nerve at the pons in patients with trigeminal neuralgia and in control subjects. SUBJECTS AND METHODS: The trigeminal nerves in 40 symptomatic patients and 114 asymptomatic control subjects were examined for the presence or absence of vascular contact at the pons by using three dimension (3D) fast inflow with steady-state precession (FISP) imaging. Imaging parameters were 35/7/15 degrees (TR/TE/flip angle) with a slab thickness of 55 mm and 64 partitions. Contrast-enhanced imaging was done in 10 of 12 patients with normal findings on an unenhanced scan. Axial, coronal, sagittal, and maximum-intensity-projection images were reviewed by two observers who had no knowledge of the clinical details. The findings on MR images were prospectively compared with the surgical findings in 25 patients. RESULTS: On the unenhanced MR images, vascular contact with the trigeminal nerve at the pons was identified in 70% of 40 nerves in patients with trigeminal neuralgia and in a further 15% following injection of contrast medium. Contact between the nerve and two vessels at the pons was seen in 10% of cases, and deformity of the nerve was present in 30% of cases. In the control group, vascular contact with the nerve was identified in 8% of 114 nerves. Contact between the nerve and two vessels or deformity of the nerve was not identified in any control subject. The difference between the two groups was highly significant regarding the presence or absence of vascular contact with the nerve at the pons (p < 0.001, x2 test), distortion of the nerve (p < .001), and contact between the nerve and two vessels (p < .001). The imaging findings were in agreement with the surgical findings regarding the presence or absence of vascular contact with the nerve in all 25 patients who had surgery. Complete or partial pain relief was achieved following microvascular decompression in all patients who had surgery. CONCLUSION: Despite the fact that vascular contact with the trigeminal nerve at the pons is not specific for trigeminal neuralgia, high-definition unenhanced and enhanced 3D FISP imaging and MR angiography at the posterior fossa are useful in determining the presence or absence of vascular contact with or deformity of, the fifth cranial nerve in patients for whom surgery is planned for treatment of trigeminal neuralgia.

Comparison of magnetic resonance angiography, duplex ultrasound, and digital subtraction angiography in assessment of extracranial internal carotid artery stenosis.

The results of a prospective study comparing ultrasound, intra-arterial digital subtraction angiography, and magnetic resonance angiography in the assessment of the degree of extracranial internal carotid artery stenosis are reported in patients with symptoms of recent carotid territory ischaemia. A total of 70 patients and 137 vessels were examined by all three techniques. The results obtained by each technique were reported blind. The mean difference (SD) for the comparison of magnetic resonance angiography and digital subtraction angiography was -0.7 (14)%, for ultrasound and digital subtraction angiography 3.1 (15)%, and for magnetic resonance angiography and ultrasound -3.8 (15)%. The level of agreement was greater for the more tightly stenosed vessels. With the assumption that the results of the digital subtraction angiogram reflect the true situation, the sensitivity and specificity in the detection of > or = 30% stenoses were 93% and 82% with ultrasound and 89% and 82% with magnetic resonance angiography; for stenoses > or = 70% 93% and 92% with ultrasound and 90% and 95% with magnetic resonance angiography; and for stenoses of 70-99% 89% and 93% with ultrasound and 86% and 93% with magnetic resonance angiography. For occlusion the values were 93% and 99% with ultrasound and 80% and 99% with magnetic resonance angiography. Increased sensitivity and specificity were obtained when analysis was confined to those vessels in which ultrasound and magnetic resonance angiography were in agreement over classification. It is thus possible to accurately categorize the degree of stenosis of the extracranial internal carotid artery from a combination of ultrasound and magnetic resonance angiography. The adoption of this combination for the investigation of patients before carotid endarterectomy removes the risk associated with conventional angiography and represents an important advance in the management of carotid stenosis.

Electrophysiologic consequences of hyperkalemic cardioplegia during surgical ischemia.

Myocardial protection strategies use cardioplegic solutions to reduce the injury induced by surgical ischemia and reperfusion. However, there is a high incidence of electrophysiologic abnormalities after cardioplegic arrest. A computerized epicardial mapping system in a porcine cardiopulmonary bypass model was used to measure the electrophysiologic consequences of different myocardial protection techniques. Both warm and cold, crystalloid and blood cardioplegic solutions were compared. The effects of hypothermia and prolonged cardiopulmonary bypass were examined in a control group that underwent a 2-hour period of hypothermia without cardioplegia or aortic cross-clamping, followed by 2 hours of normothermic reperfusion. Isochronous activation maps, unipolar electrograms, ventricular refractory periods, and pacing thresholds were measured before cardioplegic arrest and during reperfusion. Compared with the control group, crystalloid cardioplegia, but not blood cardioplegia, was accompanied by large changes in the pattern of ventricular activation and by persistent (> 2 hours) and significant slowing of the time required for complete ventricular activation. This was not the result of hypoxia. Moreover, the effective refractory period and the pacing threshold were unchanged by any cardioplegia. Our data suggest that crystalloid cardioplegia increases myocardial resistance to current flow leading to a derangement of electrical impulse propagation that may underlie arrhythmogenesis.

Coexistent trigeminal neuralgia, hemifacial spasm, and hypertension: preoperative imaging of neurovascular compression. Case report.

The case is reported of a 60-year-old woman with left-sided trigeminal neuralgia, hemifacial spasm, and hypertension. Compression of the left trigeminal, facial, and vagus nerves by the anterior and posterior inferior cerebellar arteries and a persistent trigeminal artery variant were demonstrated by magnetic resonance angiography using a novel sequence. At operation the angiographic appearances were confirmed, and decompression was performed with the placement of polyvinyl sponge at all three levels. Postoperatively, the patient had complete relief from the trigeminal neuralgia and hemifacial spasm and has sustained normotension without medication.

Electrophysiological consequences of hypothermic hyperkalemic elective cardiac arrest.

While the development of pharmacological cardioplegic solutions for myocardial protection during cardiopulmonary bypass (CPB) have significantly lengthened the safe operating time for cardiac surgical procedures, the introduction of hypothermic hyperkalemic cardioplegia (CPG) has markedly increased the incidence of postoperative arrhythmias and conduction abnormalities. Using a customized modification of a computerized mapping system, we have developed a large animal porcine model of CPB that is exquisitely sensitive to the electrophysiological (EP) derangements imposed by ischemia and cardiac arrest. This model is able to measure spatial and temporal parameters of ventricular activation with high resolution, using an array of up to 84 epicardial electrodes that can be reproducibly placed on the surface of the heart utilizing known epicardial anatomical markers (e.g., coronary arteries). With this system we have measured the spectrum of clinically observed EP disturbances caused by CPG, from slowed intraventricular conduction to complete heart block. Compared to the control group of hypothermia alone, 2 hours of crystalloid CPG arrest had a significant slowing effect on ventricular activation (p < 0.05). CPG was accompanied, in each animal, by profound changes in the spatial distribution of ventricular activation and persistent slowing of ventricular activation. Traditional EP parameters of effective refractory period and pacing threshold were unchanged by CPG. Smaller temporal and spatial changes were observed in the control group, but were always reversed by 90 minutes of warm reperfusion. We conclude that CPG induces injury of the specialized conducting system and, to a lesser degree, the myocardium. This model will afford us the opportunity to test new methods of CPG to further improve myocardial preservation during CPB.

Recurrent autonomous esophageal peristalsis in patients with chest discomfort.

Routine esophageal manometry revealed a novel pattern of esophageal motility, recurrent autonomous peristalsis, in five patients evaluated for chest discomfort and heartburn. In the absence of swallowing, esophageal peristalsis occurred at frequencies of 4-8 peristaltic sequences per minute for periods of 2-8 min. The recurrent peristaltic sequences developed spontaneously during manometry and were associated with the onset of vague chest discomfort in four patients; one patient reported no symptoms during recurrent peristalsis. Duration and propagation velocity of the recurrent peristaltic contractions differed significantly from primary peristalsis in four patients. Recurrent autonomous esophageal peristalsis is an unusual motor pattern that may be associated with vague chest discomfort. The circuit(s) mediating recurrent autonomous peristalsis are unknown.

Responses of feline gastroesophageal junction to changes in abdominal pressure.

The responses of the lower esophageal sphincter (LES), stomach, and diaphragm and their contribution to changes in the high-pressure zone (HPZ) at the gastroesophageal junction were determined during extrinsic abdominal compression or intragastric balloon distension in anesthetized cats. Abdominal compression consistently induced an increase in intraluminal end-expiratory LES and gastric pressure (P less than 0.01). Changes in LES pressure significantly exceeded the changes in gastric pressure (P less than 0.01). In contrast, the LES response during gastric distension was variable in the group of animals despite a consistent volume-dependent increase in gastric pressure. Mean LES pressure for the group was unchanged, although 33% of individual animals exhibited a decrease in LES pressure during gastric distension. Both abdominal stimuli induced sustained inhibition of crural (P less than 0.01), but not costal, diaphragmatic electromyographic activity. Vagotomy affected the LES but not the gastric or diaphragmatic responses to both stimuli. In the group of animals, the combined effect of the changes in the three measured variables on the HPZ resulted in maintenance of the antireflux barrier during abdominal compression but a significant decrease in the barrier during gastric distension.

Low dose low osmolar intravenous urography.

A prospective double blind randomised trial using 25 ml of Hexabrix 320 (ioxaglate, May and Baker), Niopam 370 (iopamidol, Merck) or Omnipaque 350 (iohexol, Nycomed) intravenous urography was carried out. The results showed no perceptible difference in the diagnostic quality of urograms with each of the media. An additional 25 ml of contrast medium was required by 4% of patients in order to obtain a satisfactory examination. We recommend that a dose of 25 ml of low-osmolar medium be used for all patients with the exception of the obese, those taking diuretics or those who have renal impairment.

Simultaneous reflex inhibition of lower esophageal sphincter and crural diaphragm in cats.

We have previously suggested that both the lower esophageal sphincter and diaphragm contribute to the high-pressure zone (HPZ) at the gastroesophageal junction. The purpose of this study in anesthetized cats was to compare changes in diaphragmatic electrical activity with changes in the intraluminal pressure profile in the HPZ following either balloon distension of the esophagus or swallowing evoked by pharyngeal stimulation. Intraluminal pressure was continuously recorded by a perfused manometric assembly anchored to the gastric fundus through an abdominal surgical approach. Integrated EMG was simultaneously measured in the costal and crural parts of the diaphragm. Our results indicate that simultaneous relaxation of the lower esophageal sphincter (LES) and crural diaphragm follows both swallowing and balloon distension of the esophagus; during swallowing both inhibitory reflexes depend on the initiation of esophageal peristalsis; crural relaxation abolishes respiratory-induced pressure oscillations in the HPZ during LES relaxation; ventilation is maintained during relaxation of the HPZ in part by continued contraction of the costal diaphragm; and different neural pathways control LES relaxation and crural relaxation. The data support the view that the crural diaphragm augments the intrinsic smooth muscle sphincter mechanism at the gastroesophageal junction and that crural relaxation may be an important factor in mouth-to-gastric transit.