Carotid endarterectomy for internal carotid artery stenosis associated with persistent primitive hypoglossal artery: efficacy of intraoperative multi-modality monitoring.

INTRODUCTION: A persistent primitive hypoglossal artery (PPHA) is a rare vascular anomaly and is usually asymptomatic. However, the PPHA may cause multi-territorial infarction when complicated by internal carotid artery (ICA) stenosis. CASE REPORT: We describe a 73-year-old male who simultaneously developed cerebral infarction in both carotid and vertebrobasilar territories due to ICA stenosis associated with an ipsilateral PPHA. The PPHA mainly provided blood flow to the vertebrobasilar territory in this case, because the bilateral vertebral arteries were markedly hypoplastic. He underwent carotid endarterectomy under internal shunting. Intraoperative multi-modality monitoring including angiography, motor evoked potential, and near infrared spectroscopy was very useful to avoid ischemic complications during surgery. The postoperative course was uneventful. CONCLUSION: It should be reminded that a persistent carotid-basilar anastomosis can cause multi-territorial cerebral infarction mimicking cardiogenic embolism and may be a candidate for aggressive prophylactic intervention, when occlusive lesions develop in the carotid artery. It is very important to monitor hemodynamic and/or electrophysiological status in both carotid and vertebrobasilar territories in order to perform carotid endarterectomy safely in such cases.

Blood-brain barrier glucose transporter: effects of hypo- and hyperglycemia revisited.

The transport of glucose across the blood-brain barrier (BBB) is mediated by the high molecular mass (55-kDa) isoform of the GLUT1 glucose transporter protein. In this study we have utilized the tritiated, impermeant photolabel 2-N-[4-(1 -azi-2,2,2-trifluoroethyl)[2-3H]propyl]-1,3-bis(D-mannose-4-ylo xy)-2-propylamine to develop a technique to specifically measure the concentration of GLUT1 glucose transporters on the luminal surface of the endothelial cells of the BBB. We have combined this methodology with measurements of BBB glucose transport and immunoblot analysis of isolated brain microvessels for labeled luminal GLUT1 and total GLUT1 to reevaluate the effects of chronic hypoglycemia and diabetic hyperglycemia on transendothelial glucose transport in the rat. Hypoglycemia was induced with continuous-release insulin pellets (6 U/day) for a 12- to 14-day duration; diabetes was induced by streptozotocin (65 mg/kg i.p.) for a 14- to 21-day duration. Hypoglycemia resulted in 25-45% increases in regional BBB permeability-surface area (PA) values for D-[14C]glucose uptake, when measured at identical glucose concentration using the in situ brain perfusion technique. Similarly, there was a 23+/-4% increase in total GLUT1/mg of microvessel protein and a 52+/-13% increase in luminal GLUT1 in hypoglycemic animals, suggesting that both increased GLUT1 synthesis and a redistribution to favor luminal transporters account for the enhanced uptake. A corresponding (twofold) increase in cortical GLUT1 mRNA was observed by in situ hybridization. In contrast, no significant changes were observed in regional brain glucose uptake PA, total microvessel 55-kDa GLUT1, or luminal GLUT1 concentrations in hyperglycemic rats. There was, however, a 30-40% increase in total cortical GLUT1 mRNA expression, with a 96% increase in the microvessels. Neither condition altered the levels of GLUT3 mRNA or protein expression. These results show that hypoglycemia, but not hyperglycemia, alters glucose transport activity at the BBB and that these changes in transport activity result from both an overall increase in total BBB GLUT1 and an increased transporter concentration at the luminal surface.

Facilitated brain uptake of 4-chlorokynurenine and conversion to 7-chlorokynurenic acid.

7-Chlorokynurenic acid (7-Cl-KYNA) and 5,7-dichlorokynurenic acid (5,7-Cl2-KYNA) are of therapeutic interest as potent glycine/N-methyl-D-aspartate NMDA) receptor antagonists, but are excluded from brain by the blood-brain barrier. We examined whether these compounds could be delivered to brain through their respective precursors, L-4-chlorokynurenine (4-Cl-KYN) and L-4,6-dichlorokynurenine (4,6-Cl2-KYN), which are amino acids. 4-Cl-KYN was shown to be rapidly shuttled into the brain by the large neutral amino acid transporter of the blood-brain barrier (K(m) = 105 +/- 14 microM, Vmax = 16.9 +/- 2.3 nmol min-1 g-1) and to be converted intracerebrally to 7-Cl-KYNA. 4,6-Cl2-KYN also expressed affinity for the transporter, but four-fold less than that of 4-Cl-KYN. In summary, the results show that because of their facilitated uptake 4-Cl-KYN and 4,6-Cl2KYN might be useful prodrugs for brain delivery of glycine-NMDA receptor antagonists.

Surgical approaches for treatment of ischaemic cerebral stroke other than moyamoya disease in children.

Ischaemic cerebral strokes in children are relatively uncommon. With the exception of patients with moyamoya disease, there is no effective treatment for these lesions. One potential approach is encephalo-duro-arterio-synangiosis (EDAS). This is a safe neurosurgical procedure that promotes spontaneous transdural anastomosis that may provide additional blood flow to ischaemic regions. We present eight children with ischaemic strokes other than moyamoya disease, and discuss surgical attempts to treat this entity. The mean age of the eight children was 3.6 years (range: 13 months to 9 years). All children presented with acute childhood hemiplegia. Ischaemic stroke had occurred in association with a head injury in three children, but without an apparent cause in five. Five children underwent stable xenon-enhanced computed tomography to evaluate cerebral blood flow and all but one patient underwent EDAS. One child with no angiographic abnormalities recovered to a normal neurological state without surgery. Following surgery, another child also fully recovered, and the remaining six children recovered with only a slight hemiparesis. Revascularization was observed on a follow-up angiogram in three children. Our surgical experiences suggest that revascularization is influenced by haemodynamic demand and recanalization of the occluded artery. We favour the use of indirect anastomosis (EDAS) for selected patients and suggest that chronic ischaemia probably contributes to surgical success.

Alterations in plasma concentrations of natriuretic peptides and antidiuretic hormone after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Hyponatremia is a common complication after subarachnoid hemorrhage. In this study we investigated the relations among hyponatremia, plasma natriuretic peptides, and antidiuretic hormone concentrations after subarachnoid hemorrhage. METHODS: Blood samples for radioimmunoassay measurement of plasma brain natriuretic peptide-like immunoreactivity, atrial natriuretic peptide-like immunoreactivity, and antidiuretic hormone were obtained every 2 to 4 days until day 14 after subarachnoid hemorrhage. RESULTS: Eleven of 20 patients with verified subarachnoid hemorrhage demonstrated mild hyponatremia (126 mEq/L < serum sodium < 135 mEq/L) during their clinical course. Atrial natriuretic peptide and antidiuretic hormone concentrations were significantly elevated on days 0 to 2 after onset of subarachnoid hemorrhage. Atrial natriuretic peptide concentrations remained high in patients who developed mild hyponatremia on days 6 to 14 after onset of subarachnoid hemorrhage. In contrast, antidiuretic hormone concentrations became significantly lower during the second week in these patients. CONCLUSIONS: Mild hyponatremia after subarachnoid hemorrhage may be attributable not to the syndrome of inappropriate secretion of antidiuretic hormone but to cerebral salt-wasting syndrome. Atrial natriuretic peptide may be a causal natriuretic factor in cerebral salt-wasting syndrome.

Mortality experience of cockpit crewmembers from Japan Airlines.

The purpose of this study was to evaluate the long-term mortality and causes of death among cockpit crewmembers. A total of 2,327 cockpit crewmembers registered at Japan Airlines between August 1, 1952, and December 31, 1988, were traced to assess mortality. Medical records were also reviewed. The mortality rates for the cockpit crewmembers were compared to those for the general Japanese population using standardized mortality ratios (SMR's). As of December 31, 1988, 59 (2.5%) of 2,327 individuals were deceased, and the leading causes of death were accidents, malignant neoplasms, and cardiovascular diseases. The overall mortality rate for the cockpit crew was significantly lower than the national standard (SMR = 0.66, p < 0.001; 95% C.I. 0.50-0.85). However, marked differences were found in cause-specific mortality, where mortality due to accidents was significantly increased (SMR = 2.43, p < 0.001; 95% C.I. 1.63-3.50), while deaths from cancer were similar, and those for cerebral vascular accidents (CVA) and coronary artery disease (CAD) were lower than comparable rates for the general population. We conclude that cockpit crewmembers had a better total mortality experience compared to the general Japanese population, except for deaths due to accidents.

Time course and clinical significance of marked left axis deviation in airline pilots.

The purpose of this study was to examine the time course and evaluate the clinical significance of marked left axis deviation (LAD) in airline pilots. The study group consisted of 30 Japan Airlines' pilots with marked LAD, identified from a group of 1,700 who are now 35 years of age or older. The mean age at examination was 48.5 +/- 5.7 years [corrected] and the mean observation period was 22.6 +/- 5.6 years [corrected]. The prevalence rate of marked LAD was 1.8%. In 20%, the axis remained unchanged, and in 70%, LAD progressed either gradually or suddenly. All subjects were examined by exercise testing and 26 had echocardiograms. Two pilots (6.7%) were found to have organic heart disease (hypertension), which was much lower than the rate reported previously. In these individuals, the onset of marked LAD was noted more than 10 years before hypertension was detected. No progression to complete left bundle branch block, nor any form of AV block, was observed among these subjects. No cardiac events or death occurred during the study period.

Recovery of circadian rhythm of plasma cortisol levels after a 3-day trip between Tokyo and San Francisco.

The objective of the present study is to investigate the change in the circadian rhythm of plasma cortisol levels following a 3-d trip and a westbound return flight from San Francisco (SFO) to Tokyo. Six healthy male students volunteered for the project. Plasma cortisol levels were monitored 4 times daily for 13 d during the experimental period. In Tokyo, the baseline pattern of cortisol concentrations showed the classical diurnal profile. During the 50-h stay in SFO, phase advancement of 8 h was observed for the initial 32 h. This was followed by a disturbance in the profile for the remaining 18-h period. After returning to Tokyo, the subjects exhibited the original diurnal pattern beginning Day 1. However, complete resynchronization was not apparent until Day 4 after the return.

The influence of transmeridian flight on human circulating lymphocytes.

We studied the influence of transmeridian flight on the number of circulating lymphocytes, which have a circadian rhythm with low values in the daytime. The number of T lymphocytes was found to be higher than the baseline value, yet its rhythmicity was maintained after eastward flight with an 8-h time difference. The number of OKB2+ as well as Leu11+ cells were suppressed after the flight. The change in the number of T lymphocytes occurred due to the increased number of OKT4+ lymphocytes. There was no correlation between the number of OKT4+ lymphocytes and the plasma cortisol level, though plasma cortisol is a major factor in regulating the number of lymphocytes. These data showed that the number of helper/inducer T lymphocytes, B cells, and natural killer cells were affected by the physical conditions experienced after the flight. The changes in T lymphocytes were independent of those of plasma cortisol levels.

Pilots with non-insulin-dependent diabetes mellitus can self-monitor their blood glucose.

The study aims to clarify the efficacy of self-monitoring of blood glucose as a tool for diabetic management in seven airline pilots with non-insulin-dependent diabetes mellitus. All were controlled with diet alone and were encouraged to measure fasting blood glucose at least three times weekly and occasional postprandial determinations for 6 months. HbAlc levels were measured every other month. After starting self-monitoring, fasting blood glucose level significantly declined from 126 +/- 18 mg.dl-1 to 109 +/- 13 mg.dl-1. HbAlc and serum lipids concentrations were also improved. The motivation of the subjects in adhering to strict diet therapy which led to the better control of diabetes was remarkable, and resulted in a lower rate of temporary disqualification from flying (17.6% vs. 7.7%). We conclude that self-monitoring of blood glucose is highly effective and should be recommended to airline pilots with non-insulin dependent diabetes mellitus for diabetes management.