Variability of pyrethroid concentrations on hard surface kitchen flooring in occupied housing.

Pyrethroids are a class of neurotoxic insecticides, and some studies have used single-time wiping of hard surface flooring to estimate indoor pyrethroid concentrations. Considering that human activities may affect concentrations, knowledge of temporal variability is needed to reduce the uncertainty of exposure estimates that are calculated using wipe sampling of pyrethroids in occupied housing. During weeks one, two, and six of a 6-week study, two wipe samples of hard surface kitchen flooring were collected in each of 50 occupied residences and used to estimate the temporal variability of eight pyrethroids and six pyrethroid degradation products. Beginning 1 month prior to sample collection, the participants kept pesticide use diaries. All pyrethroids were widely distributed among the houses, and co-occurrence of multiple pyrethroids was common structured. Application diaries and detection frequencies appeared unconnected, but the applications were correlated with measurable changes in pyrethroid concentrations. In general, degradation products were detected less frequently and at lower concentrations than their parent pyrethroids. Estimates of the intraclass correlation coefficient (ICC) for individual pyrethroids ranged from 0.55 (bifenthrin) to 0.80 (deltamethrin), and two sampling events at each residence would have been sufficient to estimate the mean concentration of most pyrethroids with an ICC of 0.80.

Kidney injury biomarkers and urinary creatinine variability in nominally healthy adults.

Environmental exposure diagnostics use creatinine concentrations in urine aliquots as the internal standard for dilution normalization of all other excreted metabolites when urinary excretion rate data are not available. This is a reasonable approach for healthy adults as creatinine is a human metabolite that is continually produced in skeletal muscles and presumably excreted in the urine at a stable rate. However, creatinine also serves as a biomarker for glomerular filtration rate (efficiency) of the kidneys, so undiagnosed kidney function impairment could affect this commonly applied dilution calculation. The United States Environmental Protection Agency (US EPA) has recently conducted a study that collected approximately 2600 urine samples from 50 healthy adults, aged 19-50 years old, in North Carolina in 2009-2011. Urinary ancillary data (creatinine concentration, total void volume, elapsed time between voids), and participant demographic data (race, gender, height, and body weight) were collected. A representative subset of 280 urine samples from 29 participants was assayed using a new kidney injury panel (KIP). In this article, we investigated the relationships of KIP biomarkers within and between subjects and also calculated their interactions with measured creatinine levels. The aims of this work were to document the analytical methods (procedures, sensitivity, stability, etc.), provide summary statistics for the KIP biomarkers in "healthy" adults without diagnosed disease (distribution, fold range, central tendency, variance), and to develop an understanding as to how urinary creatinine level varies with respect to the individual KIP proteins. Results show that new instrumentation and data reduction methods have sufficient sensitivity to measure KIP levels in nominally healthy urine samples, that linear regression between creatinine concentration and urinary excretion explains only about 68% of variability, that KIP markers are poorly correlated with creatinine (r(2) ∼ 0.34), and that statistical outliers of KIP markers are not random, but are clustered within certain subjects. In addition, we interpret these new adverse outcome pathways based in vivo biomarkers for their potential use as intermediary chemicals that may be diagnostic of kidney adverse outcomes to environmental exposure.

Different responses of cavernous malformations and arteriovenous malformations to radiosurgery.

The vascular structure of cavernous malformations (CMs) and arteriovenous malformations (AVMs) is different and they have differing clinical responses to radiosurgery. The structural differences of irradiated and non-irradiated CMs and AVMs were examined to clarify their differential responses to radiosurgery. CMs showed a greater ratio of intraluminal diameter to vessel wall thickness and a lack of subendothelial fibroblasts, myofibroblasts and smooth muscle cells compared with AVMs. Partial proteinaceous clots (19-22% of lumen) formed in CM sinusoids after radiosurgery but complete vaso-occlusion did not occur for up to 6 years after radiosurgery. In contrast, complete vaso-occlusion (91-98% of lumen) by fibrin thrombi that are permanent clots was observed in AVM vessels. Radiation-induced neuronal loss, neurofibrillary degeneration of neurons and myelin fragmentation were typical in the surrounding brain tissue of the irradiated lesions. The different structure and cellular composition of CMs and AVMs is likely to influence their responses to radiosurgery.

Barbiturate coma for severe, refractory vasospasm following subarachnoid haemorrhage.

OBJECTIVE: To document the outcome of patients treated with barbiturate coma for severe symptomatic angioplasty-resistant vasospasm. To compare mortality with that predicted by admission APACHE II score, and neurological outcome with that of historical controls treated with barbiturate coma for vasospasm, and with historical controls with delayed ischaemic deficits from vasospasm treated with nimodipine. DESIGN: Cohort study. SETTING: Neurosurgical Intensive Care Unit of tertiary referral university teaching hospital. PATIENTS: Eleven (6.7%) of 164 consecutive patients with aneurysmal SAH managed according to our protocol who were treated with thiopentone-induced burst suppression coma for severe symptomatic, angioplasty-resistant vasospasm. INTERVENTIONS: Chart, database and literature review. MEASUREMENTS AND RESULTS: All 11 patients survived to hospital discharge (mortality 0%) compared with first-day APACHE II predicted mortality of 30.6% (p=0.15). Outcome at 6 months was: good recovery 8/11 (72.7%), moderate disability 2/11 (18.2%), vegetative survival 1/11 (9.1%). Ten of 11 (90.9%) had a good neurological outcome compared with 50.6% of historical controls with delayed ischaemic deficit from vasospasm (odds ratio 9.78, 95% confidence interval 1.24-77.0, p=0.02), and 0% of previously reported patients treated with barbiturate coma for vasospasm (p < 0.01). CONCLUSION: Our results are better than previously published outcomes and suggest formal evaluation of barbiturate coma in the treatment of severe resistant symptomatic vasospasm following SAH is warranted.

A model of the pathophysiology of cerebral arteriovenous malformations by a carotid-jugular fistula in the rat.

A model of a carotid-jugular fistula in the rat was created such that the arterial feeding vessel is derived from the intracranial arterial circulation and the venous drainage communicates with a major intracranial venous drainage system. This fistula was created in 28 rats on the right side with an additional 11 rats designed as controls with a right carotid ligation and 6 rats without previous surgery. After 12 weeks convalescence, 6 rats with a carotid-jugular fistula and 6 rats without previous surgery underwent cerebral angiography. All fistulae were patent and the model was verified. All of the 33 remaining rats underwent regional cerebral blood flow (rCBF) determination by [14C]iodoantipyrine autoradiography under barbiturate anesthesia. Of the rats with the fistula, 11 had this fistula obliterated 5 min prior to rCBF determination ('closed' group) while 11 had rCBFs determined with the fistula ('open' group). The rCBF was measured from each hemisphere from 7 anatomical regions. The rCBF in the control animals ranged from a median of 82 to 112 ml/100 g/min, in the 'open fistula' group 46 to 68 ml/100 g/min, and in the 'closed' group 118 to 187 ml/100 g/min. This experimental model stimulates the pathophysiologic perturbations in the parenchyma induced by cerebral arteriovenous malformations. It supports the findings that non-infarctional hypoperfusion can result from arteriovenous malformations and that following extirpation of arteriovenous malformations hyperemia may ensue.

Chronic cerebral hypoperfusion in the rat: temporal delineation of effects and the in vitro ischemic threshold.

Acute reductions in cerebral blood flow of up to 50% do not affect neuronal function although it has been shown that reductions of a similar magnitude maintained for 26 weeks do induce neuronal changes. In vitro rat hippocampal LTP was evaluated after 10 weeks of cerebral hypoperfusion. An assessment was also made of the possible 'robustness' of hippocampal CA1 pyramidal neurons to combined in vitro hypoxic/ischemic insults because of previously shown differences in hemodynamic autoregulatory curves. No differences were found between controlled and chronically hypoperfused animals in either study. It is concluded that the changes in neuronal function induced by reductions in cerebral blood flow of less than 50% take time to develop and do not induce adaptive changes in affected neurons. The mechanism for these changes remains to be elucidated.

Pineal teratoma and its relationship to intracerebral development: case report.

A teratoma of the pineal region in a 20-year-old Australian Aborigine is presented in which an unusual location of the straight sinus and tentorium cerebelli suggests that the tumor arose before 4 months of gestation. In addition, this case provides some insight into the development of the falx cerebri, which might arise from the midline fusion of the left and right tentoria cerebelli caused by the dorsal development of the telencephalon.

The case against staged operative resection of cerebral arteriovenous malformations.

Three cases of large cerebral arteriovenous fistulae are presented in which surgical ablation was complicated by brain swelling from hyperperfusion breakthrough believed to be caused by acute intraoperative hypoperfusion superimposed on chronic preoperative hypoperfusion. On the basis of these cases, experimental data, and theoretical considerations, we seriously question the wisdom of using staged surgical resection of cerebral arteriovenous malformation to prevent complications related to alterations in cerebral hemodynamics. The reasons for this concern are: the repeated occurrence of acute-on-chronic hypoperfusion during staged resection; a lack of understanding of the time course for the correction of a disordered autoregulation; risk of hemorrhage between the initial and final resection; difficulty in assessing and substantiating flow reduction after subtotal resection; the rapidity of collateralization; the divergence of flow from large, readily accessible feeding arteries to deep penetrating vessels; and attenuation of the wall thickness in collateral vessels as a consequence of increased flow.

Microsurgery for small arteriovenous malformations of the brain: results in 110 consecutive patients.

OBJECTIVE: To examine the results of surgery in 110 consecutive patients with arteriovenous malformations (AVMs) smaller than 3 cm in diameter. These results are compared with the published results of other microsurgical series as well as with results for patients treated with focused irradiation. METHODS: From January 1989 to November 1998, 121 patients with AVMs smaller than 3 cm were treated at our institution. One hundred ten patients underwent microsurgical removal of their AVMs. The presentation, preoperative neurological status, and postoperative outcome were recorded. Follow-up was complete for all surgical cases. RESULTS: Of the 110 patients, 109 (99%) had angiographically confirmed obliteration of their AVMs. Two patients (1.8%) required reoperation for residual AVM. Two (4.3%) of 46 patients with AVMs in eloquent brain areas experienced worsening of their neurological status after surgery. One (1.6%) of 64 patients was worse neurologically after removal of an AVM in a noneloquent area. CONCLUSION: Microsurgical removal is a safe and effective treatment for the majority of AVMs smaller than 3 cm in diameter. Although the treatment is accompanied by a risk of acute onset of neurological deficits, this tends to be transient in the majority of cases. Furthermore, microsurgical excision of small AVMs offers patients immediate protection from the natural history of their vascular lesions.

A familial coincidence of pseudotumor cerebri and communicating hydrocephalus.

A family in which the mother and two of four daughters had a diagnosis of pseudotumor cerebri and one son developed communicating hydrocephalus is described. The other two daughters both have a long history of headaches but no signs of intracranial hypertension. The argument is advanced that there exists a defect of cerebrospinal fluid absorption common to pseudotumor cerebri and communicating hydrocephalus.

A ventricular infusion technique for the evaluation of treated and untreated hydrocephalus.

Patients considered to have a possible disorder of the circulation of the cerebrospinal fluid (CSF) were prospectively randomized on clinical and computed tomographic grounds into one of four categories: low probability of a disorder of circulation of the CSF (n = 14); high probability of a disorder of the circulation of the CSF (n = 10); low probability of shunt malfunction (n = 10); and high probability of shunt malfunction (n = 9). Patients with possible disorders of the circulation of the CSF who did not meet the entry criteria for each of these categories were excluded from this study. A ventricular catheter connected to a subgaleal Rickham reservoir not in continuity with a shunt system (if this was present) either was inserted into each patient or was in place from previous surgery. Infusion studies were conducted by the infusion of 1 ml/min of normal saline through a 25-gauge needle inserted through the skin into the Rickham reservoir. A separate 25-gage needle was inserted into the Rickham reservoir for continuous recording of intracranial pressure. There were 43 infusion studies that were included in the four categories. Recordings of baseline intracranial pressure for a high probability of a disorder of the circulation of the CSF did not differ significantly from a low probability of a disorder of the circulation of the CSF. Baseline intracranial pressure for a high probability of shunt malfunction was significantly higher than the low probability of a disorder of the circulation of the CSF group and the low probability of shunt malfunction group; there was, however, marked overlap in values between these groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterio-inferior sagittal sinus fistulae: case report.

The management of the case of a 9-year-old boy with progressive cognitive impairment due to arteriovenous fistulae at the apex of the inferior sagittal sinus is reported. This represents a unique location for an extraparenchymal deep central arteriovenous malformation. The patient underwent staged ablation of the lesion by surgery. The postoperative course was complicated by expansion of an aneurysmal vein of Galen undergoing thrombosis and hyperperfusion syndrome, but the patient ultimately made a satisfactory recovery.

The effects of hyperventilation on cerebral blood flow in the rat with an open and closed carotid-jugular fistula.

Perturbations in cerebral hemodynamics at the time of ablation of an arteriovenous shunt have been regarded as important in the pathogenesis of swelling and hemorrhage complicating resection of arteriovenous malformations (AVMs). A carotid-jugular fistula model in the rat had previously been investigated and found to simulate in part the nonhemorrhagic pathophysiology of a large cerebral arteriovenous fistula. Utilizing this model and measuring cerebral blood flow in 14 regions with a [14C]iodoantipyrine autoradiographic technique, the effects of hypocapnea on the cerebral circulation in opened and closed fistulas were investigated. Regional cerebral blood flow (rCBF) in control animals ranged from a median of 53 to 64 ml/100 g/min at a partial arterial carbon dioxide pressure (PaCO2) of 28 +/- 2 mm Hg and 85 to 112 ml/100 g/min at a PaCO2 of 40 +/- 5 mm Hg. In animals with an open carotid-jugular fistula created 12 weeks before the study, these median rCBF values at comparable PaCO2 levels ranged, respectively, from 15 to 39 ml/100 g/min and 50 to 68 ml/100 g/min (the 25th percentile for the open fistula in the hypocapneic group was 15 ml/100 g/min in 5 of the 14 regions studied). In contrast, median rCBF in the closed fistula group ranged from 73 to 100 ml/100 g/min in hypocapneic animals and from 118 to 187 ml/100 g/min in normocapneic animals. These results demonstrate the preservation of CO2 reactivity; hypoperfusion in the presence of a carotid-jugular fistula, hyperemia on fistula occlusion, and the potential to induce cerebral ischemia with hyperventilation in this model of a cerebral arteriovenous fistula.(ABSTRACT TRUNCATED AT 250 WORDS)

Vein of Galen malformation: diagnosis and management.

The vein of Galen malformation is a midline arteriovenous fistula with aneurysmal dilatation of the vein of Galen. The clinical details of diagnosis and treatment in 13 patients with such lesions together with a review of 232 cases collected from the literature are presented in this report. There were 132 males, 77 females, and 36 cases in which the sex was not stated. Eighty patients presented as neonates, 82 were 1 to 12 months old, 39 were 1 to 5 years old, 22 were 6 to 20 years old, and 22 were over the age of 20. The most common presenting symptoms were congestive cardiac failure (110 cases), raised intracranial pressure secondary to hydrocephalus (94 cases), cranial bruit (57 cases), focal neurological deficit (37), seizures (26 cases), and hemorrhage (25 cases). The most characteristic vascular supply to the midline fistula involved multiple bilateral vessels, although bilateral posterior cerebral and unilateral posterior cerebral supply was relatively common. The overall figures for treatment and outcome showed that 91 patients (37.1%) were treated by direct operation and 29 patients (11.3%) were treated by other forms of operation, predominantly shunting or remote vessel ligation. Forty-six patients (18.8%) were treated by medical means (digoxin, diuretics, and ventilatory support). In 79 patients (22.2%), there was no treatment or no details of treatment were available. There was an overall series mortality of 55.6% (no details were available in 33 cases) and a 37.4% mortality for surgically treated cases. After operation, there was a 46.3% incidence of significant morbidity in surviving patients. Neonatal patients fared worst, with an overall mortality of 64 of 70 cases (91.4%) where details were available. The outcome was equally bad for surgically and conservatively treated cases. Operation in the 1- to 12-month age group was more successful, but still carried a mortality of 31.7%, with a significant morbidity in approximately half of the surviving patients. Over the age of 1 year, the surgically treated patients had a 25.6% mortality and a 42.3% major morbidity in survivors. Consideration is given to some of the ways in which these figures may be improved, in particular a staged approach during the neonatal period, with the use of selective embolization or occlusion of vessels to reduce the volume of the arteriovenous shunt until the patient is older and better able to tolerate major operation.

Spinal arteriovenous malformation presenting at birth: case report.

A newborn with paraplegia and evidence of a subarachnoid hemorrhage was found to have a spinal arteriovenous malformation. The arteriovenous malformation was managed by direct surgical obliteration. This patient is the youngest ever reported to have this disorder and the youngest so treated.

Normal perfusion pressure breakthrough complicating surgery for the vein of Galen malformation: report of three cases.

Three cases are described of infants who developed malignant brain swelling (and in one case hemorrhage) after surgery for vein of Galen malformations. The cause for the brain swelling was felt to be due to hyperperfusion, or the "normal perfusion pressure breakthrough" syndrome. Although well-described for cerebral parenchymal arteriovenous malformations, cases of this complication occurring in vein of Galen malformations have not previously been reported. It is concluded from these cases that infants with large arteriovenous shunts, as attested by cardiac failure and cerebral atrophy, have an increased risk of developing this complication.

Combined endovascular stent implantation and endosaccular coil placement for the treatment of a wide-necked vertebral artery aneurysm: technical case report.

OBJECTIVE AND IMPORTANCE: We describe a case in humans of the combined application of endovascular stent placement and Guglielmi detachable coil packing in the management of a wide-necked intracranial aneurysm. CLINICAL PRESENTATION: A 56-year-old woman suffered a subarachnoid hemorrhage secondary to a large wide-necked left vertebral artery aneurysm. Because of the size of the neck of the aneurysm and the extent of its calcification evident on computed tomographic scans, it was deemed unsuitable for surgical intervention or for conventional endovascular coiling. Instead, a combined surgical and endovascular therapy was instituted. INTERVENTION: The left vertebral artery was surgically exposed and cannulated to allow for the placement of an endovascular stent across the neck of the aneurysm to act as a buttress against which Guglielmi detachable coils could be packed. The patient suffered no ill effects as a result of this procedure and made a slow but steady recovery. CONCLUSION: This report describes a case of a wide-necked intracranial artery aneurysm treated using a combination of endovascular stent implantation across an aneurysm neck and endosaccular coil placement to obliterate the aneurysm. The technique described provides another treatment to better manage the difficult entity of wide-necked intracranial aneurysms that may be unsuitable for clipping.

Successful treatment of an acute thrombosis of an intracranial vertebral artery endarterectomy with urokinase.

This is a case report of a 47-year-old man admitted with a 7-month history of disequilibrium, multiple reversible vertebrobasilar ischemic attacks, and one submaximal completed stroke in the left posterior inferior cerebellar artery distribution. Vertebrobasilar ischemic attacks continued despite anti-coagulation, and orthostatic symptomatology suggested a significant hemodynamic component contributing to the posterior circulation ischemia. Angiography confirmed bilateral high-grade stenoses of the intracranial vertebral arteries. A right intracranial vertebral artery endarterectomy was performed with electroencephalographic and somatosensory evoked potential monitoring and protection with barbiturate infusion. The arteriotomy was closed with a vein patch. Postoperatively, the endarterectomy site thrombosed. This thrombosis was completely reversed with 220,000 U of urokinase selectively infused intra-arterially at the site of thrombosis. This procedure was not complicated by hemorrhage or distal embolization. The vertebral artery was confirmed to be patent 24 hours and 7 days after the urokinase injection. The patient sustained a borderzone infarction in the right cerebellar hemisphere without neurological deficits and was discharged home well.

Chronic cerebral hypoperfusion: pathological and behavioral consequences.

OBJECTIVE: Although the effects of acute ischemic insults to the brain are well known, the effects related to chronic ischemia are poorly delineated. The pathological and behavioral changes induced by a chronic noninfarctional reduction in cerebral blood flow of 25 to 50% maintained for 6 months were assessed. METHODS: In each of 18 male Sprague-Dawley rats, an arteriovenous fistula was created in the neck via an anastomosis between the right external jugular vein and the right common carotid artery to induce cerebral hypoperfusion. Nineteen age-matched animals comprised a control group. Six months after surgery, the animals were examined using light and electron microscopic techniques, as well as via a battery of behavioral tests (motor, open field, and T-maze). RESULTS: Examination of the hippocampus by using light microscopy revealed disorganization of the CA1 sector with an increased number of astrocytes. Transmission electron microscopy of the CA1 region demonstrated neurons with increased lipofuscin pigment and central nucleoli and astrocytes with more numerous cytosolic mitochondria. Motor performance testing revealed no gross motor deficits, although open-field assessment demonstrated increased exploratory behavior in rats with fistulas. Finally, T-maze testing results suggested that errors in working memory were more common in rats undergoing chronic cerebral hypoperfusion (P < 0.05). CONCLUSIONS: These findings suggest that chronic reductions in cerebral blood flow of a magnitude previously thought to be harmless to neurons (i.e., reduced by 25-50%) do alter neuronal structure and affect whole animal behavior. Such a scenario may be responsible for a symptomatology secondary to arteriovenous steal and severe carotid stenoses. The mechanisms are still unknown.

Management of spinal dural arteriovenous malformations.

Dura-based spinal arteriovenous malformations (AVM's) are being diagnosed with increasing frequency. The optimal management of such lesions remains a topic of discussion. In an effort to guide this discussion, the authors review their experience with 17 cases of spinal dural AVM treated between January, 1984, and July, 1987. All patients presented with a slowly progressive paraparesis. The abnormalities were initially identified on myelography and confirmed by selective spinal angiography. Fourteen patients underwent endovascular embolization as a primary treatment, and a total of 18 embolization procedures were performed. After all but two of these, obliteration was confirmed at angiography. Patients' symptoms improved following 15 or these procedures but early improvement was not sustained in 10 instances; patients were unchanged after two procedures and worse after one. Follow-up angiography was performed at varying intervals after 15 of the 18 procedures, and recanalization of the previously obliterated spinal dural AVM was demonstrated in 13 instances. Eight patients ultimately underwent surgical treatment of their dura-based spinal AVM. No patient suffered deterioration of symptoms following operation. While embolization may allow angiographic obliteration of a spinal dural AVM and early clinical improvement, for the majority of patients these are not sustained. The average time to treatment failure was 5 months. Newer embolization materials will be necessary to effect permanent treatment in many of these patients.