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Inferior vena cava atresia (IVCA) is a rare vascular condition that may be treated by venous stenting. The authors report on the microsurgical removal of an intraspinally misplaced stent causing nerve root compression and neurological deficits.A 42-year-old patient with IVCA and painful cutaneous collaterals had been scheduled for treatment by stenting of the iliocaval confluence and associated venous collaterals. Initial stenting of the right iliac vein was successful; however, during recanalization of the left paravertebral plexus, the stent entered the spinal canal via extraspinal-to-intraspinal venous collaterals. Because of the use of monoplanar angiography, the stent misplacement was not seen during the procedure. Postinterventionally, the patient experienced a foot elevation weakness (grade 1/5) as well as pain and hypesthesia corresponding to the L5 dermatome. Ultrasonography ruled out a lumbosacral plexus hematoma. CT angiography showed that a stent had entered the spinal canal through the left S1 neuroforamen causing nerve root compression. The intraspinal portion of the stent was removed piecemeal via a left-sided hemilaminectomy. Venous bleeding due to the patient’s anticoagulation therapy, the stent’s sharp mesh wire architecture, and the proximity to nerve roots complicated the surgery. Postoperatively, the foot elevation improved to grade 4/5.

OBJECTIVE The number of surgeries performed for chronic subdural hematoma (CSDH) has increased. However, these changes have been poorly reported. The authors aimed to assess the national incidence of surgeries for CSDH in Finland during an 18-year time period from 1997 to 2014. They hypothesized that the incidence of CSDH surgeries has continued to increase, particularly among the elderly. METHODS A nationwide register-based follow-up study was performed using the Finnish Care Register for Health Care. All adult patients undergoing primary CSDH surgeries during 1997–2014 were included. The study population was followed up from the time of CSDH surgery until death or the end of follow-up on December 31, 2017. The incidences of CSDH surgery per 100,000 person-years were calculated separately in each age group and sex. Age standardization was performed for those 20 years of age and older with weights from the 2013 European Standard Population. Negative binomial regression models were used to assess changes in incidence rate ratios (IRRs) during the study period. RESULTS In total, 9280 patients were identified. The age-standardized incidence of CSDH surgery increased from 12.2 to 16.5 per 100,000 person-years during 1997–2014. The age- and sex-adjusted incidence of CSDH surgery increased by 30% (IRR 1.30, 95% CI 1.20–1.41). The age- and sex-adjusted incidence increased more in the older age groups, with an IRR of 1.24 for those aged 60–69 years, 1.32 for those 70–79 years, 1.46 for those 80–89 years, and 1.85 for those aged 90 years or older. The adjusted incidence did not increase for those aged 18–59 years. The sex difference (2:1 men/women) was consistent throughout the study period, with a higher incidence among men. One year after the primary surgery, 19% of the population had a resurgery, and the 1-year case fatality rate was 15%. The median age of patients increased from 73 to 76 years. CONCLUSIONS During the past 2 decades, the age- and sex-adjusted incidence of CSDH surgery has increased in Finland, with major increases for those aged 60 years or older. This increase is likely to continue in parallel with the aging population and increased life expectancies.

Background The pathophysiological basis of idiopathic normal pressure hydrocephalus (iNPH) is still unclear. Previous studies have shown a familial aggregation and a potential heritability when it comes to iNPH. Our aim was to conduct a novel case-controlled comparison between familial iNPH (fNPH) patients and their elderly relatives, involving multiple different families. Methods Questionnaires and phone interviews were used for collecting the data and categorising the iNPH patients into the familial (fNPH) and the sporadic groups. Identical questionnaires were sent to the relatives of the potential fNPH patients. Venous blood samples were collected for genetic studies. The disease histories of the probable fNPH patients (n = 60) were compared with their ≥ 60-year-old relatives with no iNPH (n = 49). A modified Charlson Comorbidity Index (CCI) was used to measure the overall disease burden. Fisher’s exact test (two-tailed), the Mann–Whitney U test (two-tailed) and a multivariate binary logistic regression analysis were used to perform the statistical analyses. Results Diabetes (32% vs. 14%, p = 0.043), arterial hypertension (65.0% vs. 43%, p = 0.033), cardiac insufficiency (16% vs. 2%, p = 0.020) and depressive symptoms (32% vs. 8%, p = 0.004) were overrepresented among the probable fNPH patients compared to their non-iNPH relatives. In the age-adjusted multivariate logistic regression analysis, diabetes remained independently associated with fNPH (OR = 3.8, 95% CI 1.1–12.9, p = 0.030). Conclusions Diabetes is associated with fNPH and a possible risk factor for fNPH. Diabetes could contribute to the pathogenesis of iNPH/fNPH, which motivates to further prospective and gene-environmental studies to decipher the disease modelling of iNPH/fNPH.

IntroductionChronic subdural haematomas (CSDHs) are one of the most common neurosurgical conditions. The goal of surgery is to alleviate symptoms and minimise the risk of symptomatic recurrences. In the past, reoperation rates as high as 20%–30% were described for CSDH recurrences. However, following the introduction of subdural drainage, reoperation rates dropped to approximately 10%. The standard surgical technique includes burr-hole craniostomy, followed by intraoperative irrigation and placement of subdural drainage. Yet, the role of intraoperative irrigation has not been established. If there is no difference in recurrence rates between intraoperative irrigation and no irrigation, CSDH surgery could be carried out faster and more safely by omitting the step of irrigation. The aim of this multicentre randomised controlled trial is to study whether no intraoperative irrigation and subdural drainage results in non-inferior outcome compared with intraoperative irrigation and subdural drainage following burr-hole craniostomy of CSDH.Methods and analysisThis is a prospective, randomised, controlled, parallel group, non-inferiority multicentre trial comparing single burr-hole evacuation of CSDH with intraoperative irrigation and evacuation of CSDH without irrigation. In both groups, a passive subdural drain is used for 48 hours as a standard of treatment. The primary outcome is symptomatic CSDH recurrence requiring reoperation within 6 months. The predefined non-inferiority margin for the primary outcome is 7.5%. To achieve a 2.5% level of significance and 80% power, we will randomise 270 patients per group. Secondary outcomes include modified Rankin Scale, rate of mortality, duration of operation, length of hospital stay, adverse events and change in volume of CSDH.Ethics and disseminationThe study was approved by the institutional review board of the Helsinki and Uusimaa Hospital District (HUS/3035/2019 §238) and duly registered at ClinicalTrials.gov. We will disseminate the findings of this study through peer-reviewed publications and conference presentations.Trial registration numberNCT04203550

Outcome and treatment-associated morbidity analysis of trigone meningioma surgery. We retrospectively assessed 27 neurosurgically treated patients (median age 63 years, range 15–84) between 1999 and 2019. The median preoperative Karnofsky Performance Scale (KPS) was 80 (range 20–100), and the majority (78%) suffered from tumour-specific symptoms. The most frequent symptoms were aphasia (n = 6), visual field deficits (n = 5), and increased intracranial pressure (n = 5). The median tumour volume was 11.2 cm3 (range 3.9–220.5). The most common approaches were the transtemporal (n = 17) and transparietal routes (n = 5). At last follow-up (median follow-up 35 months, range 3–127), the median KPS was 90 (range 30–100); eleven (42%) patients had improved, nine (35%) were unchanged, six (23%) had worsened, and one was lost to follow-up. One year after surgery, 18/21 (86%) patients had retained an activity level similar or improved compared with preoperatively. No surgery-related mortality was recorded. Postoperative new neurological deficits were seen in 13 (48%) patients; eight suffered from permanent, most commonly motor deficits (n = 4), and five of transient deficits. Permanent new motor deficits improved in the majority of affected patients (3/4) over time. New deficits were more often seen for transtemporal (8/17) than transparietal approaches (1/5). Patients with postoperative permanent new deficits had a significantly worse KPS at last follow-up (p < 0.001). The transtemporal and transparietal approaches provide good access, but the latter might provide for a better risk profile. Patients show favourable outcome, but there is a considerable risk for new neurological deficits. This must be taken into consideration for oligosymptomatic patients.

BACKGROUND: A number of randomized controlled trials have shown the benefit of drain placement in the operative treatment of chronic subdural hematoma (CSDH); however, few reports have described real-life results after adoption of drain placement into clinical practice. We report the results following a change in practice at Helsinki University Hospital from no drain to subdural drain (SD) placement after burr hole craniostomy for CSDH. METHODS: We conducted a retrospective observational study of consecutive patients undergoing burr hole craniostomy for CSDH. We compared outcomes between a 6-month period when SD placement was arbitrary (Julye December 2015) and a period when SD placement for 48 hours was routine (July-December 2017). Our primary outcome of interest was recurrence of CSDH necessitating reoperation within 6 months. Patient outcomes, infections, and other complications were assessed as well. RESULTS: A total of 161 patients were included, comprising 71 (44%) in the drain group and 90 (56%) in the non-drain group. There were no significant differences in age, comorbidities, history of trauma, or use of antithrombotic agents between the 2 groups (P > 0.05 for all). Recurrence within 6 months occurred in 18% of patients in the non-drain group, compared with 6% in the drain group (odds ratio, 0.28; 95% confidence interval, 0.09-0.87; P = 0.028). There were no differences in neurologic outcomes (P = 0.72), mortality (P = 0.55), infection rate (P = 0.96), or other complications (P = 0.20). CONCLUSIONS: The change in practice from no drain to use of an SD after burr hole craniostomy for CSDH effectively reduced the 6-month recurrence rate with no effect on patient outcomes, infections, or other complications.

Idiopathic normal pressure hydrocephalus (iNPH) is a late-onset surgically alleviated, progressive disease. We characterize a potential familial subgroup of iNPH in a nation-wide Finnish cohort of 375 shunt-operated iNPH-patients. The patients were questionnaired and phone-interviewed, whether they have relatives with either diagnosed iNPH or disease-related symptomatology. Then pedigrees of all families with more than one iNPH-case were drawn. Eighteen patients (4.8%) from 12 separate pedigrees had at least one shunt-operated relative whereas 42 patients (11%) had relatives with two or more triad symptoms. According to multivariate logistic regression analysis, familial iNPH-patients had up to 3-fold risk of clinical dementia compared to sporadic iNPH patients. This risk was independent from diagnosed Alzheimer's disease and APOE epsilon 4 genotype. This study describes a familial entity of iNPH offering a novel approach to discover the potential genetic characteristics of iNPH. Discovered pedigrees offer an intriguing opportunity to conduct longitudinal studies targeting potential preclinical signs of iNPH. (C) 2016 Elsevier B.V. All rights reserved.

Backgound/Objective: To determine the level of association between uptake of the amyloid positron emission tomography (PET) imaging agent [18F]flutemetamol and the level of amyloid-ß measured by immunohistochemical and histochemical staining in a frontal cortical region biopsy site. Methods: Seventeen patients with probable normal pressure hydrocephalus (NPH) underwent prospective [18F]flutemetamol PET and subsequent frontal cortical brain biopsy during ventriculoperitoneal shunting. Tissue amyloid-ß was evaluated using the monoclonal antibody 4G8, thioflavin S and Bielschowsky silver stain. Results: Four of the 17 patients (23.5%) had amyloid-ß pathology based on the overall pathology read and also showed increased [18F]flutemetamol uptake. [18F]Flutemetamol standardized uptake values from the biopsy site were significantly associated with biopsy specimen amyloid-ß levels (Pearson's r = 0.67; p = 0.006). There was also good correlation between the biopsy specimen amyloid-ß level and uptake of [18F]flutemetamol in the region contralateral to the biopsy site (r = 0.67; p = 0.006), as well as with composite cortical [18F]flutemetamol uptake (r = 0.65; p = 0.008). The blinded visual read showed a high level of agreement between all readers (κ = 0.88). Two of 3 readers were in full agreement on all images; 1 reader disagreed on 1 of the 17 NPH cases. Blinded visual assessments of PET images by 1 reader were associated with 100% sensitivity to the overall pathology read, and assessments by the 2 others were associated with 75% sensitivity (overall sensitivity by majority read was 75%); specificity of all readers was 100%. Conclusions: [18F]Flutemetamol detects brain amyloid-ß in vivo and shows promise as a valuable tool to study and possibly facilitate diagnosis of Alzheimer's disease both in patients with suspected NPH and among the wider population.

IntroductionAlthough a great majority of patients with cervical radiculopathy syndrome can successfully be treated non-operatively, a considerable proportion experience persistent symptoms, severe enough to require neurosurgical intervention. During the past decade, cervical spine procedures have increasingly been performed on an outpatient basis and retrospective database analyses have shown this to be feasible and safe. However, there are no randomised controlled studies comparing outpatient care with inpatient care, particularly with emphasis on the patients’ perception of symptom relief and their ability to return to normal daily activities and work.Methods and analysisThis is a prospective, randomised, controlled, parallel group non-inferiority trial comparing the traditional hospital surveillance (inpatient, patients staying in the hospital for 1–3 nights after surgery) with outpatient care (discharge on the day of the surgery, usually within 6–8 hours after procedure) in patients who have undergone anterior cervical decompression and fusion procedure. To determine whether early discharge (outpatient care) is non-inferior to inpatient care, we will randomise 104 patients to these two groups and follow them for 6 months using the Neck Disability Index (NDI) as the primary outcome. We expect that early discharge is not significantly worse than the current care in terms of change in NDI. Non-inferiority will be declared if the mean improvement for outpatient care is no worse than the mean improvement for inpatient care, by a margin of 17.3%. We hypothesise that a shorter hospital stay results in more rapid return to normal daily activities, shorter duration of sick leave and decreased secondary costs to healthcare system. Secondary outcomes in our study are arm pain and neck pain using the Numeric Rating Scale, operative success (Odom’s criteria), patient’s satisfaction to treatment, general quality of life (EQ-5D-5L), Work Ability Score, sickness absence days, return to previous leisure activities and complications.Ethics and disseminationThe study was approved by the institutional review board of the Helsinki and Uusimaa Hospital District on 6 June 2019 (1540/2019) and duly registered at ClinicalTrials.gov. We will disseminate the findings of this study through peer-reviewed publications and conference presentations.Trial registration numberNCT03979443.

ObjectiveTo evaluate the role of the copy number loss in SFMBT1 in a Caucasian population.MethodsFive hundred sixty-seven Finnish and 377 Norwegian patients with idiopathic normal pressure hydrocephalus (iNPH) were genotyped and compared with 508 Finnish elderly, neurologically healthy controls. The copy number loss in intron 2 of SFMBT1 was determined using quantitative PCR.ResultsThe copy number loss in intron 2 of SFMBT1 was detected in 10% of Finnish (odds ratio [OR] = 1.9, p = 0.0078) and in 21% of Norwegian (OR = 4.7, p < 0.0001) patients with iNPH compared with 5.4% in Finnish controls. No copy number gains in SFMBT1 were detected in patients with iNPH or healthy controls. The carrier status did not provide any prognostic value for the effect of shunt surgery in either population. Moreover, no difference was detected in the prevalence of hypertension or T2DM between SFMBT1 copy number loss carriers and noncarriers.ConclusionsThis is the largest and the first multinational study reporting the increased prevalence of the copy number loss in intron 2 of SFMBT1 among patients with iNPH, providing further evidence of its role in iNPH. The pathogenic role still remains unclear, requiring further study.

Background Desmoplastic infantile ganglioglioma is a rare tumor occurring mainly in infants and young children. Both radiological and histopathological appearances may resemble malignancy, although its clinical course is mainly benign. Methods Altogether, 5 cases of DIG have been operated on in our hospital since the first diagnosis of DIG in Finland in 1993. We evaluated their presenting symptoms, radiological and surgical findings, histologic characteristics, and follow-up. Results All patients were male. Three were less than 18 months old, and 2 were 35 and 79 months old. The most common presenting symptoms were epileptic seizures (4 cases). In 4 cases, there was a histopathologically verified single cystic tumor. In 1 case, DIG was operatively diagnosed in 2 separate locations. This patient, moreover, had 2 other lesions suspected of being DIG, including a mass originating from the ophthalmic nerve. None of the patients received adjuvant therapies. All our patients are alive after 7 to 120 months of follow-up. There were no recurrences in any of the patients after tumor resection. For the first time, we describe EGFR and MYCN amplifications in tumors which are, respectively, of their mixed glial and neuronal origin. Conclusion The clinical presentation of DIG may be more often associated with epileptic seizures than previously thought. The radiological appearance of DIG may vary from cystic to solid and from contrast-enhancing to nonenhancing. Even multiple locations of DIG have been encountered. Increasing evidence supports surgery as the treatment of choice for DIG, although oncogene amplifications have been described.

Background and Purpose —Oxidative stress is probably involved in neuronal damage induced by ischemia-reperfusion. The purpose of this study was to assess the role of antioxidant activity in cerebral ischemic stroke. Methods —Antioxidant activity of blood plasma and cerebrospinal fluid was assessed in 22 patients with cerebral hemisphere infarction that was verified and quantified by MRI. Results —Low total peroxyl radical trapping potential of plasma, but not of cerebrospinal fluid, was associated with high lesion volume and high neurological impairment assessed by scores on NIH Stroke Scale, Barthel Index, and Hand Motor Score tests. The plasma concentrations of ascorbic acid, α-tocopherol, and protein thiols were also associated with the degree of neurological impairment. Conclusions —These data suggest that the antioxidant activity of plasma may be an important factor providing protection from neurological damage caused by stroke-associated oxidative stress.

Many studies have suggested that parenteral administration of coenzyme Q 10 (Q 10 ) protects the myocardium of young experimental animals from post-ischemic reperfusion injury. Although parenteral administration, in contrast to per os supplementation, seems to elevate coenzyme Q concentrations in heart tissue, it is not suitable for prophylactic use. In addition, the incidence of ischemic events is greatest in older age. We studied the effect of Q 10 supplementation on myocardial postischemic recovery in 18-month-old Wistar rats. The treated group (n = 9) received 10 mg/kg day of Q 10 for 8 weeks in their chow while the normal chow of the control group (n = 9) contained less than 0.5 mg/kg day of Q 10 . The treatment clearly elevated plasma Q 10 concentration (286 ± 25 μmol l and 48 ± 30 μmol l , treated and controls, respectively, p 9 nor Q 10 concentrations in heart tissue were affected by the supplementation. The isolated perfused hearts were subjected to 20 minutes of ischemia and 30 minutes of reperfusion. The preischemic values of developed pressure (DP) but not contractility ( +DP Δt ) and relaxation ( −DP Δt ) were improved by Q 10 supplementation (p = 0.034, p = 0.057 and p = 0.13, respectively) while in postischemic recovery no differences were observed between the groups (p > 0.05 at all time points). Also, in myocardial flow, myocardial oxygen consumption (MVO 2 ) and myocardial aerobic efficiency (DP/MVO 2 ) the groups did not differ at any time points. Although dietary Q 10 supplementation clearly elevated plasma Q 10 concentrations in senescent rats, the coenzyme Q contents in heart tissue and myocardial recovery from ischemia were not affected. However, it is possible that the site of action for the reported beneficial effects of Q 10 is in the coronary endothelium rather than myocardium itself.

1. Age-associated deterioration of arterial function may result from long-lasting oxidative stress. Since coenzyme Q (Q10) has been suggested to protect the vascular endothelium from free radical-induced damage, we investigated the effects of long-term dietary Q10 supplementation on arterial function in senescent Wistar rats. 2. At 16 months of age, 18 rats were divided into two groups. The control group was kept on a standard diet while the other group was supplemented with Q10 (10 mg kg(-1) day(-1)). In addition, nine rats (age 2 months) also ingesting a standard diet were used as the young control group. After 8 study weeks the responses of the mesenteric arterial rings in vitro were examined. 3. Endothelium-independent arterial relaxations to isoprenaline and nitroprusside (SNP) were attenuated in aged rats. Increased dietary Q10 clearly enhanced the relaxation to isoprenaline, but did not affect the response to SNP. In addition, vasodilation of noradrenaline-precontracted rings to acetylcholine (ACh), which was also impaired in aged vessels, was improved after Q10 supplementation. Cyclooxygenase inhibition with diclofenac enhanced the relaxation to ACh only in young rats, while it abolished the difference between the old controls and Q10 supplemented rats, suggesting that the improved endothelium-dependent vasodilation observed in Q10 supplemented rats was largely mediated by prostacyclin (PGI2). 4. In conclusion, long-term Q10 supplementation improved endothelium-dependent vasodilation and enhanced beta-adrenoceptor-mediated arterial relaxation in senescent Wistar rats. The mechanisms underlying the improvement of endothelial function may have included augmented endothelial production of PGI2, increased sensitivity of smooth muscle to PGI2, or both.

Free radicals are thought to be involved in the onset of neuronal disturbances such as Alzheimer's disease, Parkinson's disease, and neuronal ceroid lipofuscinosis. It is also assumed that they play a role in cerebral injury caused by ischemia or trauma. Plasma and cerebrospinal fluid (CSF), Total (peroxyl) Radical-trapping Antioxidant Parameter (TRAP), and the known antioxidant components of TRAP, for instance, ascorbic acid, uric acid, protein sulfhydryl groups, tocopherol, and ubiquinol were analyzed and the remaining unidentified fragment was calculated in five healthy volunteers before and after 4 weeks of ascorbate and ubiquinone (Q-10) supplementation. In CSF, TRAP was significantly lower than in plasma. The major contributor to plasma's antioxidant capacity was uric acid (UA), whereas in CSF it was ascorbic acid (AA). In CSF, AA concentrations were four times higher than in plasma. Oral supplementation of AA (500 mg/d first 2 weeks, 1,000 mg/d following 2 weeks) and Q-10 (100 mg/d first 2 weeks, 300 mg/d following 2 weeks) induced a significant increase in plasma AA and Q-10. Surprisingly, in spite of the high lipophilicity of Q-10, its concentration did not change in CSF. The supplementation of AA increased its concentration in CSF by 28% (p < .05). However, the increase in AA did not result in an increase in CSF TRAP. This indicates that AA had lost one-third of its radical trapping capacity as compared to that in plasma. The facts that AA is the highest contributor to CSF TRAP and its effect on TRAP is concentration dependent could indicate that the peroxyl radical-trapping capacity of CSF is buffered by AA.

The essential role of coenzyme Q--ubiquinone--in biological energy transduction is well established. Reduced Q--ubiquinol--has also been shown to act as an antioxidant and to decrease the action of free radicals, which in turn could cause damage to structural lipids or proteins. The accumulation of lipopigments during aging in several peripheral organs and in the nervous system is considered to be related to the peroxidation of unsaturated fatty acids. An age-related decline of Q-10 has been suggested to occur in man and rats. In this study we followed the effects of life-long oral supplementation of coenzyme Q-10 on the development and life-span and pigment accumulation in peripheral tissues and the nervous system of laboratory rats. The Q-10 supplemented group showed a significant increase in Q-10 in plasma and liver, while it was unchanged in other tissues. There was no significant difference between the two groups in the development and mortality of the animals. No differences were observed in lipopigment accumulation. Our results indicate that in rats, life-long supplementation of Q-10 has no beneficial effects on life-span or pigment accumulation.

Background During cardiac arrest and after successful resuscitation a continuum of ischaemia-reperfusion injury develops. Mild hypothermia exerts protective effects in the postresuscitation phase but also alters CO 2 production and solubility, which may lead to deleterious effects if overlooked when adjusting the ventilation of the resuscitated patient. Using a multimodality approach, the effects of different carbaemic states on cerebral perfusion and metabolism were evaluated during therapeutic hypothermia. Methods Eight comatose survivors of prehospital cardiac arrest were cooled to 33°C for 24h and underwent a 60min phase of interventional lower threshold normocapnia according to temperature non-corrected pCO 2 (4.2kPa) and higher threshold normocapnia according to corrected pCO 2 (6.0kPa) in a random order. Prior to, during and after each phase, cerebral perfusion and metabolites via a microdialysis catheter were measured. Results During upper-threshold pCO 2 , an increase in middle cerebral artery mean flow velocity (MFV) and jugular bulb oxygen saturation (jSvO 2 ) were observed with a concomitant decrease in cerebral lactate concentration. Lower threshold normocapnia was associated with a decrease in MFV in most patients. In all patients jSvO 2 decreased but no change in cerebral lactate was observed. In seven patients jSvO 2 decreased below 55%. These changes were not reflected to intracranial pressure or cerebral oximetry. Conclusions During induced hypothermia, lower threshold normocapnia was associated with decreased cerebral perfusion/oxygenation but not reflected to interstitial metabolites. Upper threshold pCO 2 increased cerebral perfusion and reduced cerebral lactate. Vigilance over the ventilatory and CO 2 analysis regimen is mandatory during mild hypothermia.