Delayed Leukoencephalopathy and Foreign Body Reaction After Endovascular Treatment in Patients With Intracranial Aneurysms and Aneurysmal Subarachnoid Hemorrhage-A Systematic Review of the Literature.

Background: Delayed leukoencephalopathy and foreign body reaction are rare complications after endovascular treatment of intracranial aneurysms. However, cases are increasingly being described, given the rising case numbers and complexity. Methods: Clinical presentation, differentials, diagnostics, treatment, and formerly published data were reviewed in light of available cases. A systematic search of the literature was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. Results: This article provides an extensive literature review of previously described cases, and discusses the causes and management of this rare and delayed complication by referring to 17 articles on this topic, with a total of 50 cases with sufficient data in the literature. Furthermore, we present the case of a 53-year-old female patient with subarachnoid hemorrhage from a large anterior communicating artery aneurysm with tortuous cervical vessels who was treated with endovascular coiling and has suffered delayed leukoencephalopathy 6 weeks after discharge. Diagnostics, treatment, and clinical course of this rare complication are presented on this case and based on formerly published literature. The patient timely recovered under high dose corticosteroid treatment and follow up MRI showed almost complete remission of the described lesions within 10 days in accordance with previously published data. Conclusion: Foreign body reaction might result in delayed leukoencephalopathy, especially following complex endovascular aneurysm treatment. Early high dose followed by low dose ongoing corticosteroid treatment might result in timely remission.

Long-term Outcome and Adverse Events of Intrathecal Opioid Therapy for Nonmalignant Pain Syndrome.

OBJECTIVE: Intrathecal (IT) opioid pumps are one therapeutic cornerstone of refractory nonmalignant pain syndromes. The aim of this study was to evaluate the efficacy of and surgical and pharmacological complications of IT pumps beyond a time span of 10 years. METHODS: In this retrospective single-center cohort study, 27 patients (14 female, 13 male, age 64.0 ± 8.9 [median, 1 SD] years) were identified. Pain intensity using the numeric rating scale (NRS), pain and IT pump characteristics, and complications were analyzed. The German Pain Questionnaire was used to investigate the physical and mental health status. RESULTS: Overall time of IT therapy from first implantation to last follow-up was 20.4 ± 6.0 years. Time to implantation of the second pump (n = 18) was 10.0 ± 5.3 years, and between the second and third pump (n = 6) 6.5 ± 2.7 years; 2 patients received their fourth pump 6 years later. The NRS score was 9.0 ± 0.9 before implantation, 7.0 ± 1.8 1 year after implantation, and 4.0 ± 2.3 at the last follow-up. IT drug dose remained stable after 3 years. Opioid intoxications occurred in 3 patients (10%). One patient (3%) underwent revision surgery due to a catheter infection. Drug side effects occurred in 4 patients (14%). Our patient group had pain-related restrictions in physical activities with menial impact regarding mental and emotional stress. CONCLUSION: Even after a time span of over 15 years and several exchanges of pump systems, pain intensity was still reduced. After 3 years, IT drug dose remained unchanged with low side-effect and complication rates.

Time-related alterations of superoxide radical levels in diverse organs of bile duct-ligated rats.

The time-related alterations of superoxide radical measured in vivo by employing an ultrasensitive fluorescent assay in the liver, intestine, kidney and brain of rats with experimentally induced obstructive jaundice was investigated. Eighteen rats were randomly divided into Group A, rats subjected to sham operation, and Group B, rats subjected to bile duct ligation (BDL). Three rats from each group were subsequently killed at different time points post-operatively (1, 5 and 10 days). As compared to sham-operated, BDL rats showed a gradual increase with time of superoxide radical in the intestine, liver, kidney and brain: for animals sacrificed on the 1(st), 5(th) and 10(th) day the increase was 45%, 50% and 96% in the liver, 76%, 81% and 118% in the intestine, 64%, 71% and 110% in the kidney and 76%, 95% and 142% in the brain, respectively. This study provides direct evidence of an early appearance of oxidative stress in diverse organs, implying a uniform systemic response to biliary obstruction and emphasizing the need of early bile flow restoration.

Effect of N-acetylcysteine, allopurinol and vitamin E on jaundice-induced brain oxidative stress in rats.

We examined the possible protective effect of certain antioxidants (N-acetylcysteine, allopurinol and vitamin E) against the oxidative stress of brain tissue induced by experimental obstructive jaundice in rats. Thirty-six male Wistar rats were randomly divided into six groups; group I control, group II sham operated, group III bile duct ligated and groups IV, V, and VI in which the rats, after bile duct ligation, were given every day an intraperitoneal injection with N-acetylcysteine, allopurinol and Vit-E respectively. All rats were sacrificed on the tenth day by exsanguination and the oxidative state in samples from cortex, midbrain and cerebellum was assessed by measuring the thiol redox state and lipid peroxidation quantified by MDA measurements. The main finding was that all three antioxidants decrease lipid peroxidation in the three brain areas. Cysteine levels increased and protein thiol levels were reserved only in the group treated with N-acetylcysteine, whereas oxidized glutathione increased dramatically in the group treated with allopurinol, suggesting that each antioxidant agent had a certain influence profile on the different antioxidant defense systems. The observed effects of the antioxidants in this experimental model could also provide insight into some aspects of jaundice-induced hepatic encephalopathy in humans.

Radiculopathy after lumbar discectomy due to intraspinal retained Surgicel: clinical and magnetic resonance imaging evaluation.

BACKGROUND CONTEXT: Lumbar radiculopathy after lumbar spine surgery is an alerting sign usually caused by either a recurrent disc herniation or epidural hematoma. However, pressure on a spinal nerve root may also be exerted by a retained piece of Surgicel used to achieve hemostasis during lumbar spine surgical procedures. PURPOSE: To describe a case of lumbar radiculopathy that was caused by a piece of Surgicel left in the spinal canal after operation for lumbar disc herniation. STUDY SETTING: A case report of a retained piece of Surgicel being the cause of S1 radiculopathy. METHODS: Patient interview, medical records, imaging studies, and literature review. RESULTS: A 29-year-old man developed acute left S1 radiculopathy after a successful hemilaminectomy and discectomy operation for a L5-S1 disc herniation. In the magnetic resonance imaging studies that were performed, a postoperative hematoma could not be excluded and a reoperation revealed compression from Surgicel that was used for hemostasis. The patient was free of symptoms after reoperation. CONCLUSIONS: This case depicts the difficulty in distinguishing-by means of magnetic resonance imaging-nerve root compression caused by a postoperative hematoma and a recurrent disc herniation, from that caused by a retained Surgicel. Therefore, hemostatic agents should be meticulously used in spine surgery.

Brain oxidative stress induced by obstructive jaundice in rats.

The effect of experimental obstructive jaundice on the oxidative status of brain tissues in rats was examined. Twenty-four male Wistar rats were divided into 4 groups: Group I was the control, group II was the sham operated, and groups III and IV were bile duct ligated and killed on the 5th and the 10th day, respectively. Oxidative stress was assessed by measuring the thiol redox state (protein and nonprotein components) and lipid peroxidation level variations in samples from the cerebral cortex, midbrain, and cerebellar tissue in all animals. Results indicated the presence of oxidative stress in the jaundiced animals that was more pronounced on the 10th day as indicated by a decrease in reduced glutathione and protein thiol and an increase in protein disulphide and lipid peroxidation. A dramatic elevation of the level of total nonprotein mixed disulphide level was found specifically in the midbrain in the 10th day group. This suggests an accumulation of nonprotein disulfides other than oxidized glutathione, which remained unchanged, in this particular brain area. This study showed a correlation between experimental obstructive jaundice and the oxidative stress in the rats' brain, implying that a similar pathogenetic mechanism may play a key role in cholestatic liver disease, resulting in hepatic encephalopathy in humans.