Transient Neurological Impairment Research Articles

Improvement of Postoperative Quality of Life in Patients Over 80 Years Old With Thoracic Spinal Stenosis.

A retrospective comparative study was conducted to analyze the outcome of surgical and conservative treatment for patients over 80 years old with thoracic spinal stenosis (TSS). To evaluate the safety and efficiency of posterior spinal cord decompression surgery for over 80-year-old patients with TSS. Concerned about the risk of surgery, over 80-year-old patients with TSS are usually treated conservatively, which often leads to a decline in quality of life. So far as we know, no study demonstrates the risk and benefit of spine surgery for these patients. Over 80 years of age who underwent dorsal decompression surgery or conservative treatment due to TSS between January 2010 and November 2020 were analyzed. Sixty-four patients who completed follow-up PROM (patient-reported outcome measure) data were collected, including the mJOA (modified Japanese Orthopedic Association score) scoring system, VAS (visual analogue scale), questionnaire-based assessment of the ODI (Oswestry disability index), BI (Barthel index), and SF-36v2 (Short Form-36v2) Health Survey. The clinical characteristics, preoperative and postoperative imaging findings, operative records, complications, and individual outcomes were analyzed. Of the 64 patients, 38 underwent posterior decompression, pedicle screw fixation, and posterolateral fusion; another 26 chose conservative treatment. The baseline characteristics of the TSS patients in 2 groups show no significant differences. The clinical symptoms and imaging outcomes showed a significant improvement in the surgical group compared with the nonsurgical group, according to mJOA, VAS, ODI, BI, and SF-36v2. Cerebrospinal fluid leakage occurred in 6 patients, and transient neurological impairment occurred in 2 patients. Posterior decompression surgery for over 80-year-old patients with TSS is a safe and effective treatment, it has a good clinical outcome as well as an acceptable complication rate. However, there were no obvious improvements in quality of life or pain with conservative treatment.

Ischemic complications following surgical treatment of moyamoya disease: risk factors and prevention

One of the most difficult problems in surgical treatment of moyamoya disease is prevention of ischemic perioperative complications. The risk of these events is significantly higher compared to other cerebrovascular diseases (up to 30%). To identify unfavorable prognostic factors of perioperative cerebral ischemic complications, to determine the group of high-risk patients and to develop the guidelines for perioperative management of these patients. We analyzed clinical and diagnostic data and postoperative outcomes in 80 patients with various forms of moyamoya disease. These patients underwent 134 different interventions. Staged revascularization of both hemispheres was performed in 40 patients (80 surgeries). Most patients (n = 55) underwent combined brain revascularization (79 surgeries). Persistent postoperative complications (ischemic stroke) developed in 7 cases (5.3%). Transient neurological impairment was observed in 36 cases (27%). Statistical analysis revealed the following risk factors of perioperative complications: critical stenosis/occlusion of posterior cerebral artery (OR 9.704), severe perfusion deficit (OR 5.393) and previous TIA or ischemic stroke within 3 months prior to surgery (OR 6.433). If at least two of these signs are present, sensitivity of prognosis for postoperative complications is 80.7% and 88.6%, respectively. Patients with moyamoya disease are at high risk of perioperative complications due to complex rearrangement of collateral cerebral circulation and high sensitivity of brain to local and systemic hemodynamic changes. Patients with risk factors require careful perioperative management to exclude pathogenetic factors provoking ischemia. Early surgical treatment is advisable to reduce the risk of ischemic and hemorrhagic lesions following natural course of disease and severe perioperative complications.

Neurophysiological abnormalities in individuals with persistent post-concussion symptoms

Concussion injury results in a rapid onset of transient neurological impairment that can resolve quickly, or sometimes evolve over time, but usually resolve within seven to 10 days. However, a small but noticeable cohort (~10%) of individuals continues to experience persistent lingering effects, particularly fatigue, recognized as post-concussion symptoms (PCS). This study explored neurophysiological mechanisms in people with persistent PCS. Studies involved using self-report post-concussion fatigue scale, transcranial magnetic stimulation (TMS) and somatosensory stimulation in those with diagnosed PCS (n = 20; 36.1 ± 14.0 yr., 4 female; mean time post-concussion 15.4 ± 7.6 months) to fully recovered individuals (n = 20; 33.8 ± 6.6 yr., 2 female; post-concussion 12.9 ± 6.6 months) and healthy controls (n = 20; 37.7 ± 8.0 yr., 3 female). PCS participants demonstrated a significantly higher self-report fatigue (score: PCS 20.2 [95% CI 17.4–22.9], Recovered 6.2 [3.1–9.3], Control 2.75 [0.6–4.8]). PCS participants showed a worsening of reaction time (F2,57 = 4.214; p = 0.020) and increased reaction time variability (F2,57 = 5.505; p = 0.007). Somatosensory differences were observed for amplitude discrimination (F2,57 = 5.166; p = 0.009), temporal order judgment (F2,57 = 4.606; p = 0.014) and duration discrimination (F2,57 = 6.081; p = 0.004). Increased intracortical inhibition in TMS single pulse suprathreshold stimulation (110%: F2,57 = 6.842; p = 0.002; 130%: F2,57 = 4.900; p = 0.011; 150%: F2,57 = 4.638; p = 0.014; 170%: F2,57 = 9.845; p < 0.001) and paired pulse protocols was also seen (SICI: F2,57 = 23.390; p < 0.001, and LICI: F2,57 = 21.603; p < 0.001). Using non-invasive stimulation techniques, this novel study showed increased cortical inhibition and compromised central information processing, suggesting neural mechanisms underpinning ongoing fatigue, allowing for potential clinical rehabilitation strategies.

Management of concussion in soccer.

When participating in contact sports, (mild) head trauma is a common incident-observed in both professional and amateur sports. When head trauma results in transient neurological impairment, a sports-related concussion has occurred. Acute concussion, repetitive concussions, as well as cumulative "sub-concussive" head impacts may increase the risk of developing cognitive and behavioral deficits for athletes, as well as accelerated cerebral degeneration. While this concept has been well established for classic contact sports like American Football, Rugby, or Boxing, there is still an awareness gap for the role of sports-related concussion in the context of the world's most popular sport-Soccer. Here, we review the relevance of sport-related concussion for Soccer as well as its diagnosis and management. Finally, we provide insight into future directions for research in this field. Soccer fulfills the criteria of a contact sport and is characterized by a high incidence of concussion. There is ample evidence that these events cause functional and structural cerebral disorders. Furthermore, heading, as a repeat sub-concussive impact, has been linked to structural brain changes and neurocognitive impairment. As a consequence, recommendations for the diagnosis and management of concussion in soccer have been formulated by consensus groups. In order to minimize the risk of repetitive concussion in soccer the rapid and reliable side-line diagnosis of concussion with adoption of a strict remove-from-play protocol is essential, followed by a supervised, graduated return-to-play protocol. Recent studies, however, demonstrate that adherence to these recommendations by players, coaches, clubs, and officials is insufficient, calling for stricter enforcement. In addition, future research to solidify the pathophysiological relevance of concussion for soccer athletes seems to be needed. Advanced neuroimaging and neurochemical biomarker analyses (e.g. S100β, tau and neurofilament light (NfL)) may assist in detecting concussion-related structural brain changes and selecting athletes at risk for irreversible damage. Sports-related concussion represents a genuine neurosurgical field of interest. Given the high socioeconomic relevance, neurosurgeons should get involved in prevention and management of concussion in soccer.

An MR-based quantitative intraventricular hemorrhage porcine model for MR-guided focused ultrasound thrombolysis.

Intraventricular hemorrhage (IVH) affects approximately 50% of premature births where 50% further develop post-hemorrhagic ventricular dilation (PHVD). Patients face significant impact to long-term development if PHVD is not managed. Unfortunately, there is no accepted treatment to remove the thrombus caused by IVH. This paper describes an acute and chronic IVH model for use with magnetic resonance-guided focused ultrasound (MRgFUS) thrombolysis. A total of 12 pigs (~ 1month in age) were used in the model (eight acute and four chronic). A pre-operative brain MRI was obtained for ventricular targeting. 1.25cm3/kg of autologous blood was injected through a burr hole lateral to the midline and anterior of the coronal suture at a rate of 0.6cm3/min. A craniotomy was performed to simulate a "fontanelle". Post-operative MRI was used to calculate the clot volume. Chronic piglets were recovered, monitored daily with a neurological scoring system (NSS), and MRI scanned for 21days. The clot injection was well tolerated. The average clot size was 3987mm3 (median = 4330mm, standard deviation = 739mm3). Postmortem examination validated the presence of the clot. In the chronic animals, there was an increase in ventricular volume of 30%. Transient neurological impairment immediately followed clot injection and with onset of hydrocephalus in the chronic animals. This model establishes a measurable and targetable IVH clot in an MRI-based neonatal porcine model. The progressive post-hemorrhagic ventricular dilation in the chronic model is a potential alterable outcome from MRgFUS thrombolysis.

The efficacy of posterior hemivertebra resection with lumbosacral fixation and fusion in the treatment of congenital scoliosis: A more than 2-year follow-up study

ObjectiveHemivertebrae (HV) located at the lower lumbar or lumbosacral region often produce early trunk imbalance and long compensatory curves. Because of the biomechanical characteristics of the lumbosacral junction, the rate of instrumentation failures at the region has always been high. Our study aimed to evaluate the results of posterior HV resection with lumbosacral fixation and fusion in the treatment of congenital scoliosis and to make a preliminary analysis of the possible risk factors for instrument failures. Patients and methodsFrom 2010 to 2015, 17 patients (7 males and 10 females) with congenital scoliosis underwent HV resection with lumbosacral fixation and fusion in our department. The mean patient age was 13.2±4.4years at surgery, and the mean follow-up time was 37.6±4.6months. Clinical outcomes and related complications were assessed by reviewing medical records, operative notes, radiographic data, and scores on the SRS-22 questionnaire. ResultsThe mean Cobb angle of the segmental curve was 37.5°±12.7° preoperatively, 7.9°±5.5° postoperatively, and 7.9°±5.3° at the latest follow-up. The mean Cobb angle of the cranial compensatory curve was 39.2°±17.2°, 9.1°±9.5°, and 9.5°±10.8°, respectively. Trunk balance was improved in both the coronal (59.6%) and sagittal (58.6%) planes after surgery, and remained stable at the latest follow-up. Three domains of SRS-22, including self-image, mental health, and satisfaction, were significantly improved at the latest follow-up compared with preoperative status. Complications included one transient neurologic impairment, one superficial wound infection, and two implant failures. ConclusionsEarly posterior HV resection with short lumbosacral fixation and fusion is effective in the treatment of HV located at lower lumbar or lumbosacral region. Delayed surgical intervention may lead to longer fusion and fixation. A long lumbosacral construct using only S1 pedicle screws as distal anchors tends to accompany a high rate of implant failures.

Neurologic impairment following closed head injury predicts post-traumatic neurogenesis

In the mammalian hippocampus, neurogenesis persists into adulthood, and increased generation of newborn neurons could be of clinical benefit following concussive head injuries. Post-traumatic neurogenesis has been well documented using “open” traumatic brain injury (TBI) models in rodents; however, human TBI most commonly involves closed head injury. Here we used a closed head injury (CHI) model to examine post-traumatic hippocampal neurogenesis in mice. All mice were subjected to the same CHI protocol, and a gross-motor based injury severity score was used to characterize neurologic impairment 1h after the injury. When analyzed 2weeks later, post-traumatic neurogenesis was significantly increased only in mice with a high degree of transient neurologic impairment immediately after injury. This increase was associated with an early increase in c-fos activity, and subsequent reactive astrocytosis and microglial activation in the dentate gyrus. Our results demonstrate that the initial degree of neurologic impairment after closed head injury predicts the induction of secondary physiologic and pathophysiologic processes, and that animals with severe neurologic impairment early after injury manifest an increase in post-traumatic neurogenesis in the absence of gross anatomic pathology.

Isolated transverse sacral fractures

The limited literature available about transverse sacral fractures describes two populations of patients: one with severe associated injuries and neurologic impairment and another with insufficiency fractures after low-energy trauma. Nevertheless, we have observed that isolated sacral fractures can occur in a third group of patients without the previously described features. To describe the clinical features of a population of patients with isolated transverse sacral fractures and evaluate the results of their conservative treatment according to our experience. Retrospective cohort study. Forty-two patients with isolated transverse sacral fractures with a mean follow-up of 22 months (range, 18-24 months). Neurologic recovery, pain relief, time out of work, and disability. We included all the patients admitted at our institution for an isolated transverse sacral fracture between 1996 and 2005. The information obtained from their medical records was analyzed using an electronic spreadsheet (Microsoft Excel for Mac v.2011; Microsoft, Redmond, WA, USA). Thirty-four patients (80%) sustained a low-energy trauma, whereas only two (4.8%) presented transient neurologic impairment. Every fracture was confirmed with a sacrococcygeal computed tomography (CT) scan. All the patients referred no local pain 6 months after the accident and were able to return to their preinjury activity level. None of the patients required compensation for disability. Transverse sacral fractures should be suspected in patients referring local pain after sustaining low-energy trauma, even in the absence of risk factors for an insufficiency fracture. These injuries are difficult to detect in plain X-rays, so a sacrococcygeal CT scan is recommended. Conservative treatment is associated with excellent results in this population of patients.

Impact of high titre of antiphospholipid antibodies on postoperative outcome following pulmonary endarterectomy☆

Antiphospholipid (a-PL) antibodies, especially IgG isotype, have been associated with a variety of neurological manifestations related to thrombotic mechanism and reactivity against nervous tissues. Furthermore, high titre of a-PL antibodies has been also correlated to chronic thromboembolic pulmonary hypertension (CTEPH) and, therefore, is frequently reported in patients undergoing pulmonary endarterectomy (PEA). The impact of a-PL antibodies in postoperative outcome following PEA, however, has not been clearly evaluated yet. In this paper, we investigated the impact of a high a-PL IgG titre (HAPT) on postoperative outcome following PEA. From April 1994 to October 2008, out of 204 patients undergoing PEA at our centre, 184 were prospectively screened for a-PL antibodies. According to the preoperative IgG titre, patients were divided into two groups: Group A (high a-PL antibodies titre - HAPT) with a-PL IgG titre >10 U/ml and Group B (low a-PL antibodies titre - LAPT) with a-PL IgG titre <or=10 U/ml. Early outcomes were compared between the two groups. Twenty-eight patients (15%) were included in Group A, whereas 156 (85%) patients were included in Group B. HAPT influenced preoperative parameters as patients of Group A were younger compared to those of Group B (42+/-16 and 52+/-16 for Group A and B, respectively, P=0.001) and presented more frequently a previous history of deep venous thrombosis (DVT) (96% and 62% for Group A and B, respectively, P=0.001). The two groups were homogeneous for all other operative parameters. As far as postoperative outcome, in terms of mortality and major complications, there were no differences between the two groups. Incidence of transient neurological complications, however, was significantly different (32% and 10% for Group A and B, respectively, P=0.023). The presence of high titre of IgG isotype a-PL antibodies significantly influences preoperative characteristics of patients undergoing PEA. Furthermore, despite that no significant differences were shown in major end points, the presence of high titre of a-PL did interfere with postoperative course as caused by an increased rate of minor and transient neurological impairment (TNI). An accurate monitoring especially during hypothermic circulatory arrest (CA) period seems, therefore, mandatory in this subgroup of patients undergoing PEA.

FLOW CYTOMETRIC ASSAY TO QUANTIFY PUMP INDUCED MICROTHROMBI DURING CARDIOPULMONARY BYPASS

Almost 70% of all patients who undergo cardiopulmonary bypass (CPB) surgery suffer from neuropsychological deficits in the first postoperative week. It is speculated that this transient neurological impairment is based on microemboli, mainly due to pump-induced platelet aggregations. The aim of this study is to establish a new method to detect and quantify pump-induced platelet aggregations in an in vitro experiment. Method: Whole blood flow cytometry was used to quantify circulating platelet microaggregates derived from a centrifugal pump (Baylor Gyro C1E3) and a roller pump (Sarns Inc. 2M 6002). Each pump was tested in a mock circuit for four hours (5L/min flow against 100 mm Hg pressure head) using fresh human anti-coagulated blood (1IU heparin /ml, ACT 250 sec.). Platelets were labeled with the CD42b-PE monoclonal antibody. Platelets and platelet microaggregates were differentiated from other blood cells based on their positive PE-fluorescence. Platelet microaggregates were distinguished from single platelet by size related forward scattering. The extent of platelet aggregation was quantified by depletion of single platelets compared to control. Results: Inactivated control samples showed no platelet aggregates and were defined as 0% platelet aggregation. A positive control with ADP activated platelets (20 μM ADP) showed the presence of platelet microaggregates and resulted in >90% platelet aggregation. Extensive platelet aggregation was also observed within the roller pump group. Values for platelet aggregation increased from 0% (0 min), 8.0±3.2% (15 min) to 52.0±14.4% at the end of experiment. The values for the centrifugal pump group were significantly lower (p < 0.01); 2.0±0.9% (15 min) and 9.0 ± 2.4% (4 hours). Conclusion: Flow cytometry is able to detect and quantify platelet aggregation. This is a very useful tool to evaluate the thrombogenic resistance of prototype blood pumps in a fast, inexpensive and reliable in vitro experiment. Based on these results we speculate that the transient neuropsychological deficits after CPB are primarily due to pump derived platelet aggregation. To reduce frequency and severity of neurological complications, the use of centrifugal pumps seems to be beneficial.

Accidental injection of thiopental into the epidural space

EDITOR: A fit 46-year-old female patient with diverticulitis refractory to conservative measures was scheduled for sigmoid colectomy. An epidural catheter was sited at the L3-4 interspace and a test dose of 4 mL bupivacaine 0.5 per cent injected from a labelled 20 mL syringe containing a total of 9 mL of solution. General anaesthesia was then induced with a standard rapid sequence induction. At the start of surgery, a further bolus dose of 'bupivacaine' was administered through the epidural catheter. Immediately following the injection, the anaesthetist noted that instead of giving bupivacaine, the remaining 6 mL of thiopentone 2.5 per cent left from the induction had been inadvertently administered. The catheter was immediately aspirated, removing 1 mL of fluid and the bacterial filter was discarded. Eighty millilitres of 0.9 per cent saline drawn up through a filter needle was injected over 30 min in an attempt to dilute the solution in the epidural space. The patient remained cardiovascularly stable and surgery was continued. In recovery, the patient had no complaints and was neurologically intact. Following the incident, the epidural catheter was left in place but no further doses of local anaesthetic or analgesics were administered. The catheter was removed the following morning. In this case, a relatively small dose of 2.5 per cent thiopental had been injected through an epidural catheter while the patient was under a general anaesthetic. In awake patients, the inadvertent administration of thiopental via the epidural route has been associated with pain and other transient neurological signs [1,2] as well as signs of systemic effects [3], but permanent damage has not been described using the 2.5 per cent concentration. The high lipid solubility of thiopental and the ample vascular supply of the epidural space may favour systemic absorption, leading to rapid decline of tissue concentration in the epidural space. Provided the epidural needle or catheter has not breached the dura mater, there seems to be effective separation of the subarachnoid compartment from the epidural space [4]. This is evidenced by a number of reports of other drugs that have been administered inadvertently via the epidural route. The majority of these resulted in no or only transient neurological impairment. These include drugs such as ephedrine [2], magnesium sulphate [5], methohexital [6], ether [7], and potassium chloride [8,9]. However, despite the apparently good dural protection, serious morbidity has also been reported following epidural administration of concentrated potassium chloride solution [10] and paraldehyde [11]. Various strategies have been adopted regarding the management of accidental administration of epidural thiopental. These include injection of local anaesthetic agents in the awake patient [1], epidural epinephrine [3], steroids [3] and epidural lavage through infusion of comparatively large volumes of normal saline [1]. Common to all management strategies are attempts to dilute the drug concentration in the epidural space, to diminish absorption across the dura by influencing the pH and to control the presumed inflammatory response to the drug. However, all these efforts are entirely empirical and have not been evaluated critically under controlled conditions. In particular, the role of steroids to prevent an inflammatory reaction is controversial. Epidural steroids may carry their own risks and their role has not yet been clarified. At present, epidural corticosteroids following inadvertent injection of other inappropriate drugs cannot be universally recommended. A. WEIGERT 62 Starfield Road, London, UK G. LAWTON Department of Anaesthesia, Lewisham University Hospital, Lewisham High Street, London, UK

A method for increasing the viability of the external portion of lumbar catheters placed in the spinal subarachnoid space of rats

A method for direct catheterization of the lumbar subarachnoid space has recently been developed by Storkson et al. (1996) (J Neurosci Methods 1996;65:167–172) that may potentially improve upon the widely used method of Yaksh and Rudy (1976) (Physiol Behav 1976;17:1031–1036). This ‘catheter-through-a-needle’ technique inserts the catheter between lumbar vertebrae 5 (L5) and 6 (L6), which has been shown to reduce neurological impairment and post-surgical deaths. However, employing this technique allows the external portion of the chronic indwelling catheters to be easily damaged, resulting in ≈50% attrition within 4 days after surgery. Therefore, we developed an easy and inexpensive method for protecting the external portion of the catheter that enhances catheter viability beyond 14 days after catheter implantation while also maintaining a low injection volume (8 μl). Moreover, this modification does not significantly alter the implantation methods developed by Storkson et al. (1996) (J Neurosci Methods 1996;65:167–172) and allows for more optimal catheter materials to be incorporated. Chronically implanted catheters ( n=70) with the external portion of the catheter protected, resulted in 4% attrition 7 days after surgery and 11% attrition 14 days after surgery. Approximately 5.5% of animals implanted showed very mild and transient neurological impairment.

Cavoatrial tumor thrombectomy using cardipulmonary bypass without circulatory arrest

Of 29 patients with inferior vena caval tumor thrombus, 14 with supradiaphragmatic extension were deemed suitable for operation. Patients (age, 7.5 to 70 years) had renal cell carcinoma (n = 8), Wilms' tumor (n = 2), transitional cell carcinoma (n = 1), and adrenal carcinoma (n = 3). Seven patients had stage III disease, and 7 patients had stage IV disease. Two patients (group A) had unresectable disease at exploratory celiotomy, 4 patients (group B) underwent tumor thrombectomy without cardiopulmonary bypass, and cardiopulmonary bypass was employed in 8 patients (group C). Three of 8 group C patients had Budd-Chiari syndrome at diagnosis. Cardiopulmonary bypass with moderate hypothermia, and inferior vena caval interruption (clip or filter), was employed in all patients. There were no perioperative deaths. Transient neurological impairment was observed postoperatively in 2 patients. Coagulopathy developed in 1 patient who had hepatic encephalopathy and Budd-Chiari syndrome preoperatively and in another patient in whom protamine could not be administered. No patient had acute renal failure requiring hemodialysis. Median survival is 41 and 17 months in groups B and C, respectively. Some authors have advocated profound hypothermia and circulatory arrest in these patients. We find that satisfactory visualization and excision can be performed with cardiopulmonary bypass and moderate hypothermia, avoiding potential renal, hepatic, neurological, and septic complications associated with circulatory arrest.

Infection of rabbits with human immunodeficiency virus 1. A small animal model for acquired immunodeficiency syndrome.

Injection of rabbits with a human T cell line infected with HIV-1 caused seroconversion within 6 wk, and HIV-1 could be isolated from PBL cultures of infected rabbits. Identity of the isolated virus with HIV-1 was shown by analysis of products amplified by the polymerase chain reaction. HIV-1 infection was seen in rabbits injected with HIV-1-infected cells alone as well as in those that were first infected with HTLV-1 and subsequently with HIV-1. There were no consistent signs of disease in the rabbits infected with HIV-1 alone but HTLV-1/HIV-1-infected rabbits showed signs of illness including diarrhea and weight loss, transient neurologic impairment and, in one animal, a rapidly progressing mammary adenocarcinoma. Examination of organs taken at necropsy from both HIV-1- and HTLV-1/HIV-1-infected animals showed splenic hyperplasia and lymphocyte infiltration of the lungs, as well as moderate damage to liver and kidney in some cases.

Human exposure to styrene vapor.

Human volunteers were exposed to styrene vapor at approximately 50, 100, 200, and 375 ppm for periods of one to seven hours. Only at 375 ppm did the subjects experience significant subjective symptoms and show objective signs of transient neurological impairment. A small portion of the absorbed styrene was rapidly and exponentially excreted from the lungs in the postexposure period. A measurement of the amount of styrene present in the breath in the early postexposure period provided a means for making an estimation of magnitude of exposure. The determination of urinary hippuric acid proved to be insensitive as an indicator of exposure to this compound at these vapor concentrations.