Multimodal clinical pathways, perineural catheters, and ultrasound-guided regional anesthesia: the anesthesiologist's repertoire for the 21st century

Regional anesthesia is making a comeback because of improved technology and research that shows that its use results in less discomfort for patients and shorter hospital stays. This article provides a brief history of regional anesthesia, describes current techniques for administering it, and discusses potential benefits associated with it. It also describes Mayo Clinic's Total Joint Regional Anesthesia Clinical Pathway, a comprehensive care plan for patients undergoing joint replacement surgery that uses peripheral nerve blockade and multimodal analgesia.     

Modulatory actions of serotonin on ionic conductances of hippocampal dentate granule cells

Pressure ejection of serotonin (2 x 10(-4) M) onto dentate granule neurons in vitro produced a short-lasting membrane hyperpolarization associated with a 10-30% decrease in the input resistance. The hyperpolarization magnitude depended on the extracellular K+ concentration but not on the extra or intracellular Ca2+ concentration. It was followed by a depolarization, especially when serotonin was applied onto the perisomatic area of the neuron. The post-spike-train afterhyperpolarization, which represents a Ca2+-dependent K+ conductance, was decreased by serotonin by 10-100% and remained reduced for 2-10 min following the serotonin-induced hyperpolarization. Decreased adaptation of cell firing was also observed following serotonin application. Ca2+ action potentials evoked by intracellular depolarizing current pulses in the presence of the Na+ channel blocker tetrodotoxin and the K+ channel blocker tetraethylammonium were followed by a large afterhyperpolarization, which was markedly reduced for several minutes following serotonin application. The preceding Ca2+ action potential was either unaffected or prolonged. The hyperpolarization occurring in response to localized application of serotonin, and the reduction of the afterhyperpolarization, may represent two different mechanisms of serotonin action, probably mediated by different mechanisms. The slow time course of the late depolarization and the afterhyperpolarization depression represent modulatory effects of serotonin on dentate granule neurons.     

Multimodal imaging of residual function and compensatory resource allocation in cortical atrophy: a case study of parietal lobe function in a patient with Huntington's disease.

In a case of Huntington's disease (HD) with dementia and pronounced parieto-frontal atrophy, the functional state of the affected regions was investigated using functional magnetic resonance imaging (fMRI) and fluorodeoxyglucose-positron emission tomography (FDG-PET). It was observed that although parietal areas showed extensive atrophy and reduced resting glucose metabolism, the patient performed with similar accuracy but with longer response time in a visuospatial task compared with healthy control subjects. At the same time, the blood oxygen level-dependent (BOLD) fMRI signal in these areas, which are involved in visuospatial processing, showed a similar task-dependent modulation as in control subjects. The signal amplitude (signal percent change) of the task-dependent activation was even higher for the HD patient than in the control group. This residual functionality of parietal areas involved in visuospatial processing could account for the patient's performance in the task concerned, which contrasted with his poor performance in other cognitive tasks. The increased percent-signal change suggests that a higher neuronal effort was necessary to reach a similar degree of accuracy as in control subjects, fitting well with the longer reaction time. We propose that fMRI should be considered as a tool for the assessment of functionality of morphologically abnormal cortex and for the investigation of compensatory resource allocation in neurodegenerative disorders.     

Radical surgery of oligometastatic pancreatic cancer

Background

In metastatic disease (M1), chemotherapy (expected survival: 6–10 months) is considered the only treatment option. The aim of this study was to evaluate the outcome of curative M1 PDAC resections.

Metabolic activity of osteoarthritic knees correlates with BMI

Osteoarthritis of the knee has consistently been linked to obesity, defined as a body mass index (BMI) > 30 kg/m². It has been hypothesized that obesity may lead to osteoarthritis through increased joint pressure, accumulated microtrauma, and disruption of normal chondrocyte metabolism. These changes in chondrocyte metabolism have not been thoroughly investigated, and it is the purpose of this study to identify a relationship between BMI and altered chondrocyte metabolism in osteoarthritic tissue. Articular cartilage was harvested from the femoral condyles of patients after total knee arthroplasty, and analyzed in explant and alginate models. Glycosaminoglycan (GAG) content was measured using a dimethylmethylene blue assay and normalized to DNA content using a PicoGreen® assay. Studies have reported GAGs to be a reliable measurement of chondrocyte metabolism and osteoarthritis progression. Our results show a significant linear relationship of increasing BMI and increasing GAG content in both alginate and explant models (p < 0.001 and p = 0.001). Obese (BMI ≥ 30 kg/m²) and non-obese (BMI < 30 kg/m²) comparisons also demonstrated significant differences with higher GAG/DNA content in obese individuals compared to non-obese (p = 0.001 and p = 0.015). The study results reveal significant relationships between GAG content and BMI in this population of osteoarthritic patients. The significant difference in GAG content between the obese and non-obese patients supports the connection between osteoarthritis and obesity previously reported. Higher patient BMI (> 30 kg/m²) may be similar to dynamic compression injuries which cause increased GAG synthesis in response to cartilage damage.     

The amount of solid cerebral microemboli during carotid stenting does not relate to the frequency of silent ischemic lesions

BACKGROUND AND PURPOSE: Carotid artery stent placement (CAS) may be associated with clinically silent cerebral lesions. We prospectively evaluated the association of the number of solid cerebral microemboli during unprotected CAS with the frequency of silent cerebral lesions as detected by diffusion-weighted MR imaging (DWI). METHODS: We performed multifrequency transcranial Doppler detection of solid microemboli in the ipsilateral middle cerebral artery (MCA) during CAS in 27 consecutive patients with symptomatic high-grade carotid stenoses. No embolus protection was used in any of the cases. DWI before and 24 +/- 2 hours after CAS was used to detect new ischemic lesions. RESULTS: We detected 484 solid microemboli in 17 patients (63%). On MR imaging 24 +/- 2 hours after CAS, 6 patients (22%) had developed 13 new clinically silent DWI lesions within the ipsilateral MCA territory. In patients with Doppler evidence of solid emboli during CAS, the incidence of new DWI lesions was higher (29%) than in patients without Doppler evidence of solid emboli during the procedure (10%); this difference was not statistically significant (P = .25). The number of solid microemboli during CAS in patients with new ipsilateral DWI lesions was not significantly different from that in patients without new ipsilateral DWI lesions. CONCLUSIONS: Solid microembolism is a common event during unprotected CAS; however, the frequency of procedure-related silent cerebral lesions appears to be independent of the number of solid cerebral microemboli during the procedure.     

Prevalence of founder BRCA1 and BRCA2 mutations in unselected French Canadian women with breast cancer

The frequency of BRCA1 and BRCA2 mutations in women with breast cancer varies according to the age at diagnosis, family history of cancer, and ethnicity/country of origin. We set out to estimate the frequency of seven previously described founder mutations in BRCA1 and BRCA2 in all eligible French Canadian women diagnosed with invasive breast cancer at one Montreal hospital over a 20-month period. One hundred and ninety-two patients were eligible and 127 (66.2%) provided blood for genetic testing. We identified 4 women who carried a founder mutation (3.1%, 95% confidence interval 0.9-7.9%) in this population. Interestingly, all the mutations were in BRCA2. The mean age at diagnosis for mutation carriers was 51.2 years (range 49.1-53.5). Two of these 4 cases were lobular invasive carcinomas and 2 were ductal carcinomas, histological grade 1 or 2. Despite a small tumor size (< or =20 mm), axillary nodal involvement was present in 3 women. Estrogen receptors were strongly expressed in all cases. Two of the 4 cases reported a strong family history of breast cancer, but a family history of site-specific breast cancer was a relatively poor indicator of the presence of BRCA2 mutations. The absence of BRCA1 mutations may be a result of chance, but may also reflect different geographical origins of the most common BRCA1 mutations within the French Canadian population.