Functional MRI of the immediate impact of transcranial magnetic stimulation on cortical and subcortical motor circuits

Recent studies indicate that the cortical effects of transcranial magnetic stimulation (TMS) may not be localized to the site of stimulation, but spread to other distant areas. Using echo-planar imaging with blood-oxygenation-level-dependent (BOLD) contrast at 3 Tesla, we measured MRI signal changes in cortical and subcortical motor regions during high-frequency (3.125 Hz) repetitive TMS (rTMS) of the left sensorimotor cortex (M1/S1) at intensities above and below the active motor threshold in healthy humans. The supra- and subthreshold nature of the TMS pulses was confirmed by simultaneous electromyographic monitoring of a hand muscle. Suprathreshold rTMS activated a network of primary and secondary cortical motor regions including M1/S1, supplementary motor area, dorsal premotor cortex, cingulate motor area, the putamen and thalamus. Subthreshold rTMS elicited no MRI-detectable activity in the stimulated M1/S1, but otherwise led to a similar activation pattern as obtained for suprathreshold stimulation though at reduced intensity. In addition, we observed activations within the auditory system, including the transverse and superior temporal gyrus, inferior colliculus and medial geniculate nucleus. The present findings support the notion that re-afferent feedback from evoked movements represents the dominant input to the motor system via M1 during suprathreshold stimulation. The BOLD MRI changes in motor areas distant from the site of subthreshold stimulation are likely to originate from altered synaptic transmissions due to induced excitability changes in M1/S1. They reflect the capability of rTMS to target both local and remote brain regions as tightly connected constituents of a cortical and subcortical network.     

Cost analysis of traditional follow-up protocol versus MRI for radiographically occult scaphoid fractures: a pilot study for the Accident Compensation Corporation

AIMS: Assessment of the cost-effectiveness of early magnetic resonance imaging (MRI) for suspected radiographically occult scaphoid fractures. Methods Compare costs of patients presenting acutely with suspected scaphoid injuries (managed either with traditional follow-up radiographs and plasters) versus early MRI to exclude a fracture. Results The average medical cost for the control group was NZ470 dollars versus NZ533 dollars in the MRI group. The cost to exclude a fracture was NZ437 dollars with MRI versus NZ459 dollars for the traditional protocol. Weekly compensation costs were comparable. Conclusions The early diagnosis of clinical scaphoid fractures has clear clinical advantages. The use of MRI in this situation is cost-effective, and we recommend that it be offered as part of the routine investigative work-up available for this difficult, but common, clinical scenario.     

An investigation of the repeatability and reproducibility of ISO 11948-1 (the Rothwell method) for measuring the absorption capacity of incontinence pads

The repeatability and reproducibility (precision within and between laboratories, respectively) of an international standard method (ISO 11948-1, the Rothwell method) for measuring the absorption capacity of incontinence pads was investigated. The 74 shaped disposable bodyworn insert pads for heavy incontinence on the UK market in spring 1997 were tested in three laboratories experienced in using the method, one in each of England, Spain and Sweden. Coefficients of variation (standard deviation as a proportion of the mean) for five repeats rarely exceeded 5% within any laboratory. However, there were systematic differences between laboratories: results from the Swedish and Spanish laboratories typically exceeded those from the English laboratory by 13% and 8%, respectively. The good repeatability suggests that the method is capable of adequate precision but the poor reproducibility implies that the instructions in the standard for building and/or using the test apparatus are inadequate, leaving too much room for interpretation. Having studied the data presented here and viewed videos of the apparatus in use in five laboratories (including the three contributing to this note) the ISO working group which wrote the original standard has identified several likely sources of imprecision and is now working to revise the standard to improve its reproducibility.     

Incidence,risk factors and prognosis of stroke and TIA: the need for high-quality,large-scale epidemiological studies and meta-analyses

Stroke is a considerable clinical, social and economic burden. In recent clinical trials, a number of strategies have been shown to reduce the risk of stroke and transient ischaemic attack (TIA) in both primary and secondary prevention settings. Whether these treatments are leading to a significant reduction in the incidence of first and recurrent stroke in the clinic, however, remains unclear due to a paucity of high-quality epidemiological data. A similar lack of reliable epidemiological studies has undermined our understanding of the relationship between many potentially important vascular risk factors and stroke risk. Improvement in our knowledge of stroke epidemiology is a prerequisite for the planning of stroke services, the effective application of current stroke prevention strategies, the development of new strategies, and our understanding of the mechanisms of stroke. Future studies must take into account the clinical and pathological heterogeneity of TIA and stroke, and must be powered to allow subtype differences in risk factor relationships and prognosis to be determined reliably. In many cases, this will require meta-analysis of detailed individual patient data from multiple independent studies.     

An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis

Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p相似文献   

Actions of exogenous and endogenous IL-10 on glial responses to bacterial LPS/cytokines

The objective of this study was to investigate the actions of exogenous and endogenous IL-10 on inflammatory responses of glia. Studies were conducted in primary, mixed glial cultures from C57BL/6 (wild-type [WT]) and IL-10-deficient C57BL/6 (IL-10 knockout [KO]) neonatal mice. Activation of cultures from WT mice by bacterial lipopolysaccharide (LPS, 10 ng/ml-10 microg/ml, 24 h), caused dose-dependent increases in nitric oxide (NO) and prostaglandin E(2) (PGE(2)) release. In cultures from IL-10 KO mice, LPS elicited markedly attenuated release of NO (approximately 4-fold) and PGE(2) (approximately 17-fold). In WT cultures, co-incubation with IL-10 (10 or 100 ng/ml, 24 h) inhibited the effects of LPS on release of NO (30%) and PGE(2) (40-50%). In cultures from IL-10 KO mice, the addition of IL-10 (10 or 100 ng/ml, 24 h) completely abolished LPS-induced NO and PGE(2) release. LPS did, however, release of IL-1beta and TNF-alpha in cultures from all animals. Co-incubation of WT cultures with IL-10 (1, 10, or 100 ng/ml, 24 h) dose-dependently reduced the release of IL-1beta (by 0%, 15%, 75%, respectively). In cultures from IL-10 KO mice, co-incubation with IL-10 (1, 10, or 100 ng/ml, 24 h) completely abolished LPS induced release of IL-1beta. Co-incubation with IL-10 (1, 10, 100 ng/ml) reduced, LPS-induced TNF-alpha release dose-dependently in WT cultures (by 15%, 50% and 90%) and abolished LPS-induced TNF-alpha release in cells from IL-10 KO mice. These results indicate that in glia from WT mice, exogenous IL-10 attenuates LPS-induces release of NO, PGE(2), TNF-alpha and IL-1beta. In contrast, mixed glial cultures from IL-10 KO mice showed reduced responses to LPS, but increased sensitivity to exogenous IL-10.