Cross-cultural translation and adaptation of the Danish version of the Fugl-Meyer assessment for post stroke sensorimotor function.

PURPOSE: The Fugl-Meyer assessment (FMA) is the most widely used and recommended clinical assessment scale for evaluating sensorimotor impairments in stroke patients, but an official Danish version has not been available. This study aimed to perform a standardized translation and cross-cultural adaptation (TCCA) of the FMA into Danish. METHODS: First, a comprehensive eight-step TCCA procedure including forward and backward translation and step-wise reviewing by proof-reader and bilingual physiotherapists, to ensure conceptual and semantic equivalence was applied to develop a Danish version of the FMA. Second, inter-rater reliability of the Danish FMA was assessed in 10 subacute stroke patients. Svensson's statistical method designed for rank-based paired ordinal data to identify items showing non-systematic or systematic disagreements in relative position or concentration was used to make further improvements on translation. RESULTS: A Danish FMA version was successfully made by the step-wise TCCA procedure. The clinical validation revealed satisfactory to excellent inter-tester reliability across all items (70-100%). Significant systematic disagreement either in position or concentration or both were observed in about 20% of the items. CONCLUSIONS: The Danish version of the FMA was translated and adapted allowing for a wider standardized use of the FMA in stroke rehabilitation in Denmark.Implications for rehabilitationThe Fugl-Meyer assessment (FMA) is the most used and recommended clinical assessment scale for evaluating sensorimotor impairments in stroke patients.The translated and adapted Danish version of the FMA is now available for use in research and clinical practice in Denmark.This allows for a standardized and unified description of stroke motor recovery and severity in neurorehabilitation nationwide as well as the possibility to compare and conduct trials using FMA internationally.

Neuromuscular Electric Stimulation in Addition to Exercise Therapy in Patients with Lower Extremity Paresis Due to Acute Ischemic Stroke. A proof-of-concept randomised controlled trial.

INTRODUCTION: Exercise therapy and neuromuscular electrical stimulation (NMES) during the initial 14 days after stroke may benefit recovery of gait. We aimed to determine whether poststroke NMES of vastus medial and tibial muscles during exercise therapy is more effective than exercise therapy alone. MATERIALS AND METHODS: In this proof-of-concept randomised trial patients with first-ever acute ischemic stroke and a leg paresis (40-85 years of age) were randomised (1:1) to 10 min of daily NMES + exercise therapy or exercise therapy alone. Primary outcome was the between-group difference in change in 6 min Walk Test (6MWT) at 90 days post stroke estimated with a mixed regression model. Secondary outcomes included 10 m Walk Test, Fugl-Meyer Motor Assessment, Guralnik Timed Standing Balance, Sit to Stand, Timed Up and Go, EQ-5D-5L, Montreal Cognitive Assessment and Becks Depression Inventory. RESULTS: 50 stroke survivors (25 in each group) with a mean age of 67 years (range 43-83) were included. An insignificant between-group difference in change of 28.3 m (95%CI -16.0 to 72.6, p = 0.23, adjusted for baseline) in 6MWT at 90-days follow-up was found, in favour of the NMES group. All secondary outcomes showed no statistically significant between-group difference. The conclusion was that adding NMES to exercise therapy had no effect on poststroke walking distance measured by the 6 MWT or any of the secondary outcomes. CONCLUSIONS: In this proof-of-concept RCT, we demonstrated that NMES in addition to exercise therapy during the first 14 days after onset of ischemic stroke did not improve walking distance or any of the secondary outcomes. Future studies with a longer trial period, stratifying patients into subgroups with comparable patterns of expected spontaneous recovery - if possible within 48 h post stroke, and greater sample size, than in this study are suggestions of how rehabilitation research could go on exploring the potential for NMES as an amplifier in stroke recovery.

Influence of procedural factors on patient procedural pain in relation to diagnostic lumbar puncture.

OBJECTIVE: The aim of this study is to investigate the influence of local anesthetic (LA), operator experience level and needle type on patient procedural pain in relation to diagnostic lumbar puncture (LP). METHODS: LP was performed with either a 22 gauge traumatic needle (22 TN) or a 22 gauge atraumatic needle (22 ATN). Immediately after LP patients documented a procedural pain score (PPS) on a 10-point Likert scale. Use of LA, needle type, anesthetic time interval (ATI), number of needle insertions and the LP operator experience level were registered. ATI was defined as the time from administration of LA to first needle insertion. RESULTS: 104 patients had the LP procedure performed by 66 physicians (40 novices and 26 experienced physicians). Patients having the procedure performed by novices had a lower PPS of 2.56 if LA was administered compared to a higher PPS of 5.80 if LA was not administered (P = .046). Among experienced physicians there was no difference in PPS regardless of administration of LA. If novices administered LA, patient PPS was equal to patients having the procedure performed by an experienced operator. If novices performed the procedure with a 22 TN PPS decreased with increasing ATI (P = .01). No similar correlation was identified with the 22 ATN. CONCLUSION: Our study suggests that LP operator experience level, the needle type used and ATI may influence patient PPS. Further studies are necessary for final conclusions. These studies must consider these factors to avoid fault conclusions.

Time trends and patient selection in the use of continuous electrocardiography for detecting atrial fibrillation after stroke: a nationwide cohort study.

BACKGROUND AND PURPOSE: Clinical use of continuous electrocardiography (cECG) for detecting atrial fibrillation (AF) after stroke is unclear. In a Danish nationwide cohort, we described post-stroke time trends in outpatient cECG usage and AF incidence and characterized factors associated with cECG use. METHODS: Patients without AF discharged after their first ischaemic stroke between 2010 and 2016 were identified from Danish nationwide registries. cECG included Holter or event recording within 120 days from discharge. Cumulative incidence analysis and multivariable adjusted logistic regression were used to assess time trends and factors associated with cECG usage and AF. RESULTS: The study population comprised 39 641 patients. Cumulative use of cECG increased threefold from 3.3% [95% confidence intervals (CI), 2.8-3.8] in 2010 to 10.5% (95% CI, 9.7-11.3) in 2016. Correspondingly, cumulative incidence of post-stroke AF increased from 1.9% (95% CI, 1.5-2.3) to 2.8% (95% CI, 2.4-3.2). Of all cECG-evaluated patients, 6.3% received an AF diagnosis versus 2.2% of the unevaluated. Receiving cECG was associated with increased odds of AF (odds ratio, 3.4; 95% CI, 2.8-4.0). Lower age, milder strokes and less comorbidity were associated with increased odds of receiving cECG. In contrast, risk factors for AF were increasing age and more comorbidity. CONCLUSIONS: Post-stroke outpatient cECG use and AF incidence have increased over time, but screening rates were low. cECG use was associated with tripled odds of detecting AF. There was a disparity between factors associated with cECG use and risk factors of AF. This raise questions as to the appropriateness of the current clinical approach to post-stoke AF detection.

Semi-automatic software based detection of atrial fibrillation in acute ischaemic stroke and transient ischaemic attack.

BACKGROUND AND PURPOSE: Paroxysmal atrial fibrillation (PAF) is often asymptomatic and increases the risk of ischaemic stroke. Detection of PAF is challenging but crucial because a change of treatment decreases the risk of ischaemic stroke. Post-stroke investigations recommend at least 24-h continuous cardiac rhythm monitoring. Extended monitoring detects more PAF but is limited by costs due to manual analysis. Interpretive software might be a reasonable screening tool. The aim was to validate the performance and utility of Pathfinder SL software compared to manual analysis. METHODS: In all, 135 ischaemic stroke patients with no prior history of PAF or atrial fibrillation and who had done a 7-day continuous electrocardiogram monitoring (Holter) were included. Manual analysis was compared with Pathfinder SL software including a systematic control of registered events. RESULTS: Seventeen (12.6%) patients were diagnosed with PAF (atrial fibrillation > 30 s). Pathfinder SL software including a systematic control of events registered 16 (94.1%) patients with PAF. Manually 15 (88.2%) patients were detected with PAF. Pathfinder SL had a negative predictive value of 99% and sensitivity of 94%. CONCLUSIONS: Pathfinder SL software including a systematic evaluation of events is an acceptable alternative compared to manual analysis in PAF detection following ischaemic stroke. It is less time consuming and therefore a reliable, cheaper alternative compared to manual analysis.

Carbachol induces headache, but not migraine-like attacks, in patients with migraine without aura.

Carbachol induces headache in healthy subjects, but the migraine eliciting effect of carbachol has not previously been studied. We hypothesized that the cholinomimetic agonist carbachol would induce headache and migraine-like attacks in migraineurs. Carbachol (3 µg/kg) or placebo was randomly infused into 18 patients with migraine without aura in a double-blind crossover study. Headache was scored on a verbal rating scale from 0 to 10. Velocity in the middle cerebral artery (V(MCA)) and diameter of the superficial temporal artery (STA) were recorded. Fifteen patients experienced headache after carbachol compared with eight after placebo (P = 0.039). There was no difference in incidence of migraine-like attacks after carbachol (n = 8) compared with placebo (n = 6) (P = 0.687). Carbachol caused a decrease in V(MCA) (P = 0.044), but no change in STA (P = 0.089) compared with placebo. The study demonstrated that carbachol provocation is not a good model for experimental migraine.

Prostaglandin I2 (epoprostenol) triggers migraine-like attacks in migraineurs.

Prostacyclin [prostaglandin I(2) (PGI(2))] activates and sensitizes meningeal sensory afferents. In healthy subjects PGI(2) triggers headache in healthy subjects. However, the migraine-eliciting effect of PGI(2) has not been systematically studied in patients with migraine. We hypothesized that intravenous infusion of the stable prostacyclin analogue epoprostenol would trigger migraine-like attacks in migraineurs. We infused 10 ng kg(-1) min(-1) PGI(2) or placebo over 25 min in 12 migraineurs without aura in a controlled, double-blind, cross-over study and recorded headache intensity and associated symptoms, velocity in the middle cerebral artery (V(MCA)) and diameter in the superficial temporal artery. In the period 0-14 h, 12 subjects reported headache on PGI(2) day compared with three subjects on placebo day (P = 0.004), and six subjects fulfilled the criteria for an experimentally induced migraine-like attack compared with two subjects on placebo (P = 0.219). During infusion and post-infusion phases the AUC under the headache curve on PGI(2) was significantly larger than on placebo (P < 0.05). There was a significant V(MCA) decrease (P = 0.015) and superficial temporal artery diameter increase (P < 0.001) on PGI(2) compared with placebo. In conclusion, PGI(2) may trigger a migraine-like attack in migraine sufferers. We suggest sensitization of perivascular nociceptors and arterial dilation as the mode of action of PGI(2)-induced headache and migraine-like attacks.

Prostaglandin E2(PGE2) induces headache in healthy subjects.

The role of prostanoids in nociception is well established. The headache-eliciting effects of prostaglandin E(2) (PGE(2)) and its possible mechanisms have previously not been systematically studied in man. We hypothesized that infusion of PGE(2) might induce headache and vasodilation of cranial vessels. PGE(2) (0.40 microg kg(-1) min(-1)) or saline was infused for 25 min into 11 healthy subjects in a cross-over, double-blind study. Headache intensity was scored on a verbal rating scale from 0 to 10. In addition, we recorded mean flow in the middle cerebral artery (V(MCA)) by transcranial Doppler and diameter of the superficial temporal artery (STA) by high-resolution ultrasonography. All 11 subjects reported headache on the PGE(2) day and no subjects reported headache on the placebo day (P = 0.001). During the immediate phase (0-30 min) (P = 0.005) and the postinfusion phase (30-90 min) (P = 0.005), the area under the curve for headache score was significantly larger on the PGE(2) day compared with the placebo day. PGE(2) caused dilatation of the STA (23.5%; 95% CI 14.0, 37.8) and the MCA (8.3%; 95% CI 4.0, 12.6). We suggest that PGE(2) induces headache by activation and sensitization of cranial perivascular sensory afferents.

Changes in cerebral blood flow after acetazolamide: an experimental study comparing near-infrared spectroscopy and SPECT.

BACKGROUND AND PURPOSE: It is important to find a reliable and bedside method, which can estimate the cerebral blood flow (CBF) of patients in clinical settings. Estimation of CBF by calculating a blood flow index (BFI) using continuous wave near-infrared spectroscopy (CW-NIRS) and indocyanine green (ICG) as an i.v. tracer has been proposed to be a feasible and promising method. To validate if the BFI method can detect relative changes in CBF we compared data with the established method (133)Xenon single photon emission computer tomography ((133)Xe-SPECT). METHODS: Ten healthy subjects were investigated before and after a bolus of acetazolamide. NIRS data were obtained using a multi source detector separation configuration in order to assess a corrected BFI (BFI(corr)) value, which attempts to eliminate contamination of skin blood flow. RESULTS: Data obtained showed no significant correlation between CBF changes measured by (133)Xe-SPECT and BFI(corr) (0.133, P = 0.732). After acetazolamide, a 49% increase in CBF was detected using the (133)Xe-SPECT method, whereas no changes in any ICG variables were observed after acetazolamide. CONCLUSION: The study shows that it is not possible to obtain reliable BFI data, which reflect changes in CBF after acetazolamide infusion, using the CW-NIRS and ICG method.

The cholinomimetic agent carbachol induces headache in healthy subjects.

The parasympathetic nervous system is likely to be involved in migraine pathogenesis. We hypothesized that the cholinomimetic agonist carbachol would induce headache and vasodilation of cephalic and radial arteries. Carbachol (3 microg/kg) or placebo was randomly infused into 12 healthy subjects in a double-blind crossover study. Headache was scored on a verbal rating scale from 0-10. Velocity in the middle cerebral artery (V(MCA)) and diameter of the superficial temporal artery (STA) and radial artery (RA) were recorded. Nine participants developed headache after carbachol compared with three after placebo. The area under the curve for headache was increased after carbachol compared with placebo both during infusion (0-30 min) (P = 0.042) and in the postinfusion period (30-90 min) (P = 0.027). Carbachol infusion caused a drop in V(MCA) (P = 0.003) and an increase in STA diameter (P = 0.006), but no increase in the RA diameter (P = 0.200). In conclusion, the study demonstrated that carbachol caused headache and dilation of cephalic arteries in healthy subjects.

Sumatriptan does not affect arteriovenous oxygen differences in jugular and cubital veins in normal human subjects.

Arteriovenous anastomoses (AVAs) may open up during migraine attacks. In studies with anaesthetized and bilaterally vagosympatectomized pigs, triptans reduce AVA blood flow and increase the arteriovenous O2 difference (AVDO2). To investigate whether subcutaneous sumatriptan 6 mg could induce changes in the AVDO2, we measured the AVDO2 in the external jugular vein in healthy subjects. We also measured the AVDO2 in the internal jugular and cubital veins. There were no changes in AVDO2 after subcutaneous sumatriptan, probably because AVA blood flow is limited in humans with an intact sympathetic nervous system.

Vasoactive intestinal peptide causes marked cephalic vasodilation, but does not induce migraine.

We hypothesized that intravenous infusion of the parasympathetic transmitter, vasoactive intestinal peptide (VIP), might induce migraine attacks in migraineurs. Twelve patients with migraine without aura were allocated to receive 8 pmol kg(-1) min(-1) VIP or placebo in a randomized, double-blind crossover study. Headache was scored on a verbal rating scale (VRS), mean blood flow velocity in the middle cerebral artery (V(mean MCA)) was measured by transcranial Doppler ultrasonography, and diameter of the superficial temporal artery (STA) by high-frequency ultrasound. None of the subjects reported a migraine attack after VIP infusion. VIP induced a mild immediate headache (maximum 2 on VRS) compared with placebo (P = 0.005). Three patients reported delayed headache (3-11 h after infusion) after VIP and two after placebo (P = 0.89). V(mean MCA) decreased (16.3 +/- 5.9%) and diameter of STA increased significantly after VIP (45.9 +/- 13.9%). VIP mediates a marked dilation of cranial arteries, but does not trigger migraine attacks in migraineurs. These data provide further evidence against a purely vascular origin of migraine.

Paracetamol versus nonsteroidal anti-inflammatory drugs for rheumatoid arthritis.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are usually preferred for simple analgesics such as paracetamol for rheumatoid arthritis. It is not clear, however, whether the trade-offs between benefits and harms of NSAIDs are preferable to those of paracetamol (paracetamol is also called acetaminophen). OBJECTIVES: To compare the benefits and harms of paracetamol with NSAIDs in patients with rheumatoid arthritis. SEARCH STRATEGY: Medline Silverplatter, Embase databases were searched up until Sept 2002. Reference lists of identified articles were also searched. SELECTION CRITERIA: Randomised double-blind studies comparing paracetamol with an NSAID. DATA COLLECTION AND ANALYSIS: Decisions on inclusion of trials and data extraction were performed by the two authors independently. MAIN RESULTS: Four cross-over studies, published between 1968 and 1982, involving 121 patients, and four different NSAIDs were included. The generation of the allocation sequence and the use of methods to conceal the allocation were not described in any of the studies. The studies were double-blind but it was not clear whether the blinding was effective. Methods for collecting adverse effects were not described. The NSAIDs were preferred more often than paracetamol by the patients or the investigator. In the largest trial, 20 out of 54 patients (37%) preferred ibuprofen and 7 out of 54 (13%) paracetamol. Investigators preference (as established by joint tenderness, grip strength and joint circumference) was 17 out of 35 for diclofenac versus 5 out of 35 for paracetamol in another trial. However, because of the weaknessess in the trials, no firm conclusion can be drawn. REVIEWER'S CONCLUSIONS: When considering the trade off between the benefits and harms of non-steroidal anti-inflammatory drugs and paracetamol/acetaminophen, it is not known whether one is better than the other for rheumatoid arthritis. But people with rheumatoid arthritis and the researchers in the study did prefer non-steroidal anti-inflammatory drugs more than acetaminophen/paracetamol. There is a need for a large trial, with appropriate randomisation, double-blinding, test of the success of the blinding, and with explicit methods to measure and analyse pain and adverse effects.