The impact of physical therapy intervention of dysphagia on preventing pneumonia in acute stroke patients: A randomized controlled trial.

BACKGROUND AND OBJECTIVES: Dysphagia is a common complication following stroke. It corresponds to the development of pneumonia, which is always associated with bad prognosis, longer hospital stays and increased mortality. The aim of the study was to assess the impact of physical therapy intervention of dysphagia on preventing pneumonia in acute stroke patients. METHODS: A single-blind randomized controlled trial was carried out on 70 ischemic stroke patients with oropharyngeal dysphagia, age ranged from 49 to 65 years. They were randomly assigned to two groups (control and study) of equal number. Patients in the control group received oral care and nasogastric tube feeding, while patients in the study group received the same program in addition to the designed physical therapy program (exercises and neuromuscular electrical stimulation). The intervention program was applied for 40 min/session, 1 session/day, and 5 days/week for 4 weeks. Gugging swallowing screen (GUSS), and stroke associated pneumonia (SAP) control and prevention criteria were used to assess dysphagia and incidence of pneumonia at baseline, after two and 4 weeks of intervention for both groups. RESULTS: Before treatment, all patients were susceptible to pneumonia after two and 4 weeks of intervention; there were a significant increase in GUSS score in both groups with more improvement in favor of the study group (p < 0.05) and a statistically significant increase in incidence of SAP after 2 weeks of intervention only in the control group (p < 0.05). The results also showed a significant negative correlation between GUSS score and SAP (r = - 0.3662, p = 0.0018) IMPLICATIONS FOR PHYSIOTHERAPY PRACTICE: adding physical therapy (exercise therapy and neuromuscular electrical stimulation) to oral care and nasogastric tube feeding is effective in improving oropharyngeal dysphagia and decreasing the incidence of aspiration pneumonia in acute ischemic stroke patients.

Validity of different scoring systems in prediction of intensive care unit admission and mortality in acute organophosphate poisoning.

Background: Organophosphate compounds (OPCs) pose significant health risks, especially in developing countries with limited resources. Predicting outcomes in OPCs poisoning is crucial for guiding clinical management and reducing mortality rates. The aim of this study to evaluate the validity of different scoring systems Rapid Emergency Medicine Score, Multiple Organ Dysfunction Score, Acute Physiology and Chronic Health Evaluation Score, and Poison Severity Score in prediction of intensive care unit (ICU) admission and mortality of acute OPCs poisoning patients. Methods: A cross-sectional study was conducted on 103 patients admitted to Xx Poison Control Center between May 2022 and June 2023. Scoring systems were applied at admission, and their performance in predicting the need for ICU admission and mortality was evaluated using receiver operating characteristic (ROC) curve analysis. Results: Most patients survived (92.2%). Only 13.6% of the patients required ICU admission. Significant differences in median scores were observed between survivors and non-survivors and between patients requiring ICU admission and those who did not. Multiple Organ Dysfunction Score exhibited the highest discriminatory power for predicting both ICU admission (AUC = 0.983) and mortality (AUC = 0.999). Conclusion: The findings highlight the importance of utilizing scoring systems, particularly Multiple organ dysfunction score, for prediction of poor outcomes of acute OPCs poisoning.

Predictors for prolonged qt intervals in acute antipsychotic poisoned patients.

Background: Acute antipsychotic poisoning is correlated to a high prevalence of qt interval prolongation. Aim: This study aimed to evaluate early qt interval prolongation predictors in acute antipsychotic-poisoned patients. Methodology: This prospective cohort study enrolled 70 symptomatic patients with acute antipsychotic poisoning. Sociodemographic data, toxicological, clinical, investigation, and outcomes were collected and analyzed. The estimation of the corrected qt interval (QTc) was performed using Bazett's method. Primary outcome was normal or abnormal length of QTc interval. Secondary outcomes included duration of hospital stay, complete recovery and mortality. The corrected qt interval was analyzed by univariate and multivariate logistic regression analysis. Results: Patients were divided into groups A (normal QTc interval up to 440 msec; 58.6% of cases) and B (prolonged QTc interval ≥ 440 msec; 41.4% of cases). Patients in group B had significantly high incidences of quetiapine intake, bradycardia, hypotension, hypokalemia, and long duration of hospital stay. By multivariate analysis, quetiapine [Odd's ratio (OR): 39.674; Confidence Interval (C.I:3.426-459.476)], bradycardia [OR: 22.664; C.I (2.534-202.690)], and hypotension [OR: 16.263; (C.I: 2.168-122.009)] were significantly correlated with prolonged QTc interval. Conclusion: In acute antipsychotic poisoning, quetiapine, bradycardia, and hypotension are early clinical predictors for prolonged QTc interval.

The influence of radial extracorporeal shock wave therapy on shoulder pain and structural abnormalities in stroke patients.

Introduction: Structural abnormalities in the shoulder joint are a common complication post stroke, and the consequent pain and functional limitations become devastating quality of life problems for such patients. Shock wave therapy is a non-invasive method that can enhance the level of perfusion in ischaemic tissues, relieve inflammation, and promote healing. The aim of the study was to examine the efficacy of radial extracorporeal shock wave therapy (rESWT) on pain and disability levels in stroke patients with shoulder structural abnormalities. Material and methods: Thirty subacute stroke patients aged between 40 and 60 years were randomly allocated into 2 equal groups after signing an institutional consent form. The real rESWT group (GA) underwent rESWT in addition to a designed program of physical therapy to the shoulder joint. The control group (GB) received sham rESWT in addition to the same physical therapy program as for GA. The treatment protocol for both groups was 2 times per week for a month. Baseline and post-intervention findings in both groups were assessed and compared for primary outcomes including shoulder structural changes, pressure pain threshold (PPT), and shoulder disability, measured by ultrasonography (USS), a handheld algometer, and the shoulder pain disability index (SPADI), respectively. Results: Significant reduction of all post-treatment SPADI scores (pain, disability, and total scores) in both groups with a remarkable decrease in the rESWT group (GA) (p < 0.05). In addition, USS scores and PPT findings showed notable preference in favour of the GA group, which was demonstrated as significant decrease in USS score with an increase in PPT findings only in the rESWT group (GA) (p < 0.05). Conclusions: The addition of radial extracorporeal shock wave therapy (rESWT) to a designed physical therapy program is more efficient in reducing shoulder structural abnormalities, pain, and disability in subacute stroke patients.

Topical application of Aloe gel and/or olive oil combination promotes the wound healing properties of streptozotocin-induced diabetic rats.

Diabetic wounds are characterized by a delayed closure rate due to the excess inflammation and the inhibition of angiogenesis. Natural products derived from Aloe vera have shown great promise due to their healing magnificent properties. Olive oil is another natural product with anti-microbial and anti-inflammatory properties that may contribute to the healing process. In the present investigation, we tried to evaluate the efficacy of topical application of Aloe gel and/or olive oil in the enhancement of diabetic wounds using histological and immunohistochemical analysis. Excisional wounds were created on the back skin of streptozotocin-induced diabetic rats. Topical treatments of Aloe gel and/or olive oil were applied separately and in a combination (AVO) daily for experimental groups. Macroscopic and microscopic observations of the excision wounds were monitored at time intervals (3, 6, 9, 14 days) post-wounding. Macroscopic observations of the AVO group exhibited almost complete healing at day 14, while other groups were still in progress. Similarly, immunohistochemical analysis of the AVO group showed a mild expression pattern of NF-κB.. While, the cell proliferation (Ki-67), and angiogenesis (CD34) markers were upregulated. Conclusively, the obtained results showed that the AVO combination effectively improved the healing process in diabetic excisional wounds with significant differences in the healing kinetics compared to wounds that received Aloe gel or olive oil separately.

The ameliorative effect of kaempferol against CdCl2- mediated renal damage entails activation of Nrf2 and inhibition of NF-kB.

This study evaluated the nephroprotective effect of kaempferol against cadmium chloride (CdCl2) -induced nephropathy in rats. It also investigated if activation of Nrf2 is a common mechanism of action. Adult male rats ((150 ± 15 g) were divided into 4 groups (n = 8/each) as a control (1% DMSO, orally), control + kaempferol (200 mg/kg, orally), CdCl2 (50 mg/l in drinking water), and CdCl2 + kaempferol (200 mg/kg)-treated rats. All treatments were conducted for 8 weeks. Kaempferol significantly attenuated CdCl2-induced weight loss, reduction in kidney weights, and the injury in the glomeruli, proximal tubules, and distal tubules in the treated rats. It also significantly lowered serum levels of urea and creatinine, increased urine output and urinary creatinine levels and clearance but reduced urinary levels of albumin urinary albumin exertion (UAER), and urinary albumin/creatinine ratio (UACR) in these rats. In parallel, kaempferol downregulated renal levels of cleaved caspase-3 and Bax and unregulated those of Bcl2. In the kidney tissues of the control animals and CdCl2 rats, kaempferol significantly attenuated oxidative stress, inflammation and significantly boosted levels of manganese superoxide dismutase and glutathione. Also, and in both groups, kaempferol suppressed the nuclear levels of NF-κB p65, downregulated Keap1, and stimulated the nuclear activation and protein levels of Nrf2. In conclusion, kaempferol is a potential therapeutic drug to prevent CdCl2-induced nephropathy due to its anti-inflammatory and anti-oxidant effects mediated by suppressing NF- NF-κB p65 and transactivating Nrf2.

Salidroside inhibits insulin resistance and hepatic steatosis by downregulating miR-21 and subsequent activation of AMPK and upregulation of PPARα in the liver and muscles of high fat diet-fed rats.

This study evaluated if salidroside (SAL) alleviates high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) by downregulating miR-21. Rats (n = 8/group) were treated for 12 weeks as normal diet (control/ND), ND + agmoir negative control (NC) (150 µg/kg), ND + SAL (300 mg/kg), HFD, HFD + SAL, HFD + compound C (an AMPK inhibitor) (200 ng/kg), HFD + SAL + NXT629 (a PPAR-α antagonist) (30 mg/kg), and HFD + SAL + miR-21 agomir (150 µg/kg). SAL improved glucose and insulin tolerance and preserved livers in HFD-fed rats. In ND and HFD-fed rats, SAL reduced levels of serum and hepatic lipids and the hepatic expression of SREBP1, SREBP2, fatty acid (FA) synthase, and HMGCOAR. It also activated hepatic Nrf2 and increased hepatic/muscular activity of AMPK and levels of PPARα. All effects afforded by SAL were prevented by CC, NXT629, and miR-21 agmoir. In conclusion, activation of AMPK and upregulation of PPARα mediate the anti-steatotic effect of SAL.

Kaempferol prevents cadmium chloride-induced liver damage by upregulating Nrf2 and suppressing NF-κB and keap1.

This study evaluated the protective effect of kaempferol, a natural flavonoid, against cadmium chloride (CdCl2)-induced liver damage and examined the possible anti-inflammatory and antioxidant mechanisms of protection. Adult male rats were divided into 4 groups (each of 8 rats) as control, kaempferol (50 mg/kg/day orally), CdCl2 (15 ppm/day), and CdCl2 (15 ppm/day) + kaempferol (50 mg/kg/day). All treatments were given for 30 days. With no effect on attenuating the reduced food intake, kaempferol significantly increased body weight and lowered serum levels of liver injury markers including bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase 1 (γ-GTT1) in the CdCl2-treated rats. It also restored normal liver architectures, prevented hepatocyte, loss, and swelling and reduced inflammatory cell infiltration. These effects were associated with a reduction in mitochondrial permeability transition pore, as well as in the expression of cytochrome-c and cleaved caspase-3, markers of mitochondrial damage, and intrinsic cell death. In both the control positive and CdCl2-treated rats, kaempferol significantly lowered the hepatic levels of reactive oxygen species, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), Interleukine-6 (IL-6), and the nuclear activity and localization of NF-κB p65. Besides, kaempferol significantly increased the hepatic total and nuclear levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1, as well as levels of superoxide dismutase (SOD) and reduced glutathione (GSH) but reduced the cytoplasmic protein levels of keap1. In conclusion, the protective effect of kaempferol against CdCl2-induced hepatic damage is mediated by antioxidant and anti-inflammatory effects driven by upregulating Nrf2/HO-1 axis and suppressing the NF-κB p65 and keap1.

Cadmium chloride induces non-alcoholic fatty liver disease in rats by stimulating miR-34a/SIRT1/FXR/p53 axis.

Cadmium (Cd) is associated with non-alcoholic fatty liver disease (NAFLD). The hepatic activation of p53/miR-43a-induced suppression of SIRT1/FXR axis plays a significant role in the development of NAFLD. In this study, we have investigated CdCl2-induced NAFLD in rats involves activation of miR34a/SIRT1/FXR axis. Adult male rats were divided into 4 groups (n-8/each) as a control, CdCl2 (10 mg/l), CdCl2 + miR-34a antagomir (inhibitor), and CdCl2 + SRT1720 (a SIRT1 activator) for 8 weeks, daily. With no effect on fasting glucose and insulin levels, CdCl2 significantly reduced rats' final body, fat pads, and liver weights, and food intake. Concomitantly, it increased the circulatory levels of liver markers (ALT, AST, and γ-GTT), increased the serum and hepatic levels of total cholesterol and triglycerides coincided with increased hepatic lipid accumulation. Besides, it increased the mRNA and protein levels of SREBP1, SREBP2, FAS, and HMGCOA reductase but reduced mRNA levels of PPARα, CPT1, and CPT2. Interestingly, CdCl2 also increased mRNA levels of miR34 without altering mRNA levels of SIRT1 but with a significant reduction in protein levels of SIRT1. These effects were associated with increased total protein levels of p53 and acetylated protein of p53, and FXR. Of note, suppressing miR-34a with a specific anatomic or activating SIRT1 by SRT1720 completely prevented all these effects and reduced hepatic fat accumulations in the livers of rats. In conclusion, CdCl2 induced NAFLD by increasing the transcription of miR-34a which in turn downregulates SIRT1 at the translational level.

Salidroside induces cell apoptosis and inhibits the invasiveness of HT29 colorectal cells by regulating protein kinase R, NF-κB and STAT3.

BACKGROUND: Protein kinase R (PKR) can suppress various types of solid tumors by inducing cellular oxidative stress and apoptosis. Likewise, Slaidorside, a plant flavonoid, was shown to have anti-tumorigenesis in many solid tumors. OBJECTIVE: This study evaluated anti-tumorigenesis of Salidroside in HT29 colorectal cancer and investigated if the underlying mechanism involves activation of PKR. METHODS: Control or PKR deficient cells were cultured in DMEM media treated with 100 µM Salidroside and cell survival, apoptosis, and other biochemical-related markers were evaluated. RESULTS: Salidroside significantly reduced cell survival and proliferation and increased the release of lactate dehydrogenase (LDH) and levels of single-stranded DNA (ssDNA). It also increased the protein levels of caspases 3 and 8. Concomitantly, Salidroside increased the protein level and activity of PKR and increased the expression of its downstream targets, p-eIF2α (Ser51), p53 MAPK, and p53. On the contrary, it inhibited the nuclear activation of STAT-3 and NF-κB p65. In PKR deficient cells, the partial effects of Salidroside on cell survival, proliferation, and apoptotic markers were observed coincided with no effects on the expression of eIF-2α, and JNK, p53, p38 MAPK, and caspase 8 but with a significant decrease in the nuclear activities of STAT3 and NF-κB. CONCLUSION: Salidroside suppresses the tumorigenesis of HT29 CRC by increasing activation of eIF-2α and JNK and upregulation of p53, p38 MAPK, and caspase-8 through upregulating and activation of PKR. However, the tumor suppressor effect of Salidroside requires also inhibition of STAT3 and NF-κB in a PKR-independent mechanism.

Low frequency transcranial magnetic stimulation in subacute ischemic stroke: Number of sessions that altered cortical excitability.

BACKGROUND: Cortical reorganization between both cerebral hemispheres plays an important role in regaining the affected upper extremity motor function post-stroke. OBJECTIVES: The purpose of the current study was to investigate the recommended number of contra-lesion low frequency repetitive transcranial magnetic stimulation (LF-rTMS) sessions that could enhance cortical reorganization post-stroke. METHODS: Forty patients with right hemiparetic subacute ischemic stroke with an age range between 50-65 yrs were randomly assigned into two equal groups: control (GA) and study (GB) groups. Both groups were treated with a selected physical therapy program for the upper limb. Sham and real contra-lesion LF-rTMS was conducted for both groups daily for two consecutive weeks. Sequential changes of cortical excitability were calculated by the end of each session. RESULTS: The significant enhancement in the cortical excitability was observed at the fourth session in favor of the study group (GB). Sequential rate of change in cortical excitability was significant for the first eight sessions. From the ninth session onwards, no difference could be detected between groups. CONCLUSION: The pattern of recovery after stroke is extensive and not all factors could be controlled. Application of LF-rTMS in conjugation with a selected physical therapy program for the upper limb from four to eight sessions seems to be efficient.

Cadmium Chloride Induces Memory Deficits and Hippocampal Damage by Activating the JNK/p66Shc/NADPH Oxidase Axis.

This study investigated whether the mechanism underlying the neurotoxic effects of cadmium chloride (CdCl2) in rats involves p66Shc. This study comprised an initial in vivo experiment followed by an in vitro experiment. For the in vivo experiment, male rats were orally administered saline (vehicle) or CdCl2 (0.05 mg/kg) for 30 days. Thereafter, spatial and retention memory of rats were tested and their hippocampi were used for biochemical and molecular analyses. For the in vitro experiment, control or p66Shc-deficient hippocampal cells were treated with CdCl2 (25 µM) in the presence or absence of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor. Cadmium chloride impaired the spatial learning and retention memory of rats; depleted levels of glutathione and manganese superoxide dismutase; increased reactive oxygen species (ROS), tumor necrosis factor α, and interleukin 6; and induced nuclear factor kappa B activation. Cadmium chloride also decreased the number of pyramidal cells in the CA1 region and induced severe damage to the mitochondria and endoplasmic reticulum of cells in the hippocampi of rats. Moreover, CdCl2 increased the total unphosphorylated p66Shc, phosphorylated (Ser36) p66Shc, phosphorylated JNK, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cytochrome c, and cleaved caspase-3. A dose-response increase in cell death, ROS, DNA damage, p66Shc, and NADPH oxidase was also observed in cultured hippocampal cells treated with CdCl2. Of note, all of these biochemical changes were attenuated by silencing p66Shc or inhibiting JNK with SP600125. In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc.

Kaempferol protects against cadmium chloride-induced hippocampal damage and memory deficits by activation of silent information regulator 1 and inhibition of poly (ADP-Ribose) polymerase-1.

The neuroprotective effect of Kaempferol against cadmium chloride (CdCl2) -induced neurotoxicity is well reported. The silent information regulator 1 (SIRT1) and poly (ADP-Ribose) polymerase-1 (PARP1) are two related cellular molecules that can negatively affect the activity of each other to promote or inhibit cell survival, respectively. It is still largely unknown if the neurotoxicity of CdCl2 or the neuroprotection of Kaempferol are mediated by modulating SIRT1 and/or PAPR1 activities. In this study, we tested the hypothesis that CdCl2-induced memory deficit and hippocampal damage are associated with downregulation/inhibition of SIRT1 and activation of PAPR1, an effect that can be reversed by co-treatment with Kaempferol. Rats (n = 12/group) were divided into 4 groups as control, control + Kaempferol (50 mg//kg), CdCl2 (0.5 mg/kg), and CdCl2 + Kaempferol. All treatments were administered orally for 30 days daily. As compared to control rats, CdCl2 reduced rat's final body weights (21.8%) and their food intake (30%), induced oxidative stress and apoptosis in their hippocampi, and impaired their short and long-term recognition memory functions. Besides, the hippocampi of CdCl2-treated rats had higher levels of TNF-α (197%), and IL-6 (190%) with a concomitant increase in nuclear activity and levels of NF-κB p65 (721% & 554%). Besides, they showed reduced nuclear activity (53%) and levels (74%) of SIRT1, higher nuclear activity and levels of PARP1 (292% & 138%), increased nuclear levels of p53 (870%), and higher acetylated levels of NF-κB p65 (513%), p53 (644%), PARP1 (696%), and FOXO-2 (149%). All these events were significantly reversed in the CdCl2 + Kaempferol-treated rats. Of note, Kaempferol also increased levels of MnSOD (73.5%), and GSH (40%), protein levels of Bcl-2 (350%), and nuclear activity (67%) and levels (46%) of SIRT1 in the hippocampi of the control rats. In conclusion, Kaempferol ameliorates CdCl2-induced memory deficits and hippocampal oxidative stress, inflammation, and apoptosis by increasing SIRT1 activity and inhibiting PARP1 activity.

Impact of Patient-Surgeon Relationship on Patient's Return to Work.

BACKGROUND: Upper-limb injuries and musculoskeletal disorders represent a major economic burden for both patients and society, largely due to limitations in returning to work. We hypothesized that a positive patient-surgeon relationship may facilitate patients' recovery and lead to a faster return to work. METHODS: This longitudinal observational study comprised 219 patients, from 8 French hand trauma centers, who were 18 to 55 years of age and were on sick leave from work because of an injury or musculoskeletal disorder of the upper limb. In addition to instruments measuring patients' functional scores and quality of life, the quality of the patient-surgeon relationship was assessed at enrollment using a specific questionnaire (Q-PASREL [Quality of PAtient-Surgeon RELationship]). Six months after enrollment, the return-to-work status was assessed. Logistic and Cox regression models were developed to identify predictors of return to work (yes/no) and the time off from work in days. RESULTS: Overall, 74% of the patients who returned to work within 6 months after enrollment had a high or medium-high Q-PASREL score, whereas 64% of the patients who were still on sick leave had a low or medium-low Q-PASREL score. The odds of patients with a low or medium-low Q-PASREL score returning to work were, respectively, 95% and 71% lower than the odds of patients with a high score doing so, with a percent difference of 56% (95% confidence interval [CI] = 40% to 71%) for low versus high (odds ratio [OR] = 0.05 [95% CI = 0.02 to 0.13]) and 25% (95% CI = 6% to 44%) for medium-low versus high (OR = 0.29 [95% CI = 0.11 to 0.76]). All Q-PASREL items and scores were significantly associated with return to work. CONCLUSIONS: Patients with a lower Q-PASREL score and more severe disability were less likely to return to work within 6 months and had a longer time off from work. Efforts to improve the quality of patient-surgeon relationships may minimize the duration of sick leaves and accelerate patient recovery. LEVEL OF EVIDENCE: Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Spinal accessory nerve repair using a direct nerve transfer from the upper trunk: results with 2 years follow-up.

Spinal accessory nerve grafting requires identification of both nerve stumps in the scar tissue, which is sometimes difficult. We propose a direct nerve transfer using a fascicle from the posterior division of the upper trunk. We retrospectively reviewed 11 patients with trapezius palsy due to an iatrogenic injury of the spinal accessory nerve in nine cases. The mean age was 38 years (range 21-59). Preoperatively, patients showed shoulder weakness and limited range of motion. At a mean follow-up of 25 months, active shoulder abduction improvement averaged 57°. Trapezius muscle strength graded M4 or M5 in 10 cases and M3 in one case. No deltoid or triceps impairment was reported. Scapula kinematics was considered normal in seven patients. This technique gave satisfactory functional results and may be an alternative to spinal accessory nerve grafting for the management of trapezius palsies if direct repair is not feasible. LEVEL OF EVIDENCE: IV.

Aerobic exercises enhance cognitive functions and brain derived neurotrophic factor in ischemic stroke patients.

BACKGROUND: Stroke is a leading cause of functional impairments. High percentage of these patients will experience some degree of cognitive affection, ranging from mild cognitive impairment to dementia. OBJECTIVE: Demonstrate the role of aerobic exercises enhancing cognitive functions and its effect on Brain Derived Neurotrophic factor (BDNF) in post-ischemic stroke patients in the territory of anterior circulation. SUBJECTS AND METHODS: We included thirty Egyptian ischemic stroke patients in the territory of anterior circulation. They were divided into 2 groups; group 1 (G1) were subjected to physiotherapy program without aerobic exercises and group 2 (G2) were subjected to the same previous program followed by aerobic exercises. Both groups were subjected to pre- and post-treatment Addenbrookes's Cognitive Examination- Revised (ACER) and serum level of BDNF. RESULTS: Our results showed a significant improvement in ACER score in G2 compared to G1 post-treatment (p = 0.017). BDNF serum level significantly increased in G2 post-treatment compared to pre-treatment (p = 0.001) and compared to G1 group (p = 0.0458). ACER improvement was positively correlated to increase in serum level of BDNF (r = 0.53, p = 0.044). CONCLUSION: Aerobic exercises improve cognitive functions of ischemic stroke patients. This improvement is related to the increase in serum level of BDNF.

Reanimation of elbow extension with intercostal nerves transfers in total brachial plexus palsies.

BACKGROUND: Restoration of flexion in the elbow is the priority in the management of brachial plexus injuries. Current techniques of reconstructions, combining both nerve grafting and nerve transfer, allow more extensive repair, with additional targets: shoulder, elbow extension, hand. The transfer of intercostal nerves onto the nerve of the triceps long head is used to restore elbow extension. The aim of this retrospective study is to evaluate the results of this procedure, in total brachial plexus palsies with uninjured C5 and C6 roots. METHODS: Eleven patients with total brachial plexus injury were reviewed 24 months in average after intercostal nerves transfer. The average age of the patients was twenty-nine years. The average time to surgery after occurrence of the injury was 5 months. Triceps re-innervation and strength of elbow extension were evaluated. RESULTS: The averaged time required for triceps re-innervation after intercostal nerve transfer was 9 months. Seven patients achieved M4 elbow extension according to the Medical Research Council grading system. Two patients achieved M3 elbow extension. Two patients had poor results (M2 and M0). DISCUSSION AND CONCLUSIONS: Transfer of intercostal nerves onto the nerve of the triceps long head is a reliable procedure for the restoration of elbow extension in total brachial plexus palsy.

Digital pulley enlargement allowing early active motion following primary repair of flexor tendons.

We present a new technique of pulley enlargement that preserves its continuity without suturing. The principle of this technique is to excise 2 opposite symmetric triangles. For each of these triangles, the incision starts in the middle of the edge of the pulley and ends beyond the middle of its length. The pulley is enlarged over its entire length, both by debridement of the extremities and by plastic deformation. Although this technique precludes complete closure of the digital sheath, it spares the continuity of the pulley and thus allows early active rehabilitation.

"Stabilized arthroplasty" for old fracture dislocations of the fifth carpometacarpal joint.

The procedure of stabilized arthroplasty we present in this paper aims at a global functional restoration of old fracture dislocations of the fifth carpometacarpal joint. The conflict is eliminated by resecting the base of the metacarpal, whereas length of the fifth digit ray is restored by fusion to the adjacent fourth metacarpal. Fifth metacarpal mobility is maintained via transfer to the fourth carpometacarpal joint. The base of the fifth metacarpal is resected through a dorso-lateral approach to the fourth-fifth intermetacarpal space. The preferred plane of resection is not perpendicular to the shaft of the metacarpal but parallel to the distal articular surface of the hamatum which faces 30 degrees anteriorly. A 5 to 10 mm resection is possible without compromising the insertion of extensor carpi ulnaris. The fifth metacarpal must then be temporarily fixed by 1 or 2 intermetacarpal K-wires in the preferred position. The cortical bones on both sides of the proximal fourth intermetacarpal space must then be refreshed over 1 to 1.5 cm and the space filled with cancellous bone graft. The osteosynthesis of the lateral fusion is secured by 2 transverse screws including the 4 cortices. A temporary distal metaphyseal wire relieves forces until bone fusion. Compared with the more commonly used operative procedures, stabilized arthroplasty provides a better mobility than arthrodesis and restores metacarpal length better than nonstabilized resectional arthroplasty. Nevertheless, it can only be done given the fourth carpometacarpal joint is intact.