Background: Previous studies comparing unipolar and bipolar hemiarthroplasty for treatment of displaced intracapsular femoral neck fractures in elderly patients have often lacked methodological power and yielded conflicting clinical results. The objective of this study was to compare the clinical outcomes from each implant in a randomized cohort of elderly patients with intracapsular fracture of the femoral neck treated with a cemented hemiprosthesis.
Methods: This study is a clinical trial of 261 patients (82.0 ± 7.9 years) who were randomly assigned to one of the two treatment groups: group 1 (n = 133) received a cemented bipolar implant and group 2 (n = 128) received a unipolar head with the same stem. At 12 months post-surgery, pain and functional abilities were quantified by blinded assessors using the Oxford and Harris Hip Scores, Verbal Numerical Rating Score and Six-Minute Walk. The Mann-Whitney U-test and t-test for independent samples were used to compare results between the groups (P < 0.05).
Results: There were no significant differences in any clinical scores between the groups. Results from the Six-Minute Walk indicated no difference in functional walking ability or endurance (P = 0.446) between the groups. Self-selected pain ratings also did not differ between groups (P = 0.236). Patients receiving the unipolar prosthesis had significantly reduced abduction (P = 0.0001) and internal rotation (P = 0.047) in the operated hip compared to the non-operated hip.
Conclusion: These short-term results suggest that unipolar implants share many of the advantages of the bipolar prosthesis but can be manufactured at substantially lower cost. These implants may be appropriate for the less-active elderly patient, particularly when used with bone cement.
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Background: The therapeutic management of dementia with Lewy bodies (LBD) is a challenge given the high sensitivity to drugs in this disease. This is particularly sensitive with regard to the management of parkinsonism. In particular, treatment of motor symptoms with levodopa or dopaminergic agonists poses a risk of worsening cognitive and behavioral symptoms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Centre for Addiction and Mental Health, Toronto, ON, Canada.
Background: Dysregulated GABA/somatostatin (SST) signaling has been implicated in psychiatric and neurodegenerative disorders. The inhibition of excitatory neurons by SST+ interneurons, particularly through α5-containing GABAA receptors (α5-GABAAR), plays a crucial role in mitigating cognitive functions. Previous research demonstrated that an α5-positive allosteric modulator (α5-PAM) mitigates working memory deficits and reverses neuronal atrophy in aged mice.
View Article and Find Full Text PDFBackground: Selecting the optimal dose for clinical development is especially problematic for drugs directed at CNS-specific targets. For drugs with a novel mechanism of action, these problems are often greater. We describe Xanamem's clinical pharmacology, including the approach to dose selection and proof-of-concept studies.
View Article and Find Full Text PDFBackground: Early-onset Alzheimer's disease (EOAD) associated with amyloid precursor protein (APP) duplications or presenilin (PSEN) variants increases risk of seizures. Targeting epileptiform activity with antiseizure medicine (ASM) administration to AD patients may beneficially attenuate cognitive decline (Vossel et al, JAMA Neurology 2021). However, whether mechanistically distinct ASMs differentially suppress seizures in discrete EOAD models is understudied (Lehmann et al, Neurochem Res 2021).
View Article and Find Full Text PDFBackground: There are no cures for Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by elevation of beta-amyloid and tau proteins besides neuronal death and causing cognitive impairment. Phosphodiesterase 5 (PDE5) is a cyclic guanosine monophosphate-degrading enzyme involved in numerous biological pathways including those relevant to memory formation. PDE5 inhibition offers the potential to attenuate AD progression by acting at the downstream level of beta-amyloid and tau elevation.
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