Background And Aims: The efficacy of the erector spinae plane block (ESPB) has been demonstrated in several meta-analyses and it is increasingly being used in clinical practice. However, its mechanism of action is still not fully elucidated. Although initial anatomical studies have suggested the spread of the injectate into the paravertebral space as the main mechanism of action, more recent studies have not consistently demonstrated this. This systematic review was conducted to determine the overall proportion and extent of injectate spread following a thoracic ESPB.
Methods: PubMed, Scopus and EMBASE were searched. All studies that examined the injectate spread after a thoracic ESPB either through dissection or imaging were included. Excluded were all reviews, studies performed in paediatric patients and non-thoracic ESPBs. The primary outcome was the proportion of subjects with injectate spread in the erector spinae plane (ESP), paravertebral space (PVS), intercostal space (ICS) and epidural space (ES).
Results: This review included 29 studies involving 113 cadavers and 79 volunteers. The proportion of subjects with injectate spread in the ESP, ICS, ES and PVS was 1 (95% confidence interval, 0.97-1), 0.51 (95% CI, 0.38-0.64), 0.38 (95% CI, 0.28-0.5) and 0.57 (95% CI, 0.49-0.64) respectively. The mean spread of injectate in the ESP, ICS, ES and PVS were 9.1 (95% CI, 8.0-10.3), 5.6 (95% CI, 4.0-7.3), 3.1 (95% CI, 1.0-5.3) and 3.5 (95% CI, 2.4-4.6) spinal levels respectively.
Conclusion: Based on this study, the thoracic ESPB consistently led to injectate spread into the ESP compartment but less reliable spread into the PVS, ES and ICS compartments. There is also preliminary evidence that an increased time to assessment may be associated with an increased spread of injectate into the PVS.
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http://dx.doi.org/10.1016/j.jclinane.2023.111304 | DOI Listing |
J Hepatol
January 2025
Centre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, EH16 4UU, United Kingdom. Electronic address:
Background & Aims: Hepatocyte transplantation has shown promise for genetic diseases of the hepatocytes but to date has shown limited efficacy for non-genetic forms of severe liver injury. Limited cell engraftment and poor function of donor hepatocytes in recipient livers impacts the clinical utility of hepatocyte cell therapy. The mechanisms underpinning this are poorly understood.
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December 2024
Washington University School of Medicine, Saint Louis, MO, USA.
Background: A recent case report described an individual who was a homozygous carrier of the APOE3 Christchurch (APOE3ch) mutation and resistant to autosomal dominant Alzheimer's Disease (AD) caused by a PSEN1-E280A mutation. Whether APOE3ch contributed to the protective effect remains unclear.
Method: We generated a humanized APOE3ch knock-in mouse and crossed it to an amyloid-β (Aβ) plaque-depositing model.
Alzheimers Dement
December 2024
Oregon Health & Science University, Portland, OR, USA.
Background: Dementia with Lewy Bodies (DLB) is one of the most common Alzheimer's Disease (AD)-related dementias and it is defined by the presence of abnormal cytoplasmic inclusions composed of aggregated α-synuclein (αsyn) in neuronal soma, known as Lewy bodies (LB). LB often coexists with AD type pathology such as amyloid-β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau in several LB dementias, including Parkinson's Disease Dementia and Lewy Body variant AD. These co-pathologies likely represent a spectrum of various contributions of shared mechanisms that underlie these diseases.
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December 2024
VA Puget Sound GRECC, Seattle, WA, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia and one of the most devastating neurodegenerative diseases. In the last decades, a large proportion of AD patients have been described as having aberrant accumulation of TDP-43 protein, a well-established driver of neurodegeneration. This TDP-43 proteinopathy in AD can co-occur in neurons with the main hallmarks of the disease, toxic amyloid oligomers and neurofibrillary tangles containing hyperphosphorylated Tau, and correlates with rapid progression and worse prognosis.
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December 2024
Byrd Alzheimer's Center & Research Institute, Tampa, FL, USA.
Background: BIN1, the second strongest GWAS risk factor for late-onset Alzheimer's disease (AD), encodes a nucleocytoplasmic adaptor protein that plays many roles in multiple tissue and cell types. It is known that BIN1 can directly bind to tau in vitro, and neuronal BIN1 expression decreases in patients with AD. Accumulation of intracellular hyperphosphorylated tau is a hallmark pathogenic feature of AD and related tauopathies.
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