Trans-axillary thoracic outlet decompression.

Thoracic outlet syndrome (TOS) is a group of conditions thought to be caused by the compression of neurovascular structures going to the upper extremity. TOS is a difficult disease to diagnose, and surgical treatment remains challenging. Many different surgical techniques for the treatment of TOS have been described in the literature and many reasonable to good outcomes have been reported, which makes it hard for surgeons to determine which techniques should be used.

Surgical approaches for thoracic outlet decompression in the treatment of thoracic outlet syndrome.

Thoracic outlet syndrome (TOS) is a controversial and uncommon syndrome. Three different diagnoses can be made based on the compressed structure: arterial TOS, venous TOS, and neurogenic TOS. Diagnosing TOS, especially neurogenic TOS, remains difficult since a single diagnostic tool does not exist.

General Overview and Diagnostic (Imaging) Techniques for Neurogenic Thoracic Outlet Syndrome.

Thoracic outlet syndrome is an uncommon and controversial syndrome. Three different diagnoses can be made based on the compressed structure, arterial TOS, venous TOS, and neurogenic TOS, though combinations do exist as well. Diagnosing NTOS is difficult since no specific objective diagnostic modalities exist.

Reliability and validity of the standardized elevated arm stress test in the diagnosis of neurogenic thoracic outlet syndrome.

Objective: We developed a standardized elevated arm stress test (sEAST) meter to standardize patients' posture and measure additional grip and fatigue parameters. In the present prospective cohort study, we aimed to determine the reliability and validity of the sEAST in the diagnosis of neurogenic thoracic outlet syndrome (NTOS).

Methods: Patients evaluated for NTOS between October 2018 and February 2020 were included and performed the sEAST.

Reliability and validity of the elevated arm stress test in the diagnosis of neurogenic thoracic outlet syndrome.

Objectives: The objective of this retrospective analysis of prospectively collected data was to assess the test-retest reliability and validity of the elevated arm stress test (EAST) as measured by the duration in a cohort of patients with suspected neurogenic thoracic outlet syndrome (NTOS).

Methods: Patients evaluated for NTOS between January 2017 and September 2018 were identified. Test-retest reliability by the intraclass correlation coefficient was determined for duration of the EAST.

Surgery Versus Continued Conservative Treatment for Neurogenic Thoracic Outlet Syndrome: the First Randomised Clinical Trial (STOPNTOS Trial).

Objective: Neurogenic thoracic outlet syndrome (NTOS) is one of the most controversial clinical entities in medicine. Several major case series have shown promising results of surgery; however, solid scientific evidence is lacking. The aim of this trial was to objectify the effect of thoracic outlet decompression (TOD).

Redo surgery for neurogenic thoracic outlet syndrome is useful.

Objectives: Surgery for neurogenic thoracic outlet syndrome (NTOS) has shown good outcome in numerous case series. However, 5% to 30% of patients will have persistent or recurrent symptoms, caused by incomplete first rib resection, reattachment of residual scalene muscle, fibrous scarring around the brachial plexus, or a wrong NTOS diagnosis. In patients with a sound diagnosis of recurrent or persisting NTOS, not responding to conservative measures, a secondary procedure can be considered.

Thoracic outlet decompression surgery for Gilliatt-Sumner hand as a presentation of neurogenic thoracic outlet syndrome.

Background: Chronic compression of the inferior trunk of the brachial plexus can result in severe pain and progressive atrophy and weakness of the musculature of the forearm and hand, known as Gilliatt-Sumner hand (GSH). The objective of treatment for these patients is to stop further atrophy and pain. Restoration of motor function has been thought to be seldom achieved.

Duplex Ultrasound Studies Are Neither Necessary or Sufficient for the Diagnosis of Neurogenic Thoracic Outlet Syndrome.

Background: Duplex ultrasound (DU) is used in the diagnosis of neurogenic thoracic outlet syndrome (NTOS) to measure compression of the subclavian artery (SCA) which is thought to strengthen the NTOS diagnosis. However, the value of DU in NTOS remains unclear.

Methods: A retrospective review of a prospectively acquired database from the TOS center of the Catharina Hospital Eindhoven was performed of patients referred between January 2017 and December 2019.

Variability in electrodiagnostic findings associated with neurogenic thoracic outlet syndrome.

Introduction/aims: Neurogenic thoracic outlet syndrome (NTOS) is a heterogeneous and often disputed entity. An electrodiagnostic pattern of T1 > C8 axon involvement is considered characteristic for the diagnosis of NTOS. However, since the advent of high-resolution nerve ultrasound (US) imaging, we have encountered several patients with a proven entrapment of the lower brachial plexus who showed a different, variable electrodiagnostic pattern.

Feasibility and Outcomes of a Multidisciplinary Care Pathway for Neurogenic Thoracic Outlet Syndrome: A Prospective Observational Cohort Study.

Objective: The North American Society for Vascular Surgery (SVS) reporting standards for neurogenic thoracic outlet syndrome (NTOS) were published in 2016 to produce consistency in the diagnosis and treatment of NTOS, but outcomes resulting from following these standards are not yet available. The results of a standardised multidisciplinary care pathway for NTOS based on the North American SVS reporting standards for NTOS are reported.

Methods: Patients referred between August 2016 and December 2019 with suspected NTOS were evaluated in this single center prospective cohort study.

Surgical management of post-thrombotic syndrome in chronic venous thoracic outlet syndrome.

Objective: Venous thoracic outlet syndrome (VTOS) is considered chronic when symptoms and venous stenosis or occlusion are present for >3 months after the initial primary upper extremity deep vein thrombosis event. Many of patients with chronic VTOS receive conservative treatment. However, a subset of these patients will have persistent post-thrombotic syndrome symptoms because of underlying causative anatomy.

Same Admission Hybrid Treatment of Primary Upper Extremity Deep Venous Thrombosis with Thrombolysis, Transaxillary Thoracic Outlet Decompression, and Immediate Endovascular Evaluation.

Background: Multiple algorithms exist for treating acute primary upper extremity deep venous thrombosis (pUEDVT) caused by venous thoracic outlet syndrome (VTOS). In this case series, we present the results of our dedicated same admission treatment algorithm.

Methods: All patients between January 2015 and December 2019 with an established acute upper extremity deep venous thrombosis (symptoms <14 days) caused by VTOS were treated according to an algorithm consisting of same admission thrombolysis, transaxillary thoracic outlet decompression (TA-TOD) with extensive venolysis, and venography.

Interfascial Plane Blocks Reduce Postoperative Pain and Morphine Consumption in Thoracic Outlet Decompression.

Background: Postoperative analgesia in patients undergoing transaxillary thoracic outlet decompression (TATOD) is challenging because of the invasive surgery, the complex innervation of the axillary region, and the preoperative use of opioids by many patients. Commonly, postoperative pain is managed with additional opioids that introduce well-known sideeffects. To investigate the analgesic efficacy of 2 novel regional anesthesia techniques, we performed a retrospective study comparing the combined pectoral block type 1 and erector spinae block (PECS 1 + ESB) and the pectoral block type 2 (PECS 2) and systemic intravenous opioids regimen (no block) in patients undergoing TATOD.

Familial predisposition of thoracic outlet syndrome: does a familial syndrome exist? Report of cases and review of literature.

Introduction: Neurogenic thoracic outlet syndrome (NTOS) is caused by compression of the brachial plexus. The clinical presentation of NTOS is characterized by symptoms of pain, paresthesia, numbness or muscle weakness in the neck, arm or hand.

Methods: In this case report, five patients were diagnosed with NTOS.

[Neurogenic thoracic outlet syndrome].

Neurogenic thoracic outlet syndrome (nTOS) is a type of thoracic outlet syndrome (TOS) where compression of the brachial plexus is responsible for development of upper-extremity, head and neck symptoms. We present a 16-year-old and a 34-year-old patient with nTOS. Diagnosis in both cases was done by following the recently published reporting standards for (n)TOS.

Intact working memory in non-manifesting LRRK2 carriers--an fMRI study.

Cognitive impairments are prevalent in patients with Parkinson's disease. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of genetic Parkinsonism. Non-manifesting carriers of the G2019S mutation in the LRRK2 gene were found to have lower executive functions as measured by the Stroop task.

Reorganization of corticostriatal circuits in healthy G2019S LRRK2 carriers.

Objective: We investigated system-level corticostriatal changes in a human model of premotor Parkinson disease (PD), i.e., healthy carriers of the G2019S LRRK2 mutation that is associated with a markedly increased, age-dependent risk of developing PD.

A voxel-based morphometry and diffusion tensor imaging analysis of asymptomatic Parkinson's disease-related G2019S LRRK2 mutation carriers.

Background: Patients with Parkinson's disease have reduced gray matter volume and fractional anisotropy in both cortical and sub-cortical structures, yet changes in the pre-motor phase of the disease are unknown.

Methods: A comprehensive imaging study using voxel-based morphometry and diffusion tensor imaging tract-based spatial statistics analysis was performed on 64 Ashkenazi Jewish asymptomatic first degree relatives of patients with Parkinson's disease (30 mutation carriers), who carry the G2019S mutation in the leucine-rich repeat kinase 2 (LRRK2) gene.

Results: No between-group differences in gray matter volume could be noted in either whole-brain or volume-of-interest analysis.

Neural correlates of executive functions in healthy G2019S LRRK2 mutation carriers.

Introduction: The G2019S mutation in the leucine rich repeat kinase 2 (LRRK2) gene is prevalent among Ashkenazi Jewish patients with Parkinson's disease (PD). Cognitive deficits are common in early stage PD. We aimed to characterize the effect of the G2019S mutation on neural mechanisms of executive function processing by testing whether healthy mutation carriers who are an "at risk" population for the future development of PD differed from non-carriers on an functional magnetic resonance imaging (fMRI) Stroop interference task.

Cerebral pathological and compensatory mechanisms in the premotor phase of leucine-rich repeat kinase 2 parkinsonism.

Compensatory cerebral mechanisms can delay motor symptom onset in Parkinson's disease. We aim to characterize these compensatory mechanisms and early disease-related changes by quantifying movement-related cerebral function in subjects at significantly increased risk of developing Parkinson's disease, namely carriers of a leucine-rich repeat kinase 2-G2019S mutation associated with dominantly inherited parkinsonism. Functional magnetic resonance imaging was used to examine cerebral activity evoked during internal selection of motor representations, a core motor deficit in clinically overt Parkinson's disease.

Compensatory activity in the extrastriate body area of Parkinson's disease patients.

Compensatory mechanisms are a crucial component of the cerebral changes triggered by neurodegenerative disorders. Identifying such compensatory mechanisms requires at least two complementary approaches: localizing candidate areas using functional imaging, and showing that interference with these areas has behavioral consequences. Building on recent imaging evidence, we use this approach to test whether a visual region in the human occipito-temporal cortex-the extrastriate body area-compensates for altered dorsal premotor activity in Parkinson's disease (PD) during motor-related processes.