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1.
Eplasty ; 23: e67, 2023.
Article in English | MEDLINE | ID: mdl-38229962

ABSTRACT

Background: Though traumatic digital amputations are common, outcomes data are scarce. The FRANCHISE study clarified functional outcomes after digital amputation, but little information is available regarding mental health outcomes. The aims of this study were to document patient-reported mental health outcomes after traumatic digital amputation, elucidate the relationship between mental health and functional outcomes, and determine which patient/injury attributes conferred risk of unfavorable mental health outcomes. Methods: This was a descriptive, retrospective study of 77 patients with history of single digit, non-thumb traumatic amputation. Eligible patients completed Patient-Reported Outcomes Measurement Information System (PROMIS) Upper Extremity, Pain Interference, Anger, Anxiety, and Depression computer adaptive tests, and a short questionnaire recorded handedness, demographics, and worker's compensation status. Results: Correlation across the 3 PROMIS mental health domains (Anger, Anxiety, Depression) was uniformly strong and statistically significant. Correlation between the PROMIS mental health and functional (Upper Extremity and Pain Interference) scores was statistically significant but much weaker. Multivariable analysis revealed younger age and a worker's compensation claim had independent statistically significant predictive value for worse PROMIS Anger, Anxiety, and Depression scores. Female sex was also found to independently predict PROMIS Anxiety. Conclusions: By identifying patients at increased risk for feelings of anger, anxiety, and depression after digital amputation, anticipatory counseling can be provided. Anger, anxiety, and depression are very likely to coexist in the same patient; when responding to a patient who exhibits 1 element of this triad, the surgeon should be aware that the other 2 elements are likely to be present, even if not obvious.

2.
J Hand Surg Eur Vol ; 47(5): 461-468, 2022 05.
Article in English | MEDLINE | ID: mdl-34496665

ABSTRACT

The purpose of this study was to quantify the stigma associated with digital amputation and examine factors associated with it. One hundred and sixty-four digital amputees completed the Neurological Quality of Life-Stigma questionnaire and a battery of Patient-Reported Outcome Measurement Information System instruments. Multivariable analysis examined factors associated with stigma experience. The mean observed stigma score of 47 (SD 8, range 36-64) was similar to the mean value of the normal population. Younger age, a worker's compensation claim and depression were each independently associated with a more severe experience of stigma after digital amputation. Socioeconomic variables, anatomical details and mechanism of injury were not independently associated with stigma. Digital amputation is not highly stigmatizing overall. Surgeons should consider referring at-risk patients to a mental health provider for support during the coping and adjustment process after amputation.Level of evidence: III.


Subject(s)
Amputees , Amputation, Surgical , Humans , Quality of Life , Risk Factors , Surveys and Questionnaires
3.
Neurorehabil Neural Repair ; 35(5): 431-443, 2021 05.
Article in English | MEDLINE | ID: mdl-33754913

ABSTRACT

Following traumatic peripheral nerve injury, adequate restoration of function remains an elusive clinical goal. Recent research highlights the complex role that the immune system plays in both nerve injury and regeneration. Pro-regenerative processes in wounded soft tissues appear to be significantly mediated by cytokines of the type 2 immune response, notably interleukin (IL)-4. While IL-4 signaling has been firmly established as a critical element in general tissue regeneration during wound healing, it has also emerged as a critical process in nerve injury and regeneration. In this context of peripheral nerve injury, endogenous IL-4 signaling has recently been confirmed to influence more than leukocytes, but including also neurons, axons, and Schwann cells. Given the role IL-4 plays in nerve injury and regeneration, exogenous IL-4 and/or compounds targeting this signaling pathway have shown encouraging preliminary results to treat nerve injury or other neuropathy in rodent models. In particular, the exogenous stimulation of the IL-4 signaling pathway appears to promote postinjury neuron survival, axonal regeneration, remyelination, and thereby improved functional recovery. These preclinical data strongly suggest that targeting IL-4 signaling pathways is a promising translational therapy to augment treatment approaches of traumatic nerve injury. However, a better understanding of the type 2 immune response and associated signaling networks functioning within the nerve injury microenvironment is still needed to fully develop this promising therapeutic avenue.


Subject(s)
Inflammation , Interleukin-4 , Nerve Regeneration/physiology , Peripheral Nerve Injuries , Signal Transduction/physiology , Animals , Humans , Inflammation/drug therapy , Inflammation/immunology , Inflammation/metabolism , Interleukin-4/immunology , Interleukin-4/metabolism , Nerve Regeneration/drug effects , Peripheral Nerve Injuries/drug therapy , Peripheral Nerve Injuries/immunology , Peripheral Nerve Injuries/metabolism , Peripheral Nerve Injuries/physiopathology , Signal Transduction/drug effects
4.
Front Physiol ; 9: 708, 2018.
Article in English | MEDLINE | ID: mdl-29971011

ABSTRACT

Osteoarthritis (OA) is a debilitating inflammation related disease characterized by joint pain and effusion, loss of mobility, and deformity that may result in functional joint failure and significant impact on quality of life. Once thought of as a simple "wear and tear" disease, it is now widely recognized that OA has a considerable metabolic component and is related to chronic inflammation. Defects associated with primary cilia have been shown to be cause OA-like changes in Bardet-Biedl mice. We examined the role of dysfunctional primary cilia in OA in mice through the regulation of the previously identified degradative and pro-inflammatory molecular pathways common to OA. We observed an increase in the presence of pro-inflammatory markers TGFß-1 and HTRA1 as well as cartilage destructive protease MMP-13 but a decrease in DDR-2. We observed a morphological difference in cartilage thickness in Bbs1 M390R/M390R mice compared to wild type (WT). We did not observe any difference in OARSI or Mankin scores between WT and Bbs1M390R/M390R mice. Primary cilia appear to be involved in the upregulation of biomarkers, including pro-inflammatory markers common to OA.

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