Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 7 de 7
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
J Clin Med ; 10(5)2021 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-33804565

RESUMO

Thoracic outlet syndrome comprises a group of disorders that result in compression of the brachial plexus and subclavian vessels exiting the thoracic outlet. Symptoms include pain, paresthesia, pallor, and weakness depending upon the compromised structures. While consensus in diagnostic criteria has not yet been established, a thorough patient history, physical exam, and appropriate imaging studies are helpful in diagnosis. General first-line therapy for thoracic outlet syndrome is a conservative treatment, and may include physical therapy, lifestyle modifications, NSAIDs, and injection therapy of botulinum toxin A or steroids. Patients who have failed conservative therapy are considered for surgical decompression. This article aims to review the epidemiology, etiology, relevant anatomy, clinical presentations, diagnosis, and management of thoracic outlet syndrome.

2.
Psychopharmacol Bull ; 51(1): 94-109, 2021 Jan 12.
Artigo em Inglês | MEDLINE | ID: mdl-33897066

RESUMO

Purpose of Review: This comprehensive review discusses the adverse effects known today about marijuana, for either medical or recreational use. It reviews the role of cannabis in the treatment of chronic pain, cognitive and neurological adverse effects, special cases and addiction. Recent Findings: Cannabinoids work through the endocannabinoids system and inhibit the release of GABA and glutamate in the brain, impact neuromodulation, as well as dopamine, acetylcholine and norepinephrine release. They affect reward, learning and pain. The use of cannabis is increasing nationally and world-wide for both recreational and medicinal purposes, however, there is relatively only low quality evidence to the efficacy and adverse effects of this. Cannabis and its derivatives may be used for treatment of chronic pain. They are via CB1 receptors that are thought to modulate nociceptive signals in the brain. CB2 receptors in the DRG likely affect pain integration in the afferent pathways, and peripherally CB2 also affects noradrenergic pathways influencing pain. A large proportion of users may see more than 50% of chronic pain alleviation compared with placebo. Cannabis affects cognition, most notably executive function, memory and attention, and may deteriorate the boundary between emotional and executive processing. Cannabis impairs memory in the short run, which become more significant with chronic use, and may also be accompanied by poorer effort, slower processing and impacted attention. It is generally believed that long-term use and earlier age are risk factor for neurocognitive deficits; neuroimaging studies have shown reduced hippocampal volume and density. Executive functions and memory are worse in adolescent users versus adults. Cannabis addiction is different and likely less common than other addictive substances, but up to 10% of users meet criteria for lifetime cannabis dependence. Addiction patterns may be linked to genetic and epigenetic differences. It is still unclear whether abstinence reverses patterns of addiction, and more research is required into this topic. Summary: Cannabis use has become more abundant for both medical and recreational use. It carries likely benefits in the form of analgesia, anti-emesis and improved appetite in chronic patients. The evidence reviewing adverse effects of this use are still limited, however, exiting data points to a clear link with neurocognitive deterioration, backed by loss of brain volume and density. Addiction is likely complex and variable, and no good data exists to support treatment at this point. It is becoming clear that use in earlier ages carries a higher risk for long-term deficits. As with any other drug, these risks should be considered alongside benefits prior to a decision on cannabis use.

3.
Curr Pain Headache Rep ; 25(1): 6, 2021 Jan 25.
Artigo em Inglês | MEDLINE | ID: mdl-33495883

RESUMO

PURPOSE OF REVIEW: Loin pain hematuria syndrome (LPHS) is rare and seldom diagnosed, yet it has a particularly significant impact on those affected. This is a review of the latest and seminal evidence of the pathophysiology and diagnosis of LPHS and presents the typical clinical presentation and treatment options available. RECENT FINDINGS: LPHS is typically found in young women with characteristic symptoms, including severe recurrent flank pain and gross or microscopic hematuria. The majority of patients will experience crippling pain for many years without effective therapy, often requiring frequent use of narcotic medication. However, the lack of conclusive pathophysiology, in conjunction with the rarity of LPHS, has prohibited the development and trial of definitive treatment options. Nevertheless, in order to combat this rare but severe disease, management strategies have continued to evolve, ranging from conservative measures to invasive procedures. This review presents an overview of the current hypotheses on the pathophysiology of LPHS in addition to summarizing the management strategies that have been utilized. Only 30% of LPHS patients will experience spontaneous resolution, whereas the majority will continue to face chronic, crippling pain. Several methods of treatment, including invasive and non-invasive, may provide an improved outcome to these patients. Treatment should be individually tailored and multi-disciplinary in nature. Further research is required to further elucidate the pathophysiology and develop new, specific, treatment options.

4.
Best Pract Res Clin Anaesthesiol ; 34(3): 493-506, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33004161

RESUMO

Chronic pain syndromes cost the US healthcare system over $600 billion per year. A subtype of chronic pain is neuropathic pain (NP), which is defined as "pain caused by a lesion or disease of the somatosensory system," according to the International Association for the Study of Pain (IASP). The pathophysiology of neuropathic pain is very complex, and more research needs to be done to find the exact mechanism. Patients that have preexisting conditions such as cancer and diabetes are at high-risk of developing NP. Many NP patients are misdiagnosed and receive delayed treatment due to a lack of a standardized classification system that allows clinicians to identify, understand, and utilize pain management in these patients. Medications like tricyclic antidepressants, serotonin-norepinephrine reuptake Inhibitor (SNRIs), and gabapentinoids are first-line treatments followed by opioids, cannabinoids, and other drugs. There are limited studies on the treatment of NP.

5.
Best Pract Res Clin Anaesthesiol ; 34(3): 507-516, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33004162

RESUMO

Chronic pain is typically defined as pain that persists after acute tissue damage and inflammation or as pain that follows a chronic disease process and lasts more than three months. Because of its debilitating impact on the quality of life of patients, recent research aims to investigate the mechanisms behind nociception to discover novel therapeutic agents to alleviate pain. One such target is the neuropeptide calcitonin gene-related peptide (CGRP), which has shown to play an integral role in migraine pathophysiology. Effective treatments of migraines with CGRP antagonists have stimulated our efforts toward checking a possible involvement of CGRP in nonheadache pain conditions such as hypertension, congestive heart failure, Alzheimer's disease, and vascular ischemia. Here, we provide a brief overview of chronic pain, with a particular emphasis on the role of CGRP as a fundamental mediator of nociceptive pain as well as a target for novel therapeutic agents.

6.
Psychopharmacol Bull ; 50(2): 56-67, 2020 May 19.
Artigo em Inglês | MEDLINE | ID: mdl-32508368

RESUMO

Purpose of Review: This is a comprehensive review of the association between cannabis use and psychological disorders. It reviews the latest and seminal evidence that is available and attempts to conclude the strength of such association. Recent Findings: Cannabis is a flowering plant with psychoactive properties, attributed to cannabinoids that naturally occur within the plant. These act through the CB1 and CB2 receptors to inhibit GABA and glutamate release, as well through other forms of neuromodulation through the modulation of the endocannabinoid system (eCBs); a system that is otherwise involved in different pathways, including reward, memory, learning, and pain. Recent societal changes have increased the use of both medical and recreational cannabis. Patients with mental illness are considered more vulnerable and are prone to reward-seeking behavior. Cannabis use disorder (CUD) has been shown to have an increased prevalence in individuals with mental illness, creating an explosive cocktail. Approximately 1 in 4 patients with schizophrenia are also diagnosed with CUD. Cannabis use is associated with 2-4 times the likelihood of developing psychosis in healthy individuals. It has also been associated with multiple poor prognostic factors in schizophrenia, as well as in patients with a history of psychosis who do not meet diagnostic criteria for schizophrenia. Cannabis has been linked with anxiety; THC has been shown to elicit anxiety; however, anxiety is also a trigger for cannabis use. However, a recent large meta-analysis did not find a convincing link between cannabis and anxiety. This was reiterated in a recent epidemiological study that did not find such a correlation; however, it did identify a link between cannabis use, substance disorder, alcohol use disorder, drug use disorder, and nicotine dependence. Similarly, contradicting data exists regarding the link of depression and cannabis use. Summary: Cannabis use is increasing with recent societal shifts; however, its interaction with mental health is less well understood. CUD is highly prevalent in individuals with mental health disorders, especially those with other substance abuse disorders. There is evidence to support that cannabis use may trigger and worsen psychosis and schizophrenia. The link with depression and anxiety is less clear and needs further investigation. Personality disorder is linked with substance use disorder and shares similar risk factors with CUD.

7.
Am J Physiol Heart Circ Physiol ; 316(1): H145-H159, 2019 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-30362822

RESUMO

Myocardial hypertrophy is an independent risk factor for heart failure (HF), yet the mechanisms underlying pathological cardiomyocyte growth are incompletely understood. The c-Jun NH2-terminal kinase (JNK) signaling cascade modulates cardiac hypertrophic remodeling, but the upstream factors regulating myocardial JNK activity remain unclear. In this study, we sought to identify JNK-activating molecules as novel regulators of cardiac remodeling in HF. We investigated mixed lineage kinase-3 (MLK3), a master regulator of upstream JNK-activating kinases, whose role in the remodeling process had not previously been studied. We observed increased MLK3 protein expression in myocardium from patients with nonischemic and hypertrophic cardiomyopathy and in hearts of mice subjected to transverse aortic constriction (TAC). Mice with genetic deletion of MLK3 (MLK3-/-) exhibited baseline cardiac hypertrophy with preserved cardiac function. MLK3-/- mice subjected to chronic left ventricular (LV) pressure overload (TAC, 4 wk) developed worsened cardiac dysfunction and increased LV chamber size compared with MLK3+/+ littermates ( n = 8). LV mass, pathological markers of hypertrophy ( Nppa, Nppb), and cardiomyocyte size were elevated in MLK3-/- TAC hearts. Phosphorylation of JNK, but not other MAPK pathways, was selectively impaired in MLK3-/- TAC hearts. In adult rat cardiomyocytes, pharmacological MLK3 kinase inhibition using URMC-099 blocked JNK phosphorylation induced by neurohormonal agents and oxidants. Sustained URMC-099 exposure induced cardiomyocyte hypertrophy. These data demonstrate that MLK3 prevents adverse cardiac remodeling in the setting of pressure overload. Mechanistically, MLK3 activates JNK, which in turn opposes cardiomyocyte hypertrophy. These results support modulation of MLK3 as a potential therapeutic approach in HF. NEW & NOTEWORTHY Here, we identified a role for mixed lineage kinase-3 (MLK3) as a novel antihypertrophic and antiremodeling molecule in response to cardiac pressure overload. MLK3 regulates phosphorylation of the stress-responsive JNK kinase in response to pressure overload and in cultured cardiomyocytes stimulated with hypertrophic agonists and oxidants. This study reveals MLK3-JNK signaling as a novel cardioprotective signaling axis in the setting of pressure overload.


Assuntos
Cardiomegalia/metabolismo , MAP Quinase Quinase Quinases/genética , Sistema de Sinalização das MAP Quinases , Animais , Débito Cardíaco , Cardiomegalia/patologia , Cardiomegalia/fisiopatologia , Células Cultivadas , Humanos , MAP Quinase Quinase 4/metabolismo , MAP Quinase Quinase Quinases/antagonistas & inibidores , MAP Quinase Quinase Quinases/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/fisiologia , Inibidores de Proteínas Quinases/farmacologia , Piridinas/farmacologia , Pirróis/farmacologia , Ratos , Ratos Sprague-Dawley , Remodelação Ventricular
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...