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1.
Pain Manag ; 5(2): 107-16, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25806905

RESUMO

Chronic postsurgical pain (CPSP) may develop after any surgical procedure, and is a common feature after abdominal and pelvic surgery with a prevalence varying between 10 and 40%. The pathological mechanisms leading to chronic CPSP are probably inflammation, tissue and nerve damage and alterations in central pain processing. The mechanisms in chronic postsurgical abdominal and pelvic pain are poorly studied and research has largely focused on reporting of prevalence and describing risk factors, including patient characteristics, psychological factors, surgical procedure and pre- and acute postoperative pain. In this review, the most important risk factors are discussed, and aiming for preventive, personalized health care, possible methods for prediction of susceptibility and potential strategies for diminishing chronic postsurgical abdominal and pelvic pain are provided.


Assuntos
Dor Abdominal/epidemiologia , Dor Crônica/epidemiologia , Dor Pós-Operatória/epidemiologia , Dor Pélvica/epidemiologia , Dor Abdominal/prevenção & controle , Dor Crônica/prevenção & controle , Feminino , Humanos , Masculino , Dor Pós-Operatória/prevenção & controle , Dor Pélvica/prevenção & controle , Fatores de Risco
2.
World J Gastroenterol ; 21(1): 47-59, 2015 Jan 07.
Artigo em Inglês | MEDLINE | ID: mdl-25574079

RESUMO

Pain in chronic pancreatitis (CP) shows similarities with other visceral pain syndromes (i.e., inflammatory bowel disease and esophagitis), which should thus be managed in a similar fashion. Typical causes of CP pain include increased intrapancreatic pressure, pancreatic inflammation and pancreatic/extrapancreatic complications. Unfortunately, CP pain continues to be a major clinical challenge. It is recognized that ongoing pain may induce altered central pain processing, e.g., central sensitization or pro-nociceptive pain modulation. When this is present conventional pain treatment targeting the nociceptive focus, e.g., opioid analgesia or surgical/endoscopic intervention, often fails even if technically successful. If central nervous system pain processing is altered, specific treatment targeting these changes should be instituted (e.g., gabapentinoids, ketamine or tricyclic antidepressants). Suitable tools are now available to make altered central processing visible, including quantitative sensory testing, electroencephalograpy and (functional) magnetic resonance imaging. These techniques are potentially clinically useful diagnostic tools to analyze central pain processing and thus define optimum management approaches for pain in CP and other visceral pain syndromes. The present review proposes a systematic mechanism-orientated approach to pain management in CP based on a holistic view of the mechanisms involved. Future research should address the circumstances under which central nervous system pain processing changes in CP, and how this is influenced by ongoing nociceptive input and therapies. Thus we hope to predict which patients are at risk for developing chronic pain or not responding to therapy, leading to improved treatment of chronic pain in CP and other visceral pain disorders.


Assuntos
Analgésicos/uso terapêutico , Dor Crônica/tratamento farmacológico , Manejo da Dor/métodos , Pancreatite Crônica/tratamento farmacológico , Animais , Sistema Nervoso Central/efeitos dos fármacos , Sistema Nervoso Central/fisiopatologia , Dor Crônica/diagnóstico , Dor Crônica/etiologia , Dor Crônica/fisiopatologia , Procedimentos Clínicos , Humanos , Medição da Dor , Percepção da Dor/efeitos dos fármacos , Limiar da Dor/efeitos dos fármacos , Pancreatite Crônica/complicações , Pancreatite Crônica/diagnóstico , Pancreatite Crônica/fisiopatologia , Valor Preditivo dos Testes , Resultado do Tratamento
3.
Neurol Int ; 2(1): e4, 2010 Jun 21.
Artigo em Inglês | MEDLINE | ID: mdl-21577340

RESUMO

Fatigue and exercise intolerance are symptoms in children with metabolic myopathy. Frequently this is combined with muscle pain in children with mitochondrial myopathy. Offering therapeutic advice remains challenging in this patient group. Here we describe five children above the age of four years, with normal intelligence, myopathy, exercise intolerance, motor developmental delay, and fatigue, who were diagnosed with a mitochondrial dysfunction. Based on the positive experience of condition training in adults with mitochondrial disease and inactivity, aerobic exercise training was advised for all the children. Because of the lack of clear protocols for individualized mitochondrial myopathies, regular training was initiated. The Movement Assessment Battery of Children, the Jamar dynamometer for grip force, and the Bruce protocol treadmill test were applied for evaluation. No patient showed significant disease progression on a weekly scheme of strength training or on aerobic training during periods varying between 6 and 18 months. Only one out of the five patients has shown an improvement after a period of structured, aerobic training, demonstrating good compliance and motivation over the course of 18 months. Some patients developed severe muscle pain after explosive exercise. Even in a relatively homogenous, intelligent group of patients and motivated parents, we could not reach full compliance. With our case studies, we would like to draw attention to the importance and pitfalls of movement therapy in children with mitochondrial disease.

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