Chronic Fatigue and Acute Rhabdomyolysis

Author(s):  
Ros Quinlivan ◽  
Pascal Laforêt

Chronic fatigue syndrome is usually idiopathic, management involves a multi-disciplinary approach, advice on pacing activities and cognitive behavioral therapy. Metabolic myopathies that cause exercise intolerance may lead to a fatigue syndrome due to deconditioning, other neuromuscular disorders presenting with paroxysmal fatigue and weakness such as the myasthenic syndromes and channelopathies can occasionally be mistaken for a metabolic disorder. Acute rhabdomyolysis, a potentially life-threatening complication, has many causes both acquired and genetic. Urgent treatment is required and prevention of future episodes requires a careful search for an underlying genetic cause.

2021 ◽  
Vol 8 ◽  
pp. 204993612110093
Author(s):  
Sonia Poenaru ◽  
Sara J. Abdallah ◽  
Vicente Corrales-Medina ◽  
Juthaporn Cowan

Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection. A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings. The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses. There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.


Life ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 43
Author(s):  
Josef Finsterer

The aim of this review is to summarize and discuss recent findings and new insights in the etiology and phenotype of metabolic myopathies. The review relies on a systematic literature review of recent publications. Metabolic myopathies are a heterogeneous group of disorders characterized by mostly inherited defects of enzymatic pathways involved in muscle cell metabolism. Metabolic myopathies present with either permanent (fixed) or episodic abnormalities, such as weakness, wasting, exercise-intolerance, myalgia, or an increase of muscle breakdown products (creatine-kinase, myoglobin) during exercise. Though limb and respiratory muscles are most frequently affected, facial, extra-ocular, and axial muscles may be occasionally also involved. Age at onset and prognosis vary considerably. There are multiple disease mechanisms and the pathophysiology is complex. Genes most recently related to metabolic myopathy include PGM1, GYG1, RBCK1, VMA21, MTO1, KARS, and ISCA2. The number of metabolic myopathies is steadily increasing. There is limited evidence from the literature that could guide diagnosis and treatment of metabolic myopathies. Treatment is limited to mainly non-invasive or invasive symptomatic measures. In conclusion, the field of metabolic myopathies is evolving with the more widespread availability and application of next generation sequencing technologies worldwide. This will broaden the knowledge about pathophysiology and putative therapeutic strategies for this group of neuromuscular disorders.


2001 ◽  
Vol 40 (11) ◽  
pp. 1158-1161 ◽  
Author(s):  
Akinori MASUDA ◽  
Takashi NAKAYAMA ◽  
Takao YAMANAKA ◽  
Kenji HATSUTANMARU ◽  
Chuwa TEI

1994 ◽  
Vol 18 (Supplement_1) ◽  
pp. S112-S112
Author(s):  
Andrew R. Lloyd ◽  
Ian Hickle ◽  
Alan Brockman ◽  
Catherine Hickie ◽  
Andrew Wilson ◽  
...  

2021 ◽  
Vol 6 (3) ◽  
pp. 472-478
Author(s):  
Adwitiya Ray ◽  
Neharika Saini ◽  
Ravi Parkash

Coronavirus disease 2019 (COVID-19) is a viral infection that causes various respiratory, gastrointestinal, and vascular symptoms. The acute illness phase lasts for about 2-3 weeks. However, there is increasing evidence that a percentage of COVID-19 patients continue to experience long-lasting symptoms characterized by fatigue, dyspnea, myalgia, exercise intolerance, and sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. Similar symptoms are reported by patients who having myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS). ME/CFS pathology is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. There is a resemblance between post-acute COVID-19 symptoms and ME/CFS. However, at present, there is inadequate evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies. Keywords: chronic fatigue syndrome, COVID-19, human coronavirus, myalgic encephalomyelitis, post-infectious fatigue, review.


2020 ◽  
Author(s):  
Jihyun Lee ◽  
Suzanne D Vernon ◽  
Patricia Jeys ◽  
Weam Ali ◽  
Andrea Campos ◽  
...  

Abstract Background. Lightheadedness, fatigue, weakness, heart palpitations, cognitive dysfunction, muscle pain, and exercise intolerance are some of the symptoms of orthostatic intolerance (OI). There is substantial comorbidity of OI in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome). The 10-minute NASA Lean Test (NLT) is a simple, point-of-care method that can aid ME/CFS diagnosis and guide management and treatment of OI. The objective of this study was to understand the hemodynamic changes that occur in ME/CFS patients during the 10-minute NLT. Methods. A total of 150 ME/CFS patients and 75 age, gender and race matched healthy controls (HCs) were enrolled. We recruited 75 ME/CFS patients who had been sick for less than 4 years (<4 ME/CFS) and 75 ME/CFS patients sick for more than 10 years (>10 ME/CFS). The 10-minute NLT involves measurement of blood pressure and heart rate while resting supine and every minute for 10 minutes while standing with shoulder-blades on the wall for a relaxed stance. Spontaneously reported symptoms are recorded during the test. ANOVA and regression analysis were used to test for differences and relationships in hemodynamics, symptoms and upright activity between groups.Results. At least 5 minutes of the 10-minute NLT were required to detect hemodynamic changes. The <4 ME/CFS group had significantly higher heart rate and abnormally narrowed pulse pressure compared to >10 ME/CFS and HCs. The <4 ME/CFS group experienced significantly more OI symptoms compared to >10 ME/CFS and HCs. The circulatory decompensation observed in the <4 ME/CFS group was not related to age or medication use. Conclusions. Circulatory decompensation characterized by increased heart rate and abnormally narrow pulse pressure was identified in a subgroup of ME/CFS patients who have been sick for <4 years. This suggests inadequate ventricular filling from low venous pressure. The 10-minute NLT can be used to diagnose and treat the circulatory decompensation in this newly recognized subgroup of ME/CFS patients. The >10 ME/CFS group had less pronounced hemodynamic changes during the NLT possibly from adaptation and compensation that occurs over time. The 10-minute NLT is a simple and clinically useful point-of-care method that can be used for early diagnosis of ME/CFS and help guide OI treatment.


Author(s):  
Aziz Shaibani

Undue fatigability is common in neuromuscular clinics, but nonneuromuscular causes are much more common than neuromuscular causes. Generalized fatigue is commonly caused by anemia, hypothyroidism, obstructive sleep apnea, depression, chronic fatigue syndrome (CFS), uremia, chronic obstructive pulmonary disease (COPD), and other diseases. Physiological fatigue is accentuated by neuromuscular disorders. Most strikingly, myasthenia gravis (MG) causes undue fatigue of the ocular, chewing, swallowing, and breathing muscles. However, amyotrophic lateral sclerosis (ALS), myopathies, and motor neuropathies are also associated with abnormal fatigue. Central causes like multiple sclerosis are notorious for fatigue. It is hard to measure fatigue because it is subjective and varies with the psychological status. Myasthenia hardly causes isolated fatigue.


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