Chronic fatigue is an underdiagnosed condition in children, particularly those with neuromuscular illnesses. The mechanism and treatment of chronic fatigue in this special population may differ from those of the adult population. More research is necessary to fully understand and best address the role of this problem in children with special health care needs.
In recent years, medical research has taken a great interest in chronic fatigue affecting adults. Multiple theories as to possible etiologies have been examined, and various treatments have been studied. Despite this, many questions still remain regarding this common but complex phenomenon. It is hoped that further research will guide its management and significantly improve the lives of patients impacted by this disabling illness.
Unfortunately, the focus on adult chronic fatigue overshadows the lack of attention to evaluating this condition in the pediatric population. This deficiency is particularly worrisome, as chronic fatigue in a child would theoretically have different implications when compared with that in an adult. If the child’s play and school activities were to be limited secondary to fatigue, the physical, educational, and social development of that child could be delayed. One study reported that these children demonstrated increased absence from school (20-60 days), with subsequent decline in academic performance, reduction in extracurricular activities, and adverse effects on peer relationships.
Although it appears that this oversight is slowly being addressed, more information regarding this subset would prove valuable, as children seem to be affected to a similar extent as adults. The overall prevalence of this underdiagnosed pediatric ailment has been approximated as 1.2% to 1.9%, which is comparable to the prevalence of chronic fatigue in adults. Like adults, those children typically affected are female with a ratio of 2:1 as compared to males. They tend to be in their early teenage years and from an upper middle-class background. Additionally, a history of relatives suffering from chronic fatigue or a past medical history of asthma may be noted. Emotional problems, such as anxiety or depression, can further increase the risk. Associated symptoms can include headaches, muscle pains, fever, and exercise-induced fatigue. Frequently, the illness is self-limited, but a minority of children may be persistently or severely affected.
One reason for the failure of physicians to correctly diagnose this condition may be the child’s inability to clearly articulate the chief complaint. Usually a parent concerned by the child’s inactivity brings the matter to a physician’s attention. This clinical situation can be further compounded if the child suffers from a concurrent neuromuscular illness. Children with special health care needs may be most affected by chronic fatigue and least diagnosed. It is especially important to consider this disorder in such a specific population, as these children are often already delayed in physical and social function and, thus, stand to suffer worse outcomes.
Differentiation of fatigue versus sleepiness versus weakness
Other symptoms such as sleepiness or weakness may be confused for chronic fatigue. It is important to differentiate fatigue from these separate entities as treatment may differ. This can prove difficult, because fatigue is a subjective and abstract concept. Fatigue implies an extreme mental and physical exhaustion independent of exertion, disease, or the amount of sleep, whereas sleepiness implies a problem with the sleep/wake cycle itself. Despite being separate entities, these 2 conditions can coexist. Weakness more typically implies a defect in neuromuscular function. This should be objectively measured by motor strength testing.
Differential diagnosis
A vast array of diseases can imitate chronic fatigue (see Table 1 for a noninclusive list of possible diagnoses). For this reason, it is imperative to rule out any active medical or psychiatric conditions that may lead to a misdiagnosis of chronic fatigue. It is advisable to perform a thorough history, including mental status examination, as well as a physical examination when evaluating a patient with fatigue. A minimum battery of laboratory screening tests, including complete blood count with leukocyte differential; erythrocyte sedimentation rate; electrolytes, alanine aminotransferase, total protein, albumin, alkaline phosphatase, calcium, phosphorus, glucose, blood urea nitrogen, and creatinine; thyroid-stimulating hormone; and urinalysis, should be performed.
| Cardiology arrhythmia | Chronic heart failure, cardiac defect |
| Endocrine | Cushing’s disease, diabetes mellitus, obesity |
| ENT | Allergic rhinitis, sinusitis |
| GI Crohn’s disease | Intussusception |
| ID | EBV, HIV, human herpes virus, lyme disease, parvovirus, polio |
| Neurology | Chronic fatigue syndrome, central fatigue, cerebral palsy, disseminated encephalomyelitis, multiple sclerosis, stroke, traumatic brain injury |
| Neuromuscular diseases | Amyotrophic lateral sclerosis, Charcot-Marie-Tooth disease, Guillan-Barré syndrome, immune neuropathy, myopathy, muscular dystrophy, myasthenia gravis, myotonic dystrophy |
| Oncology | Leukemia, lymphoma, solid tumor |
| Psychiatric | Anxiety, depression, psychosomatic disorders |
| Pulmonary | Cystic fibrosis, sarcoidosis, sleep-disordered breathing |
| Rheumatology | Fibromyalgia, juvenile rheumatoid arthritis, systemic lupus erythematosus |
Differential diagnosis
A vast array of diseases can imitate chronic fatigue (see Table 1 for a noninclusive list of possible diagnoses). For this reason, it is imperative to rule out any active medical or psychiatric conditions that may lead to a misdiagnosis of chronic fatigue. It is advisable to perform a thorough history, including mental status examination, as well as a physical examination when evaluating a patient with fatigue. A minimum battery of laboratory screening tests, including complete blood count with leukocyte differential; erythrocyte sedimentation rate; electrolytes, alanine aminotransferase, total protein, albumin, alkaline phosphatase, calcium, phosphorus, glucose, blood urea nitrogen, and creatinine; thyroid-stimulating hormone; and urinalysis, should be performed.
| Cardiology arrhythmia | Chronic heart failure, cardiac defect |
| Endocrine | Cushing’s disease, diabetes mellitus, obesity |
| ENT | Allergic rhinitis, sinusitis |
| GI Crohn’s disease | Intussusception |
| ID | EBV, HIV, human herpes virus, lyme disease, parvovirus, polio |
| Neurology | Chronic fatigue syndrome, central fatigue, cerebral palsy, disseminated encephalomyelitis, multiple sclerosis, stroke, traumatic brain injury |
| Neuromuscular diseases | Amyotrophic lateral sclerosis, Charcot-Marie-Tooth disease, Guillan-Barré syndrome, immune neuropathy, myopathy, muscular dystrophy, myasthenia gravis, myotonic dystrophy |
| Oncology | Leukemia, lymphoma, solid tumor |
| Psychiatric | Anxiety, depression, psychosomatic disorders |
| Pulmonary | Cystic fibrosis, sarcoidosis, sleep-disordered breathing |
| Rheumatology | Fibromyalgia, juvenile rheumatoid arthritis, systemic lupus erythematosus |
Definition of chronic fatigue
Although chronic fatigue syndrome is an individual entity in the differential diagnosis of chronic fatigue, it may be helpful to examine this syndrome to formulate a working definition of chronic fatigue. According to the Centers for Disease Control and Prevention, to receive a diagnosis of chronic fatigue syndrome, a patient must satisfy 2 criteria:
- 1.
Experience severe chronic fatigue for at least 6 months duration with no known causative medical conditions
- 2.
Concurrently have at least 4 of the following symptoms: substantial impairment in short-term memory or concentration; sore throat; tender lymph nodes; muscle pain; multijoint pain without swelling or redness; headaches of a new type, pattern, or severity; lack of refreshing sleep; and postexertional malaise lasting more than 24 hours
These symptoms must be persistent or recurrent during the 6 or more consecutive months of illness. Additionally, they must not have predated the fatigue.
Length of time is used to differentiate prolonged fatigue from chronic fatigue. Prolonged fatigue can be defined as lasting 1 month or longer, whereas chronic fatigue implies persistent or relapsing fatigue of 6 or more consecutive months.
Although there is a significant research gap in the difference between chronic fatigue syndrome in children versus adults, there is 1 study that showed that outpatient rehabilitation significantly improved the prognosis of chronic fatigue syndrome in children and adolescents plagued with this illness.
Analysis of fatigue secondary to neurologic impairments
Cerebral Palsy
Children with cerebral palsy (CP), especially the spastic variants, can be severely affected by fatigue. The mechanism behind fatigue in children with CP is not just on a muscular level but on a whole-body energy expenditure level. Fatigue consequently affects school function, home life, extracurricular activities, and socialization with peers.
Body mechanics as a whole in children with CP cause weakness to the affected muscles. However, on a single muscle level, limbs of children with CP actually show less fatigability. Studies comparing CP versus control muscles have shown that individual spastic muscles fatigue to a lesser extent than unaffected muscles. It has been proposed that muscles affected with CP have an increase in type I muscle fibers. This is likely an adaptation to meet metabolic demands, as these muscles use the same motor units more repetitively and for longer durations during standing and ambulation. Unfortunately, less fatigability on the single muscle level does not translate into less fatigue overall. On the contrary, spastic CP is associated with poorer functioning as well as with lower levels of activity and participation as measured by the gross motor function classification system. Although agonist muscles are less fatigable individually, they also have a deficit in the volume of muscle activation, causing a decrease in force production. Force is further affected by co-activation. When an agonist muscle fires, co-activation by the antagonist muscle has been observed. This also causes a decrease in peak force production. Therefore, the combination of decreased muscle activation plus co-activation of antagonist muscles causes an overall weakness in children with CP.
The weakness of impaired biomechanical efficiency seen in CP also translates into a higher oxygen (O 2 ) requirement when comparing individuals with CP verses those without CP in matched activities. For example, in a hemiplegic child versus a matched control, an activity such as walking will show a decrease in walking velocity, increased muscle weakness, decreased force production, and antagonist co-activation, all leading to higher O 2 requirements. Due to higher O 2 requirements, the child with CP will have an increase in energy expenditure and, therefore, be quicker to fatigue.
Increase in muscle fatigue has not only been measured by energy expenditure but also by self-reporting from parents of children with CP. Studies have shown that children with a more severe diagnosis have an increased incidence of fatigue as reported by their parents. Pain also appears to be a major contributor to fatigue with a direct correlation between the amount of pain and the amount of fatigue. There is also an inverse relationship between pain and fatigability and with quality of life (QOL) issues such as school functioning.
Improvements in pain and prevention strategies of fatigability are ways to help improve the QOL in a child with CP. Treatment options for pain management and spasticity include muscle relaxants, such as botulinum toxin A, diazepam, and baclofen, as well as improvement of muscle strength and flexibility through physical therapy. Fatigue-specific interventions often focus on decreasing energy expenditure. Adaptive equipment has been found to be particularly helpful in decreasing energy expenditure. Children with CP who require a wheelchair for mobility should be specially fitted with a customized wheelchair that takes the individual child’s needs into consideration and subsequently provides them with the maximum upper-extremity function coupled with the most energy conservation. If a child is ambulating but needs the assistance of a walker, studies have shown that although there is no difference in walking velocity or cadence between anterior and posterior walkers, there is an increase in upright positioning and decrease in oxygen consumption rates when a posterior walker is used. Therefore, in terms of fatigability, a posterior walker would be recommended for energy conservation. For the child ambulating without an assistive device, which is commonly seen in a child with hemiplegia, studies have shown that the addition of an ankle-foot-orthosis can be useful in controlling deformities, improving the child’s gait efficiency from toe walking to a heel-toe gait, and subsequently reducing energy expenditure. See Table 2 for options in decreasing fatigue in children with CP.
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