Symptom Burden in Persons With Spinal Cord Injury

Department of Rehabilitation Medicine, University of Washington Seattle, Seattle, Washington, United States
Archives of Physical Medicine and Rehabilitation (Impact Factor: 2.57). 06/2007; 88(5):638-45. DOI: 10.1016/j.apmr.2007.02.002
Source: PubMed


To determine (1) the frequency, severity, and reported course of 7 symptoms in persons with spinal cord injury (SCI) and (2) the association between these symptoms and patient functioning.
Postal survey.
A survey that included measures of the frequency, severity, and recalled course of pain, fatigue, numbness, weakness, shortness of breath, vision loss, and memory loss, as well as a measure of community integration and psychologic functioning was mailed to a sample of persons with SCI. One hundred forty-seven usable surveys were returned (response rate, 43% of surveys mailed).
The frequency and average severity of each symptom was computed, and the frequencies of each type of reported course were noted. Analyses estimated the associations among the symptoms, and between symptom severity and measures of patient functioning.
The most common symptoms were pain, weakness, fatigue, and numbness. All symptoms were reported to remain the same or to get worse more often than they were reported to improve once they began. Pain, weakness, fatigue, and memory loss were the symptoms most closely associated with patient functioning.
Patients with SCI must deal with a number of secondary complications in addition to any disability caused by the injury itself. Of 7 symptoms studied, pain, weakness, and fatigue appeared to be most common and most closely linked to patient social and mental health functioning. Research is needed to identify the causal relationships between perceived symptoms and quality of life in patients with SCI and to identify effective treatments for those symptoms shown to impact patient functioning.

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Available from: Mark P Jensen, Mar 05, 2014
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    • "This finding was surprising in light of previous research that suggests that low frequency (a/h) NF training can result in increases in self-reported energy levels, at least in some individuals (Raymond et al. 2005; see also Kayiran et al. 2010). More research is needed to determine if this finding represents random variation in fatigue levels in our sample, or if there is a systematic effect of the NF protocols used in this study and increases in fatigue (which can be a very bothersome symptom for many individuals with SCI; Cook et al. 2011; Jensen et al. 2007b). The current study has a number of important limitations that should be considered when interpreting its results. "
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    ABSTRACT: Chronic pain, usually refractory to analgesics, is a significant problem for many individuals with spinal cord injury (SCI). Preliminary studies suggest that electroencephalography (EEG) biofeedback (also known as neurofeedback, NF) has the potential to help patients with otherwise refractory chronic pain. However, there remain many unanswered questions about the effects and mechanisms of this treatment. We studied 13 individuals with SCI and chronic pain with NF. Ten of the 13 individuals completed 4 sessions each of three different neurofeedback protocols assigned in random order for a total of 12 NF sessions. All three protocols had similar immediate effects on pain intensity. In addition, the participants reported modest pre- to post-treatment decreases in worst pain and pain unpleasantness following completion of the 12 NF sessions. These improvements were maintained at 3-month follow-up. The majority of the participants felt they benefited from and were satisfied with the treatment. No significant effects on measures of other outcome domains (sleep quality, pain interference and fatigue) were observed, although there was a non-significant trend for an increase in fatigue. Finally, pre- to post-treatment changes in EEG bandwidth activity, consistent with the training protocols, were observed in θ and α but not β frequencies. The findings provide preliminary support for the potential efficacy of NF for the treatment of SCI-related pain, and suggest that further clinical studies are warranted.
    Applied Psychophysiology and Biofeedback 03/2013; 38(2). DOI:10.1007/s10484-013-9214-9 · 1.13 Impact Factor
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    • "In a study of people with phantom limb pain, pain catastrophizing was also shown to significantly contribute to wind-up-like pain when anxiety and depression were controlled for (Vase, et al., 2011) Pain catastrophizing has been found to be positively associated with pain-related disability among those with spinal cord injury, cerebral palsy, phantom limb pain, muscular dystrophy and multiple sclerosis (Borsbo, et al., 2009; Douglas, Wollin, & Windsor, 2008; Engel, et al., 2000; Hill, et al., 1995; Miro, et al., 2009; Molton, et al., 2009; Nicholson Perry, Nicholas, & Middleton, 2009; Nicholson Perry, Nicholas, Middleton, et al., 2009; Osborne, et al., 2007). Psychological functioning among people with spinal cord injury, multiple sclerosis, phantom limb pain, muscular dystrophy and cerebral palsy has been found to be negatively associated with pain catastrophizing (Douglas, et al., 2008; Engel, Jensen, & Schwartz, 2006; Engel, et al., 2000; Hanley, et al., 2004; Hill, et al., 1995; Miro, et al., 2009; Molton, et al., 2009; Nicholson Perry, Nicholas, & Middleton, 2009; Nicholson Perry, Nicholas, Middleton, et al., 2009; Osborne, et al., 2007; Smedema, Catalano, & Ebener, 2011; Ullrich, Jensen, Loeser, & Cardenas, 2007; Wollaars, et al., 2007). Pain catastrophizing has also been shown to mediate the relationship between pain severity and psychological distress and pain-related disability among people with spinal cord injury (Ullrich, et al., 2007). "
    Pain Management - Current Issues and Opinions, 01/2012; , ISBN: 978-953-307-813-7
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    • "Many neuropathies that lead to a loss of sensitivity also produce neuropathic pain. These include diabetes (Daulhac et al., 2006; Pabbidi et al., 2008), chemotherapeutic neuropathy (Polomano and Bennett, 2001; Ledeboer et al., 2007b), spinal cord injury (Jensen et al., 2007), and CNS infections (Rowbotham and Fields, 1996; Macleod et al., 2002). We here demonstrate this EAE model shares characteristic symptoms of both reduced sensitivity to touch and mechanical allodynia seen in other neuropathies. "
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    ABSTRACT: Multiple Sclerosis (MS) is an autoimmune inflammatory disease that presents clinically with a range of symptoms including motor, sensory, and cognitive dysfunction as well as demyelination and lesion formation in brain and spinal cord. A variety of animal models of MS have been developed that share many of the pathological hallmarks of MS including motor deficits (ascending paralysis), demyelination and axonal damage of central nervous system (CNS) tissue. In recent years, neuropathic pain has been recognized as a prevalent symptom of MS in a majority of patients. To date, there have been very few investigations into sensory disturbances in animal models of MS. The current work contains the first assessment of hind paw mechanical allodynia (von Frey test) over the course of a relapsing-remitting myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE) rat model of MS and establishes the utility of this model in examining autoimmune induced sensory dysfunction. We demonstrate periods of both decreased responsiveness to touch that precedes the onset of hind limb paralysis, and increased responsiveness (allodynia) that occurs during the period of motor deficit amelioration traditionally referred to as symptom remission. Furthermore, we tested the ability of our recently characterized anti-inflammatory IL-10 gene therapy to treat the autoimmune inflammation induced behavioral symptoms and tissue histopathological changes. This therapy is shown here to reverse inflammation induced paralysis, to reduce disease associated reduction in sensitivity to touch, to prevent the onset of allodynia, to reverse disease associated loss of body weight, and to suppress CNS glial activation associated with disease progression in this model.
    Brain Behavior and Immunity 10/2008; 23(1):92-100. DOI:10.1016/j.bbi.2008.09.004 · 5.89 Impact Factor
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