ReviewFatigue after subarachnoid haemorrhage: A systematic review
Introduction
The incidence of non-traumatic subarachnoid haemorrhage (SAH) is approximately 9 cases per 100,000 person-years and has remained relatively stable during the last 40 years [1]. Advances in management have increased the chances of survival after SAH from 48% to 65% over the last three decades [1]. The incidence of SAH is highest in people aged between 40 and 60 years, which means that any adverse long term effects will have affect survivors' ability to continue their previous social roles, including returning to work [2]. Thus, understanding the long-term consequences of SAH is important so that services can be planned to meet the needs of these people. Fatigue is one such potential long-term consequence. It is well established that fatigue is common in other neurological conditions, including ischaemic stroke, and that fatigue can be extremely debilitating [3].
There are several ways to categorise fatigue. Fatigue could be divided into ‘normal’ and ‘pathological’ fatigue. Normal fatigue is defined as “a state of general tiredness that is the result of overexertion and can be ameliorated by rest”, whilst “pathological” fatigue is “a state characterized by weariness unrelated to previous exertion levels and is usually not ameliorated by rest” [3]. Pathological fatigue is a symptom of many diseases [3], [4].
Fatigue in neurological disorders such as multiple sclerosis and Parkinson's disease is often associated with depression and sleep disturbances [4], but it may develop in the absence of these known potential causes, indicating that other, as yet unknown, factors may be implicated [1]. There are several putative pathological mechanisms that might, in theory, trigger fatigue after SAH. Systemic inflammation may alter neurotransmitter signalling in the brain through changing activity of enzymes such as indoleamine 2,3-dioxygenase, while disruption of fronto-subcortical neurocircuits due to complications of SAH such as delayed ischaemia or hydrocephalus may lead to the subtle impairment of attention and arousal and subsequent fatigue [4], [5]. Neuroendocrine changes may also contribute to the development of fatigue in patients after SAH [6]. Currently, the mechanisms of fatigue after SAH are unknown and hence no reliable treatments are available [1], [7].
The aims of this systematic review were:
- 1.
To assess the frequency, severity and time course of fatigue after SAH.
- 2.
To identify factors associated with the development of fatigue after SAH, namely patients' demographics, baseline characteristics of SAH, sleep disturbances, psychological factors (such as anxiety, depression, cognitive impairment), complications (for example neuroendocrine changes, hydrocephalus or delayed ischaemia) of SAH and comorbidities.
- 3.
To evaluate the impact of fatigue on patients' daily lives after SAH.
Section snippets
Searches
One author (MK) conducted searches in MEDLINE (from 1966), EMBASE (from 1980), CINAHL (from 1937), AMED (from 1885), PsychInfo (from 1806) on October 15, 2010 and in PubMed (from 1950) on February 20, 2011 (Appendix 1). The same author (MK) read every title and abstract and obtained full texts of potentially relevant papers. He then applied inclusion and exclusion criteria to each of the full texts. Any uncertainties were discussed with a second reviewer (GM). He also scrutinised reference
Results
The electronic search identified 4935 citations (Fig. 1.). Twenty seven full texts were retrieved for detailed evaluation. Fourteen studies which either did not report fatigue or did not contain primary data were excluded (Fig. 1). Thirteen studies (total number of participants — 737, subject number ranged from 10 to 141) describing 11 cohorts (data from three of the cohorts were used in six publications [13], [14], [19], [20], [21], [22]) fulfilled our inclusion criteria [10], [11], [12], [13]
Discussion
To our knowledge this is the first systematic review of fatigue after SAH. We found 13 studies (n = 737) which met our inclusion criteria. Their quality ranged from low to maximal scores, but overall was relatively high: only three studies had scores less than 18 out of 22. Importantly, the studies on which we based most of our conclusions about associates of fatigue after SAH were of high quality [11], [18], [21].
The frequency of fatigue in the included studies varied greatly; this is likely to
Conflict of interest
None.
Acknowledgment
This work was supported by European Federation of Neurological Societies' Scientific Fellowship to MK.
The following are the supplementary materials related to this article.
Supplementary materials related to this article can be found online at doi: 10.1016/j.jpsychores.2011.12.008.
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