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Infectious Disease and Neurocognition
Table 22.3 Continued
Ref. Ye a r N Diagnostic
criteria
45 2013 Review Prefers
ACR 2010 to
ACR 1990
46 2018 Review NA UK
Notes: a e diagnostic criteria here are listed according to their commonly referred to names. eir descriptions
appear in Appendix 1 and their full citations appear in the references section.
Abbreviations: ACR, American College of Rheumatology; CBT, cognitive behavioral therapy; CFS, chronic fatigue
syndrome; DEU, Germany EEG, electroencephalogram; ERP, event- related potential(s); FM, bromyalgia; FMS,
bromyalgia syndrome; GnRH, gonadotropin- releasing hormone; N, number of subject; NA, not applicable; NIH,
National Institutes of Health; NIRS, near- infrared spectroscopy; NLD, the Netherlands; Ref., reference; SF36, Short
Form 36 Health Survey; TSH, thyroid- stimulating hormone; UK, United Kingdom; USA, United States of America.
Reference citation key: 1. Glass and Park, 2001; 2. Glass, 2006; 3. Glass, 2009; 4. Minelli and Vaona, 2012; 5. Gelonch
et al., 2013; 6. Bell et al., 2018;7. Wu et al., 2018; 8. Innes and Sambamoorthi, 2020; 9. Ibraheem et al., 2021; 10. Wolfe
et al., 2021; 11. Joustra et al., 2022; 12. Leavitt and Katz, 2014; 13. Gil- Ugidos et al., 2021; 14. Gelonch et al., 2018; 15.
Gelonch et al., 2017; 16. Leavitt and Katz, 2008; 17. Munoz Ladron de Guevara et al., 2018; 18. Kratz et al., 2020; 19.
Cherry et al., 2014; 20. Pidal- Miranda et al., 2018; 21. Tesio et al., 2015; 22. Sletvold et al., 1995; 23. Williamson and
Larner, 2016; 24. Katz et al., 2004; 25. Medina et al., 2019; 26. Nishioka et al., 2016; 27. Galvez- Sánchez et al., 2018;
28. Samartin- Veiga et al., 2019; 29. Gonzalez- Villar et al., 2017; 30. Curatolo et al., 2017; 31. Santos et al., 2018; 32.
Silva et al., 2017; 33. Chou et al., 2018; 34. Alanoglu et al., 2005; 35. Walitt et al., 2016; 36. Blanco et al., 2019; 37. Qu
et al., 2021; 38. Lin et al., 2021; 39. Barcelo- Martinez et al., 2018; 40. Ge et al., 2019; 41. Shmygalev et al., 2014; 42.
D’Souza et al., 2021; 43. Wood et al., 2009; 44. Minelli and Vaona, 2012; 45. Gelonch et al., 2013; 46. Bell et al., 2018.
Location Results
a
Spain Reviews the literature from 1995
to 2012. Few studies of cognitive
function in patients with FM were
found, and those found mostly
use small samples. e studies
demonstrate decits mainly in
working memory and complex
attentional function. Long- term
memory and executive functions are
also impaired. e degree of pain
seems directly related to cognitive
dysfunction
Meta- analysis that included 37
USA
studies. FM was signicantly
and negatively associated with
performance on all domains of
cognitive function: inhibitory
control (g = 0.61), memory (g = 0.51
for short- term, 0.50 for long- term
memory), and set shiing (g = 0.30)
e terms used to describe the impairments are descriptive and to some extent
overlap but most likely are not duplicative. e terms we have gleaned include attentional domain (Lin et al., 2021), cognitive symptoms (Qu et al., 2021), executive
function (Alanoğlu et al., 2005; González- Villar et al., 2017), executive domain (Lin
et al., 2021), executive function– attention (Santos et al., 2018), executive function–
long- term memory (Santos et al., 2018), executive function– working memory
(Santos et al., 2018), executive function– shiing and updating (Santos et al., 2018),
naming colors decit (Miró et al., 2011), nonspecic information processing deficit (Karper, 2007), reading words decit (Miró et al., 2011), short- term memory
Fibromyalgia and Chronic Fatigue 379
attention (Kratz et al., 2020), short- term memory processing (Kratz et al., 2020),
speed test decits (Miró et al., 2011) task performance (Qu et al., 2021), and visuospatial working memory (Williamson & Larner, 2016).
At least ten articles reviewing cognitive impairments associated with FM were
published between 2001 and 2021 by researchers residing in seven dierent countries and utilizing diering search strategies. All these articles support an association
between some kind of cognitive impairment and FM. erefore, the association of
cognitive impairment with FM seems to be withstanding both the test of time and
the examination of researchers in dierent countries utilizing dierent search strategies, although the specics of the cognitive impairment or impairments associated
with FM vary.
We both acknowledge and caution that the dierences in cognitive impairments
reported in the literature by researchers in dierent countries may be attributable
to dierent laboratories and dierent researchers using dierent descriptions of the
same cognitive domains or that the dierences in cognitive domains aected may be
attributable to the specic tests administered. Despite these dierences, Ibraheem
et al. (2021) performed a meta- analysis of 29 studies and discussed cognitive impairment as a function of disease pathophysiology (not noting the potential role infection or considering coexisting diagnoses in the patient population).
Further but indirect support for an association of cognitive impairment with FM
comes from the comparison of FM’s cognitive impairment to that of other chronic,
pain- associated diseases such as rheumatic diseases (Walitt et al., 2016) and rheumatoid arthritis specically (Joustra et al., 2022).
Several investigators have hypothesized that the cognitive dysfunction seen in FM
is due to brain sensitization (Leavitt & Katz, 2008; Medina et al., 2019). But studies
attempting to elucidate the pathology underlying cognitive dysfunction reveal multiple preliminary ndings with no profoundly compelling single mechanism.
Our search strategy revealed only one study that raises the possibility that the cognitive dysfunction associated with FM arises from an anatomical abnormality. Van
Koulil et al. (2010) found a correlation in the reduction in gray matter density in the
parahippocampal gyri and cingulate cortex with the cognitive dysfunction accompanying FM. All other identied studies suggest altered physiological or pathological mechanisms, or both.
Eorts have been made to correlate altered brain electrical activity with FM’s cognitive dysfunction. Both reduced frontal brain electrical activity (Muñoz Ladrón de
Guevara et al., 2018) and increased “neural noise” (Nishioka et al., 2016) have been
reported. Auditory event potentials show prolonged latencies and reduced amplitudes (Wood et al., 2009). ese reports, which detect altered electrical activity via
electrophysiological methods, are supported by near infrared spectroscopy studies,
which show reduced brain activity in the frontal regions of FM patients (D’Souza
et al., 2021). Further support for the belief that the cognitive dysfunction of FM
arises from decreased brain electrical activity comes from the studies of SamartinVeiga et al. (2019), Chou et al. (2018), and Ge et al. (2019), who nd that electrical
Infectious Disease and Neurocognition
stimulation of the brain reduces cognitive impairment. Possibly related is the nding
that loss of olfaction correlates with cognitive impairment (Bell et al., 2018).
e severity of FM- associated cognitive dysfunction appears to be alterable to
some extent. Neuroendocrine hormones (Wu et al., 2018) and cortisol levels (BarcelóMartinez et al., 2018; Lin et al., 2021; Qu et al., 2021) have been found to inuence FMassociated cognitive dysfunction. FM patients who smoke have been found to have
more severe cognitive dysfunction (Gelonch et al., 2018). However, statin therapy and
its associated muscle pain have been shown not to increase cognitive dysfunction in
FM (Pidal- Miranda et al., 2018). e possibility of non- pharmacological therapy to
improve cognitive dysfunction in FM patients has been proposed but has not been
conclusively demonstrated. Both cognitive behavioral therapy and exercise therapy
have been proposed (Barceló- Martinez et al., 2018; Blanco et al., 2019; Curatolo et al.,
2017) but await conrming and more robust clinical trials.
Table 22.4 lists the frequency of the domains in which decits have been found in
the studies we have presented here and the descriptors used to describe those domain decits.
Not surprisingly, the most frequently found descriptor of cognitive dysfunction
in FM patients is “poor cognition.” Other common descriptors are losses of “executive function,” “processing speed,” and “attentional control.” ere are other, less
frequently used descriptors that most likely arise from a lack of uniformity in the
instruments used for cognitive testing. We note the report of “olfactory impairment” in one citation that is of signicance in lieu of the nding of olfactory impairment in patients experiencing Covid- 19 and long Covid (Boscolo- Rizzo et al., 2022;
Whitcro & Hummel, 2020). Linkage of cognitive impairment to viral infection is
interesting because the loss of senses, including hearing, smell, and sight, has been
linked elsewhere to the risk of cognitive decline (Devanand, 2016; Nagarajan et al.,
2022; Uchida et al., 2019).
Myalgic encephalomyelitis/ chronic fatigue
syndrome and cognitive dysfunction
Our search of PubMed using the search terms (chronic fatigue syndrome) or (myalgic encephalomyelitis) or (ME/ CFS) and (cognitive dysfunction) yielded 257 citations. Inspection of the titles narrowed the number of citations to 54 and reading
the abstracts and/ or actual publications further narrowed the number of relevant
citations presented to 20 articles (Table 22.5). Our intent is to demonstrate the
linkage of ME/ CFS to cognitive dysfunction and, to the extent possible, indicate how
it has been characterized and what possibly inuences it. At the outset, we state that
some of the retrieved citations we have excluded are early works claiming that there
are or were no cognitive dierences between ME/ CFS patients and healthy controls. We are unable to oer an explanation as to why these early ndings were negative but believe that the preponderance of more recent evidence supports cognitive
Fibromyalgia and Chronic Fatigue 381
Table 22.4 Frequency of domain deficits occurring in cited fibromyalgia
studies
Descriptor of cognitive domain Number of published papers
Poor cognition 9
Executive function 6
Processing speed 6
Attentional control 5
Short- term memory 4
Long- term memory 3
Verbal 3
Working memory 2
Impaired control of attention 1
Dysfunction parallels severity 1
Episodic memory 1
Semantic memory 1
Olfactory impairment 1
Manipulation 1
Orientation 1
Spatial reference memory 1
Recall 1
Information processing 1
Reading speed 1
Color naming 1
dysfunction in ME/ CFS patients. Possibly the more recent ndings of cognitive dysfunction in ME/ CFS patients aligns with the improved tools to assess the various
domains and parameters of cognition.
Reports concerning cognitive impairment associated with ME/ CFS began in 1995
and continue to the present time. e papers presented below were published between 1997 and 2022 and include a meta- analysis of 748 papers by a multi- national
team of authors spanning Europe published in 2022. at paper concludes that cognitive dysfunction is present in patients with ME/ CFS. We also nd support for this
conclusion in the number of countries in which researchers have found similar associations: Australia, Belgium, France, Italy, Japan, Netherlands, Norway, Romania,
Serbia, Spain, the United Kingdom, and the United States of America (Figure 22.5).
Infectious Disease and Neurocognition
Table 22.5 Summary of studies finding cognitive impairments associated with myalgic
encephalomyelitis/ chronic fatigue syndrome
Ref. Ye a r N Country Diagnostic
criteria
a
Reviews
1 2022 40 studies
analyzed
France
Italy
CDC 1994 or
earlier criteria
Romania
Serbia
UK
2 2001 Review Belgium Clinical case
denition not an
inclusion criterion
Results
Aected are visuospatial
immediate memory, verbal
memory (storage, retrieval,
recognition) and visual
memory (recovery) and a
low eciency in attentional
abilities. Executive
functions are little or not
aected. Instrumental
functions preserved
Review of neurocognitive
studies shows that slowed
processing speed, impaired
working memory, and poor
learning of information are
the most prominent features
of cognitive dysfunction in
CFS patients. ere is no
specic pattern of cerebral
abnormalities unique
to ME/ CFS. ere is no
overwhelming evidence
that the fatigue of ME/
CFS is related to cognitive
performance, nor is the
decreased performance
attributable to depression
and anxiety
3 1997 Review USA Advocates using
subgroups
e most consistently
documented
neuropsychological
impairments are in
the areas of complex
information processing
speed and eciency.
General intellectual
abilities and higher order
cognitive skills are intact
Clinical cognitive assessments in adults
4 2019 236 Norway CDC 1994 Patients had problems
mainly in the domains
of psychomotor
speed and attention
measured by objective
neuropsychological tests
Table 22.5 Continued
Fibromyalgia and Chronic Fatigue 383
Ref. Ye a r N Country Diagnostic
criteria
a
Results
5 2014 68 Spain ACR 1990 50 percent of CFS patients
exhibited impairment
in attention and motor
functioning, and nearly
40 percent showed
impairment in speed
information processing
and executive functioning.
Fatigue predicted
attention and executive
functioning impairment,
and emotional factors
predicted verbal memory
dysfunction
6 2011 25 Belgium CDC 1988
CDC 1994
CFS patients had slower
phasic alertness and
impaired working, visual,
and verbal episodic
memory compared to
controls
7 1999 29 Belgium Oxford 1991
CDC 1988
CDC 199
CFS patients have
normal phasic arousal
level and visual selective
attention requiring
shifting of attention in the
visuospatial field. They
have reduced information
processing speed and
efficiency and attentional
dysfunction. Patients
have poor performance
on recall of verbal
information that is due to
poor initial storage rather
than to a retrieval failure
8 2022 2461 Netherlands CDC 1994 Cognitive task performance
was poorer in individuals
with CFS versus controls
without disease and
controls with a medical
disorder
(continued)
Infectious Disease and Neurocognition
Table 22.5 Continued
Ref. Ye a r N Country Diagnostic
criteria
a
Results
9 2006 43 USA CDC 1994 CFS patients with
signicant complaints of
mental fatigue exhibited
signicant impairment in
spatial working memory
and sustained attention
(rapid visual information
processing) when
compared to CFS patients
with low complaints
of mental fatigue and
non- fatigued subjects.
Performance was impaired
only in the nal stages of
the test, indicating greater
cognitive fatigability in
these patients
Factors aecting cognitive impairment in ME/ CFS patients
10 1998 12 USA CDC 1994 e sensory reactivity and
acquisition of conditioned
reex responses were
measured. Patients with
CFS exhibited normal
sensitivity and responsivity
to acoustic stimuli but
displayed impaired
acquisition to a delayed
paradigm of the eye blink
response suggesting
organic brain dysfunction
11 2020 128 Netherlands
USA
CDC 1994 Working memory was
impaired aer head- up tilt
testing
12 2018 43 Australia CDC 1994 CFS patients showed
significantly longer
reaction times but no
significant difference in
accuracy to the Stroop
Color– Word task.
Blood oxygenation level
dependent changes in
response to the Stroop
task in ten regions of the
brain were significantly
lower in CFS patients
Table 22.5 Continued
Fibromyalgia and Chronic Fatigue 385
Ref. Ye a r N Country Diagnostic
criteria
a
13 2006 Not reported USA No clinical case
denition cited
Results
Long- term and working
memory impairments.
CFS patients have slow
information- processing,
and FM patients have
impaired control of
attention. Neuroimaging
studies demonstrate
cerebral abnormalities
with increased neural
recruitment during
cognitive tasks
14 2006 41 USA CDC 1994 Relative to CFS patients
in the normal- NKCA
subgroup, low- NKCA
patients reported less vigor,
more daytime dysfunction,
and more cognitive
impairment. Low- NKCA
patients performed less
on objective measures
of cognitive functioning
relative to normal- NKCA
patients
15 2012 30 Australia CDC 1994 CFS patients showed no
decits in performance
accuracy but were
signicantly slower. CFS
patients showed low and
unresponsive heart rate
variability, greater HR
reactivity, and prolonged
HR recovery aer cognitive
challenge suggesting
that reduced vagal tone
inuences cognitive
function
16 2019 51 UK CDC 1994 Comorbidity with major
depression is not itself
responsible for the
reductions in cognitive
performance seen in ME/
CFS patients
(continued)
Infectious Disease and Neurocognition
Table 22.5 Continued
Ref. Ye a r N Country Diagnostic
criteria
a
17 2020 25 Australia Pediatric case
denition 2006
Results
Resting- state functional
magnetic resonance
imaging used to evaluate
intrinsic connectivity,
cognitive function,
and subjective fatigue,
before and aer a period
of cognitive exertion
in adolescent ME/ CFS
patients. No dierence
found between patients
and controls for intrinsic
functional connectivity,
sustained attentional
performance, processing
speed, and increased
subjective fatigue as a result
of cognitive exertion
18 2011 52 Spain CDC 1994 e cognitive impairment
in CFS is independent of
disease duration. ere is no
increase in severity of decits
with disease duration
Clinical cognitive assessments in children and adolescents
19 2011 50 Japan Pediatric case
denition 2006
Children with CFS had
reduced motor skills.
Selective and alternative
attention, and spatial
working memory decit
discriminates CFS patients
from control subjects with
70.5% accuracy (p = 0.007)
20 2015 120 Norway New onset,
3 months. Chronic
relapsing fatigue
Adolescents have impaired
processing speed, working
memory, cognitive
inhibition response, and
verbal learning. ese
decits are unaected by
adjustments for symptoms
of depression, anxiety
traits, and sleep problems
Notes: a e diagnostic criteria here are listed according to their commonly referred to names. eir descriptions
appear in Appendix 1 and their full citations appear in the references section.
Abbreviations: CDC, Centers for Disease Control and Prevention (USA); CFS, chronic fatigue syndrome; FM, bromyalgia; HR, heart rate; ME/ CFS, myalgic encephalomyelitis/ chronic fatigue syndrome; N, number of subjects;
NKCA, natural killer cell activity; Ref., references.
Reference citation key: 1. Aoun Sebaiti et al., 2022; 2. Michiels and Cluydts, 2001; 3. Tiersky et al., 1997; 4. Rasouli
et al., 2019; 5. Santamarina- Perez et al., 2014; 6. Constant et al., 2011; 7. Michiels et al., 1999; 8. Joustra et al., 2022;
9. Capuron et al., 2006; 10. Servatius et al., 1998; 11. van Campen et al., 2020; 12. Shan et al., 2018; 13. Glass, 2006; 14.
Siegel et al., 2006; 15. Beaumont et al., 2012; 16. Robinson et al., 2019; 17. Josev et al., 2020; 18. Santamarina- Perez
et al., 2011; 19. Kawatani et al., 2011; 20. Sulheim et al., 2015.
Fibromyalgia and Chronic Fatigue 387
Figure 22.5 Countries in which studies suggesting linkage of myalgic encephalomyelitis/
chronic fatigue syndrome to cognitive impairment have studied and are cited in the manuscript
are shown in dark grey.
us far, individual cognitive dysfunction studies have tended to employ small
sample sizes and varying cognitive assessment instruments. We, therefore, nd it
dicult to summarize with condence the precise domains of cognitive function
impaired by ME/ CFS. Nor do we have increased condence in some studies over
others. Consistently reported cognitive decits found in multiple studies seem to be
impaired processing speed (Beaumont et al., 2012; Glass, 2006; Michiels & Cluydts,
2001; Michiels et al., 1999; Rasouli et al., 2019; Santamarina- Perez et al., 2014;
Sulheim et al., 2015; Tiersky et al., 1997), impaired verbal memory (recall) (Aoun
Sebaiti et al., 2022; Constant et al., 2011; Michiels et al., 1999; Santamarina- Perez
et al., 2011; Sulheim et al., 2015), and attention decits (Aoun Sebaiti et al., 2022;
Kawatani et al., 2011; Santamarina- Perez et al., 2014). One study suggests impaired
motor function as cause of cognitive impairment (Santamarina- Perez et al., 2014),
which lends itself to the notion that cognitive function can be aected by multiple
physiologic functions including movement, which can make it challenging to denitively dene a causation of the cognitive symptoms reported in ME/ CFS.
ere have been few explorations of the pathophysiological causes of these dysfunctions, but possibilities we have gleaned from the literature include low natural
killer cell activity that exacerbates cognitive dysfunction (Siegel et al., 2006), poor
utilization of oxygen in regions of the brain causing cognitive dysfunction (Shan
et al., 2018), and decreased tissue perfusion caused by a reduction of vagal tone and/
or altered heart rate variability (Beaumont et al., 2012). One preliminary study raises
the possibility of slowed synaptic transmission (Servatius et al., 1998).
We have identied two studies of cognitive dysfunction in children and adolescents with ME/ CFS (Kawatani et al., 2011; Sulheim et al., 2015) but none that directly compare the cognitive dysfunction found in children and adolescents with
that found in adults. Nevertheless, until such comparative studies are performed,