Volgens een recente studie van Watanabe, werkzaam bij het Riken Instituut, en collega's
is er wel degelijk sprake van ontsteking van de hersenen (encephalo-myelitis, de
E van ME) in "CVS".
Waar diverse (bio)psychosocialisten de naam afwijzen op basis van "het misleidende karakter",
toonden Watanabe en mede-onderzoekers m.b.v. positron emissietomografie (PET)-scans aan:
Interessante citaten uit het studierapport:
De "proefkonijnen":
Nine patients who fulfilled the international diagnostic criteria for CFS and ME
were recruited from the Fatigue Clinical Center at Osaka City University Hospital, Osaka, Japan.
Het betreft hier dus patiėnten die aan de internationale consensus-criteria voor ME voldoen.
Het zou interessant zijn te weten of neuro-inflammatie ook aanwezig is
bij CVS-patiėnten die niet aan de ME-criteria voldoen (CVS/niet-ME).
De resultaten:
Table 2
Regional 11C-(R)-PK11195 BPND in CFS/ME Patients and Healthy Controls
|
Region
|
CFS/ME
|
Healthy control
|
P
|
Increase (%)
|
|
Midbrain
|
0.181 ± 0.027
|
0.123 ± 0.024
|
0.0001
|
47
|
|
Pons
|
0.155 ± 0.030
|
0.107 ± 0.028
|
0.0021
|
45
|
|
Thalamus
|
0.097 ± 0.021
|
0.058 ± 0.023
|
0.0013
|
66
|
|
Cingulate
|
0.010 ± 0.008
|
0.003 ± 0.003
|
0.0353
|
199
|
|
Amygdala
|
0.057 ± 0.031
|
0.031 ± 0.025
|
0.0586
|
85
|
|
Hippocampus
|
0.053 ± 0.023
|
0.029 ± 0.017
|
0.0212
|
81
|
De grootste afwijkingen komen voor in de gyrus cinguli,
hippocampus en amygdala,
hersengebieden die volgens de studie gerelateerd zijn aan "depressie" en cognitieve symptomen.
[T]he concentration of interferon-g tended to be higher in CFS/ME patients than in healthy controls
(1.66 ± 2.77 vs. 0.00 ± 0.00 pg/mL, P=0.0740).
The concentration of
tumor necrosis factor-a (0.80 ± 0.63 vs. 0.45 ± 0.80 pg/mL, P=0.3735),
interleukin-1b (1.02 ± 0.99 vs. 0.40 ± 0.60 pg/mL, P=0.1129), and
interleukin-6 (0.60 ± 0.56 vs. 0.75 ± 1.10 pg/mL, P=0.7277)
was similar between the groups.
De cytokinenivo's in het serum van patiėnten weken, m.u.v. IFN-γ,
niet significant af van gezonde proefkonijnen.
This suggests that neuroinflammation should be assessed using PET
rather than by measuring peripheral proinflammatory cytokines.
Mede gezien de technische complicaties m.b.t. cytokine-onderzoek (levensduur) en deze uitkomsten,
zou encefalomyelitis niet m.b.v. bloedonderzoek. maar via PET-scans vastgesteld moeten worden.
De (mogelijke) oorzaken:
Although the mechanisms underlying neuroinflammation in CFS/ME are unclear,
one plausible mechanism is overactivity of neurons.
To compensate for functional loss associated with CFS/ME,
patients have to exert greater effort to perform daily activities,
resulting in enhanced neural activation.
Overactivation of N-methyl-D-aspartate receptors caused by enhanced neural activation
results in production of proinflammatory cytokines, reactive oxygen species, and nitrogen species
that cause inflammation.
Another plausible mechanism is the immunologic response to the initial infectious process,
which can also induce the production of the proinflammatory cytokines,
reaction oxygen species, and nitrogen species that cause neuroinflammation.
De auteurs schetsen twee mogelijke oorzaken van neuro-inflammatie:
Commentaren:
Klik op betreffende logo om het commentaar te kunnen lezen:
Neuroinflammation in patients with chronic fatigue syndrome/Myalgic Encephalomyelitis:
an 11C-(R)-PK11195 PET study.
J Nucl Med. 2014 Mar 24. doi: 10.2967/jnumed.113.131045.
Nakatomi Y, Mizuno K, Ishii A, Wada Y, Tanaka M, Tazawa S, Onoe K, Fukuda S,
Kawabe J, Takahashi K, Kataoka Y, Shiomi S, Yamaguti K, Inaba M, Kuratsune H, Watanabe Y.
Abstract
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disease
characterized by chronic, profound, disabling, and unexplained fatigue.
Although it is hypothesized that
brain inflammation is involved in the pathophysiology of CFS/ME,
there is no direct evidence of neuroinflammation in patients with CFS/ME.
Activation of microglia or astrocytes is related to neuroinflammation.
11C-(R)-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline-carboxamide (11C-(R)-PK11195)
is a ligand of PET for a translocator protein that is expressed by activated microglia or astrocytes.
We used 11C-(R)-PK11195 and PET to investigate
the existence of neuroinflammation in CFS/ME patients.
METHODS:
Nine CFS/ME patients and 10 healthy controls
underwent 11C-(R)-PK11195 PET and completed questionnaires
about fatigue, fatigue sensation, cognitive impairments, pain, and depression.
To measure the density of translocator protein,
non-displaceable binding potential (BPND) values were determined
using linear graphical analysis
with the cerebellum as a reference region.
RESULTS:
The BPND values of 11C-(R)-PK11195
in the cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons
were 45%-199% higher in CFS/ME patients than in healthy controls.
In CFS/ME patients, the BPND values of 11C-(R)-PK11195
in the amygdala, thalamus, and midbrain
positively correlated with cognitive impairment score,
the BPND values in the cingulate cortex and thalamus
positively correlated with pain score, and
the BPND value in the hippocampus
positively correlated with depression score.
CONCLUSION:
Neuroinflammation is present in widespread brain areas in CFS/ME patients and
was associated with the severity of neuropsychologic symptoms.
Evaluation of neuroinflammation in CFS/ME patients
may be essential for understanding the core pathophysiology and
for developing objective diagnostic criteria and effective medical treatments.
KEYWORDS:
11C-(R)-PK11195, chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME),
neuroinflammation, positron emission tomography (PET)
PMPMID: 24665088
http://jnm.snmjournals.org/content/early/2014/03/21/jnumed.113.131045.abstract
Met dank aan Manja, die mij attendeerde op deze nieuwe studie.
|
