Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A neurological entity?, by Inigo Murga Gandasegui, Larraitz Aranburu Laka, Pascual-Angel Gargiulo, Juan-Carlos Gomez-Esteban, Jose-Vicente Lafuente Sanchez in Medicina Vol 57, #10, p 1030, Sep 27, 2021 [doi.org/10.3390/medicina57101030]
Review abstract:
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disorder of unknown physiopathology with multisystemic repercussions, framed in ICD-11 under the heading of neurology (8E49). There is no specific test to support its clinical diagnosis.
Our objective is to review the evidence in neuroimaging and dysautonomia evaluation in order to support the neurological involvement and to find biomarkers serving to identify and/or monitor the pathology. The symptoms typically appear acutely, although they can develop progressively over years; an essential trait for diagnosis is ‘central’ fatigue together with physical and/or mental exhaustion after a small effort.
Neuroimaging reveals various morphological, connectivity, metabolic, and functional alterations of low specificity, which can serve to complement the neurological study of the patient. The COMPASS-31 questionnaire is a useful tool to triage patients under suspect of dysautonomia, at which point they may be redirected for deeper evaluation.
Recently, alterations in heart rate variability, the Valsalva maneuver, and the tilt table test, together with the presence of serum autoantibodies against adrenergic, cholinergic, and serotonin receptors were shown in a subgroup of patients. This approach provides a way to identify patient phenotypes. Broader studies are needed to establish the level of sensitivity and specificity necessary for their validation.
Neuroimaging contributes scarcely to the diagnosis, and this depends on the identification of specific changes. On the other hand, dysautonomia studies, carried out in specialized units, are highly promising in order to support the diagnosis and to identify potential biomarkers. ME/CFS orients towards a functional pathology that mainly involves the autonomic nervous system, although not exclusively.
5. Conclusions
The neurobiopathological substrate of ME/CFS is unknown. There currently is no neuroimaging finding or specific laboratory test to establish the diagnosis. Changes reported in volumetry, cerebral blood flow, anatomy, and functional connectivity, at rest as well as in response to stimuli reveal the existence of brain dysfunctions, whose meaning is yet to be determined. The interpretation of findings is complicated by the lack of a consensual study protocol.
The available evidence on the involvement of the autonomic nervous system
(sympathetic/parasympathetic imbalance) indicates that the neurologist plays an essential role in the clinical evaluation of the syndrome and highlights the potential benefits of dysautonomia units for a better understanding of these dysfunctional pathologies.
