Abstract
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS and Gulf War Illness (GWI) share features of post-exertional malaise (PEM), exertional exhaustion, or postexertional symptom exacerbation. In a two-day model of PEM, submaximal exercise induced significant changes in activation of the dorsal midbrain during a high cognitive load working memory task (Washington 2020) (Baraniuk this issue). Controls had no net change. However, ME/CFS had increased activity after exercise, while GWI had significantly reduced activity indicating differential responses to exercise and pathological mechanisms. These data plus findings of the midbrain and brainstem atrophy in GWI inspired a review of the anatomy and physiology of the dorsal midbrain and isthmus nuclei in order to infer dysfunctional mechanisms that may contribute to disease pathogenesis and postexertional malaise. The nuclei of the ascending arousal network were addressed. Midbrain and isthmus nuclei participate in threat assessment, awareness, attention, mood, cognition, pain, tenderness, sleep, thermoregulation, light and sound sensitivity, orthostatic symptoms, and autonomic dysfunction and are likely to contribute to the symptoms of postexertional malaise in ME/CFS and GWI.
Highlights
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) [1,2] and Gulf WarIllness (GWI) [3,4] share features of post-exertional malaise, fatigue that is not relieved by rest, unrefreshing and non-restorative sleep, total body pain, and systemic hyperalgesia and decreased quality of life
The region of interest in the midbrain extended from the left to right periaqueductal gray (PAG) and to the adjacent right midbrain reticular formation (MRF), inferior colliculus (IC), and lateral lemniscus, and caudally to the right lateral isthmus4.oTf 2h2e opposing directions of responses in ME/CFS versus Gulf WarIllness (GWI) indicated different molecular mechanisms were perturbed by exercise in the two diseases
Review of the midbrain nuclei provides a novel perspective on potential neural pathologies affecting periaqueductal gray, parabrachial complex, inferior colliculus, oculomotor and visual systems in threat assessment, anxiety, negative emotion, pain and tenderness, and other aspects of the ME/CFS and GWI clinical experiences
Summary
Illness (GWI) [3,4] share features of post-exertional malaise (exertional exhaustion), fatigue that is not relieved by rest, unrefreshing and non-restorative sleep, total body pain, and systemic hyperalgesia and decreased quality of life. Exercise caused dissociation of the DMN with aberrant anterior node activation in both ME/CFS and GWI These dynamic changes in the medial prefrontal cortex may be objective evidence of postexertional malaise. The region of interest in the midbrain extended from the left to right periaqueductal gray (PAG) and to the adjacent right midbrain reticular formation (MRF), inferior colliculus (IC), and lateral lemniscus, and caudally to the right lateral isthmus4.oTf 2h2e opposing directions of responses in ME/CFS versus GWI indicated different molecular mechanisms were perturbed by exercise in the two diseases. The anterior rim of the midbrain contains the cerebral peduncles with ascending nerve tracts to the thalamus and cortex, and descending corticospinal, corticopontine, and sensory information from the spinal cord dorsal columns to the thalamus (spinothalamic tract) and the lateral lemniscus that carries auditory information from cochlear nuclei to the inferior colliculus. AA rreevviieeww ooff eeaacchh nnuucclleeaarr rreeggiioonn pprroovviiddeess aa ffrreesshh ppeerrssppeeccttiivvee ffoorr iinntteerrpprreettiinngg tthhee ccuurrrreenntt rreessuullttss aanndd ggeenneerraattiinngg nneeww hhyyppootthheesseess ffoorr ppoosstteexxeerrttiioonnaall mmaallaaiissee,, MMEE//CCFFSS,,aannddGGWWII
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
