An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome, by Klaus J Wirth, Carmen Scheibenbogen & Friedemann Paul in Journal of Translational Medicine volume 19, no: 471 (2021)
There is accumulating evidence of endothelial dysfunction, muscle and cerebral hypoperfusion in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS).
In this paper we deduce the pathomechanisms resulting in central nervous pathology and the myriad of neurocognitive symptoms. We outline tentative mechanisms of impaired cerebral blood flow, increase in intracranial pressure and central adrenergic hyperactivity and how they can well explain the key symptoms of cognitive impairment, brain fog, headache, hypersensitivity, sleep disturbances and dysautonomia.
Excerpt from Introduction
ME/CFS is classified as a neurological disease. This is based on neurological symptoms including mental fatigue, impaired cognition, psychomotor slowing, disturbed sleep, hypersensitivities to noise, light and smells, headache, pain and paresthesias and severe dysautonomia.
Many symptoms are, however, not obviously explained by neurological pathology including the cardiovascular situation with orthostatic intolerance, hypovolemia and a low activity of the renin–angiotensin–aldosterone system (RAAS), or the impaired muscle function (reduced handgrip strength and fatigability) and energetic disturbance. This co-occurrence of seemingly unrelated symptoms and findings prompts to look for a unifying explanation (the most parsimonious explanation).
The authors discuss:
- Decreased cerebral blood flow (CBF)
- Disturbed local blood flow regulation and neurovascular coupling
- Increase in intracranial pressure
- Disturbances of reflexes and autonomic function, hypervigilance and hypersensitivity to sensory stimuli such as light, noises and smells and brain fog
- Hypocapnia, hyperventilation, respiratory alkalosis and possible consequences for skeletal muscle metabolism
- Sleep disturbances and non-restorative sleep
Neurological symptoms in ME/CFS can be severe and debilitiating, but no clear specific brain pathology or lesions have been detected so far. Whether neuroinflammation or a brain stem pathology exists—where dysautonomia may have its origin as the primary disturbance eliciting ME/CFS—remains to be shown.
Decreased CBF, disturbed local blood flow regulation and neurovascular coupling, central adrenergic hyperactivity, hypocapnia and increase in intracranial presssure seem to play a strong role in the pathophysiology of the neurological symptoms in ME/CFS (Fig. 1). They can well explain cognitive impairment, brain fog, headache, psychomotor slowing, ataxia and loss of coordination of movements, hypersensitivity, sleep disturbances and dysautonomia.