Disease Mechanisms and Clonidine Treatment in Adolescent Chronic Fatigue Syndrome.

At baseline, patients with CFS had a lower number of steps per day, digit span backward score, and urinary cortisol to creatinine ratio. They had a higher fatigue score, heart rate responsiveness, plasma norepinephrine level , and serum C-reactive protein concentration compared with healthy controls. There were no significant differences regarding blood microbiology evaluation.

Adolescent CFS is associated with enhanced sympathetic nervous activity, low-grade systemic inflammation, attenuated hypothalamus-pituitary-adrenal axis function, cognitive impairment, and large activity reduction, but not with common microorganisms. Low-dose clonidine attenuates sympathetic outflow and systemic inflammation in CFS but has a concomitant negative effect on physical activity; thus, sympathetic and inflammatory enhancement may be compensatory mechanisms. Low-dose clonidine is not clinically useful in CFS.

Neuromuscular strain as a contributor to cognitive and other symptoms in chronic fatigue syndrome: hypothesis and conceptual model

Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we use the more general term “neuromuscular strain.”
Neuromuscular restrictions are common in CFS, and many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination.
In this paper we submit that neuromuscular strain is a previously unappreciated peripheral source of sensitizing input to the nervous system, and that it contributes to the pathogenesis of CFS symptoms, including cognitive dysfunction.