- Last Updated: 05 December 2015 05 December 2015
Brain and neuro-endocrine functioning
I.Treasaden (London, UK) looked at volumetric changes in regional grey and white matter in CFS using Voxel 3D MRI techniques. He compared 26 CFS patients with controls. In the CFS patients there was reduced grey matter in the occipital lobes (associated with visual processing), in the right angular gyrus (involved in perceptual sequence learning, conscious awareness of actions) and in the posterior division of the left parahippocampalgyrus (associated with memory function and retrieval). There was also reduction of white matter in the left occipital lobe. This data helps to confirm a neurological diagnosis, and needs to be correlated with biochemical changes.
That there is evidence for reduced aldosterone in those with CFS was presented by R.Boneva (Atlanta, USA). Many of the symptoms in some CFS patients do overlap with those of Addison’s disease. These include orthostatic intolerance, orthostatic tachycardia and heat/cold intolerance. Maintenance of blood volume may be poor and this is dependent on regulation by aldosterone and mineralocorticoid receptors in the brain. In this study of 70 CFS patients and 212 controls, those with CFS had comparatively lower aldosterone levels. A previous study (Wichita) had reported higher plasma renin levels. Further studies should measure aldosterone response to salt restriction and postural changes.
A.Miller (Atlanta, USA) presented 2 papers. The first was on behalf of J.Jones (Atlanta, USA) using functional MRI (fMRI). It has been suggested that CFS symptoms may be linked to altered cognitive or pre-cognitive processing in the CNS. This study investigated the sense of “self” and “illness-related semantic information”. The focus was on the right anterior insula, an area associated with awareness and self-related processing. Conclusions were that there is a real alteration of body physiology in CFS. The interoceptive landscape is acquired cognitively and precognitively in an altered way, enhancing the prominence of symptoms related to fatigue.
The second paper demonstrated decreased basal ganglia activity in CFS associated with fatigue by fMRI. Results compared to controls, showed decreased activation in the right caudate and right globuspallidus. The decreased activation in the right globuspallidus was significantly correlated with increased mental fatigue, general fatigue and reduced activity. Dopamine has a central role in basal ganglia regulation, so alterations in dopamine metabolism may be involved. Dopamine transmission and metabolism in these areas may be due to activated immune pathways. Pharmacologic strategies targeting dopamine and the basal ganglia may be therapeutic possibilities.
J.Dyke (New York, USA) discussed a new brain imaging technique known as arterial spin labelling MRI was used to compare regional cerebral blood flow (rCBF) in CFS, patients with major depression (MDD) and healthy controls. The 2 patient groups were psychotropic-medication free for 1 week prior to scanning. rCBF was significantly decreased in CFS in the left anterior cingulate cortex and the right lingual region compared to controls, while those with MDD had a trend towards significantly lower rCBF in the left anterior cingulate cortex. rCBF for CFS and MDD did not differ significantly. It is unclear whether the hypoperfusion in rCBF in CFS would account for previous observation of increased ventricular lactate. This increase could be due to oxidative stress, mitochondrial dysfunction or decreased rCBF.
The conference ended with an excellent over view by Anthony Komaroff (Boston, USA). He mentioned an informal meeting which had taken place to discuss multicentre research initiatives. He stressed the importance of a variety of initiatives pulling clinicians and researchers together. Forms, laboratory tests etc. need to be standardised. He pointed out that “Research Needs Money”.