Brain Injury and the Chronic Fatigue Syndrome Brain

Brain Injury can happen many ways. The most common is blunt force trauma, typically from a car accident, called Traumatic Brain Injury (TBI) or from a stroke . TBI and stroke is easy for most people to understand and be emphatic towards.  In general the half-life of TBI preventing employment is 2 years [reference]. The rate of recovery depends on many issues and the ability to be employed is often dependent on the ability of the person or their recovery therapist to be adaptive. I know because I have been thru the process three times!

In the case of Chronic Fatigue Syndrome, it is not the result of an one instance in time like TBI.  It is the ongoing consequence of the disease process and has some unique characteristics such as loss of brain mass. As readers may know, I have had CFS three times – each time with significant cognitive loss (1st time going from a triple 1st class honors student to barely passing my courses the following year). The last time with CFS, the SPECT scan was (mis)read as early Alzheimer’s – which “agreed” with general memory issues.  An evaluation by a subsequent neurologist who was familiar with CFS, dismissed that diagnosis because my memory issues did not match Alzheimer’s — in fact those issues have been decreasing year after year since recovery started.

In this first post, I will give the facts, what may scare some of you but should be accepted and you should move on to acting upon this. In the second post, I will give my view on recovery strategies for brain injury (with reference to literature).

Brain Injury in Chronic Fatigue Syndrome

First the bad news, the scary news — far worst than brain injury from someone that suffered an automobile accident or a fall.

  • “most of the studies found gray matter (GM) volumes reduced in some brain regions in CFS”[2015]
  • Patients with chronic fatigue syndrome have reduced absolute cortical blood flow [2006].
  • “Most patients showed autonomic nervous system dysfunction and circadian rhythm disturbances, similar to those observed in jet lag. Radiological imaging studies (SPECT, Xe-CT, and MRS) revealed decreased blood flow in the frontal and thalamic areas, and accumulation of choline in the frontal lobe.” [2004]
  • “Neuroinflammation is present in widespread brain areas in CFS/ME patients and was associated with the severity of neuropsychologic symptoms.” [2014]
  • “Patients with AIDS dementia complex had the largest number of defects (9.15 per patient) and healthy patients had the fewest defects (1.66 per patient). Patients with chronic fatigue syndrome and depression had similar numbers of defects per patient (6.53 and 6.43, respectively). In all groups, defects were located predominantly in the frontal and temporal lobes.” [1994]
  • “CFS subjects showed less perfusion in the anterior cingulate region, the change in CFS subjects’ activation of the left anterior cingulate region during the PASAT was greater than that observed for healthy subjects.” [2003]
  • Patients with chronic fatigue syndrome have reduced absolute cortical blood flow.[2006]
  • ” reports of WM [white Matter] volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits.”[ Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression.[2015]
  • “Neuroimaging and EEG research has documented brain dysfunction in cases of CFS. Therefore, a quantitative EEG was done, comparing her to a normative data base. This revealed excessive left frontal theta brainwave activity in an area previously implicated in SPECTresearch.” [2001]
  • “Bilateral white matter atrophy is present in CFS… Right hemispheric increased FA[piecewise fractional anisotropy] may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.” [2015]
  • “Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness.” [2000]
  • “symptoms of fatigue in CFS subjects were associated with reduced responsivity of the basal ganglia, possibly involving the disruption of projections from the globus pallidus to thalamic and cortical networks.” [2014]
  • ” neurocognitive testing in CFS has demonstrated deficits in speed and efficiency of information processing, attention, concentration, and working memory.” [2013]
  • “many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis–in both of which conditions chronic fatigue is characteristically present.” [1997]
  • ” in chronic fatigue syndrome patients, there is discordance between SPET brain perfusion and 18F-FDG brain uptake.” [1998]
  • “CFS patients showed a significant hypometabolism in right mediofrontal cortex (P = 0.010) and brainstem (P = 0.013) in comparison with the healthy controls. Moreover, comparing patients affected by CFS and depression, the latter group showed a significant and severe hypometabolism of the medial and upper frontal regions bilaterally (P = 0.037-0.001), whereas the metabolism of brain stem was normal. Brain 18FDG PET showed specific metabolism abnormalities in patients with CFS in comparison with both healthy controls and depressed patients.” [1998]
  • ” In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T(1) -weighted MR and white matter volume, group × hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation.” [2011]
  • Sjögren syndrome presenting with encephalopathy mimicking Creutzfeldt-Jakob disease.[2013] Sjogren Syndrome is often co-morbid with CFS
  • Brainstem perfusion is impaired in chronic fatigue syndrome. [1995]
  • “The EEG abnormality is slow alpha wave contaminants on slow wave background, which is identical to EEG of CFS. The results clearly imply that CFS is not a hysterical or psychogenic disease, and that fibromyalgia may be a central fundamental of CFS. Fibromyalgia, however, has distinct features such as no antecedent inflammatory process and no endemics. Therefore, the syndrome has features distinct from, in addition to common features to CFS. It is also very difficult to distinguish CFS from depression. The above-mentioned features can be observed in depression. Now, study of brain blood flow or metabolism by PET or SPECT can be a possible tool for establishment of the CFS identity.” [1992]
  • “The BP(ND) values of (11)C-(R)-PK11195 in the cingulate cortex, hippocampus, amygdala, thalamus, midbrain, and pons were 45%-199% higher in CFS/ME patients than in healthy controls.” [2014] via PET Scan

Bottom Line:

Next time that someone says “CFS is your head”, do not disagree, instead haul out the above and say that they are correct, it is physical disruption of the brain!