The implication wasn't SSRIs, it was for drugs that control or limit amounts of monoamines (quite different).
The activity of the serotonin pathways was investigated by three research groups back in the 90s (including well known UK psychiatrists who each took part in two of the studies). They found
elevated activity and the papers hypothesised that this may be a causative factor in the experience of fatigue.
Similarly, no SSRI has ever demonstrated a benefit for depression in CFS patients in double blinded RCTs at reasonable follow up intervals. (but the broader targeting MAOIs are effective)
The Japanese tried to do a bunch of gene expression stuff, but their studies were flawed as their patients had taken antidepressants long-term before hand, so the finding of lowered Serotonin receptor expression was not a specific finding as the same finding is found in the general population who have taken antidepressants long term. Yes, taking antidepressants long term leads to permanent brain chemistry changes - something that your doctor probably didn't tell you.
In the 2000s, well known UK psychatrists W and S tried to explain away their results in light of the Japanese research, ignoring the flaw
Serotonin etc all play important roles in immune response.
http://www.ncbi.nlm.nih.gov/pubmed/10080856 and many other reviews.
I think the measurements of the neurotransmitters is a symptom, not a cause. Drugs that target these neurotransmitters, eg neuroleptics or other classes that have other effects will just cause more problems than they will solve. The reason why they are still being considered is that scientists still don't have a clue when it comes to understanding fatigue. Drugs that prevent damage are a different question. I would also predict that if any of these drugs do magically work, it will be due to reasons (eg protective effects) other than what is currently understood about that drug.