A reader wrote:
“Need your brain.
- GastroCrom is Cromoglicic Acid ” is traditionally described as a mast cell stabilizer, …prevents the release of inflammatory chemicals such as histamine from mast cells.”
Tramadol ” is an opioid pain medication…
- “As of 2015 tramadol was not approved in the United States for fibromyalgia. Based on three small trials with weak study design, there is fair evidence for tramadol as a second line treatment.” It also “increase central serotonin neurotransmission. “
- “Earlier studies suggest that CFS may be associated with genetic variability in genes important for serotonin (5-HT) signaling [3,4].” 
- “Chronic fatigue syndrome (CFS) or Myalgic Encephalomyelitis (ME) is characterized by…autoimmunity to serotonin” 
- Aspartame ==> glutamate: I could only find studies indicating no evidence   , but did find
- ” Plasma phenylalanine concentrations were significantly higher (p less than 0.05, paired t test) after ingestion of meals containing aspartame” 
- “Aspartame has conflicting evidence with two positive and two negative provocation studies [for causing headaches]. Observational studies provide modest evidence that gluten- and histamine-containing foods as well as alcohol may precipitate headaches in subgroups of patients.” 
- “Selective serotonin reuptake inhibitors (SSRIs) are often prescribed in patients with postural tachycardia syndrome (POTS), and act at synaptic terminals to increase monoamine neurotransmitters.” 
- ‘Pharmacologic treatment is recommended on a case-by-case basis, and can include… , mineralocorticoid agents to increase blood volume, and serotonin reuptake inhibitors.”  (for mineralocorticoid see above diagram)
The two drugs acts strongly on two different aspects of CFS:
- Excessive histamine is reduced (probably, microbiome associated)
- Improved serotonin signalling (possibly DNA associated), which may also impact POTS
They may act on other aspects but that is difficult to evaluate given the dominant aspects that they are known to act upon.
Second Question – Calcium Channels
Now the explicit question about Calcium Channels.
- “It is suggested that chronic fatigue syndrome/fibromyalgia is caused by virus injury to the calcium channels leading to larger quantities than usual of calcium ions entering the striated muscle cells.”
- “Circulating autoimmune antibodies may produce symptoms of muscular fatigue by reacting with acetylcholine receptors or calcium binding channels … We were unable to detect any pathogenic antibodies.” 
- ” We also report for the first time,… as well as decreased intracellular calcium within specific conditions in CFS/ME patients.” 
- “Given the important roles of calcium (Ca2+) and acetylcholine (ACh) signalling in B cell activation and potential antibody development, we aimed to identify relevant single nucleotide polymorphisms (SNPs) and genotypes in isolated B cells from CFS/ME patients…. identified a number of SNPs and genotypes in genes… These may …. suggest a role for Ca2+ dysregulation in AChR and TRP ion channel signalling in the pathomechanism of CFS/ME.” 
- “TRPM3 activity and function in NK cells in CFS/ME patients is impaired, resulting in changes in Ca2+ ion concentration in the cytosol and intracellular stores which may, in turn, change the NK cells’ activation threshold.” 
My take is that the impact of the two drugs mentioned above with calcium channel (still speculative, the “may” keyword) is far less than their impact on two established aspects of CFS. It may be there, but these two drugs are not suitable to demonstrate that calcium channels (versus other things) is involved or effective for treatment.