There is moderate evidence for use as a second-line treatment for fibromyalgia but it is not FDA approved for this use; however, its use is approved for treatment of fibromyalgia as a secondary painkiller by the NHS.Its analgesic effects take about one hour to come into effect and 2 to 4 h to peak after oral administration with an immediate-release formulation. On a dose-by-dose basis, tramadol has about one-tenth the potency of morphine (thus 100 mg is commensurate with 10 mg morphine but may vary) and is practically equally potent when compared with pethidine and codeine. For pain moderate in severity, its effectiveness is equivalent to that of codeine at low doses, and hydrocodone at very high doses; for severe pain it is less effective than morphine.These painkilling effects last about 6 h. The potency of analgesia varies considerably as it depends on an individuals genetics. People with specific variants of CYP2D6 enzymes may not produce adequate amounts of the active metabolite (desmetramadol) for effective pain control.Sleep medicine physicians sometimes prescribe tramadol (or other opiate medications) for refractory restless legs syndrome (RLS); that is, RLS that does not respond adequately to treatment with first-line medications such as dopamine agonists (like pramipexole) or alpha-2-delta (α2δ) ligands (gabapentinoids), often due to augmentation. Contraindications
Tramadol may not provide adequate pain control for individuals with certain genetic variants of CYP2D6 enzymes as they metabolize tramadol to the inactive molecule. These genetic polymorphisms are not currently routinely tested for in clinical practice.
People who are at an increased risk of acquiring particular fungal infections in general may also be at an increased risk of developing fungal meningitis, as the infection may in some cases spread to the central nervous system. People residing in the Midwestern United States, and Southwestern United States and Mexico are at an increased risk of infection with Histoplasma and Coccidioides, respectively. Diagnosis
If suspected, fungal meningitis is diagnosed by testing blood and cerebrospinal fluid for pathogens. Identifying the specific pathogen is necessary to determine the proper course of treatment and the prognosis. Measurement of opening  pressure, cell count with differential, glucose and protein concentrations, Grams stain, India ink, and culture tests should be performed on cerebrospinal fluid when fungal meningitis is suspected. Treatment
Fungal meningitis is treated with long courses of high dose antifungal medications. The duration of treatment is dependent upon the causal pathogen and the patients ability to stave off the infection; for patients with a weaker immune system or diabetes, treatment will often take longer. Prognosis
Prognosis depends on the pathogen responsible for the infection and risk group. Overall mortality for Candida meningitis is 10-20%, 31% for patients with HIV, and 11% in neurosurgical cases (when treated). Prognosis for Aspergillus and coccidioidal infections is poor. Outbreaks
As of November 5, 2012, the CDC reported that 409 patients had laboratory-confirmed fungal meningitis caused by injections with contaminated medication. There had been 30 fatalities. A black mold, Exserohilum rostratum, was found in 45 of these cases.