Using medication as a diagnostic tool
Christoff Trüter
Spousal caregiver
Over the centuries, doctors have devised a magnitude of methods to diagnose illnesses, from early clinical observations and skin prick tests, all the way through to X-rays, blood tests, ECGs, lumbar punctures, biopsies, mammograms, ultrasounds, endoscopies, stress tests, genetic testing, CT scans, MRIs, and functional imaging like PET scans, just to name a few.
One intriguing approach I’ve come across is the use of pharmaceuticals, where medication is administered to see if symptoms improve, which can help confirm a suspected diagnosis.
Disclaimer
This article is not suggesting that medication can diagnose disease. A treatment response does not prove a diagnosis, nor does a lack of response rule one out.
Rather, it explores a simple question: when a treatment produces a meaningful, repeatable change in symptoms, should that observation influence how we think about a diagnosis?
A classic example is giving levodopa (which replenishes dopamine levels in the brain) to patients with suspected Parkinson’s disease, to support the diagnosis.
In my wife’s case, this was never done deliberately; however, through the help of our very sympathetic GP, we introduced several medications to help treat her symptoms, which might inadvertently shed some light and offer clues to doctors who are willing to have a deeper look.
Here is a list of medications currently used:
- Atkineton (biperiden)
One of the earliest medications added to her regimen, Atkineton, works by blocking acetylcholine receptors in the brain. It has been quite effective in treating her tremors. - Neurika 75 (pregabalin)
She uses Neurika 75 in moderation to treat neuropathic pain. Although it isn’t always 100% effective, it remains one of the more important medications in her regimen. - Prednisone
A corticosteroid, commonly used to treat autoimmune diseases, was a recent addition to her treatment. It suppresses the immune system and reduces inflammation through its cortisol-like effects. -
Morphine (used acutely, not chronically)
During a recent ER visit, morphine administration triggered severe shaking and tremors—a paradoxical response indicating abnormal CNS excitability and possible underlying neurological dysfunction.
The before last-mentioned (prednisone) addition had a dramatic effect; whereas she was previously becoming more and more fatigued as the day went on, she suddenly had much more energy and could function significantly better both during the day and at night, which is at odds with the literature around FND treatment.
When I informed her neurologist about the improvement, he acknowledged it but attributed it to a general steroid effect rather than considering whether it might provide a clue worth investigating. In an email, he wrote:
The response to steroids is great news.
Use this moment to remind her nothing is broken or permanent.
Steroids are like adrenaline, let’s see how this plays out and continue on the steroids. Remember that steroids have side effects and the dose given should be the minimum effective dose.
At that point, the underlying cause of her symptoms had not been established. Yet despite not knowing what was causing them, and despite her condition being progressive, he was still prepared to state that nothing was broken and nothing was permanent. That reassurance was not supported by the steroid response. Prednisone may produce a general increase in energy, but it can also suppress inflammation and immune activity. The response did not prove an inflammatory condition, but neither did it justify dismissing that possibility or declaring the condition harmless and reversible.
This illustrates the point of this post. A medication response may provide a possible clue without diagnosing anything. The appropriate response to uncertainty is to remain uncertain and investigate relevant possibilities, not to use an unexplained improvement to reinforce a conclusion that has itself never been established.
The response to medication suggests the possibility of an underlying organic issue, such as neurological, inflammatory, or autoimmune, which warrants further investigation. Their effectiveness implies that a real biological cause might be at play, which potentially contributes to the CNS reflex described by the FND diagnosis and points to treatable conditions.
For those jumping the placebo gun, on the days she forgets to take her prednisone, her energy drops dramatically, and when she skips Atkineton, her tremors worsen, challenging the claims that this is merely a placebo effect.
