Neurological disorders, neurological damages, and progressive neurological dysfunction are all possible side effects of antidepressant use.
And, in fact, acute neurological dysfunction is the standard and clinically desired outcome of antidepressant use, which begins with the first dose administered. Continued use may be considered “neurodegenerative” in some contexts or cases, but the degeneration may not always last beyond the treatment and withdrawal syndrome periods and does not constitute a disorder unto itself except as carved into specific subsets of symptoms.
Whether diseases considered independent entities, such as Parkinson’s, are within that scope of neurological side effects is not always agreed upon, because there may be differing causal factors (in terms of precipitating elements or mechanical functioning). So, while there are side effect clusters referred to by phrases like “Parkinsonian tremor”, “pseudo-Parkinsonism”, or “drug-induced Parkinsonism”, whether they are considered the ‘disease proper’ is sometimes more a matter of semantics than experience, symptomologically speaking.
Since we do not understand the origin of most neurodegenerative conditions, and the side effects of antidepressants can newly appear, or worsen, over the course of treatment, discontinuation, or post-use, differentiating between entities by citing the innately chronic or worsening nature of a disease not inherently attributed to drugging is not sufficient to distinguish drug-induced Parkinsonism from Parkinson’s that has no clear cause.
Some people do experience a reduction in neurological problems caused by antidepressants, after spending time off them and recovering, but it is not a guarantee, and withdrawal states or damages and dysfunction that persist or become more apparent post-discontinuation can give the appearance of a neurodegenerative process even if someone is essentially in a state of healing overall. And, of course, some changes or damages can lead to worsening problems, though the mechanics and outcomes are poorly studied, if studied at all.
Drug-induced Parkinsonian symptoms specifically have been seen to improve, continue, or worsen in respective groups of patients, meaning there is no predefined course in the short or long terms. Since antidepressants, and other psychotropics that are known to cause neurological side effects (including Parkinsonism in particular), can cause significant neuroplastic changes and are fundamentally neurotoxic, we cannot necessarily identify drug-induced states as non-degenerative or free from morphological alterations in trying to distinguish them from Parkinson’s as a primary condition.
Continuing with the example of Parkinson’s, drugs are considered the second leading cause of Parkinsonian symptoms, behind the greater and most probably heterogeneous category of “primary” Parkinson’s—an idiopathic presentation of symptoms and pathology without any perspicuous medical events being connected, eg drugging with psychotropics. So, even in that distinction we are dealing more with a semantic division than a practical one except that drug-induced Parkinsonism can diminish over time for some patients—that the underlying dysfunction seems to differ in at least some cases does not really get the patient anywhere.
Antidepressants are psychotropics, neurotoxins, and the source of dysfunctional changes on the physiological, biochemical, systemic, and epigenetic levels. This can give rise to new or worsening neurological conditions. Since we don’t understand the conditions we attempt to treat with antidepressants, don’t understand why they do what they do, and don’t understand primary neurological disorders in question, saying exactly what it is that people have when these side effects occur is far more speculative than simply pointing out that it does happen and it should be a consideration when weighing the risks and potential benefits of using antidepressants.
As for that article specifically, it presents information with a variety of potential implications for the increased rate of Parkinson’s seen in antidepressant users (not all of which were mentioned by the authors themselves):
-Early undiagnosed Parkinson’s might involve depressive symptoms for some patients.
-Early undiagnosed Parkinson’s might involve symptoms misdiagnosed as depressive for some patients.
-Parkinson’s might be itself misdiagnosed at a higher rate in patients who have used antidepressants, perhaps at least partly due to their significant rate of neurological side effects (which include various movement disorders).
-Something(s) might be contributing to both Parkinson’s and depression, (or something diagnosed as depression).
-Depression might sometimes create or contribute to a potential for Parkinson’s.
-Drugs might create sometimes or create or contribute to a potential for Parkinson’s.
-Depression might sometimes worsen or exploit a latent potential for Parkinson’s.
-Drugs might sometimes worsen or exploit a latent potential for Parkinson’s.
We face a similar conundrum in dealing with other pharmaceutical neurotoxins, for example antipsychotics and methamphetamine, and the difficulties endemic to our low level of neurobiological and neuropathological understanding mean that we will probably not have definitive research about the roles such drugs play anytime soon.