When people think about Parkinson’s disease, they picture the tremor, the shuffle, the stiffness. What gets less attention is what’s happening on the inside. Depression and anxiety are among the most common non-motor symptoms of Parkinson’s, and for many people they weigh on quality of life at least as heavily as the movement problems. They’re also frequently missed, brushed off as an understandable reaction to a difficult diagnosis rather than treated as the clinical conditions they are.

Ketamine has entered the Parkinson’s conversation from two different directions—one about mood, one about movement—and it’s worth keeping them straight. We’ll walk through both, and we’ll be clear about where the evidence is solid and where it’s still early.

The Mood Burden of Parkinson’s

Depression is thought to affect roughly a third to as many as half of people with Parkinson’s at some point, and anxiety commonly travels with it. This isn’t only a psychological response to a hard diagnosis, though that’s part of it. Parkinson’s involves the loss of dopamine-producing neurons and broader changes in brain chemistry—including serotonin and norepinephrine systems—that directly affect mood regulation. In other words, the same disease process that drives the movement symptoms also disturbs the circuits that keep mood steady.

Standard antidepressants are the usual first step and help some patients. But response is inconsistent in Parkinson’s, side effects can be harder to tolerate, and many people remain depressed despite a fair trial. That leaves a real gap, and it’s the same gap that drives interest in ketamine for treatment-resistant depression more broadly.

Why Ketamine Is Being Considered for Mood

Ketamine acts on the glutamate system through the NMDA receptor and, downstream, appears to restore synaptic connections within hours to days rather than the weeks SSRIs require. Our explainer on how ketamine works goes into the mechanism, but the relevant point for Parkinson’s is that it reaches depression by a route independent of the dopamine pathways that the disease has already damaged.

Because ketamine has a solid record in treatment-resistant depression, and because depression in Parkinson’s is so often treatment-resistant, it’s a logical option to weigh. We’d frame it honestly as an individualized conversation, not a Parkinson’s-specific proven therapy—most of the recent research spotlight has actually been on movement, with mood improvement reported alongside.

The Movement Story: Levodopa-Induced Dyskinesia

The more surprising line of research concerns movement—specifically levodopa-induced dyskinesia. Levodopa is the cornerstone medication for Parkinson’s, but after years of use many people develop dyskinesia: involuntary, sometimes writhing movements that emerge as a complication of the very drug controlling their symptoms. It’s a genuinely difficult problem with limited good options.

Here ketamine has shown real promise. Early clinical work found that subanesthetic ketamine infusions produced long-lasting reductions in dyskinesia—and in depression—in people with Parkinson’s, with benefits reported to persist for weeks to months after treatment. A 2025 study in the journal Brain looked at the mechanism and found that ketamine appears to disrupt abnormal motor cortex activity and promote lasting neuroplasticity.

Sub-anaesthetic ketamine rescued the decoupling of motor cortex activity from movement seen in Parkinson’s dyskinesia, pointing to a mechanism involving disruption of abnormal cortical activity and long-lasting neuroplasticity. — Summarized from a 2025 study, Brain (Oxford Academic)

The FDA has cleared an investigational new drug application to study ketamine for levodopa-induced dyskinesia, with phase 2 trials planned. That’s a meaningful step, but the key word is investigational. Notably, the dyskinesia research has often relied on longer continuous infusions—in animal models the movement benefit appeared only with extended dosing, not a brief injection—which is a different protocol from a standard antidepressant session. So the movement application is not something being delivered routinely in outpatient clinics; it lives in formal research settings for now.

What We Do and Don’t Offer

It’s worth being direct about our lane. At Music City Ketamine, our focus is the mood side—depression and anxiety, including the depression and anxiety that accompany Parkinson’s—using the established subanesthetic infusion approach. We are not a Parkinson’s movement-disorder program, and we don’t present ketamine as a treatment for the core tremor, stiffness, and slowness of the disease, or as a substitute for dopaminergic medication and the care of a movement-disorder neurologist.

The dyskinesia research is exciting, and we’re glad to talk about it, but we’ll always point people toward the trial and specialist settings where that work is happening rather than imply we can replicate it. Where we can genuinely help is when depression or anxiety is dragging down someone’s life with Parkinson’s and the usual medications haven’t been enough.

The Safety Questions That Come First

Parkinson’s adds specific considerations to the usual ketamine screening:

You can read more about how we approach candidacy in is ketamine therapy safe and about the situations where we decline in when we decline ketamine for a patient. A Parkinson’s diagnosis doesn’t automatically close the door, but it raises the bar for individualized screening, and we strongly prefer to coordinate with the treating neurologist.

How We’d Approach It

If depression or anxiety has taken hold alongside Parkinson’s, a careful evaluation looks at the whole picture: how long since diagnosis, current motor and cognitive status, blood pressure control, the full medication list, and what antidepressants have already been tried. Because the experience of an infusion can feel unfamiliar—and because cognitive and movement symptoms can shape it—the environment matters. That’s part of why Marla stays present during infusions, and why our therapy dogs, Walter White and Wilma, are part of the room.

The hours and days after each session, the neuroplastic window, deserve attention too. Rest, gentle routine, and supportive follow-up—ideally alongside ongoing Parkinson’s care—can help any mood gains settle in. And relief from depression often has a ripple effect: someone who feels less weighed down tends to engage more with exercise and physical therapy, which are cornerstones of living well with Parkinson’s.

An Honest Bottom Line

Parkinson’s carries a heavy, under-recognized mood burden, and standard antidepressants often fall short. Ketamine offers a different mechanism and a genuine record in treatment-resistant depression, which makes it a reasonable option to discuss for the mood side. The movement research—especially for levodopa-induced dyskinesia—is one of the more intriguing developments in the field, but it’s still investigational and belongs in trial and specialist settings for now.

If you or someone you love is facing depression or anxiety alongside Parkinson’s, we’d be glad to talk it through honestly—clear about what the evidence supports, what it doesn’t, and how we’d work with your neurologist to keep everything safe. You can also read more about our approach to depression and anxiety treatment.