Direct answers, hedged only where hedging is warranted

Ask who is physically present during the session and what their credential is, whether monitoring is continuous or intermittent, how the dose is determined and whether it is adjusted between sessions, what the plan is if you do not respond after the induction course, whether they will coordinate with your existing prescriber, what integration support is included and whether it costs extra, and what the total cost looks like across twelve months rather than per session. All of that can be established in one phone call, and the willingness to answer plainly is itself informative.

A single intravenous infusion in the United States commonly costs between four hundred and eight hundred dollars, which puts a six-session induction course somewhere between roughly two and a half and five thousand dollars. That figure excludes the initial consultation, any psychiatric evaluation billed separately, integration therapy where it is not bundled, and the maintenance sessions that frequently follow. Asking a clinic for an annualised estimate covering the first twelve months produces a far more useful number than a per-session price.

Commercial insurance rarely reimburses intravenous ketamine for depression because administration for mood indications is off-label. The associated psychiatric evaluation is sometimes billable, and it is worth asking a clinic to identify exactly which components can be submitted. Esketamine is different: because it holds FDA approval for treatment-resistant depression, coverage is genuinely plausible, subject to prior authorisation and documented failure of previous treatments.

The evidence is considerably thinner than for treatment-resistant depression. PTSD has some promising early trials, smaller and fewer than the depression literature, with durability unresolved. Anxiety is frequently advertised but more thinly evidenced, and is often treated as an adjunct rather than a primary target. Being clear about the strength of evidence for a specific indication is more useful than a general statement about whether ketamine works.

Ketamine has been FDA-approved as a general anaesthetic since 1970. Its use for depression and other mood indications is off-label, which is legal and routine across medicine but means it has not been through the approval process for that specific use. Esketamine, sold as Spravato, is the exception: it was approved in 2019 for treatment-resistant depression in adults alongside an oral antidepressant, in 2020 for depressive symptoms in adults with major depressive disorder and acute suicidal ideation or behaviour, and in January 2025 as a standalone monotherapy for treatment-resistant depression.

In 2023 the FDA issued a public warning about compounded ketamine products used at home without monitoring, citing risks including sedation, dissociation, airway compromise and the absence of any clinician present if something goes wrong. Telehealth has a legitimate role in this field for consultation, screening, follow-up and integration therapy, and it materially improves access for people far from a clinic. Using it to supply a dissociative anaesthetic to an unmonitored patient is a different proposition, and the distinction is worth insisting on.

Ketamine has a long anaesthetic safety record, and the subanaesthetic doses used for mood indications are a fraction of surgical doses. During a session, transient dissociation, nausea, and modest rises in blood pressure and heart rate are common, which is why continuous monitoring is standard. Serious risks concentrate in specific groups: uncontrolled hypertension, a personal or family history of psychosis or bipolar disorder, certain cardiac conditions, and significant substance use history all change the calculation. Long-term safety data for repeated low-dose psychiatric use is thinner than the anaesthetic safety data, and that distinction is worth holding onto.

Screening typically identifies several groups for whom the risk profile changes materially: people with uncontrolled hypertension, those with a personal or family history of psychosis, people with bipolar disorder outside of careful supervision because of the risk of precipitating a manic episode, those with certain cardiac or hepatic conditions, people who are pregnant, and those with significant untreated substance use disorder. A programme that does not ask about these before scheduling has skipped the assessment that determines whether treatment is appropriate at all.

A standard induction course is six sessions delivered over two to three weeks, though this convention comes from early trial protocols rather than from comparative research establishing that six is optimal. Some programmes offer four and some extend to eight. What happens afterwards is the less-discussed part: response is often not permanent, and many patients move onto maintenance sessions every two to six weeks. Any clinic presenting six sessions as a complete treatment without discussing maintenance has described half of what is involved.

Most people describe a sense of distance from the body, an altered perception of time, and sometimes visual distortion. It typically builds partway through an infusion and resolves within twenty to thirty minutes of the drip finishing. People who know in advance that this is expected, temporary and monitored generally find it far less alarming than those who encounter it unprepared. The infusion can be slowed or stopped if someone becomes distressed, and knowing that beforehand is itself a useful part of preparation.

No, and this is not negotiable. Driving is prohibited for the remainder of the day after any ketamine administration. Arranging a ride home is part of booking rather than an afterthought, and across a six-session induction it means arranging somebody else's time repeatedly. Esketamine carries the same restriction with its own REMS requirement that patients not drive until the day after treatment.

Conventional antidepressants work primarily on monoamine systems and typically need four to six weeks before any effect can be assessed. Ketamine acts on the glutamate system, principally as an antagonist at the NMDA receptor, and where it produces an effect that effect is often visible within hours to days. The proposed downstream mechanism involves increased brain-derived neurotrophic factor and a temporary rise in synaptic connectivity, which researchers describe as a window of heightened neuroplasticity.