Ketamine Clinic

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Ketamine-Assisted Psychotherapy

The Craig Clinic offers ketamine-assisted psychotherapy (KAP) at 74 Harley Street for adults whose depression, post-traumatic stress disorder or anxiety disorder has not responded adequately to conventional treatment. The service is consultant psychiatrist led. Professor Craig undertakes every assessment, sets the treatment plan and retains medical oversight throughout.

Psychotherapeutic work is led by Annushka Shani, a Jungian analyst, who co-leads the clinic.

Approximately a third of patients with major depressive disorder do not achieve an adequate response to standard antidepressant and psychological treatment. Ketamine is currently one of the best evidenced pharmacological options for this group, and the clinic was established in response to that clinical gap.

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The Development of the Service

Professor Craig established a ketamine clinic for depression at King Edward VII’s Hospital in 2022, among the first in central London. That service provided intravenous ketamine to patients with treatment-resistant depression under psychiatric supervision and generated the clinical experience on which the present programme is built.

In 2026, in partnership with Cambridge Biotherapies, Professor Craig established the current service with Annushka Shani. The change is one of model rather than of drug. Where the earlier clinic was primarily an infusion service, treatment is now offered as ketamine-assisted psychotherapy, with the pharmacological and psychotherapeutic components planned together from the outset and psychotherapy treated as integral to the treatment rather than as an adjunct to it.

Cambridge Biotherapies is a USA based private treatment centre founded in 2016 by Dr Daniel A. Brenner, providing ketamine infusion, ketamine-assisted psychotherapy and transcranial magnetic stimulation. The two services refer patients to one another where clinical need or geography makes that appropriate, and Dr Brenner contributes to clinical discussion of complex cases, bringing substantial experience in this area of practice. Clinical responsibility for patients treated at Harley Street rests with Professor Craig throughout.

The Clinical Team

Professor Michael Craig undertakes all psychiatric assessment, prescribing and medical oversight for the clinic.

Annushka Shani is a Jungian analyst and a member of the Society of Analytical Psychology, registered with the British Psychoanalytic Council under registration number 20455. She delivers the preparation and integration psychotherapy and co-leads the clinic.

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Who May be Suitable for KAP?

We accept referrals from GPs, consultant psychiatrists, clinical psychologists and other registered clinicians, and we also accept self-referrals. Presentations we assess include:

  • Treatment-resistant depression
  • Post-traumatic stress disorder, including complex PTSD
  • Generalised and refractory anxiety
  • OCD unresponsive to standard care
  • Persistent suicidal ideation
  • Existential distress in the context of life-limiting illness
  • Comorbid presentations of the above

Suitability is determined at assessment. Patients who are not suitable candidates are told so directly and alternative treatment options are discussed, including rTMS where indicated.

How Does Ketamine Work?

Ketamine is a non-competitive antagonist at the N-methyl-D-aspartate (NMDA) receptor, a glutamate receptor central to synaptic plasticity, learning and emotional regulation. Altered glutamatergic signalling in the prefrontal cortex, hippocampus and amygdala is implicated in the persistence of depressive cognition and of traumatic memory.

Blockade of tonic NMDA receptor activity produces a rapid rise in synaptic glutamate, activation of AMPA receptors and downstream mTOR signalling, which in turn increases synthesis and release of brain-derived neurotrophic factor (BDNF). The result is increased synaptogenesis in prefrontal and limbic circuits. A systematic review by Kang and colleagues, covering 139 preclinical and clinical publications, found consistent evidence that ketamine increases the molecules involved in neuroplasticity, including glutamate, AMPA receptors, mTOR and the BDNF and TrkB pathway, and that these changes accompany rapid improvement in mood. The mechanism is nonetheless not settled, and restoration of deficits in neuroplasticity is best understood as the most parsimonious account rather than a proven pathway. What is not in doubt is that it differs fundamentally from that of monoaminergic antidepressants, which accounts for the speed of response.

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The Neuroplastic Window

The working premise of ketamine-assisted psychotherapy is that the period following administration is one of heightened capacity to form new associative pathways and to revise entrenched patterns of thought and affect, and that psychotherapy delivered inside it consolidates more readily than psychotherapy delivered at an arbitrary interval. Integration sessions are therefore timed to the 48 to 72 hours after dosing.

This is a clinical rationale rather than a measured biological interval. Animal and molecular work supports a time-limited increase in plasticity markers, but human data are less clear cut. A 2024 review by Pardossi and colleagues of BDNF in patients treated with ketamine and esketamine found that most studies report a rise in plasma BDNF after intravenous ketamine while others do not, and that studies remain small. The timing used here follows the observed course of the clinical response rather than a precisely defined window, and the page states the position on that basis rather than claiming more than the evidence supports.

What Does the Evidence Show?

Treatment-resistant depression

Ketamine is one of only a small number of interventions shown to outperform placebo or sham treatment for treatment-resistant depression in randomised controlled trials. A 2024 network meta-analysis by Saelens and colleagues in Neuropsychopharmacology examined 69 randomised trials and 10,285 participants across 25 treatments, and identified ketamine, electroconvulsive therapy, repetitive transcranial magnetic stimulation, theta burst stimulation, minocycline and aripiprazole as the treatments with a higher response rate than control. In the largest pooled safety and outcome analysis of intravenous ketamine in this population, reported by Wan, Murrough and colleagues, 205 infusions given at 0.5 mg/kg over 40 minutes to 97 patients produced a response rate of 67%, response being defined as a 50% or greater reduction in Montgomery Asberg Depression Rating Scale score. Response definitions and trial populations vary, most of the outcome data are short term, and these figures should not be read as a prediction of individual outcome.

The antidepressant effect emerges within 24 hours of a single infusion, which no conventional antidepressant approaches. Its main limitation is durability. The effect of a single administration is transient, and it is this that provides the rationale both for a course of treatment rather than an isolated infusion, and for integrating psychotherapy.

Post-traumatic stress disorder

Ketamine acts on the amygdala, hippocampus and prefrontal circuitry that subserves encoding and retrieval of traumatic memory. A 2024 systematic review and meta-analysis by Kwan and colleagues in CNS Spectrums, covering 44 studies of ketamine across psychiatric disorders other than mood disorders, found statistically significant reductions in PTSD symptom severity on both the PTSD Checklist for DSM-5 and the Clinician-Administered PTSD Scale, and in obsessive compulsive symptoms on the Yale-Brown Obsessive Compulsive Scale. The evidence base here is smaller and less mature than in depression and the studies are heterogeneous. Where ketamine is combined with trauma-focused psychotherapy during the integration phase, effects appear better sustained at follow up.

Suicidal ideation

Ketamine is distinctive among psychiatric medications in reducing suicidal ideation rapidly and to a degree that is at least partly independent of its effect on mood. Clinically meaningful reductions have been documented within hours of a single intravenous infusion. This makes it a useful option where rapid stabilisation is the priority, though it does not substitute for the usual measures required to manage acute risk.

Why is Psychotherapy Part of the Treatment?

The limited durability of ketamine given alone is the reason psychotherapy is built into the programme. A systematic review of ketamine-assisted psychotherapy by Drozdz and colleagues, covering 17 studies and 603 participants, concluded that psychotherapy provided before, during and after ketamine administration can both amplify and prolong benefit, and that it was precisely the short-lived effect of ketamine as a drug that prompted this line of work. Protocols vary considerably in route, dose, frequency and psychotherapeutic modality, and larger randomised trials are still needed.

Ketamine reliably brings symbolic, imagistic and unconscious material to the surface, and the psychotherapeutic traditions that already have a method for working with non-ordinary states and with dream and symbolic content are well suited to this task. Jungian analysis is one of the orientations identified in the KAP training literature for this reason. Psychotherapy at the clinic is delivered by a senior practitioner with both analytic training and specific training in psychedelic-assisted psychotherapy.

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Routes of Administration

There is no fixed protocol. Route, dose, titration strategy and session frequency are set at assessment and reviewed as treatment proceeds.

Intravenous Infusion

Intravenous racemic ketamine gives the most predictable pharmacokinetics and allows real-time titration. Psychoactive effect begins at 5 to 10 minutes, peaks at 20 to 30 minutes and resolves within 60 to 90 minutes. This is the most extensively studied route in treatment-resistant depression and in acute suicidal ideation.

Infusions are given in a dedicated private room with continuous cardiovascular monitoring and a senior clinician present throughout. Dosing starts at 0.5 mg/kg over 40 minutes and is adjusted according to tolerability and response. A course typically comprises two to six infusions over 2 to 8 weeks. Patients must be accompanied home and must not drive for 24 hours.

Intravenous administration is preferred where there is significant functional impairment, where suicidal ideation requires rapid stabilisation, or where speed and magnitude of antidepressant response is the primary consideration.

Oral and sublingual ketamine

Oral and sublingual dosing produces a slower onset at 30 to 45 minutes, a lower peak plasma concentration and a longer, more diffuse plateau. Bioavailability is lower than by the intravenous route but an antidepressant effect is documented for both.

The resulting state is generally less disorienting and remains more accessible to psychotherapeutic dialogue during the session, with richer imagery and dream material reported afterwards. Where the psychotherapeutic component is the main treatment vector, this route may be preferable.

Unsupervised or at-home dosing is not offered. All ketamine administration takes place on clinic premises under supervision.

Intranasal esketamine

Esketamine nasal spray is the only ketamine preparation licensed in the United Kingdom for treatment-resistant depression, given alongside an oral antidepressant. It can be arranged for patients for whom it is the more appropriate option, and is discussed at assessment where relevant. It is administered under supervision with a period of post-dose observation.

Intranasal esketamine

Esketamine nasal spray is the only ketamine preparation licensed in the United Kingdom for treatment-resistant depression, given alongside an oral antidepressant. It can be arranged for patients for whom it is the more appropriate option, and is discussed at assessment where relevant. It is administered under supervision with a period of post-dose observation.

The Treatment Pathway

No ketamine is administered without prior psychiatric assessment, medical screening and a confirmed clinical indication. The sequence below is the standard pathway and is adapted to individual circumstances.

1

Psychiatric assessment

A 60 to 90 minute evaluation with Professor Craig covering psychiatric and medical history, current presentation, previous treatment and clinical indication. Contraindications are reviewed systematically.

2

Medical screening

Baseline cardiovascular assessment, blood pressure, and a structured review of medical comorbidity, substance use and current medication for interactions relevant to ketamine. Liaison with the GP or treating physician is arranged where indicated. Baseline liver function and urinary symptoms are documented.

3

Preparation

One or more preparation sessions with Annushka Shani to establish the therapeutic relationship, provide a framework for what the dosing session involves, and clarify the patient’s intentions for it. Preparation is treated as clinically substantive rather than procedural and influences both the depth and the safety of what follows.

4

Dosing sessions

Given in a private clinical room under continuous physiological monitoring and medical supervision. The psychotherapist may be present in a supportive, non-directive role, attending to the patient’s affective state, providing grounding where needed and noting material for integration.

5

Integration

Integration sessions are held in the 48 to 72 hours after each dosing session. Imagery, affect, relational themes and subsequent dream material are worked through in depth. Longer-term psychotherapeutic work beyond the acute programme can be arranged for patients who wish to continue.

6

Review and discharge planning

Professor Craig conducts a formal psychiatric review on completion. Decisions on maintenance treatment, tapering or discharge back to the existing clinical team are made with the patient. A clinical summary is sent to the referrer or GP as required.

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Side Effects and Risks

Ketamine is well tolerated by most patients at the doses used in psychiatric practice, and effects during a session are transient and resolve as the drug clears. Expected effects and side effects include:

  • Dissociation, perceptual change and altered sense of time during administration
  • Transient rise in blood pressure and heart rate
  • Nausea and vomiting
  • Dizziness, unsteadiness and blurred vision
  • Headache
  • Anxiety or distress during the session
  • Fatigue for the remainder of the day

Risks associated with repeated or prolonged use, principally urinary tract and bladder injury, hepatobiliary abnormalities, cognitive effects and dependence, are dose and frequency related. Programmes are therefore time limited, doses conservative, and cumulative exposure kept to the minimum needed for clinical benefit. Urinary and hepatic symptoms are reviewed at each attendance and treatment is stopped if they emerge. Written aftercare guidance is provided and adverse event protocols are in place.

The rise in blood pressure is modest at the doses used in psychiatry. Pooled data from 2,252 ketamine or esketamine treatments across 15 studies give a mean increase of 12.6 mmHg systolic and 8.5 mmHg diastolic, transient in each case, which is why blood pressure is monitored throughout and why uncontrolled hypertension is a contraindication.

When is Ketamine not Suitable?

Ketamine is well tolerated by most patients at the doses used in psychiatric practice, and effects during a session are transient and resolve as the drug clears. Expected effects and side effects include:

  • Psychotic illness, or a history of psychosis
  • Uncontrolled hypertension, or significant cardiac or cerebrovascular disease
  • Raised intracranial pressure
  • Current ketamine or other substance misuse, or dependence
  • Significant hepatic impairment or established ketamine-related urinary tract injury
  • Pregnancy and breastfeeding
  • Certain dissociative disorders, assessed individually

Suitability in bipolar disorder, in personality disorder and in patients on concurrent psychotropic medication is determined case by case at assessment.

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Clinical Governance

Ketamine is administered only after written informed consent, medical screening and psychiatric assessment confirming indication. Physiological monitoring is maintained throughout every session. The premises at which intravenous ketamine is administered are registered with the Care Quality Commission. Prescribing follows General Medical Council guidance on unlicensed and off-label prescribing, and published expert consensus on ketamine use in psychiatric practice.

Referrals and Enquiries

A brief referral letter or clinical summary is helpful but is not required in order to make contact. All enquiries are treated confidentially. The clinic is private and does not hold NHS contracts. Fees are set out on the Fees and Terms page and are discussed at the point of assessment.

References

Sources are listed in the order in which the page draws on them. All were located on PubMed and DOIs are given so the citations can be held on file for substantiation purposes.

  • Kang MJY, Hawken E, Vazquez GH. The mechanisms behind rapid antidepressant effects of ketamine: a systematic review with a focus on molecular neuroplasticity. Frontiers in Psychiatry 2022;13:860882. doi:10.3389/fpsyt.2022.860882
  • Pardossi S, Fagiolini A, Cuomo A. Variations in BDNF and their role in the neurotrophic antidepressant mechanisms of ketamine and esketamine: a review. International Journal of Molecular Sciences 2024;25(23):13098. doi:10.3390/ijms252313098
  • Saelens J, Gramser A, Watzal V, Zarate CA, Lanzenberger R, Kraus C. Relative effectiveness of antidepressant treatments in treatment-resistant depression: a systematic review and network meta-analysis of randomized controlled trials. Neuropsychopharmacology 2024;50(6):913-919. doi:10.1038/s41386-024-02044-5
  • Wan LB, Levitch CF, Perez AM, Brallier JW, Iosifescu DV, Chang LC, Foulkes A, Mathew SJ, Charney DS, Murrough JW. Ketamine safety and tolerability in clinical trials for treatment-resistant depression. Journal of Clinical Psychiatry 2015;76(3):247-252. doi:10.4088/JCP.13m08852
  • Kwan ATH, Lakhani M, Singh G, Le GH, Wong S, Teopiz KM, Dev DA, Manku AS, Sidhu G, McIntyre RS. Ketamine for the treatment of psychiatric disorders: a systematic review and meta-analysis. CNS Spectrums 2024:1-8. doi:10.1017/S1092852924000580Lamontagne SJ, Ballard ED, Zarate CA. Effects of stress on endophenotypes of suicide across species: a role for ketamine in risk mitigation. Neurobiology of Stress 2022;18:100450. doi:10.1016/j.ynstr.2022.100450
  • Drozdz SJ, Goel A, McGarr MW, Katz J, Ritvo P, Mattina GF, Bhat V, Diep C, Ladha KS. Ketamine assisted psychotherapy: a systematic narrative review of the literature. Journal of Pain Research 2022;15:1691-1706. doi:10.2147/JPR.S360733
  • Vankawala J, Naples G, Avila-Quintero VJ, Ramirez KL, Flores JM, Bloch MH, Dwyer JB. Meta-analysis: hemodynamic responses to sub-anesthetic doses of ketamine in patients with psychiatric disorders. Frontiers in Psychiatry 2021;12:549080. doi:10.3389/fpsyt.2021.549080
  • Sholevar R, Kromka W, Beaussant Y. Ketamine and ketamine-assisted psychotherapy for psychiatric and existential distress in patients with serious medical illness: a narrative review. Journal of Palliative Medicine 2025;28(7):967-981. doi:10.1089/jpm.2024.0346

Racemic ketamine given by infusion or by the oral and sublingual route is not licensed in the United Kingdom for the psychiatric indications described and is prescribed off-label. Intranasal esketamine is licensed for treatment-resistant depression. Information on this page is general and does not constitute medical advice. A formal psychiatric assessment is required before any treatment can be offered.

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