JOURNEY CLINICAL PSYCHIATRY PC
JOURNEY CLINICAL PSYCHIATRY CA PC
JOURNEY CLINICAL PSYCHIATRY TX PC
By signing below, you consent to receive psychiatric medication management services through Journey Clinical Psychiatry PC and/or Journey Clinical Psychiatry CA PC (“Journey”). Psychiatric medication management services may involve psychiatric medications such as, but not limited to, ketamine, SSRIs (Selective serotonin reuptake inhibitors), SNRIs (serotonin and norepinephrine reuptake inhibitors), TCAs (Tricyclic antidepressants), MAOIs (Monoamine oxidase inhibitors), Atypical antidepressants, other anxiolytics, mood stabilizers, benzodiazepines, stimulants, hypnotics and additional agents as applicable. Your Journey provider will discuss with you all of the medication options available to treat your current condition. Your Journey provider will present information in language that you can understand. You will learn how the medication works, its dosage, frequency, expected benefits, possible side effects, drug interactions, and any withdrawal affects you may experience if you stop taking the medication abruptly. By the end of the discussion, you will have all the information you need to make an informed decision as to which medication is right for you.
You acknowledge that patients will have varying success in treatment depending on the severity of their complaints and not everyone is a good candidate for psychiatric medication management. Psychiatric medication management requires strict adherence to dosage and frequency, close follow-up, and sometimes regular blood tests. Your ability to adhere to medication treatment will be taken into consideration in your Journey provider agreeing to provide you with medication management services. You understand that, although your Journey provider may conclude that certain psychiatric medications may help you, there are no guarantees that your condition will improve from psychiatric medication management. You understand that sometimes a patient may have to try several different psychiatric medications before they experience an improvement in symptoms.
You acknowledge that some possible treatments may not be approved by the FDA for treatment of your specific condition, and that this off-label use may have additional risks along with uncertain benefits. You are aware of and understand the risks of this treatment and that there may be limited evidence for potential benefits. With this knowledge, you have choosen to participate in this treatment.
You understand that psychiatric medications can have significant side effects which your Journey provider has discussed with you. You understand that medication treatment could have effects on your brain, body, consciousness, emotions, actions, sleep, memory, judgment, coordination, stamina, and sexuality. You confirm that you will review information about any given treatment and will ask your provider any questions or clarify any concerns. You also confirm that you have been given an opportunity to decline any suggested treatment.
You hereby waive any and all claims against Journey or your treatment provider, including any additional members, directors, officers, employees, agents, or related parties of Journey or your provider, for the use of such treatments in your psychiatric care. This agreement will also be directed to your heirs and assigns. You voluntarily enter this agreement, waiver, and release to allow your treatment with any potential off-label and not FDA-approved uses of medications along with their indicated uses. This agreement, waiver, and release pertains to various medications which may be prescribed as part of your treatment.
Overview
Ketamine is a dissociative class compound, with an FDA schedule III designation. It is indicated for and commonly used as an anesthetic medication. Ketamine has been found to be helpful for treating depression, even in individuals who have not responded to other interventions. It has a unique effect, in that it can work very rapidly, with individuals frequently seeing improvement in their depression within hours. However, ketamine response is not guaranteed and even in responders, the therapeutic effect from a single treatment is time-limited, with relapse typically occurring within a span of several days to one or two weeks in the absence of concomitant maintenance strategies.
Maintenance strategies must therefore be employed to extend the duration of the treatment response to a meaningful length of time. In severely symptomatic patients, this is most often accomplished by administering a series of ketamine treatments in relatively close succession (for example, severely symptomatic patients often receive 4 to 6 treatments spaced out over two to three weeks), which has been shown to extend the duration of effect, from a span of days to weeks, up to a span of weeks to months, in some cases even longer. Concomitant use of psychotherapy and / or conventional antidepressant medication in conjunction with ketamine pharmacotherapy has also been shown to prolong the duration of treatment effect in recent studies. Less symptomatic patients may not require as many or as frequent ketamine sessions to sustain therapeutic effect, as those who are more severely symptomatic and impaired.
The ongoing beneficial effects that can result from ketamine treatment include general mood improvement, lessening of anhedonia and reduction/resolution of suicidal ideation. Improvements in levels of anxiety and behavioral patterns of sleep, appetite and energy can also be realized. Ketamine has also demonstrated benefit in anxiety conditions, including PTSD, and may improve patterns of obsessive thinking or rumination. Coupling these biological effects with psychotherapy and behavioral change is designed to maximize the depth and duration of these benefits.
Off-label use
Ketamine does not have an indication for treatment of depression, anxiety or any other psychiatric condition by the FDA. Therefore, the provision of ketamine for these conditions is an ‘off-label’ use. This is a legal prescribing practice and occurs quite commonly – up to 20% of prescriptions written every year in the US are for off-label indications, by some measures. Two examples among many include the use of tricyclic antidepressants for pain and antihistamines for insomnia.
Mechanism
The most current evidence indicates that ketamine operates chiefly on the glutamate neurotransmitter system in the central nervous system (i.e. brain and spinal cord), which consists of the neurotransmitter glutamate and its two principal receptor molecules located on the surface of nerve cells, known as the NMDA receptor (NMDA-R) and AMPA receptor (AMPA-R). Ketamine exerts its effects by both stimulating the release of glutamate into the neuronal synapse (the space that exists between two brain cells (neurons) that are adjacent to and hence in communication with one another) and antagonizing the binding of glutamate at the NMDA-R on the post-synaptic neuron. This has the effect of shunting glutamate preferentially through the AMPA-R system. This in turn triggers a cascade of intracellular events that ends with the upregulation of another neurotransmitter, BDNF, at key sites in the brain associated with executive functioning, memory and emotion regulation.
Increased levels of BDNF promote the formation of new synapses in these areas, which promotes the formation of new circuits between and among neighboring neurons, ultimately enhancing overall brain functioning and flexibility. This effect is termed an enhancement of the brain’s ‘neuroplasticity’, which is to say the brain’s ability to form novel connections among its constituent neurons, and hence novel patterns of thinking, feeling and behaving, in response to environmental stimuli. Enhancement of neuroplasticity produces both an intrinsic antidepressant response and creates a window of time during which the brain is more responsive to interventions such as psychotherapy, which ultimately felt to contribute strongly to the acute and ongoing effects of treatment.
Route of Administration
Ketamine can be administered in a variety of ways: via an intravenous ketamine infusion (IV), an intramuscular injection (IM), a subcutaneous injection (SC) intranasally, orally and sublingually as a dissolving wax troche or rapid dissolving tablet. Routes vary in the onset of action, bioavailability (i.e. how much is absorbed into the systemic circulation) and clearing time through the system for each individual. While there is generally a predictable response based on past administration, it is possible that patients may experience variable physiological and subjective experiences with the same dose.
Source: The Ketamine Papers, Chapter “Intravenous Ketmamine Steven P. Levine MD”, p 292
Footnote 1: derived from Journey Clinical Psychiatry, PC (“Journey”) clinicians’ private practice experience
Ketamine has an elimination (beta) half-life of 2.5 hours. Its acute subjective effects, however, are mediated by its alpha half-life of 10-15 minutes, which is the time it takes for ketamine to cross into the brain and back out into the systemic circulation across the blood-brain barrier. It is excreted through the kidneys. A small percentage is unchanged, while the majority is converted, upon circulation through the liver, into its primary active metabolites, norketamine and hydroxynorketamine, which may play an additional role in mediating the antidepressant effects and can be detected in the urine for up to a week after treatment.
Dosing protocols
There are a variety of dosing protocols in practice. The initial wave of research into ketamine’s antidepressant effects has been largely focused on the provision of 0.5mg/kg of ketamine by IV infusion over 45 minutes, in a repeated series consisting of 2/week for 3 weeks, often in the office of an anesthesiologist. In this model, the treatment effect relies predominantly on ketamine’s intrinsic pharmacologic properties, with little attention paid to the role of concomitant psychotherapy in leveraging ketamine’s neuroplasticity-enhancing effects in the time immediately after and between treatments.
More recent protocols have been explored and described in the literature, which include provision of ketamine by a sublingual or intramuscular route in the presence of a psychotherapist, with the express intention of leveraging not only ketamine’s intrinsic antidepressant effects, but also the enhancement of brain neuroplasticity, in order to render psychotherapeutic interventions more effective and long-lasting.
Effect
Ketamine effects can be designated as occurring at time of dosing–i.e. acute–and ongoing–i.e. beyond the time it takes for ketamine to be metabolized and excreted, noting that longer acting metabolites persist up to a week.
The acute subjective effects of ketamine dosing can range from sub-perceptual disturbances in cognitive processing and body sensation to full dissociative states in which one feels separate from the body and thoughts dissolve fully. Research evidence suggests that some level of dissociation may be correlated with treatment response for depression.
These experiences are classified as non-ordinary states of consciousness, and may represent novel experiences for patients. It is possible that some patients may experience a departure from their usual mind and physical state as challenging or unsettling in the moment. The treatment environment, supportive therapist stance and dosing protocol is designed to optimize the positive nature of the subjective experiences induced by ketamine.
Initial dosing (i.e. 100-200mg sublingual ketamine) is designed to place patients in a ‘trance’ state that is often described as a “glass of wine effect”. At higher doses (i.e. 300-800mg sublingual ketamine), the dissociative effect becomes more pronounced, and patients may experience more ego-transcendent types of experiences, which some people describe as spiritual, and these can also be profoundly therapeutic in some cases.
Depending on the patient’s experience and the desired effects, dosing can be adjusted upward or downward over the course of subsequent treatment sessions, in consultation with the ketamine prescriber.
Ketamine-Assisted Psychotherapy
The outcome of Ketamine-Assisted Psychotherapy, like all psychedelic-assisted psychotherapy modalities, is greatly influenced by factors summarized as the ‘set and setting’ of the experience. ‘Set’ refers to the mindset, or internal environment, of the experiencer of the non-ordinary state of consciousness produced by the psychedelic; this includes the experiencer’s beliefs, intentions, emotional state, etc. ‘Setting’ refers to the external environment in which the experiencer is located at the time of the psychedelic-assisted psychotherapy session; this includes not only the physical aesthetics of the environment itself, which are important, but also the interpersonal dynamics that exist between the experiencer and anyone else in the space, such as their therapist, the experiencer and therapist’s culture, etc.
In this implementation model, ketamine is dosed in a comfortable office setting, using sublingual lozenges in the form of a rapid dissolving tablet or wax-based troche. A peaceful, safe, calming environment characterized by trust between patient and therapist, and entered into with the proper set of intentions, beliefs, expectations and so on, can set the stage for an experience that can be significantly more therapeutic than pharmacologic treatment alone, particular when pharmacologic treatments are conducted in highly sterile, medicalized environments such as anesthesiologist’s clinic, as they nowadays often are.
Additionally, when these conditions are met, the non-ordinary states of consciousness induced by the ketamine frequently provide for more material to work with in therapy than is ordinarily the case with unassisted psychotherapy alone, especially in the context of a long term psychotherapeutic relationship.
This treatment model is offered after evaluation of a patient’s response to medication, psychotherapy, and the appropriateness of other, more conventional treatment modalities – e.g., in the case of depression, SSRIs / SNRIs, ECT, TMS, etc. The patient has a right to refuse or discontinue ketamine treatment at any point during the treatment course. The expected outcome from treatment may vary from non-response to a robust and sustained response. There are adverse effects potentially associated with the treatment, discussed below. Long-term maintenance of benefit from treatment may require ongoing ketamine dosing, ongoing unassisted psychotherapy, use of other medications, or some combination of all of these. On the other hand, a single or subsequent dosing of ketamine does not automatically imply the need for ongoing provision of this treatment.
Medical clearance for treatment:
In addition to its psychological and anesthetic effects, ketamine also has ‘sympathomimetic’ properties, which means it acts to mimic some of the effects of the sympathetic branch of the autonomic nervous system. In practical terms what this means is that it has the effect of elevating both blood pressure and heart rate. Typically these elevations are relatively mild (10-20 mmHg increases in both systolic and diastolic blood pressure; 10-20 bpm increases in heart rate) and brief (30-90 minutes, depending on dose and route of administration). As such, for a person with healthy cardiovascular status, ketamine poses very little risk in this regard, exerting a stress on the cardiovascular system roughly equivalent to mildly vigorous physical exercise, such as running briskly up a flight of stairs.
Prior to administration of ketamine, you will be evaluated by your prescriber, a medical professional, who will interview you and review your medical and psychiatric history, in order to identify factors that may place you at higher risk of adverse effects from a ketamine dosing experience. From a medical standpoint, risk-conferring conditions are generally chronic conditions that are vulnerable to exacerbation into states of acute instability by the sympathomimetic effects of ketamine, because even mild and transient elevations in blood pressure and heart rate can destabilize conditions such as poorly controlled hypertension, poorly controlled glaucoma, poorly controlled arrhythmias, etc.
For the same reason, your evaluating clinician will instruct you to refrain from the use of other sympathomimetic medications, such as stimulants (e.g., Adderall, Ritalin, etc.), on the day of a ketamine treatment session, so as to avoid any additive sympathomimetic effects.
Another potential risk of ketamine, unrelated to its sympathomimetic effects, is its propensity to cause bladder inflammation and dysfunction, although serious and permanent bladder damage has only been reported in people in situations where ketamine is used very frequently at high doses for a prolonged period of time, such as in someone suffering from ketamine addiction. While the pattern of dosage and frequency used in ketamine infusion therapy or ketamine-assisted psychotherapy does not cause bladder irritation in most people and has never been reported to cause severe or permanent bladder damage, people with a history of bladder problems (e.g., cystitis), might be more prone to suffering bladder irritation when receiving ketamine. This irritation is rare and is typically mild and transient, but for some people it can be distressing enough to outweigh the benefits of ketamine treatment.
In some cases, the evaluating medical professional may determine that a patient requires consultation with another medical specialist, such as a primary care physician, a cardiologist or a urologist, to either inform the decision of whether it would be safe to proceed, or to initiate treatments targeted at controlling conditions that are elevating risk, e.g. performing an EKG to evaluate the current status of someone with a history of cardiac arrhythmia, initiating antihypertensive medication for someone with poorly-controlled hypertension, or recommending prophylactic treatment to minimize the symptoms of ketamine-associated cystitis.
Ketamine is typically not recommended for use during pregnancy due to a lack of data from controlled studies in humans. For this same reason, the Federal Drug Administration has not assigned a pregnancy risk category to ketamine. Because it currently remains unclassified, it is best to avoid ketamine use while pregnant or breastfeeding unless, upon discussion with your prescribing clinician, it is determined that the benefits far outweigh the risks, which is not inconceivable but would be a relatively rare circumstance.
Adverse and side effects associated with treatment:
As described above, ketamine increases sympathetic tone in the vasculature and can raise blood pressure and heart rate, which has associated risks with adverse outcomes linked to stroke and arrhythmias, resulting in loss of function and possibly death.
Ketamine exhibits very minimal suppression of respiratory drive, however it is rarely reported to cause laryngospasm, although this is extremely rare outside of pediatric populations, and has only been reported at relatively high doses administered by intramuscular or intravenous injection.
Ketamine has a risk of abuse, i.e. escalated use despite adverse outcomes. It generally has low reinforcement properties (such as those observed with stimulants) and no physiological withdrawal syndrome (such as that observed with opiates or benzodiazepines). Therefore, it is atypical for patients to crave use and demonstrate behaviors to obtain it, although some people may develop a psychological craving for the temporary escape and acute symptom relief that ketamine provides, particularly those who are using it outside of the context of a therapeutic relationship. Ketamine does result in some physiologic tolerance (needing higher doses for the same effect), though this is often easily managed by planning judicious amounts of time between dosing sessions.
At anesthetic doses (1-4mg/kg dosed by IM or IV), the following side effects are most commonly reported, and may occur at lower doses, i.e. sublingual dosing of 100-200mg, but are less likely:
Effects resolve completely in nearly all patients within 2-4 hours (IM, IV, sublingual if spit), or 6-12 hours (oral or sublingual if swallowed).
From a psychiatric standpoint, ketamine confers the risk of potentiating or exacerbating symptoms of psychosis in people with a personal history of primary psychotic illness (e.g. schizophrenia or schizoaffective disorder). For this reason, patients with these diagnoses are not appropriate candidates for ketamine therapy. Unlike conventional antidepressants, ketamine has not been shown to precipitate manic episodes in people with a history of bipolar disorder if they are taking ketamine while depressed. However, ketamine can exacerbate manic symptoms in someone who is already in a state that is acutely manic or mixed (manic and depressive symptoms occurring at the same time). Patients with a history of bipolar disorder will therefore be carefully screened by their evaluating clinician to ensure they are not experiencing elements of mania prior to initiating ketamine treatment and throughout the treatment course.
Management of Adverse Effects:
Because your ketamine treatment will be taking place under the observation of a psychotherapist who is not a trained medical provider, it is important to understand that you will need to play an active role in ensuring your own medical safety during your dosing session, under the guidance of the medical provider who is prescribing the ketamine. Primarily this will consist of adhering to all the safety recommendations outlined in this document and communicated to you by your ketamine prescriber at the time of that evaluation.
Your ketamine prescriber will direct you to a video recorded by Journey Clinical that demonstrates how to correctly use a blood pressure cuff. You will be asked to measure your blood pressure and heart rate using this cuff prior to self-administration of the sublingual ketamine, and report these values to your psychotherapist, whose job it is to record them.
Based on your medical history and cardiovascular risk factors, your ketamine prescriber will provide you and your psychotherapist with upper limits for your blood pressure and heart rate measurements, above which it is recommended that you do not proceed with self-administration of ketamine.
If the initial reading of these measurements are above the parameters set forth by your prescriber, your psychotherapist may guide you through some controlled breathing exercises or other methods designed to alleviate any acute anxiety you may be feeling, which can falsely elevate blood pressure and heart rate. After this, you may re-check your blood pressure and heart rate to see if they have normalized.
If your blood pressure and heart rate have not normalized following these methods, then you agree not to proceed with self-administration of ketamine, and your KAP session will need to be canceled. It may be rescheduled only after you have sought consultation with your primary care provider for further workup and management of these vital sign abnormalities.
Your psychotherapist or your after-care/support person may activate emergency response systems, i.e. call 911, if there is any indication of a medical emergency during the course of a ketamine-assisted psychotherapy session.
With respect to nausea, approximately 10% of patients who receive ketamine by IM or IV injection will develop significant nausea; this percentage is somewhat higher when ketamine is taken by the sublingual route, especially when it is swallowed. For this reason, at the time of your initial evaluation, your ketamine prescriber will also prescribe a small supply of an anti-nausea medication called ondansetron (Zofran), and will discuss with you during your evaluation whether and when you should take it in order to minimize or prevent nausea from occurring during your ketamine experience.
Generally, if you are prone to motion sickness or to becoming nauseated from other medications, it is a good idea to take ondansetron as a preventative measure 1-2 hours prior to your first, and all subsequent, ketamine sessions. People without a known propensity for nausea may choose to forgo this precaution for their first ketamine session, to see whether it is necessary to take prior to subsequent sessions. If nausea does occur during that first dosing session, taking ondansetron during the session can help alleviate the symptoms within about 30-60 minutes, and it should be taken as a preventative measure prior to all subsequent ketamine sessions.
Preparation
Prior to treatment:
Outline of a standard KAP session
Preparation: 0-15 minutes
Dosing: Onset 15-30 minutes
Trance state: 30-45 minutes: Generally restful, volitionally non-verbal, supported by soothing music and eye shades to promote inward focus
Early Integration Phase: 30-45 minutes: Opportunity for reflection and discussion
Disengagement from treatment
At any point in the treatment course, you may disengage from the defined and recommended process – i.e. sit up and take off the eye shades. However, by signing this consent form, you are agreeing not to leave the office of your psychotherapist until he or she feels it is safe for you to do so. You may request that your defined aftercare support person assume custody at any point during the treatment, with full release into care to be determined by the psychotherapist conducting the session.
Aftercare
Ongoing and concurrent treatment
For the duration of your treatment relationship with your Journey prescriber, you are agreeing to remain engaged in an ongoing and concurrent treatment with a psychotherapist, who will be working in a collaborative treatment relationship with you and your prescriber. The termination or interruption of collaborative treatment will result in termination of further ketamine prescriptions from your Journey prescriber. If for whatever reason you are unhappy with your psychotherapist but would like to continue pursuing ketamine-assisted psychotherapy, let your prescriber know, as he or she may be able to facilitate connecting you with another psychotherapist.
Ketamine disposal
If you choose to discontinue KAP prior to using all of your prescribed ketamine, you acknowledge and agree that you will follow the applicable state disposal guidance for any unused ketamine.
Final declaration
In signing this agreement, I recognize that I have established a treatment relationship with a Journey Clinical Psychiatry PC, Journey Clinical Psychiatry CA PC, Journey Clinical Psychiatry TX PC prescriber of ketamine for ketamine-assisted psychotherapy. I understand that I have alternative treatment options beside ketamine for my condition. I understand that I may not respond or have a favorable response to ketamine treatment and there are risks, contraindications, and side effects associated with the treatment, as further described herein, some of which may be permanent.
I understand that a Journey Clinical Psychiatry PC, Journey Clinical Psychiatry CA PC, Journey Clinical Psychiatry TX PC prescriber will outline the dosing for the ketamine prescribed to me, the setting in which I should self-administer the ketamine, and the appropriate range for my vitals. I agree that I will not self-administer the prescribed ketamine outside of these guidelines.
Treatment may be terminated by Journey Clinical Psychiatry PC, Journey Clinical Psychiatry CA PC, Journey Clinical Psychiatry TX PC based on clinical factors, including and not limited to concerns regarding poor fit with treatment, low likelihood of response, lack of adherence to treatment agreements and recommendations, concern for diversion, patient behaviors and risk factors exceeding an acceptable level of risk to patient safety, and lack of sufficient collaboration with a KAP therapist. Provision of treatment does not automatically imply future treatment.