Author: Gary Jackson

Unveiling The Duration: How Long Does Ketamine-Induced Psychosis Last?

However, brain imaging SPECT studies reported that THC did not lead to a significant increase in dopamine release even though the dose was sufficient for participants to experience psychotic symptoms, suggesting a non-central role for striatal DA in THC-elicited psychosis (42). In line with this knowledge, in their randomized, double blind clinical trial, Morgan et al. (36) administered cannabinoids by inhalation to 48 cannabis users; they planned four sessions, THC (8 mg), THC (8 mg) + CBD (16 mg), CBD 16 mg and placebo. They found an increase in psychotomimetic symptoms following administration of THC alone and the combination of THC and CBD, especially negative, perceptual distortions, and cognitive disorganization.

• Summary of major mechanism of action, nature of evidence and prevalence of psychotic symptoms for each substance.
• When compared to adult males, juvenile male rats are less sensitive to ketamine’s antidepressant effects.
• This effect set in just 1 hour after their first dose and lasted as long as 1 month after their last dose.
• Below, get the details on the potential benefits and risks of trying ketamine for treatment-resistant depression, plus guidance on getting a prescription from a qualified mental health professional.
• Along the same line, using magnetoencephalography (MEG), subjects’ ratings of a “blissful state” during a low-dose ketamine infusion (0.25 mg/kg bolus, 0.375 mg/kg/1 h, i.v.) correlated positively with increased frontoparietal activation (Muthukumaraswamy et al., 2015).

This protein plays a role in neuroplasticity, or your brain’s ability to adapt as you experience new things. By supporting neuroplasticity, ketamine may help change negative thought patterns that contribute to depression. These approaches don’t always relieve severe depression symptoms, including thoughts of suicide — and that’s where ketamine could make a difference. Treatment-resistant depression refers to depression symptoms that don’t respond to two or more types of antidepressant medication. Especially in the presence of altered mental status, CNS infections such as meningitis and encephalitis, and CNS malignancies also merit consideration.

Potential clinical implications

This creates an imbalance of excitatory and inhibitory signals in the central nervous system, which affects sensory perception. Below, get the details on the potential benefits and risks of trying ketamine for treatment-resistant depression, plus guidance on getting a prescription from a qualified mental health professional. The complexity of achieving diagnostic clarity in cases of suspected drug-induced psychosis and the need for medically supervised detox means that residential treatment programs specializing in dual diagnosis treatment are typically the best setting in which to begin the recovery process.

The presence of co-occurring mental health conditions can also impact the duration of ketamine-induced psychosis. Individuals with pre-existing mental health disorders, such as depression or anxiety, may be more likely to experience prolonged psychosis symptoms. The interaction between ketamine and these underlying conditions can complicate the recovery process and extend the duration of psychosis. Chronic exposure to a higher dose of ketamine (20 mg/kg, i.p.) is necessary to elicit an antidepressant-like response in juvenile male mice (Parise et al., 2013).

What to Know About Ketamine Therapy for Depression

Studies examining ketamine self-administration at low doses have not yet examined the molecular mechanisms underlying ketamine’s reinforcing effects. These molecular changes induce a hyperexcitable state in the NAc, which is also observed following chronic exposure to other drugs of abuse such as alcohol, another NMDAR-antagonist (Ron and Barak, 2016). It is therefore important to examine whether these molecular changes will also occur at therapeutic low doses of ketamine, and it is particularly important to further delve into the molecular mechanisms mediating the reinforcing properties of chronic exposure to low-dose ketamine as a treatment for depression. This differential sensitivity to ketamine in both sexes at the juvenile period could be explained by levels of circulating gonadal hormones. In support of this idea is the fact that the locomotor-activating effects of low-dose ketamine in preadolescent animals (McDougall et al., 2017).

Juvenile male rats injected with an effective antidepressant dose of ketamine (20 mg/kg, i.p.) were more sensitive to its acute locomotor-activating effects as compared to adults (Parise et al., 2013; Rocha et al., 2017). However, sensitization to the locomotor activating effects of ketamine occurred in both adolescent and adult male rats (Rocha et al., 2017). At lower doses of ketamine (3–10 mg/kg, i.p.), which is an ineffective antidepressant dose in male juvenile rats, adult, but not juvenile male rats, developed ketamine-induced sensitization to its locomotor activating effects (Wiley et al., 2008).