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About Ketamine

Why Ketamine

IT IS ESTIMATED that somewhere between 30 to 60% of people being treated for depression with traditional antidepressants do not experience improvement in their symptoms. These commonly prescribed drugs work by altering levels of chemicals in the brain’s monoamine system i.e. neurotransmitters such as serotonin, dopamine and norepinephrine. Typically, many weeks are required to increase the dose to the recommended therapeutic dose range or blood level, and then weeks more of observing for effect.  If there is no response or insufficient response, the drug is then tapered down slowly, over the same long period of time,  and perhaps a second or third drug is prescribed in similar fashion. Many people experience undesirable side effects as well – weight gain, sexual dysfunction or lack of libido, drowsiness. The SSRI’s are the most commonly prescribed antidepressants/anti-anxiety drugs; tricyclics and MAO inhibitors are older medications but are still occasionally prescribed.

KETAMINE has been used by anesthesiologists since 1970. Its safety profile as an adjunct to anesthesia is well known. Its effect on mood disorders has been documented in multiple studies and has been used with increasing frequency to treat unipolar depression, bipolar depression, situational depression such as post-partum depression, post traumatic stress disorder and generalized anxiety disorder. A dose (based on body weight) is given intravenously, and the beneficial effects often occur within hours of administration. When given as recommended there appears to be a variable but sustained effect in almost 80% of patients. Follow up “booster” treatments may be indicated at intervals which vary based on the individual's response.

KETAMINE works on the brain in a way different from traditional antidepressants. Rather than targeting an imbalance of various chemical neurotransmitters, it appears to enhance regeneration of brain cell connections – increasing dendritic growth and branching – that have atrophied or been destroyed due to prolonged stress, depression, or genetic predisposition. The phenomenon of regrowth is referred to as neuroplasticity, and the potential to revive dormant brain connections has astounding implications in both psychiatry and neurology.

KETAMINE is an NMDA (n-methyl-d-aspartate) antagonist in the pathways of the brain involving the amino acid glutamate. Ketamine activates neural connections particularly in the hippocampus. The hippocampus lies deep in the brain and is largely associated with mood but also long and short-term memory. It isn’t clear yet precisely how the glutamatergic path works in restoring neural connections in the hippocampus – it may involve gene expression, for instance – but it is a finely tuned system that responds quickly, within hours, to very small doses of ketamine. Vegetative symptoms, anhedonia (inability to experience pleasure) and the inclination to dwell on negative thoughts have been shown to improve quickly.

KETAMINE’S speed of onset is evidenced by its use in emergency rooms to treat acute suicidal ideation.