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Update: New Ketamine Clinic Coming Soon to Panama City Beach Learn More

The human brain is the most complex entity known to man, with roughly 86 billion neurons, and it serves as the pain control center for our life. If you’re suffering from emotional or physical pain that won’t go away after standard treatment, you can benefit from an alternative medicine like ketamine.

WHAT EXACTLY IS KETAMINE?

Ketamine was first produced as an anesthetic in 1962 and was licensed for human use by the US Food and Drug Administration eight years later. The medicine is still used as an anesthetic for small surgical operations and as a sedative for irritable or disturbed people nowadays. Ketamine has been the topic of extensive research and controversy over the last four decades regarding its efficacy in treating symptoms of mental disease such as bipolar disorder, depression, anxiety, and PTSD.

THE EFFECTS OF KETAMINE ON THE BRAIN

The effect of ketamine on the glutamate system is one of the keys to its potential therapeutic efficacy in helping the brain control pain. Glutamate is a brain neurotransmitter that regulates a huge portion of our neurological system. You may have long-term depression if glutamate receptors are hyperactive, but ketamine works by blocking glutamine receptors. One of the reasons the medicine may work to lessen chronic inflammation associated with depression is because it has powerful anti-inflammatory qualities.

Ketamine’s therapeutic effect on the brain is a hot topic of controversy. Researchers know that ketamine has been shown to alleviate some of the symptoms of mental illnesses such as anxiety, depression, posttraumatic stress disorder, and physical discomfort associated with chronic pain, but even scientists who are wary of its potential benefits advocate for more thorough testing.

KETAMINE AFFECTS WHAT PART OF THE BRAIN?

Ketamine has the potential to alter several parts of the human brain, although research into the drug’s effectiveness in these areas is still ongoing.

Ketamine affects the following areas of the brain:

The medial prefrontal cortex

The frontal lobe contains the medial prefrontal cortex (MPFC). Persistent pain has an impact on decision-making, self-control, risk and fear processing, emotion regulation, and control over amygdala activity. This part of the brain is in charge of emotion-driven behavior.

Amygdala

The Amygdala is located in the frontal region of the temporal lobe, near the hippocampus. Pain affects the brain’s decision-making abilities, as well as its ability to determine punishment vs reward, memory, and emotional responses. This part of the brain is crucial in the development of emotional disorders.

Gray Periaqueductal

In the tegmentum of the midbrain, the Periaqueductal gray surrounds the cerebral aqueduct.

Cortex of the anterior cingulate

The frontal area of the cingulate cortex houses this. It’s here that our brain goes into overdrive when it comes to pain, doing the majority of the heavy lifting. Autonomic functions, attention allocation, morals and ethics, anticipating rewards, managing impulses, decision-making, emotion, and interpreting physical pain are all influenced by this region.

Hippocampus

The Hippocampus is found in the temporal lobe of the medial temporal lobe. The brain works on memory consolidation, spatial orientation, navigation, emotion, and learning in this area. The Hippocampus is part of the limbic system, and it undergoes alterations as a result of the brain’s recognition of chronic pain.

Accumbens nucleus

The Nucleus accumbens is located in the forebrain’s basal region. Aversion, reward, motivation interpretation, reinforcement learning, and the brain’s interpretation and reaction to addiction all take place here. The malleability of the nucleus accumbens controls the shift from acute to chronic pain, according to studies.

Glutamate and GABA Levels Are Rebalanced With Ketamine

Another function of glutamate in the brain is the production and balance of GABA, a relaxing neurotransmitter. Overactive glutamate receptor genes can lead to a GABA imbalance, which can lead to mental health issues. Anxiety can be caused by high glutamate levels and low GABA, while depression can be caused by glutamate and GABA depletion. Ketamine operates in three stages to correct this imbalance:

  1. Phase 1: Immediate Effects
    Ketamine affects the brain’s opiate receptors during this period, which can affect depressive symptoms. During this stage, patients are often relaxed, pain-free, and have a sedative-like sensation.
  2. Phase 2: Long-Term Effects
    Glutamate receptors are enhanced in phase two, which aids in the restoration of normal glutamate and GABA levels. Patients are often at ease after treatment at this phase. During this time, patients may have emotions of invulnerability.
  3. Phase 3: Return to Baseline
    The brain’s reaction to ketamine induces new neural receptors formation when the levels have stabilized, which may aid in resetting the depressed brain. Ketamine may be especially beneficial for people who are depressed and have suicidal thoughts.

Ketamine also helps people cope with stress by reducing inflammation and increasing stress resilience.

The brain undergoes structural changes as a result of stress. Ketamine counteracts these alterations by encouraging synaptic formation in depressed brain areas including the prefrontal cortex and hippocampus, which control behavior, mood, personality development, and memory.

Ketamine Treatment for Depression in Florida

Despite the fact that ketamine has been present for about 60 years, its therapeutic utility in the treatment of mental disease symptoms has only been studied for roughly 20 years. Treatments like ketamine can help lessen distress from bipolar disorder, depression, anxiety, and other mental health illnesses depending on your illness, symptoms, and under ideal settings.

We can assist you or a loved one with questions concerning the clinical usage of ketamine. Get in touch with one of our Florida Ketamine Clinics right now to discover more about our cutting-edge new treatments.