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How the brain works · 02

Neuro-Chemistry

Neurotransmitters are released by Neuro EP signals. Understanding the synapse explains how medications work, and why they so often come with trade-offs.

How neurochemistry works

Individual microscopic neurons connect to form pathways at specialized junctions called synapses.

When a neuron receives an electrical signal, it releases a chemical neurotransmitter into the synapse. That neurotransmitter stimulates the next neuron, which generates its own electrical signal to pass along to other neurons.

How neuropharmacology works

Most neuro-active drugs work at the synapse by increasing or decreasing neurotransmitters. Many can accomplish goals similar to Neuro EP treatments: increasing brain activity when it’s too low, or decreasing it when it’s too high.

Some medications have very beneficial effects for specific brain conditions, and they work faster than training the brain to make similar improvements.

Problems with neuropharmacology

Why medications come with trade-offs

Despite their benefits, neuro-active medications can cause several problems at the same time.

The effect is temporary

The benefit occurs only after each dose and quickly fades, requiring the next dose. This creates dependence on the medication, often for the rest of your life.

Your brain fights back

Your brain often works to counteract the drug. After long-term use, stopping can leave symptoms worse than before. For example, long-term pain medication can leave pain worse than if it had never been taken.

They affect the whole brain

Medications travel to every part of your brain, not just the part that needs help. Lowering activity in the Pain Network also lowers it in memory, attention, judgment and problem-solving networks.

The Neuro EP difference: treatments like neurofeedback decrease elevated activity only in the network that needs it, such as the Pain Network, without affecting other parts of your brain. That’s how they avoid the whole-brain side effects that can keep people from doing the things they used to do.

Common neuro-active medications

The intended target, and the unintended one

Every medication below reaches its intended brain area, and every other area too. Here’s what that means in practice.

Chronic pain

Oxycodone (Percocet), morphine and other opioids

Target neurotransmitter: Stimulates mu-opioid inhibitory receptors throughout the brain, similar to the neurotransmitters beta-endorphin and endomorphin-1 and -2

Target area & benefit

Mu-opioid inhibition reduces activity in the Pain Network, reducing pain perception

Unintended areas & side effects

Mu-opioid inhibition in the prefrontal cortex causes poor attention, cognition, motivation and judgment

Chronic pain

Gabapentin (Neurontin) and pregabalin (Lyrica)

Target neurotransmitter: Reduces excitatory neurotransmitters, especially glutamate, throughout the brain

Target area & benefit

Reduced glutamate in the Pain Network can reduce pain perception

Unintended areas & side effects

Reduced glutamate in the frontal lobes and cerebellum can cause dizziness, poor cognition, brain fog, imbalance and fatigue

Chronic pain, depression, anxiety

Duloxetine (Cymbalta)

Target neurotransmitter: Increases serotonin (5-HT) and norepinephrine (NE) throughout the brain

Target area & benefit

Increased inhibition in the Pain Network can reduce pain perception

Unintended areas & side effects

Increased NE in the frontal lobes and limbic areas may cause paradoxical anxiety, agitation and/or insomnia

Parkinson’s disease

Benztropine (Cogentin)

Target neurotransmitter: Decreases acetylcholine (ACh) throughout the brain

Target area & benefit

Decreased ACh in the striatum rebalances dopamine and ACh to improve tremors

Unintended areas & side effects

Decreased ACh in the temporal lobes, especially the hippocampus, can cause poor memory, confusion, brain fog, dry mouth, or even dementia with chronic use

Insomnia, anxiety

Diphenhydramine (Benadryl, ZzzQuil), doxylamine (Unisom, NyQuil), hydroxyzine (Vistaril, Atarax)

Target neurotransmitter: Blocks histamine (H1) and acetylcholine (ACh) throughout the brain

Target area & benefit

Blocking H1 and ACh in arousal areas of the hypothalamus and reticular activating system causes sleepiness

Unintended areas & side effects

Blocking ACh in the temporal lobes, especially the hippocampus, can cause poor memory, confusion, brain fog, dry mouth, or even dementia with chronic use

Insomnia

Zolpidem (Ambien)

Target neurotransmitter: GABA agonist, which inhibits brain activity throughout the brain

Target area & benefit

Acts on cortical, thalamic and hypothalamic arousal networks to induce sleep

Unintended areas & side effects

GABA-mediated inhibition in the frontal and temporal lobes, including the hippocampus, can cause amnesia, confusion, disorientation, poor coordination, sleep-walking, sleep-driving and other unusual behaviors

Insomnia, anxiety

Lorazepam (Ativan), alprazolam (Xanax), diazepam (Valium)

Target neurotransmitter: GABA agonist, which inhibits brain activity throughout the brain

Target area & benefit

Acts on arousal networks to induce sleep, and on the amygdala and limbic system to temporarily reduce anxiety

Unintended areas & side effects

GABA-mediated inhibition in the frontal and temporal lobes can cause poor memory or amnesia, confusion, poor coordination, poor attention, feeling “drunk,” dependence, withdrawal and addiction

Parkinson’s disease

Levodopa + carbidopa (Sinemet, Crexont) and pramipexole (Mirapex)

Target neurotransmitter: Increases dopamine (DA) throughout the brain

Target area & benefit

Increased DA in the substantia nigra and striatum improves movement (bradykinesia and rigidity)

Unintended areas & side effects

Increased DA in the frontal lobes and limbic system can cause hallucinations, paranoia, agitation or psychosis

Agitation, paranoia, hallucinations, psychosis, schizophrenia

Haloperidol (Haldol), risperidone (Risperdal)

Target neurotransmitter: Inhibits dopamine (DA) throughout the brain

Target area & benefit

Decreased DA in the frontal lobes and mesolimbic system improves agitation and psychosis

Unintended areas & side effects

Decreased DA in the substantia nigra and basal ganglia can cause Parkinsonism or tardive dyskinesia; in frontal and limbic areas it can cause loss of motivation, brain fog and emotional blunting

This information is educational. Never start, stop or change a medication without talking to your prescribing provider.

Continue exploring

Neuro-Anatomy Structure and location in the brain Neuro-Chemistry Neurotransmitters and medications You are here Neuro-Physiology Brainwave power, frequency and connectivity Non-Neuronal Control Glial cells that support the brain

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