06/02/2026
🚑👍💉
𝙌𝙪𝙚𝙨𝙩𝙞𝙤𝙣- “𝙒𝙝𝙮 𝙞𝙨 𝙩𝙝𝙚𝙧𝙚 𝙩𝙝𝙞𝙨 𝙚𝙢𝙚𝙧𝙜𝙚𝙣𝙘𝙚 𝙥𝙝𝙖𝙨𝙚 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 𝙩𝙝𝙚 𝙥𝙖𝙞𝙣 𝙙𝙤𝙨𝙚 𝙖𝙣𝙙 𝙙𝙞𝙨𝙨𝙤𝙘𝙞𝙖𝙩𝙞𝙫𝙚 𝙙𝙤𝙨𝙚?”
Great question!
This is one of those ketamine topics that clicks once you stop expecting the dose response to be smooth.
Ketamine does not flip a single switch as the dose rises. It shuts brain systems down in layers. The middle layer is where things get weird.
Ketamine is a 🍌
I learned this lesson the hard way.
I had a patient who was fine. Then suddenly not fine at all.
Eyes wide. Thrashing. Crying. Trying to climb off the stretcher.
Vitals stable. Oxygen good. Nothing else changing.
Except the ketamine dose.
I remember thinking, why is this drug so unpredictable?
It wasn’t the drug.
It was the dose range I parked in.
That call forced me to finally understand what ketamine actually does to the brain.
🧠 CORE IDEA. DIFFERENT BRAIN CIRCUITS DROP OUT AT DIFFERENT DOSES
Ketamine blocks NMDA receptors, but NMDA-dependent circuits do not all fail at the same time. As the dose increases, ketamine affects brain systems in a predictable order.
1️⃣ LOW DOSE. ANALGESIA. PAIN DOSE
🟢 Targets spinal cord and thalamic pain pathways
🟢 Reduces central sensitization
What the patient looks like
🙂 Awake
🙂 Oriented
🙂 Often calm
🧠 Cortical integration stays intact
Key takeaway
Pain signals are dampened, but the brain stays connected.
2️⃣ MEDIUM DOSE. EMERGENCE OR DYSPHORIC PHASE. THE WEIRD ZONE
This is the phase most people are asking about.
Here is what is happening physiologically.
🔹 Prefrontal cortex starts to lose control
🧠 Executive function weakens
🧠 Emotional regulation degrades
🧠 Sensory input loses normal filtering
🔹 Limbic system stays active
🔥 Emotions fire without context
🔥 Fear, euphoria, paranoia, or vivid imagery can surface
🔹 Default mode network destabilizes
⚠️ Sense of self begins to fragment
⚠️ Consciousness remains present
What you see
🚨 Patient is awake but cognitively unmoored
🚨 Hallucinations
🚨 Agitation
🚨 Crying or laughter
🚨 Panic
This is not true dissociation yet.
Key point
This is partial cortical shutdown.
3️⃣ HIGHER DOSE. DISSOCIATIVE ANESTHESIA
At this point enough cortical and thalamocortical circuits are offline.
🧠 Sensory input no longer integrates into awareness
🧠 Patient disconnects from the external world
🧠 The observer network shuts down
Clinically
👁️ Nystagmus
🧍 Catalepsy
🪫 Minimal response to stimuli
😌 Often less agitation than the emergence phase
Key takeaway
Once the brain fully lets go, behavior often becomes quieter and more stable.
🧩 WHY THE EMERGENCE PHASE EXISTS
Partial cortical shutdown is worse than full shutdown.
❌ Too awake to be unconscious
❌ Too disconnected to stay oriented
❌ Emotional circuits still firing
❌ Logical control going offline
This imbalance produces
🚨 Dysphoria
🚨 Hallucinations
🚨 Agitation
🚨 “Bad trips”
You see the same pattern with hypoxia, alcohol, and sleep deprivation. Awareness degrades before consciousness disappears.
💊 WHY BENZOS HELP. AND WHY THEY DO NOT CANCEL KETAMINE
Benzodiazepines
🟢 Suppress limbic overactivity
🟢 Restore inhibitory balance
🟢 Smooth the transition through the middle zone
They do not block ketamine analgesia.
They do not reverse dissociation.
They quiet emotional noise during the handoff.
🚑 TAKE AWAY
If you sit in the middle dose range
⚠️ You will see agitation
⚠️ You will see emergence reactions
⚠️ You will think ketamine is unpredictable
If you commit to
✅ True analgesic dosing
✅ Or true dissociative dosing
Ketamine suddenly feels predictable.
That emergence phase is not random.
It is the brain pushing back before it fully disconnects.
That patient taught me this lesson in real time.
I have not forgotten it since.
🪜SIMPLE DOSAGE 🪜
• 0.1 – 0.3 mg/kg → Analgesia
• 0.4 – 0.8 mg/kg → Partial dissociation / emergence
• 1 – 2 mg/kg → Full dissociation
REFERENCES 📚
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Unresponsiveness, unconsciousness, and dissociated states.
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Low-dose ketamine for acute pain management in the emergency setting.
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DOI: 10.1016/j.emc.2022.12.004
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DOI: 10.1097/ACO.0000000000001171
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DOI: 10.1176/appi.ajp.2022.22010072
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