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MM's avatar

Doc,

Thanks for these posts - very much appreciated.

Question: how does a benzo make a cataonic patient more alert? I would imagine any GABAergic depressant would have the opposite effect.

Martin Greenwald, M.D.'s avatar

The neurobiology of catatonia is not fully understood, but dysfunction in the GABA-A system in parts of the frontal and parietal cortex probably plays a role, as does glutamate hyperactivity and the NMDA receptor. Even though catatonic people often appear sedated or don't move much, that can be the effect of what is essentially a neurobiologically hyperactive syndrome. But we still have lots to learn.

This article may be of interest.

https://neuro.psychiatryonline.org/doi/10.1176/jnp.2009.21.4.371

Sarah  Hawkins (she/her)'s avatar

I haven’t been as severe as your patient above, but when I developed psychosis I remember feeling my reading speed slow down and stop as my mind became overwhelmed with so much internal noise and fear as internal prompts turned into more frightening voices that I thought must be real because where could they be coming from otherwise? My second episode was caused by a head injury, and again, very similar symptoms this time caused by the inflammation- again I couldn’t hold the gist of the paragraph I had read and follow the words in the sentence at the same time. It became too difficult, something I felt was a core skill of mine. Gone.

MM's avatar

Fascinating - thanks for the share.

Seems like the glutamate system is coming into focus as the basis for a number of psychiatric disorders. Perhaps the mechanism here is similar to that of ketamine and its recently-discovered efficacy in depression.

Jim Ryser's avatar

This reminded me of a patient with NMS back when I was rotating with one of the best psychiatrists I’d worked with. She was so caring and amazing at her skills. They gave the patient benzos and the patient perked up by the next day; out of the ICU a day after that. Love this post.

Martin Greenwald, M.D.'s avatar

A fortunate response, given that many cases of NMS do not go well, sadly.

Gia Yan's avatar

This is an absolute must do now for anyone treating Catatonia. Thank you for this.

Sarah  Hawkins (she/her)'s avatar

The pictures look like hemisphere damage

Jenean McBrearty's avatar

Just a suggestion: Don't wait until paragraph 6 to let your readers know the ailment your patient suffers with. I realize it's the style/habit of CNF to delay relevant information (for some unknown pseudo-literary reason), but I would have been clearer about that you were describing had you have started the article with "I have treated patients with catatonia before. It's symptoms range from wearing funny hats to dancing in the moonlight ....(whatever they are), and in this instance Annie's seemed to be (stabilized? Intractable? Misdiagnosed?).

Also, you said there was a shift change and you never saw Annie again. Could you have followed her progress anyway?

Roman S Shapoval's avatar

I'm not a doctor, but I wonder, if patients were treated with sunlight, especially UV-A, would this help replenish their neurotransmitters and allow their own internal clocks to work efficiently once more?:

https://romanshapoval.substack.com/p/why-obesity-starts-in-the-eye

Sidenote- GABA is also lowered as dopamine is lowered from blue-light toxicity of our devices, screens etc.

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Sep 10, 2025
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Paul Summergrad,M.D.'s avatar

I had the same reaction and thought this was going to be a post about stroke and hemiagnosia …..

Martin Greenwald, M.D.'s avatar

Sorry for the late response! An astute observation. Yes there have been functional imaging studies in Catatonia that IIRC implicate the fronto-parietal network among other things, and visuo-spatial construction is consistently impaired. This review may be helpful (?) but there are others.

https://pubmed.ncbi.nlm.nih.gov/38484496/