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.
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.
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.
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?:
This is an absolute must do now for anyone treating Catatonia. Thank you for this.
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.
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
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.
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.
The pictures look like hemisphere damage
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.