Question from a Member:
[Regarding a young female who has been in a catatonic stupor for over two years] Neurologists saying it is not neurological and psychiatrists saying it is not psychiatric. She stays in a stuporous state.The brain shows mild atrophy spots They are trying to find if long-term catatonia can contribute to that.
How commonly are brain imaging abnormalities found?
Brain imaging abnormalities are very common in catatonia, occurring in more than 75% of cases! (Haroche et al., 2020). These include findings in both the structure and function of the brain. Below, I’ll summarize the main findings in the structure and function one-by-one.
What is found on structural brain imaging of the brain (MRI, CT)?
(MRI= Magnetic Resonance Imaging. CT Computerized Tomography)
In published case reports, the most common structural finding was diffuse lesions of white matter, that is, white matter lesions in a wide range of brain regions (Haroche et al., 2020).
There are only a few published systematic studies using structural imaging. The main finding in these studies was diffuse cerebral atrophy (Haroche et al., 2020).
But, catatonia can also be associated with focal cerebral atrophy. For example, a middle-aged woman with recurrent catatonia and other behavioral changes was later found to have frontal lobe atrophy on brain imaging (Russ and Russakoff, 1980).
The presence of cerebral atrophy should not lead to discouragement in terms of treatment. For example, a young man with schizophrenia who had severe catatonia was found to have diffuse cerebral atrophy, but he was successfully treated with a combination of clozapine, high dose lorazepam, divalproex,, and amantadine (Ene-Stroescu et al., 2014).
What is found on functional brain imaging (fMRI, SPECT, PET, MRS)?
fMRI = functional Magnetic Resonance Imaging. SPECT = Single-Photon Emission Computed Tomography. PET = Positron Emission Tomography. MRS = Magnetic Resonance Spectroscopy.
In published case reports, the most common findings on functional imaging were frontal, temporal, or basal ganglia hypoperfusion (low blood flow; Haroche et al., 2020).
In hypokinetic catatonia (which is what we typically think of when we speak of catatonia), increased neural activity in premotor areas has been found in imaging studies (Walther et al., 2019).
What about after catatonia is successfully treated?
When catatonia is successfully treated clinically, in general, these functional abnormalities tend to improve as well, at least partially (Haroche et al., 2020).
But, in systematic studies using functional brain imaging, after catatonic episodes, hypoactivation of the orbitofrontal cortex, hyperactivation of the medial prefrontal cortex, and dysconnectivity between frontal and motor areas have been reported (Haroche et al., 2020).
Bottom line
The majority of patients with catatonia have abnormalities on brain imaging and most commonly, the findings on brain imaging are diffuse, that is, in many parts of the brain.
So, though brain imaging can sometimes be helpful, it doesn’t always provide strong clues to any particular etiology of the catatonia. For example, in the patient our Member asked about, the finding of “mild atrophy spots” on brain imaging doesn’t help too much.
Related Pages
Which antipsychotics should be preferred for catatonia?
Lorazepam for catatonia: How much? How long?
How to carry out the Lorazepam Challenge Test in catatonia
How to use ECT for catatonia
References
Ene-Stroescu V, Nguyen T, Waiblinger BE. Successful treatment of catatonia in a young man with schizophrenia and progressive diffuse cerebral atrophy. J Neuropsychiatry Clin Neurosci. 2014 Winter;26(1):E21-2. doi: 10.1176/appi.neuropsych.13010007. PMID: 24515696.
Haroche A, Rogers J, Plaze M, Gaillard R, Williams SC, Thomas P, Amad A. Brain imaging in catatonia: systematic review and directions for future research. Psychol Med. 2020 Jul;50(10):1585-1597. doi: 10.1017/S0033291720001853. Epub 2020 Jun 16. PMID: 32539902.
Ruff RL, Russakoff LM. Catatonia with frontal lobe atrophy. J Neurol Neurosurg Psychiatry. 1980 Feb;43(2):185-7. doi: 10.1136/jnnp.43.2.185. PMID: 7359156; PMCID: PMC490497.
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