Structural alterations of amygdala and hypothalamus contribute to catatonia

Fritze, Stefan; Brandt, Geva A.; Kubera, Katharina M.; Schmitgen, Mike M.; Northoff, Georg; Geiger-Primo, Lena S.; Tost, Heike; Meyer‐Lindenberg, Andreas; Hirjak, Dušan

doi:10.1016/j.schres.2022.05.003

Cited by 14 publications

(7 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There are however studies conducted for other patient groups, which included hypothalamic subregions analysis in vivo: anterior-inferior hypothalamus has been found to be smaller in patients with catatonia 53 and different volumes in lateral or ventromedial nuclei were seen to be associated with very low birth weight individuals. 54 …”

Section: Discussionmentioning

confidence: 99%

Hypothalamic Subunit Volumes in Schizophrenia and Bipolar Spectrum Disorders

Ruggeri,

Nerland,

Mørch-Johnsen

et al. 2024

Schizophrenia Bulletin

View full text Add to dashboard Cite

Background The hypothalamus is central to many hormonal and autonomous nervous system pathways. Emerging evidence indicates that these pathways may be disrupted in schizophrenia and bipolar disorder. Yet, few studies have examined the volumes of hypothalamic subunits in these patient groups. We compared hypothalamic subunit volumes in individuals with psychotic disorders to healthy controls. Study Design We included 344 patients with schizophrenia spectrum disorders (SCZ), 340 patients with bipolar disorders (BPD), and 684 age- and-sex-matched healthy controls (CTR). Total hypothalamus and five hypothalamic subunit volumes were extracted from T1-weighted magnetic resonance imaging (MRI) using an automated Bayesian segmentation method. Regression models, corrected for age, age2, sex, and segmentation-based intracranial volume (sbTIV), were used to examine diagnostic group differences, interactions with sex, and associations with clinical symptoms, antipsychotic medication, antidepressants and mood stabilizers. Study Results SCZ had larger volumes in the left inferior tubular subunit and smaller right anterior-inferior, right anterior-superior, and right posterior hypothalamic subunits compared to CTR. BPD did not differ significantly from CTR for any hypothalamic subunit volume, however, there was a significant sex-by-diagnosis interaction. Analyses stratified by sex showed smaller right hypothalamus and right posterior subunit volumes in male patients, but not female patients, relative to same-sex controls. There was a significant association between BPD currently taking antipsychotic medication and the left inferior tubular subunits volumes. Conclusions Our results show regional-specific alterations in hypothalamus subunit volumes in individuals with SCZ, with relevance to HPA-axis dysregulation, circadian rhythm disruption, and cognition impairment.

show abstract

Section: Discussionmentioning

confidence: 99%

Hypothalamic Subunit Volumes in Schizophrenia and Bipolar Spectrum Disorders

Ruggeri,

Nerland,

Mørch-Johnsen

et al. 2024

Schizophrenia Bulletin

View full text Add to dashboard Cite

show abstract

“…More recently, studies have explored the neurobiological underpinnings of catatonia using advanced imaging techniques[ 28 - 30 ]. Structural magnetic resonance imaging studies have revealed that catatonia was associated with widespread reductions in gray-matter volume, including in the orbitofrontal, cingulate, and visual cortices and the insula when compared with healthy individuals.…”

Section: Research Developments In the Field Of Catatoniamentioning

confidence: 99%

“…Patients with catatonia demonstrated hypergyrification in the motor, premotor, and somatosensory cortices compared with controls; however, no differences in cortical thickness were observed between patients with catatonia and controls[ 29 ]. In addition, patients with catatonia were found to have significantly smaller volumes in the anterior inferior hypothalamus, the cortical nucleus of the amygdala, and the hippocampal fimbria[ 30 ]. Furthermore, patients with catatonia exhibited poor functional activation of the supplementary motor area, primary and secondary motor cortices, inferior parietal cortex, and basal ganglia during self-initiated movements[ 31 , 32 ].…”

Section: Research Developments In the Field Of Catatoniamentioning

confidence: 99%

First 150 years of catatonia: Looking back at its complicated history and forward to the road ahead

Csihi,

Ungvari,

Caroff

et al. 2024

World J Psychiatry

View full text Add to dashboard Cite

Karl Ludwig Kahlbaum (1828-1899) was the first to conceptualize and describe the main clinical features of a novel psychiatric illness, which he termed catatonia in his groundbreaking monograph published 150 years ago. Although Kahlbaum postulated catatonia as a separate disease entity characterized by psychomotor symptoms and a cyclical course, a close examination of his 26 cases reveals that most of them presented with motor symptom complexes or syndromes associated with various psychiatric and medical conditions. In his classification system, Kraepelin categorized catatonic motor symptoms that occur in combination with psychotic symptoms and typically have a poor prognosis within his dementia praecox (schizophrenia) disease entity. Because of the substantial influence of Kraepelin’s classification, catatonia was predominantly perceived as a component of schizophrenia for most of the 20th century. However, with the advent of the psychopharmacotherapy era starting from the early 1950s, interest in catatonia in both clinical practice and research subsided until the early 2000s. The past two decades have witnessed a resurgence of interest in catatonia. The Diagnostic and Statistical Manual of Mental Disorders Fifth Edition, marked a paradigmatic shift by acknowledging that catatonia can occur secondary to various psychiatric and medical conditions. The introduction of an independent diagnostic category termed “Catatonia Not Otherwise Specified” significantly stimulated research in this field. The authors briefly review the history and findings of recent catatonia research and highlight promising directions for future exploration.

show abstract

“…Many cases have clearly related autoimmunity to the onset of catatonia: anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, autoimmune thyroid disorders, multiple sclerosis, and systemic lupus erythematosus (Rogers et al, 2019 ; Durns et al, 2020 ). Other authors pinpointed alterations of the limbic system like lower volumes of the amygdala and the hypothalamus as the arise of the affective component of catatonia (Fritze et al, 2022 ). Furthermore, a widely known hypothesis is anomalies in dopamine and GABAergic circuitries result in deficits of top-down modulation (Northoff, 2002 ).…”

Section: Introductionmentioning

confidence: 99%

Molecular and cellular mechanisms leading to catatonia: an integrative approach from clinical and preclinical evidence

Ariza-Salamanca

Corrales-Hernández

Pachón-Londoño

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

This review aims to describe the clinical spectrum of catatonia, in order to carefully assess the involvement of astrocytes, neurons, oligodendrocytes, and microglia, and articulate the available preclinical and clinical evidence to achieve a translational understanding of the cellular and molecular mechanisms behind this disorder. Catatonia is highly common in psychiatric and acutely ill patients, with prevalence ranging from 7.6% to 38%. It is usually present in different psychiatric conditions such as mood and psychotic disorders; it is also a consequence of folate deficiency, autoimmunity, paraneoplastic disorders, and even autistic spectrum disorders. Few therapeutic options are available due to its complexity and poorly understood physiopathology. We briefly revisit the traditional treatments used in catatonia, such as antipsychotics, electroconvulsive therapy, and benzodiazepines, before assessing novel therapeutics which aim to modulate molecular pathways through different mechanisms, including NMDA antagonism and its allosteric modulation, and anti-inflammatory drugs to modulate microglia reaction and mitigate oxidative stress, such as lithium, vitamin B12, and NMDAr positive allosteric modulators.

show abstract

Structural alterations of amygdala and hypothalamus contribute to catatonia

Cited by 14 publications

References 55 publications

Hypothalamic Subunit Volumes in Schizophrenia and Bipolar Spectrum Disorders

Hypothalamic Subunit Volumes in Schizophrenia and Bipolar Spectrum Disorders

First 150 years of catatonia: Looking back at its complicated history and forward to the road ahead

Molecular and cellular mechanisms leading to catatonia: an integrative approach from clinical and preclinical evidence

Contact Info

Product

Resources

About