Neurobiological Approach of Catatonia and Treatment Perspectives

Ellul, Pierre; Choucha, Walid

doi:10.3389/fpsyt.2015.00182

Cited by 42 publications

(31 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Brain‐imaging studies in catatonic cases have shown major alterations in right hemispheric neural networks, specifically medial and lateral orbitofrontal networks and the posterior parietal cortex (Northoff, ). This particular network may be abnormally modulated by altered functional interactions in GABAergic transmission due to the decreased GABA receptor density, resulting in a lack of inhibition and decreased top‐down control (Ellul & Choucha, ). This may account for the interplay among motor and behavioral alterations observed in clinical experiences and cognitive processing in patients with catatonia.…”

mentioning

confidence: 99%

Is motor imagery different in catatonic schizophrenia?

et al. 2017

View full text Add to dashboard Cite

show abstract

mentioning

confidence: 99%

Is motor imagery different in catatonic schizophrenia?

et al. 2017

View full text Add to dashboard Cite

show abstract

“…The exact pathophysiology of catatonia is still unknown. However it is widely agreed that low gamma-aminobutyric acid (GABA A ) activity in the orbitofrontal cortex, low dopamine D 2 receptor activity, alterations in the N-methyl-D-aspartate (NMDA) receptor glutamatergic system, and high serotonin 1A (5-HT 1A ) receptor activity may contribute to the development of symptoms [7,8].…”

Section: Discussionmentioning

confidence: 99%

Rapid efficacy of aripiprazole in the treatment of catatonic depression/catatonia with consideration of the drug’s unique receptor profile: a case report

Sichert

Volz

2020

Fortschr Neurol Psychiatr

View full text Add to dashboard Cite

Catatonia is a widespread problem in psychiatric hospitals as approximately 10% of patients present with catatonic symptoms upon admission. Catatonia carries the risk of severe, even fatal complications. The first line treatment is usually electroconvulsive therapy (ECT) or benzodiazepines, but ECT may not be readily available and benzodiazepines may not always be effective. We describe the case of a patient presenting with severe symptoms of catatonic depression who completed a 3-day course of 25 mg aripiprazole that rapidly resolved his catatonic symptoms. Several cases have already been reported where administration of aripiprazole successfully resolved catatonic symptoms after other treatment options had failed. Aripiprazole’s efficacy and advantages may lie in its unique receptor profile. It acts as a dopamine D2 receptor (D2 R) antagonist and partial D2 R agonist depending on the precise cellular milieu, which may explain its efficacy and favourable side effect profile compared to other antipsychotics used to treat catatonia. Aripiprazole also partially agonises D3 receptors and serotonin 2 C receptors (5-HT2 C), which may contribute to its antidepressant properties. Aripiprazole enhances gamma-aminobutyric acid (GABA) transmission in certain brain areas, and it is widely agreed that low GABA activity may contribute to catatonic symptoms. Pharmacokinetics studies show that peak plasma levels are reached rapidly, within 2–3 hours of intramuscular administration and 4–6 hours of oral administration. Administration of high-dose aripiprazole (>25 mg/day) should be considered as a viable alternative to ECT and benzodiazepines in patients presenting with catatonic symptoms. Aripiprazole also carries a much lower risk of complications compared to other antipsychotics.

show abstract

“…Also, clozapine could modulate glutamate and GABA neurotransmission. [13][14][15] Alternatively, but not exclusively, the effect of clozapine could derive from its enhanced antipsychotic properties. …”

Section: -12mentioning

confidence: 99%

“…10 A daily dose between 300 and 750 mg may be required to achieve efficacy, 10,11 and relief from catatonic symptoms is observed within 2-7 weeks of treatment. [10][11][12] The neurobiology of catatonia is complex, [13][14][15] and clozapine may be effective through its actions at various biological junctures of this neurobiology. 10,16 It is possible that the net effect of clozapine on dopamine neurotransmission (low D2 receptor occupancy coupled with increased dopamine release in the striatum via the stimulation of 5-HT 1A receptors) contributes to the anticatatonic effects of clozapine.…”

mentioning

confidence: 99%

Clozapine for the management of persistent catatonia

Tabbane¹,

Halayem²,

Joober³

2016

jpn

View full text Add to dashboard Cite

A 42-year-old man with a diagnosis of undifferentiated schizophrenia has been hospitalized several times since age 23 for psychotic relapses, usually in the context of nonadherence to medication.During the last relapse, he was concerned about many plots being planned against him for vague reasons. He experienced catatonic symptoms, including rigid postures, resistance to eating and drinking, immobility, mutism and staring, and displayed periods of unexplained aggressiveness. Physical examination revealed waxy flexibility with no extrapyramidal symptoms or fever. He had a score of 24 on the Bush-Francis Catatonia Rating Scale (BFCRS), which is compatible with a severe form of catatonia.Even in a patient with psychiatric illness, a plethora of medical conditions can be associated with catatonia. This emphasizes the importance of ruling out a somatic cause.1,2 The patient was assessed by an internist and a neurologist, and no clinical abnormalities were identified. Laboratory results, including MRIs and electroencephalography (EEG) scans were unremarkable.Because the patient refused intravenous injections, lorazepam was initiated orally and was rapidly titrated up to 6 mg daily for more than 15 days, without any effect. However, higher doses were not tolerated. Subsequently, the patient accepted intramuscular injections, which resulted in partial and transitory remission of the catatonic symptoms for a few hours. After a gradual discontinuation of benzodiazepines (BZD), electroconvulsive therapy (ECT) was initiated. Two series of treatments of 20 sessions each with unitemporal followed by bitemporal electrode placement were completed with no significant improvement, and the score on the BFCRS remained between 20 and 24.Risperidone (4-6mg/d) and aripiprazole (20mg/d) were each used for a period of at least 6 weeks but were not able to alleviate catatonia symptoms. Parkinsonism was systematically assessed and corrected using anticholinergic agents as needed. Finally clozapine was initiated and gradually titrated to 400 mg over a period of 5 weeks. A significant decrease in the BFCRS score (final score of 4) was observed after 5 weeks, allowing for long-deferred care and discharge from the hospital.In contrast to acute catatonia, chronic catatonia is less responsive to first-line treatments, including lorazepam and ECT, especially in the context of schizophrenia.2-7 Using lorazepam for longterm periods has been proposed as a therapeutic option, although the therapeutic response may be slower, taking months rather than days. 2,4 It is generally recommended to discontinue antipsychotics (APs) in patients presenting with catatonia, as APs increase parkinsonism, leading to a potential aggravation of catatonia and an increase in the risk of neuroleptic malignant syndrome (NMS). 2,4,8However, atypical APs are known to have weak γ-aminobutyric acid (GABA) agonist activity and serotonin (5-HT 2 ) antagonism that could stimulate dopamine release in the prefrontal cortex and alleviate catatonic symptoms. 9 In the event that the...

show abstract

Neurobiological Approach of Catatonia and Treatment Perspectives

Cited by 42 publications

References 48 publications

Is motor imagery different in catatonic schizophrenia?

Is motor imagery different in catatonic schizophrenia?

Rapid efficacy of aripiprazole in the treatment of catatonic depression/catatonia with consideration of the drug’s unique receptor profile: a case report

Clozapine for the management of persistent catatonia

Contact Info

Product

Resources

About