Periodic Catatonia Research Articles

Periodic Catatonia: A Tangled Spectra within Neuropsychiatry

Catatonia was first described by Kahlbaum in 1874. Subsequently, in 1908, Kraepelin delineated a cyclical pattern of catatonia in a group of patients with Schizophrenia. Further ahead, in 1938, Gjessing demonstrated the role of nitrogen phasic change in synchronous syntonic cases of periodic catatonia. However, Stokes et al., in 1941, demonstrated it to be a result of steady accumulation rather than a phasic change in nitrogen balance. There are no reliable prevalence figures for periodic catatonia. Prominent diagnostic manuals have not given this diagnostic entity a separate nosological status, despite evidence of a discrete metabolic profile. This case series elucidates periodic catatonia in different psychiatric disorders and how a separate diagnostic criterion could help in early detection and management. We narrate three case reports of catatonic manifestations in two young adolescents and one young adult male, with no underlying medical condition. The first case report highlights intermittent brief periods of catatonic excitement beginning with acute anxiety and followed by fainting spells. The second case report narrates an acute onset manic episode which alternates with the catatonic episode. The third case report shows seasonal advents of catatonia. The pharmacological intervention itself was adequate enough to resolve the catatonic symptoms. The three cases give a purview of catatonic manifestations with differential phenomenology. The treatment of catatonia bears challenges owing to a lack of awareness and differential response to available pharmacotherapy.

Periodic Catatonia: An Atypical Presentation of a Common Diagnosis among Older Adults

Periodic Catatonia: An Atypical Presentation of a Common Diagnosis among Older Adults

Ремиссии при периодической кататонии

At the current stage of the formation of concepts of endogenous psychoses, due to the change in the clinical paradigm – the expansion of the boundaries of catatonia to a level involving the inclusion of a wide range of periodically manifesting motor disorders (varying in severity), the study of remissions that form after attacks of periodic catatonia is of particular relevance. The aim of the study is to develop a typology of remissions formed after the onset of periodic catatonia attacks, which occur in the clinical space of schizophrenia and schizophrenic spectrum disorders (RSHS). Research methods: clinical and catamnestic (observation for more than 3 years after the onset of seizures), psychometric (BFCRS, SANS, GAF), statistical. The study material consisted of 30 patients diagnosed with schizophrenia and RSHS (ICD-10; DSM-5) who are under outpatient supervision after inpatient treatment of periodic catatonia attacks in departments 1 and 2 of the Federal State Budgetary Institution of the National Clinical Hospital. Results: within the framework of this study, a new approach to the systematics of remissions has been developed, which is based not only on remissions reflecting a certain stage in the development of the endogenous process (slowing down, stabilization, reduction of symptoms) and social and labor maladaptation, but also remissions, in the formation of which the dynamics of personality disorders participates. In accordance with this, 2 types of remissions are distinguished: 1) remissions with personalized motor phenomena – type of personality development (psychasthenic/hypochondriac circle), prolonged; 2) symptomatic remissions, with signs of ongoing course, with symptoms of catatonia mitis.

Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology.

The British Association for Psychopharmacology developed an evidence-based consensus guideline on the management of catatonia. A group of international experts from a wide range of disciplines was assembled. Evidence was gathered from existing systematic reviews and the primary literature. Recommendations were made on the basis of this evidence and were graded in terms of their strength. The guideline initially covers the diagnosis, aetiology, clinical features and descriptive epidemiology of catatonia. Clinical assessments, including history, physical examination and investigations are then considered. Treatment with benzodiazepines, electroconvulsive therapy and other pharmacological and neuromodulatory therapies is covered. Special regard is given to periodic catatonia, malignant catatonia, neuroleptic malignant syndrome and antipsychotic-induced catatonia. There is attention to the needs of particular groups, namely children and adolescents, older adults, women in the perinatal period, people with autism spectrum disorder and those with certain medical conditions. Clinical trials were uncommon, and the recommendations in this guideline are mainly informed by small observational studies, case series and case reports, which highlights the need for randomised controlled trials and prospective cohort studies in this area.

Periodic catatonia in schizophrenia spectrum disorders

Typological differentiation of periodic catatonia in schizophrenia and schizophrenia spectrum disorders (SSD), in particular, schizoaffective disorder. Seventy-four patients with the verified diagnosis of schizophrenia and SSD (ICD-10 items F20, F21) were studied. The clinical, psychometric (BFCRS, SANS) and statistical methods were used. Clinical and psychometric study of seizures of periodic catatonia was carried out at the following stages: 1) manifestation of a seizure; 2) the maximum severity of psychopathological disorders. Also, at the end of the seizure, an additional assessment of the severity of negative symptoms was carried out using the SANS. Three forms of periodic catatonia have been identified: hypokinetic, parakinetic, multikinetic. Clinical distinguishing indicators of periodic catatonia seizurs have been established (protracted - two-stage - form of seizures; the phenomenon of «secondary catatonia»). The psychometric study revealed significant differences between the variants of periodic catatonia seizures in terms of the severity of motor phenomena (at both stages of the seizure) and negative disorders. BFCRS scores at the first stage of seizures were as follows: hypokinetic - 9.7±0.4; parakinetic - 12.8±0.9; multikinetic - 32.3±1.6 (the differences were found between 1 and 2 (p<0.05); between 1 and 3, as well as 2 and 3 (p<0.01)). BFCRS scores at the second stage of seizures were 12.1±0.8; 19.9±1.2 and 47.7±1.9, respectively,with the differences between 1 and 2 (p<0.05); between 1 and 3, and also 2 and 3 (p<0.01). The scores on the SANS anhedonia-asociality subscale were 1.9±0.2 for hypokinetic; 2.3±0.3 for parakinetic and 3.2±0.2 for multikinetic with the differences between 1 and 2, 1 and 3, 2 and 3 (p<0.01). Periodic catatonia is the clinical entity that includes a complex of progressively worsening seizures, the psychopathological systematics of which takes into account the clinical structure of motor disorders, their affiliations with positive and negative dimensions, and functional activity.

Late-onset periodic catatonia with atypical course: A diagnostic quandary

ABSTRACT We describe a case of late-onset periodic catatonia with atypical course in an elderly male with onset at the age of 70 years with brief episodes of sudden agitation lasting for a few hours of the day, followed by immobility, mutism, ambitendency, withdrawal, and urinary incontinence for the next few days. Four such episodes with complete recovery over the next few days and no residual behavioral symptoms lasting for several years (up to 7 years) without any long-term prophylactic psychotropic use. During the fourth such episode, the patient presented to our facility with a similar abrupt onset of symptoms. All biochemical investigations and neuroimaging findings were found to be noncontributory. On clinical examination, a diagnosis of periodic catatonia was suspected, which was later confirmed by immediate response to the intravenous diazepam challenge given under vitals monitoring in a high-dependency unit setting.

Subtyping chronic catatonia: Clinical and neuropsychological characteristics of progressive periodic catatonia and chronic system catatonias vs. non-catatonic schizophrenia

Catatonia has been defined by ICD-11 as a nosologically unspecific syndrome. Previous neuropsychiatric conceptions of catatonia such as Wernicke-Kleist-Leonhard's (WKL) one, have isolated chronic catatonic entities, such as progressive periodic catatonia (PPC) and chronic system catatonias (CSC). This study aimed at comparing the clinical and neuropsychological features of PPC, CSC and non-catatonic patients, all diagnosed with a schizophrenia spectrum disorder (SSD).The clinical and cognitive measures were compared among 53 SSD patients, first by separating catatonic (C-SSD, n = 27) and non-catatonic patients (NC-SSD, n = 26), and second, by separating PPC (n = 20), CSC (n = 6) and NC-SSD patients. Bayes factors were used to compare the model with 1 or 2 catatonic groups.We found that PPC had a more frequent schizo-affective presentation, higher levels of depression and less positive psychotic symptoms than both CSC and NC-SSD. CSC patients had an earlier illness onset, a poorer cognitive functioning, and higher antipsychotics doses than both PPC and NC-SSD. Most differences between C- and NC-SSD were accounted by characteristics of either PPC or CSC. The model with 2 catatonic groups clearly outperformed that with 1 catatonic group.Our results point to a substantial clinical heterogeneity of ‘catatonia’ within the SSD population and suggest that distinguishing (at least) 2 chronic catatonic phenotypes (PPC and CSC) may represent a relevant step to apprehend this heterogeneity. It is also a more parsimonious attempt than considering the around 32.000 distinct catatonic presentations resulting from the combinations of 3 out of 15 polythetic criteria for ICD-11 catatonia.

A Brain Imaging-Based Diagnostic Biomarker for Periodic Catatonia: Preliminary Evidence Using a Bayesian Approach

Periodic catatonia (PC) is a psychomotor phenotype with a progressive-remitting course. While it can fit any disorder diagnosis of the schizoaffective spectrum, its core features consist of a mix of hypo- and hyperkinesias resulting in distortions of expressive movements such as grimacing and parakinesias. The replication of cerebral blood flow (CBF) increases in the left supplementary motor area (L-SMA) and lateral premotor cortex (L-LPM) in acute and remitting PC patients indicates that these increases could be used as diagnostic biomarkers. In this proof-of-concept study, 2 different MRI sequences were repeated on 3 separate days to get reliable measurement values of CBF in 9 PC and 26 non-PC patients during different cognitive tasks. Each patient was compared to 37 controls. In L-SMA [–9; +10; +60] and L-LPM [–46; –12; +43], a test was positive if the t value was >2.02 (α < 0.05; two tailed). The measurements had good analytical performance. Regarding the tests, their sensitivities and specificities were significantly different from the chance level on both measures, except for L-SMA sensitivities. When combining all the tests, among regions and methods, sensitivity was 98% (95% credible interval [CI] 76–100%) and specificity 88% (72–97%). Bayesian inferences of its negative predictive values for PC were >95% regardless of the context, while its positive predictive values reached 94% but only when used in combination with clinical criteria. The case-by-case analysis suggests that non-PC patients with neurological motor deficits are at risk to be false positive.

Maintainance ECT for Recurrent Catatonia-A Case Report

Abstract Catatonia was first described by Kahlbaum as a disorder of movement and speech .Kraeplin grouped catatonia along with other sub types of schizophrenia. In ICD-10 catatonia is mentioned as sub type of schizophrenia. DSM-5 gives independent status to catatonia. Catatonia may be caused by many medical conditions ,but in psychiatry it is associated more with mood disorders and schizophrenia. There are certain conditions with recurrent catatonia like the Periodic catatonia .We present a case of 35year old woman who has recurrent catatonia for the past 15 years .She was diagnosed with catatonic schizophrenia initially, treated with adequate trials of different antipsychotics , mood stabilisers and benzodiazepines with poor response. For the past several years she is being given maintainance ECT to which she is showing good response. ECT is effective in the treatment of recurrent catatonia and can be maintained. Key words – recurrent catatonia, maintainance ECT, good response

Maintainance ECT for Recurrent Catatonia-A Case Report

Abstract Catatonia was first described by Kahlbaum as a disorder of movement and speech .Kraeplin grouped catatonia along with other sub types of schizophrenia. In ICD-10 catatonia is mentioned as sub type of schizophrenia. DSM-5 gives independent status to catatonia. Catatonia may be caused by many medical conditions ,but in psychiatry it is associated more with mood disorders and schizophrenia. There are certain conditions with recurrent catatonia like the Periodic catatonia .We present a case of 35year old woman who has recurrent catatonia for the past 15 years .She was diagnosed with catatonic schizophrenia initially, treated with adequate trials of different antipsychotics , mood stabilisers and benzodiazepines with poor response. For the past several years she is being given maintainance ECT to which she is showing good response. ECT is effective in the treatment of recurrent catatonia and can be maintained. Key words – recurrent catatonia, maintainance ECT, good response

Personalized rTMS improves chronic and treatment resistant catatonias–A proof of concept study

Introduction Chronic and treatment resistant catatonias are orphans’ pathologies. No treatment has ever been developed or is currently in the pipeline for these conditions. As a toolbox, rTMS might correct abnormal brain activity in relation with psychomotor disorders provided the knowledge on where and how to modulate it using functional brain imaging (RETONIC, NCT03116425 ). Methods Twelve patients were recruited. Their abnormal regions were outlined thanks to 3 MRI sessions using ASL sequences performed during different tasks. They were compared to 38 normal controls (threshold P Results We report on the first 10 patients, 2 are currently finishing the study. Eight patients had the periodic catatonia phenotype according to Leonhard. All had the previously reported hyperperfusion in the left central and precentral cortices. The inhibitory modulation of this region improved all patients but one according to the Clinical Global Impression–Improvement scale (minimally to very much improved) mostly by alleviating apathy. More various anomalies were observed in the prefrontal regions which correction led to a minimal improvement in two patients. One patient much worsened under control stimulation. The two last patients had Leonhard's manneristic catatonia phenotype. Both had a complex pattern of hypoperfusion in the prefrontal regions. Its modulation much improved the most severely affected patient while the modulation of the placebo regions much worsened his condition. The other patient had no significant change whatever the treatment arm. Conclusion Considering that rTMS outperformed electroconvulsive therapy in 2 patients, it deserves a more systematic assessment.

A double dissociation between two psychotic phenotypes: Periodic catatonia and cataphasia

Schizophrenia as a single liability model was confronted to the multiple psychotic phenotypes model proposed by the Wernicke-Kleist-Leonhard school, focusing on two: periodic catatonia (PC) and cataphasia (C). Both are stable and heritable psychotic phenotypes with no crossed liability and are coming with the buildup of specific residual symptoms: impairment of psychomotricity for PC and a specific disorganization of thought and language in C. Regional cerebral blood flow (rCBF) was used as a biomarker. We attempted to refute the single phenotype model by looking at relevant and specific rCBF anomalies for PC and C, that would exceed anomalies in common relative to controls (CTR), i.e. looking for a double dissociation. Twenty subjects with PC, 9 subjects with C and 27 matched controls had two MRI QUIPSS-II arterial spin labeling sequences converted in rCBF. One SPM analysis was performed for each rCBF measurement and the results were given as the conjunction of both analysis. There was a clear double dissociation of rCBF correlates between PC and C, both being meaningful relative to their residual symptomatology. In PC: rCBF was increased in the left motor and premotor areas. In C: rCBF was decreased bilaterally in the temporo-parietal junctions. Conversely, in both (schizophrenia): rCBF was increased in the left striatum which is known to be an anti-psychotics' effect. This evidence refuts the single schizophrenia model and suggests better natural foundations for PC and C phenotypes. This pleads for further research on them and further research on naturally founded psychotic phenotypes. Clinical trialName of the registry: ClinicalTrials.govIdentification: NCT02868879

Poster Number: NR 35 - When a Benzodiazepine Can Help Save a Life: Periodic and Malignant Catatonia in an Aging Veteran

Introduction: Background: Catatonia is a syndrome defined by immobility, rigidity, mutism, posturing, stupor, negativism, staring, and echolalia. This syndrome is commonly associated with psychiatric disorders but can also be associated with neurologic and general medical illnesses. Catatonia can be further categorized into subtypes such as malignant catatonia (MC), a rare but fulminant and progressive type of catatonia characterized by autonomic instability. MC shares clinical and pathophysiological features with other syndromes such as Neuroleptic Malignant Syndrome (NMS). Thus, diagnosis of MC can be delayed, which increases morbidity and mortality. Furthermore, catatonia can be periodic, meaning symptoms can occur, then resolve but later return. Literature suggests that the interval time between episodes of periodic catatonia varies from 4.5 to 20 months with the average interval being 10.7 months. Current evidence supports benzodiazepines and electroconvulsive therapy (ECT) as the standard treatment for the various forms of catatonia.

Molecular hypotheses to explain the shared pathways and underlying pathobiological causes in catatonia and in catatonic presentations in neuropsychiatric disorders

The pathobiological causes, the shared cellular and molecular pathways in catatonia and in catatonic presentation in neuropsychiatric disorders are yet to be determined. The hypotheses in this paper have been deduced from the latest scientific research findings and clinical observations of patients with genetic disorders, behavioral phenotypes and other family members suffering mental disorders. The first hypothesis postulates that catatonia and the heterogeneity of catatonic signs and symptoms involve nucleolar dysfunction arising from abnormalities of the brain-specific, non-coding micro-RNA, SNORD115 genes (either duplications or deletions) which result in pathobiological dysfunction of various combinations in the downstream pathways (possibly along with other genes in these shared pathways). SNORD115 controls five genes CRHR1, PBRM1, TAF1, DPM2, and RALGPS1 as well as the alternative splicing of serotonin 2C receptor. SNORD115 abnormalities with varying downstream multigene involvement would account for catatonia across the life span within some subtypes of autism spectrum disorders, schizophrenia, bipolar and major depressive disorder, psychosis, genetic disorders, and in immune disorders such as anti-N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis as well as the susceptibility to the neuroleptic malignant syndrome (NMS) if environmentally triggered. Furthermore, SNORD115 genes may underlie a genetic vulnerability when environmental triggers result in excess serotonin producing the serotonin syndrome, a condition similar to NMS in which catatonia may occur. Dysfunction of SNORD115-PBRM1 connecting with SMARCA2 as well as other proven schizophrenia-associated genes might explain why traditionally catatonia has been classified with schizophrenia. SNORD115-TAF1 and SNORD-DPM2 dysfunction introduce possible clues to the parkinsonism and increased creatinine phosphokinase in NMS, while abnormalities of SNORD115-RALGPS1 suggest links to both anti-NMDAR encephalitis and the proven predisposing catatonic SHANK3 gene. The second hypothesis postulates that periodic catatonia (PC) on 15q15 involves abnormalities of vacuolar protein sorting 39 (VPS39), a proven de novo schizophrenic gene in this chromosomal locus and part of the HOPS complex. These will impact the autophagic and endocytic pathways, thereby lowering lysosomal degradation. VPS39 mutations may be considered also to disrupt lysosome-mitochondria tethering and transport of lipids and calcium through membrane contact sites (MCSs). To account for the periodicity in PC it is speculated that the mammalian equivalent of the vacuole and mitochondria patch (vCLAMP) would be altered by VPS39 mutations and subsequently followed by the mammalian equivalent of endoplasmic reticulum mitochondria encounter structure (ERMES) restoring mitochondrial homeostasis. Future precision psychiatry will require accurate pathophysiologically-defined psychiatric diagnoses to accelerate the discovery of specific molecular-targeted medications to improve therapeutic outcomes.

Periodic catatonia with long-term treatment: a case report

BackgroundPeriodic catatonia has long been a challenging diagnosis and there are no absolute guidelines for treatment when precipitating factors are also unclear. We report a schizophrenia patient with periodic catatonia with a 15-year treatment course. A possible correlation between decreased daylight exposure and periodic attacks has been observed.Case presentationWe describe a 49-year-old woman with periodic catatonia associated with schizophrenia with 15 years of follow-up. The patient was treated with the antipsychotics risperidone, haloperidol, loxapine and quetiapine, but catatonia still relapsed once per year during the first few years of her disease course. The treatment was consequently been switched to clozapine due to fluctuated psychotic illness, and a longer duration of remittance was achieved. Lorazepam-diazepam protocol was used for rapid relief of catatonic symptoms, and was able to significantly shorten the duration of the symptoms. In addition, we observed a possible correlation between catatonic episodes and decreased daylight exposure during the 15-year duration.ConclusionsSuccessful treatment of acute periodic catatonia was achieved with a lorazepam-diazepam protocol, and the patient remained in remission for a longer duration under clozapine treatment. Besides, the possibility of decreased daylight exposure acting as a precipitating factor was observed during our 15 years of follow-up.

Catatonic syndrome: From detection to therapy

IntroductionCatatonia is a psychomotor syndrome which can include motor, mental, behavioral and vegetative symptoms. Exclusively associated with schizophrenia until the 1970s, catatonia still remains an under-diagnosed syndrome with significant morbidity and mortality. Literature findingsAs a result of its different forms and developments, catatonic syndrome can be associated with many organic and psychiatric etiologies and confused with a variety of diagnoses. In addition to its organic complications, malignant catatonia can also be extremely severe. Several diagnostic scales are described, those of Bush and Peralta being the most widely used. Despite the recent development of the DSM-5, we can regret the lack of progress in the international classifications concerning both the recognition of the etiological diversity of this syndrome and in the clinical and therapeutic approaches to it. The diagnosis is based solely on clinical data, and needs to be completed by information from paraclinical settings, particularly with respect to detecting organic etiology. The first-line treatment is still based on the use of certain benzodiazepines or benzodiazepine-like agents such as lorazepam, diazepam and zolpidem. If the first or second line fails, or in case of malignant catatonia, electroconvulsive therapy is recommended. For the periodic form, no large-sample study has been performed on long-term treatment. A few case reports suggest the use of lithium in periodic catatonia, specifically to prevent recurrent episodes or at least to extend the inter-episode intervals. Other studies are in favor of the use of benzodiazepines, with disagreement between gradual discontinuation and long-term treatment. Concerning the management of catatonia in patients with schizophrenia, for whom first-line benzodiazepines are often insufficient, certain atypical antipsychotics such as clozapine or quetiapine appear efficient. These data are also applicable to children and adolescents. ConclusionOften neglected by practitioners, catatonic syndrome remains a common entity of which it is important to be aware, especially in case of rapid installation of the symptoms. Diagnostic scales should be used and a lorazepam test should be performed to avoid delaying the diagnosis. Second-line therapy requires further study. This concerns in particular diazepam, anti-NMDA (N-methyl-D-aspartate) and rTMS (repetitive transcranial magnetic stimulation). Some specificities of catatonia, such as the periodic form and cases in patients with schizophrenia, also require further evaluations.

La catatonie dans tous ses états

Catatonia is a frequent but unrecognized syndrome. Described in the late nineteenth century by the German psychiatrist Karl Kahlbaum, catatonia has experienced some nosological twists including the attachment to schizophrenia by Emil Kraepelin and Eugen Bleuler. It was not until the mid-nineteenth century that clinicians recognize catatonia related to other etiologies including somatic ones. This paradigm shift has helped to rediscover this syndrome, to find a treatment algorithm and try to understand its pathophysiology. From a diagnostic point of view, we will see that a few cardinal signs may be retained: inhibition and rigidity, stereotypies, aimless agitation, negativity and ambivalence. The treatment of catatonia must be twofold: to relieve the catatonic state, and to treat the cause. Among symptomatic treatments, some benzodiazepines (such as lorazepam) and zolpidem are generally very effective and provide a diagnostic test. If that fails, electroconvulsive therapy is the main second line treatment. Regarding the cause of catatonia, one should distinguish psychiatric disorders: mood disorders, schizophrenia, autism and periodic catatonia; and numerous organic causes among which we will highlight anti-NMDAR (N-Methyl-D-aspartate glutamate receptor) encephalitis. Treating the cause should be undertaken as quickly as possible in parallel with the treatment of the catatonic state, except for neuroleptics which may worsen catatonia if administered early. Catatonia corresponds to a dysfunction of the circuits involved in voluntary movement in response to fear, most often in the form of stupor but sometimes in a furious form. The lateral orbitofrontal cortex, in default in catatonia, and carrier of GABA-A receptors, would be heavily involved in this primitive reaction which it should inhibit by interaction with the median orbitofrontal cortex and the amygdala.

Periodic Catatonia after Thyroid Cancer

Periodic Catatonia after Thyroid Cancer

The role of Pannexin gene variants in schizophrenia: systematic analysis of phenotypes.

Pannexins are a group of brain-expressed channel proteins thought to be regulators of schizophrenia-linked pathways including glutamate release, synaptic plasticity and neural stem proliferation. We got evidence for linkage of a catatonic phenotype to the PANX2 locus in a family study. Aim of our study was to evaluate the role of Pannexins in schizophrenia and clinical phenotypes, particularly with regard to periodic catatonia. We genotyped six single-nucleotide polymorphisms at PANX1, five at PANX2 and three at PANX3 in 1173 German cases with schizophrenia according to DSM-5 and 480 controls. Our sample included 338 cases with periodic catatonia corresponding to Leonhard's classification. Association with schizophrenia according to DSM-5 was limited to genotype rs4838858-TT [p=0.02, odds ratio (OR) 3.1] and haplotype rs4838858T-rs5771206G (p=0.02, OR 2.7) at PANX2. We found no significant association with clinical phenotypes. Our limited findings do not support a major contribution of PANX1-3 to disease risk of schizophrenia according to DSM-5. We cannot confirm an association of the PANX2 loci at chromosome 22q13 with periodic catatonia.

Petre Tomescu and His Early Studies in Catatonic Schizophrenia

Petre Tomescu (born 1890, died 1972) was a professor of Psychiatry, and Dean of the Faculty of Medicine from Bucharest. He was one of the first psychiatrists in Romania to be highly influenced by the hereditary theories of mental pathology and eugenics, proposing a different interpretation and treatment of mental disorders compared to his predecessors. His scientific work included studies in the areas of epilepsy, physiopathology of adrenergic substances, psychotechnic examinations, excretion and metabolism of alcohols, and so on. One of the main areas of study was however the catatonic syndrome. For example, in an article from 1929, Tomescu continued the researchers conducted by Bourgignon and de Jong regarding catatonia induced by Bulbocapnine on animals, by testing it on cats, dogs, chickens, and rabbits. In another study, conducted together with his mentor Al. Obregia, he described a series of particular cases of periodic catatonia, either as an evolutive stage of periodic psychosis, or alternating with manic syndrome. One of his most interesting, however practically unknown results, was proving a positive response in patients with schizophrenic catatonia to Harmine, a monoamine oxidase inhibitor. The purpose of this presentation is to present these forgotten studies, and to emphasise the role Tomescu had in the development of Romanian psychiatry in the Interwar period. Acknowledgment: This work was supported by a grant of the Romanian National Authority for Scientific Research, CNDI– UEFISCDI, PN-II-RU-TE-2012-3-44