Catatonia is an uncommon and heterogeneous psychomotor syndrome. It can be not only the manifestation of a psychiatric disorder but also a wide range of medical conditions. The malignant catatonia is a subtype of catatonia which includes dysautonomic signs such as hyperthermia or hemodynamic instability, and because most of the affected patients are taking antipsychotics or antidepressants previously, it can be confounded with medical conditions such as neuroleptic or serotonin syndrome.

To present a case of malignant catatonia admitted in a medical ward

The present study is a case report of a patient admitted with initial diagnosis of serotonin syndrome in a medical ward of our hospital and referred to the consultation and liaison psychiatry (CLP) unit. We also searched previously case reports, series and systematic reviews about catatonia secondary to medical conditions and hyperthermia catatonia.

Ms. TN is a 71-year-old woman, with prior history of major depressive disorder. One month ago she was admitted in a psychiatric ward of another hospital for a depressive episode with psychotics features, and was treated with escitalopram 10mg/day, vortioxetine 10mg/day, mirtazapine 15mg/day, trazodone 50mg/day, quetiapine 700mg/day and haloperidol 5mg/day. She had a worsening of depressive symptoms with suicidal thoughts, negativism and psychomotor retardation, and subsequently hyperthermia, rigidity, mydriasis, tachicardia and increased bowel sound. She was tranfered to our medical ward, and diagnosed of serotonin syndrome. She was stopped all the psychiatric drugs and was treated with dantrolene and support measures. After 10 days without antidepressants or antipsychotics she maintened the same symptomatology and was referred to our CLP unit. The psychopathological evaluation showed stupor, mutism, waxy flexibility and negativism, and she responded to a challenge test with intravenous clonazepam 0,5mg. She was diagnosed of malignant catatonia and was started oral clonazepam 2mg/day. Although there was a partial response, she did not tolerate higher doses because of sedation and finally was treated with electroconvulsive therapy (ECT). She dad a remission of catatonic symptoms after only two sessions of ECT.

Malignant catatonia can be confounded with other medical conditions such as serotonin or neuroleptic syndromes. All of them can have catatonic signs, and it is important to recognize them (a challenge test with a benzodiacepine can be helpful). The key to distingish malignant catatonia from them is that some of the catatonic signs (negativism and psychomotor retardation) happened before the dysautonomic signs. Also, it is uncommon that a serotonin syndrome persisted more than 3-5 days after the suspension of antidepressants. Consultation and liaison psychiatrists can help for the differential diagnosis and management of patients with suspected catatonia in medical wards.

None Declared

The discovery of second-generation antipsychotics represented an authentic breakthrough for the management of psychotic disorders. Nevertheless, they still don’t adequately manage some aspects of these disorders, such as negative symptoms (NS), cognitive impairment, or extra-pyramidal symptoms (EPS). New-generation antipsychotics present different pharmacological mechanisms and have been reported to ameliorate these aspects. Among them, cariprazine acts as a D2/D3 partial agonist with variable affinity with serotoninergic receptors, and many studies show its efficacy for preventing and treating positive symptoms as well as for the management of NS and EPS.

To report a case of a patient diagnosed with schizophrenia with highly invalidating antipsychotic-induced EPS that remitted after switching to cariprazine, while maintaining clinical stability. To review literature about cariprazine and its relationship with NS and EPS.

We describe the case of a 66-year-old woman diagnosed with schizophrenia and under treatment with three-month injectable paliperidone 175mg. During her follow-up at outpatient clinic, she presented a progressively highly invalidating non-trembling parkinsonian syndrome attributable to medication. Paliperidone plasmatic levels were within therapeutic range. An antipsychotic switch was agreed, and cariprazine was started.

The switch from a second-generation antipsychotic to cariprazine entailed the remission of a highly invalidating EPS while improving some of the NS and maintaining psychopathological stability.

Assessing and differentiating NS and EPS is of an utmost importance during the follow-up of patients under antipsychotic treatment. Cariprazine is an interesting alternative when treating patients diagnosed with psychotic disorders that present mostly NS and antipsychotic-induced EPS.

No significant relationships.

Anticholinergic syndrome (AS) is a complication that can appear due to different drugs with antimuscarinic effects, such as antihistamines, alkaloids, antipsychotics, tricyclic antidepressives or anesthetics, and it is characterized by urinary retention, dry mouth and skin, mydriasis, low-grade fever, and confusion or coma.

To describe a clinical case of AS admitted to our hospital.

We present a case report of a patient with schizophrenia who presented an anticholinergic syndrome. We also searched for previous studies of AS using a pubmed query.

A 53-year-old male was admitted for a psychotic decompensation to another hospital in Barcelona. The usual treatment at home was amisulpride 1200mg/d, olanzapine 30mg/d and lormetazepam, and haloperidol 6mg/d and clotiapine 40mg/d were added to treat the decompensation. Then, the patient started to present mydriasis, mucocutaneous dryness, low-grade fever, slight hypertension and tachycardia, repeated retentions of urine, confusion, unintelligible speech and agitation, so he was referred to our hospital. Once he was admitted, haloperidol was withdrawn and support measures (bladder catheterization, fluid therapy, etc.) were applied. After a few days, most of the mentioned alterations were stabilized, but the psychotic symptoms, such as thought and behavioural disorganization, persisted and required electroconvulsive therapy, with subsequent improvement.

AS is a relatively frequent side effect of psychiatric medication, which diagnosis is clinical, so, we must be capable to identify it and initiate early treatment to prevent possible complications. The first step, as reflected in the case described, is to stop the causative drugs, and apply support measures. Additionally, physostigmine can be used, as it is an effective antidote.

No significant relationships.

Mood episodes in bipolar disorder (BD) are still identified with subjective retrospective reports and scales. Digital biomarkers, such as actigraphy, heart rate variability, or ElectroDermal activity (EDA) have demonstrated their potential to objectively capture illness activity.

To identify physiological digital signatures of illness activity during acute episodes of BD compared to euthymia and healthy controls (HC) using a novel wearable device (Empatica´s E4).

A pragmatic exploratory study. The sample will include 3 independent groups totalizing 60 individuals: 36 BD inpatients admitted due to severe acute episodes of mania (N=12), depression (N=12), and mixed features (N=12), will wear the E4-device at four timepoints: the acute phase (T0), treatment response (T1), symptoms remission (T2) and during euthymia (T3; outpatient follow-up). 12 BD euthymic outpatients and 12 HC will be asked to wear the E4-device once. Data pre-processing included average downsampling, channel time-alignment in 2D segments, 3D-array stacking of segments, and random shuffling for training/validation sets. Finally, machine learning algorithms will be applied.

A total of 10 patients and 5 HC have been recruited so far. The preliminary results follow the first differences between the physiological digital biomarkers between manic and depressive episodes. 3 fully connected layers with 32 hidden units, ectified linear activation function (ReLU) activation, 25% dropout rate, significantly differentiated a manic from a depressive episode at different timepoints (T0, T1, T2).

New wearables technologies might provide objective decision-support parameters based on digital signatures of symptoms that would allow tailored treatments and early identification of symptoms.

No significant relationships.

Trichotillomania is a disorder (estimated prevalence 0.5-2.0%) with common onset in childhood, rarely seen in adulthood, characterized by the repetitive pulling out of one’s own hair leading to hair loss and functional impairment, associated with other comorbidities: major depression (39-65%), anxiety disorder (23-32%), SUDs (15-19%), OCD (13-27%).

To present a case of late-onset trichotillomania in a 60-year-old woman.

The present study is a case report of a patient visited in outpatient psychiatry for trichotillomania. We also searched previously case reports, series and systematic reviews of clinical trichotillomania using a pubmed query.

This is a 60-year-old morbidly obese woman diagnosed with dysthymia, binge eating disorder and histrionic personality disorder. She explained a worsening of anxiety associated with work problems of one year of evolution and, for six months, the beginning of the plucking of eyebrow hairs and scabs to decrease this symptom, with inability to avoid the behaviour and without eating the hairs. The mental evaluation highlighted psychic anxiety, hypothymia, low self-esteem and feelings of failure and did not suggest a delirium. We started treatment with topiramate up to 150mg/day which was not successful. After that we switched to fluoxetine up to 60mg/day associated to psychotherapy observing a slight gradual improvement.

The clinical presentation suggested the diagnosis of trichotillomania in the context of dysthymia. No particular medication demonstrates efficacy in the treatment of trichotillomania. Preliminary evidence suggests treatment effects of clomipramine, NAC and olanzapine based on individual trials with small sample sizes. Research findings also recommend psychotherapy based on habit reversal.

No significant relationships.

Pseudobulbar affect (PBA) is an emotional disorder characterized by uncontrollable outbursts of laughing and/or crying. It is caused by lesions that damage pathways in the frontal lobe and descending to the brain stem, basis pontis and cerebellum. The main causes are neurodegenerative diseases.

To present a case of PBA secondary to cerebral toxoplasmosis.

The present study is a case report of a patient admitted for HIV-related toxoplasmosis to our hospital. We also researched previous case reports of PBA secondary to CNS infection using a pubmed query.

Mr. JA is a 38-year-old male, with no prior psychiatric or medical history. He reported having had same-sex sexual encounters previously. He was admitted for ataxia and dysarthria in a medical unit, and diagnosed of HIV infection, with a CD4 count of 19 cells/μL. The MRI showed a lesion of 22x19x18mm with ring enhancement predominantly in basis pontis, compatible with toxoplasmosis(Image1). Treatment with sulfadiazine, pyrimethamine and dexamethasone was initiated. After five days of hospitalization he was referred to Consultation-Liaison Psychiatry for involuntary and uncontrollable outbursts of laughing and crying, insomnia, but no other psychopathological symptoms. Therefore, citalopram 20mg per day was started, with reduction on the frequency of outbursts.

The clinical presentation suggested the diagnosis of PBA due to cerebral toxoplasmosis. Although we found no previous reports of PBA related to HIV infection or toxoplasmosis, the location of the toxoplasmosis lesion is congruent with the typical damaged pathways in PBA. To our knowledge, this is the first report about PBA secondary to HIV-related toxoplasmosis.

No significant relationships.

Cardiovascular events (CVE) are infrequent adverse effects in patients receiving electroconvulsive therapy (ECT). Nonetheless, it constitutes a threat for patient’s life and may compromise continuing ECT.

To describe a case of acute-onset atrial fibrillation under combined therapy with ECT and venlafaxine.

We present a 76-year-old man diagnosed of delusional disorder and without any previous CVE, who was hospitalized in our acute psychiatric unit by major depressive episode with psychotic symptoms resistant to pharmacological treatment (valproic-acid 100mg/d, haloperidol 6mg/d, venlafaxine 300mg/d). ECT was initiated presenting atrial fibrillation after first session of ECT, requiring amiodarone and anticoagulant treatment for stabilization. Second session of ECT was delayed for three-weeks, worsening the psychiatric symptoms. Haloperidol was discontinued initiating lurasidone with better cardiovascular profile.

CVE occur in 2% of the patients receiving ECT, being acute arrhythmia the most frequent one. Among them, few cases of atrial fibrillation (AF) under ECT have been reported. It has been hypothesised that initial vagal response followed by catecholamine surge secondary to ECT could facilitate the development of AF. In addition venlafaxine, an antidepressant drug, may also predispose to arrhythmia in high-risk individuals. High doses of venlafaxine (>300mg/d) combined with ECT have been related with an increment of CVE.

Although clinically effective for the treatment of major depression disorder, combined therapy of ECT and venlafaxine could precipitate the start of a CVE in genetically susceptible individuals. Therefore, identify and clarify potential risk factors other than previous history of CVE is critical to reduce morbidity and mortality in these patients.

No significant relationships.

Lurasidone is an atypical antipsychotic agent with potential antidepressant effects through its antagonist activity at the 5-HT7 receptor. Although treatment-emergent affective switch (TEAS) induced by second-generation antipsychotics are not frequent, several cases have been reported. To our knowledge, there is no evidence of lurasidone-induced TEAS.

To describe a case of lurasidone-induced mania.

We describe a clinical case of a patient admitted to our psychiatric outpatient unit who developed a manic episode, presumably induced by the introduction of lurasidone. We also conduct a review of the literature on this subject.

A 37-year-old man diagnosed with obsessive-compulsive disorder (OCD) and an alcohol use disorder was hospitalized due to OCD decompensation with depressive symptomatology and suicidal thoughts, and for alcohol detoxification process. Since he had a previous history of clomipramine-induced TEAS, he was started on lurasidone up to 111mg to avoid the use of antidepressants, showing a progressive improvement of depressive symptoms. Thus, the patient was discharged when alcohol detoxification process was completed. Eight days after discharge, the patient began to show manic symptoms, so he had to be readmitted. Lurasidone was discontinued and valproic acid up to 1000mg/day as mood stabilizer was added, presenting a positive remission of manic symptoms.

According to our experience, lurasidone may have induced an affective switch in this patient. Based on our findings, patients and psychiatrists should monitor possible lurasidone-induced mood switching. However, further research is needed in order to back-up this one case report findings.

No significant relationships.

The Coronavirus Disease 2019 (COVID-19) can affect mental health in different ways. There is little research about psychiatric complications in hospitalized patients with COVID-19.

The aim of the study was to describe the psychiatric clinical profile and pharmacological interactions in COVID-19 inpatients referred to a Consultation-Liaison Psychiatry (CLP) unit.

This is a cross-sectional retrospective study, carried out at a tertiary hospital in Spain, in inpatients admitted because of COVID-19 and referred to our CLP Unit from March 17,2020 to April 28,2020. Clinical data were extracted from electronic medical records. The patients were divided in three groups depending on psychiatric diagnosis: delirium, severe mental illness (SMI) and non-severe mental illness (NSMI).

Of 71 patients included (median [ICR] age 64 [54-73] years; 70.4% male), 35.2% had a delirium, 18.3% had a SMI, and 46.5% had a NSMI. Compared to patients with delirium and NSMI, patients with SMI were younger, more likely to be institutionalized and were administered less anti-COVID19 drugs. Mortality was higher among patients with delirium (21.7%) than those with SMI (0%) or NSMI (9.45%). The rate of side effects due to interactions between anti-COVID19 and psychiatric drugs was low, mainly drowsiness (4.3%) and borderline QTc prolongation (1.5%).

Patients affected by SMI were more often undertreated for COVID-19. However, the rate of interactions was very low, and avoidable with a proper evaluation and drug-dose adjustment. Half of the patients with SMI were institutionalized, suggesting that living conditions in residential facilities could make them more vulnerable to infection.

No significant relationships.

Dhat Syndrome is a culture-bound entity frequent in the Indian subcontinent. It is characterized by somatic symptoms, together with depressive and anxiety features, specifically focused on the belief of losing semen through urine1.

To describe an atypical Dhat Syndrome case in European cultural context,and to determine the appropriate diagnostic frame and subsequent therapeutic approach.

We present the case of a 37-year-old Indian man attended in our psychiatric outpatient unit mainly due to somatic complaints (gastrointestinal, sexual dysfunction, weakness, and dizziness). He interpreted his problem as possibly due to diabetes and hypothyroidism, and specifically from sugar loss in urine. Organic diseases were excluded.

Although considered as culture-bound, Dhat syndrome has been classified as a subtype of depression, anxiety disorder, somatoform disorder2,3,4, and even a prodromal phase of schizophrenia5. Antidepressants and benzodiazepines are the most recommended pharmacological treatments1. Antipsychotic agents have been used when clear psychotic symptoms were present (auditory hallucinations,delusions)5. Nonetheless, paliperidone 6mg/d was initiated at baseline, with good response and partial remission of the symptoms at two weeks, despite the absence of clear psychotic features. Culturally-informed cognitive-behavioural therapy, as well as sexual education could be beneficial were planned and initiated1.

Data on Dhat Syndrome is scarce, yet agreement exist in considering the cultural context of the patient to avoid diagnostic delays. The adequate treatment remains uncertain. Antipsychotics may be a potential treatment. Further research is necessary to clarify the nature of this syndrome but European clinicians must be aware of culturally-mediated psychiatric manifestations which are increasingly prevalent due to globalization.

No significant relationships.