Theory of Mind (ToM) is defined as the cognitive ability that infers other’s mental states (Premack & Woodruff. J Behav Brain Sci 1978; 1 515-526).The interest in the study of ToM distinguishing its affective and cognitive components has been growing. Its study in psychopathology has been evolved from its original studies in autism spectrum disorders (ASD), schizophrenia (SCZ) and, borderline personality disorder (BPD), to other mental disorders like major depressive disorder (MDD), bipolar disorder (BP), anorexia nervosa (AN) and social anxiety disorder (SAD).

1) review the most commonly used instruments for ToM assessment; 2) to compile the evidence on ToM deficits across mental disorders. For both objectives, target disorders are previously mentioned.

The search was carried out on the PubMed, PsycInfo and Scopus databases, using the terms “Theory of mind”, “Mentalization” and the previously mentioned mental disorders and pertinent thesaurus. Articles in English, published since 2010 were considered. A 2-step strategy (first, article screening and full reading) was followed to select articles of interest.

Reading the Mind in the Eyes (Baron-Cohen et al., J Child Psychol Psychiatry 2001; 42 241-251) and Movie for the Assessment of Social Cognition (Dziobeck et al. J Autism Dev Disord 2006; 36 623-636) were the most commonly used tasks to assess ToM. Regarding mental disorders, studies showed deficits in cognitive and affective ToM skills in ASD, SCZ, BPD, MDD and BP. Hypomentalization was mainly observed in ASD and MDD, while BPD and SCZ were featured by errors associated with hypermentalization. Studies in AN and SAD are scarce, but they mainly highlight a cognitive ToM deficit, with hypomentalization in AN and hypermentalization in ASD. In all of them, depressive symptomatology seems to be a critical moderator of ToM performance.

Although ToM impairments are well described for some mental disorders, more research is needed to reach solid conclusions for others. The use of different and heterogeneous ToM assessment instruments can strongly influence the results of studies. The study of ToM is essential to gain a better understanding of the diseases and to develop effective treatments targeting specific ToM deficits.

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A feeling as ancient as humankind, having been documented in the Bible, represented by mythological figures and appearing as a recurrent theme in art and literature, jealousy is a complex emotion that is non-discriminatory and often associated with negative feelings ranging from insecurity, suspicion, rage, fear to humiliation. Commonly associated with romantic relationships, it typically arises when one perceives a threat, either real or imagined, from a third party in regards to possession or perceived security. Jealousy, like other aspects of the human experience, varies in its expression and intensity, ranging from an adaptive response to a potentially dangerous psychopathological symptom.

The authors aim to describe jealousy and discuss the spectrum on which it appears, ranging from an adaptive response to a psychopathological manifestation.

A brief non-structured literature review was carried out with recourse to various databases such as Pubmed as well as complimentary literary sources when deemed pertinent.

Described as a defensive reaction that is expressed as a cognitive, emotional and behavioural response to a perceived threat, jealousy has been discussed in various arenas of thought ranging from evolutionary psychology to philosophy to psychiatry to representation in the arts. It is a difficult term to define as it is a feeling expressed through diverse emotions and behaviours originating from various contexts as well as varying in its intensity. The literature demonstrates that jealousy can exist as an adaptive response, with evolutionary explanations, to a psychopathological expression either as obsessive jealousy or morbid jealousy, also known as Othello’s Syndrome. Each carries its own particularities in terms of expression, clinical significance and intervention. The more often described delusional jealousy, is characterized by the presence of strong, false beliefs that the partner is unfaithful, whereas obsessive jealousy, less commonly described, presents with unpleasant, ego-dystonic and irrational jealous ruminations that the partner could be unfaithful. These thoughts are often accompanied by compulsive verification of the partners’ behaviour. Treatment interventions in these cases are varied and present implications in prognosis.

Jealousy is a complex emotional state and has been described as part of the universal human experience, with research indicating its existence across various cultures. The expression of this emotional experience as well as its potential manifestation types should be taken into consideration by the mental health practitioner when carrying out an evaluation, as treatment interventions and prognosis may vary depending on the presentation.

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Borderline personality disorder (BPD) is associated with severe suffering and insomnia disorder (ID) (Fertuck et al., 2016; Galbiati et al., 2020).

The aim was to investigate the negative association between self-reported physical activity (PA) and the severity of BPD with ID acting as a mediator (St-Amour et al., 2021).

The role of ID within the association of PA with BPD was tested using mediation analysis with the statistical program R 4.3 (N = 120; RStudio Team, 2020).

Table 1

Mediation analysis results

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Accordingly, ID does not appear to affect the association of PA and BPD severity whereas fewer PA and severe ID can nonetheless have a positive association with the symptoms of BPD in independent ways.

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The early diagnostic of schizophrenia and other psychosis is very important for the early therapeutic interventions.

The aim is to describe the connection between the prodromal stage of psychosis and clinical features.

74 patients with late-onset psychosis (mean age 64,33±9, 2 male; age of onset 55,3±11,2): late-onset schizophrenia (LOS) (n=49, mean age 63,0±8,47, age of onset 53,9±9,56), late-onset schizoaffective disorder (LOSaD) (n=17, mean age 62,4±6,5, age of onset 54,6±10,6, 2 male), late onset delusion disorder (LODD) (n=8, mean age 76,6±4,3, age of onset 65,2±17,0). Psychopathological, statistical methods were applied.

Allocated 4 types of prodromal stage – 1st without psychopathological signs (n=24, 33%), 2nd – with affective signs like disturbances of mood, anxiety (n=18, 24%), 3rd – with paranoid signs like acute stress-related paranoid reactions without medication; 4th - with schizoid signs with overvaluated ideas. In the 1st group next syndromes prevailed: with secondary persecutory mood-congruent delusions (n=10, 41,7%); with auditory second-person pseudohallucinations with sistematyzed persecutory delusions (n=9, 37,5%); with only systematized persecutory delusions (n=1, 4,1%); with bizzarre delusions (n=3, 12,5%) and with polymorphic symptoms, include different hallucinations, catatonia disorders and with some oneiroid state signs (n=1, 4,1%). In this group 9 patients were diagnosed with LOS (37,5%); 12 patients with LOSaD (50%) and 3 patients with LODD (12,5%). The 2nd group was presented with auditory second-person pseudohallucinations with sistematyzed persecutory delusions (n=5, 27.7%), with secondary persecutory delusions with delusion mood (n=11, 61%), with systemized persecutory delusional - 5.5% (n=1) and with catatonia (n=1, 5.5%). In this group 12 patients were diagnosed with LOS (66%), 5 patients with LOSaD (28%) and 1 patient with LODD (5.5%). In the 3rd group these syndromes prevailed: with auditory second-person pseudohallucinations with sistematyzed persecutory delusions (n=7, 63%), with secondary persecutory delusions with delusion mood - in 2 cases (18.2%), with bizarre delusions - in 2 cases (18.2%). 12 patients were diagnosed with LOS (n=10.91%) and 1 patient with LODD (1.9%). The 4th group was presented with auditory second-person pseudohallucinations with sistematyzed persecutory delusions (n=5, 23.8%), with secondary persecutory delusions with delusion mood (n=3, 14.3%), with bizarre delusions (n=6, 28.6%), with systemized persecutory delusions (n=1, 4.7%), with catatonia (n=2, 9.5%) and with polymorphic symptoms (n=4, 20%). 18 patients were diagnosed with LOS (85.7%) and 3 patients - with LODD (14.3%).

There are different types of prodromal stage in late-onset psychosis that concluded with clinical features.

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The neuroleptic malignant syndrome is a rare but potentially the most dangerous complication of neuroleptic use. The first descriptions of this disorder were given by Delay and colleagues in the 1960s, calling it “hypertonic akinetic syndrome” and characterizing it with hyperthermia, extrapyramidal symptoms, altered mental status, and autonomic dysfunction. Current knowledge unequivocally shows that NMS most often occurs with the use of first-generation antipsychotics, especially in parenteral form. After the appearance of this disorder, the usual practice is to transfer the patient to monotherapy with clozapine, excluding antipsychotics from the chemical group that led to NMS.

However, there are isolated reports of the occurrence of this syndrome in patients on concomitant therapy of clozapine with lithium salts.

The main objective is to present possible case of NMS in patients with concomitant use of clozapine and lithium

Case report: M. K., born in 1984, graduated from high school, unmarried, without permanent employment. In 2003, after the parenteral application of Depo preparation, he developed NMS. He was hospitalized at the Institute of Psychiatry in Belgrade when he was diagnosed with psychosis of the schizophrenic cycle. After discharge from the hospital, stable clinical remission persists with maintenance therapy with clozapine. In July 2018, after a short stay abroad, he developed a pronounced behavioral disorganization and was forced to be admitted to our institution.

On admission and in the initial phase of hospital treatment, the clinical picture is dominated by intense psychomotor restlessness, acoustic hallucinatory experiences, dysphoric-euphoric mood, and uncontrolled verbal and physical aggression towards medical staff and other patients. He was treated with clozapine, which was gradually titrated up to 600 mg daily, with benzodiazepine support (lorazepam 10 mg p.d.) without significant improvement, medical sedation, and lithium salts were introduced into the therapeutic protocol.

Immediately afterward, psychomotor inhibition occurs, accompanied by somnolence, mild hypotension, sinus tachycardia, and subfebrile temperatures, without signs of muscle stiffness. Lab. analysis of CpK 628, other findings within reference values. Excluded psychopharmaceuticals from the therapeutic protocol, introduced detox. procedures and III generation cephalosporins, after which the patient’s condition stabilizes.

It is important to bare in mind the possibility of NMS in patients with concomitant use of clozapine and lithium

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Tardive dyskinesia is usually persistent, irreversible involuntary movement of the tongue, lips, face, trunk and extremities in patients taking long-term dopaminergic antagonist drugs. Although it is mostly associated with the use of neuroleptics, cases of tardive dyskinesia existed before the discovery of these agents. Patients with schizophrenia and other neuropsychiatric disorders are particularly at risk for tardive dyskinesia because they are exposed to neuroleptics and anticholinergic agents for longer periods than healthy individuals. Free radicals are thought to be probably involved in the pathogenesis of tardive dyskinesia. Vitamin E is a fat-soluble antioxidant, and it is thought to be effective in the treatment of antipsychotic-associated tardive dyskinesia, as it has a cytotoxic free radical-binding effect.

In this poster presentation, it was aimed to evaluate the clinical results of the treatment of tardive dyskinesia with high-dose vitamin E in four inpatients with serious mental illness and long-term antipsychotic use. In addition, the treatment of tardive dyskinesia will be discussed in the light of current literature data.

In the case report, there are three patients with schizophrenia and one with mild mental retardation. They were treated with 1600 IU of vitamin E per day. The patients continued their vitamin E treatment for 90 days. The severity of tardive dyskinesia of the patients was measured by Abnormal Involuntary Movement Scale (AIMS).

At the end of the 90 day treatment, the AIMS measurements of the subjects decreased 72,7%, 73,3%, 72,2% and 80% respectively.

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In our clinic, we observed that patients using long-term typical antipsychotics were prescribed antipsychotics in unindicated situations or in high doses, patients with high risk for tardive dyskinesia were not taken into consideration when planning treatment, and we encountered cases of tardive dyskinesia despite the widespread use of atypical antipsychotic drugs in hospitalized patients. The use of benzodiazepines is restricted especially in elderly individuals due to their side effects and the risk of addiction in long-term use. Although the clinical importance of vitamin E is unknown, it is preferred because it can be used with a low risk of side effects, considering that it can prolong bleeding time. Although the results of a review of tardive dyskinesia treatment do not suggest that vitamin E reliably improves tardive dyskinesia symptoms, our experience shows that patients benefit from vitamin E treatment. In this regard, there is a need for studies that will be conducted with a large sample and compare the effectiveness of vitamin E with the treatments known to be effective in tardive dyskinesia.

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Neuroleptic malignant syndrome is a rare but also life-threatening adverse reaction associated with mostly antipsychotic use. It is mostly related with the administration of D2 dopamine receptor-blocking antipsychotics or sudden discontinuation of antiparkinsonian drugs.

In this article, we present a 55-year-old male patient diagnosed with schizophrenia who was admitted to the emergency department with acute onset confusion and fever. He had been on haloperidol and quetiapine treatment for several years.

His Creatine kinase (CK) levels were elevated (2928 - 11462 U/l within 1 day. U/l). She was admitted to the intensive care unit with an initial diagnosis of NMS. The patient’s all antipsychotic treatment was discontinued.

At a follow-up examination after 6 days, myoglobin, CK, and leukocyte values were noted to start decreasing. The rigidity and altered mental status improved after 6 days. After 9 days he was discharged. He was admitted to the psychiatry outpatient clinic. He was suffering from auditory hallucinations therefore the antipsychotic treatment has been started and it was planned to reach the target dose of 10mg olanzapine PO by increasing the weekly dose to 2.5 mg. However, due to the increase in the patient’s auditory hallucinations, the treatment was rearranged and the target dose of 15mg was reached. After that, the patient’s positive symptoms regressed significantly. The patient has been on 15 mg olanzapine treatment for the last 1 year with no positive symptoms.

What is the most appropriate treatment choice after NMS? There is no easy, single answer to this question. Although we were aware that there have been reported NMS cases with olanzapine use for this patient it was chosen since it is one of the second-generation antipsychotics that the patient did not use by examining the treatment history. This case shows that this syndrome may develop even after a long and stable neuroleptic treatment and the patient may continue to benefit from different antipsychotic treatments.

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Risperidone is a benzisoxazole derivative and is an antipsychotic drug that is frequently used in psychiatric disorders with high binding to 5HT-2A, D2, α1-adrenergic and α2-adrenergic receptors. It is a second generation antipsychotic and the most common side effects are known as extrapyramidal symptoms, weight gain, sedation, hyperprolactinemia, dizziness, insomnia, anxiety and nausea. Edema has been reported in a few cases as a side effect of risperidone in the literature.

In this case report, we aimed to present a case of peripheral edema developed in a patient using escitalopram combined with risperidone and to review the literature on this subject.

A 48-year-old male presented to the outpatient psychiatry clinic with symptoms of difficulty in controlling his irritability and anger, damaging the things around him, depression, loss of interest and desire, sleep disturbance, fatigue, and feelings of worthlessness. The patient also applied to the psychiatry outpatient clinic with similar symptoms 5 months ago, and had been on sertraline 50 mg/day and quetiapine 25 mg/day since then. But it was learned that he did not benefit, so his treatment was adjusted as escitalopram 10 mg/day and risperidone 1 mg/day. The patient, who came to the outpatient clinic control after 1 month and did not describe a similar complaint before, described peripheral edema that developed approximately 2 weeks after he started using psychiatric medication. On examination, 3+ pretibial peripheral edema was detected. Since the patient had a previous history of escitalopram use, it was recommended to continue escitalopram 10 mg/day treatment, and risperidone 1 mg/day was discontinued and he was called for control.

It was observed that the edema completely resolved within 2 weeks following the discontinuation of risperidone treatment.

In conclusion, risperidone is an antipsychotic frequently used in clinical practice, and edema is a rare but important side effect and can be encountered even at low doses. Despite the low incidence, this side effect should be considered by clinicians. There is a need for controlled studies that explain the relationship between risperidone and edema, elucidate the mechanism of edema and investigate its incidence.

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Long-acting injectable antipsychotics have demonstrated advantages over therapeutic adherence and can reduce the rates of relapses and due to treatment discontinuation. The novel presentation of paliperidone palmitate six-month (PP6M) can simplify the treatment to two injections per year.

The purpose of the present research is to describe the profile of patients receiving this novel treatment in our area. For this, a descriptive study has been carried out.

We have collected and analyzed data from a total of 8 patients from the global long-acting injectable nursing registry in our area. The data collection was from May 2022 to October 2022.

Fig. 1: Sociodemographic characteristics and Fig. 2: Clinical characteristics.

None of the patients required hospitalization at the time of the study, although this work team considers that it is early to make conclusions in this regard. No serious or minor adverse effects were reported in any of the cases during the time of the investigation, apart from one case of mild sedation.

The clinical characteristics of most patients were psychopathological stability and good adherence to previous treatment. Although this study shows that the drug was also used in patients who did not meet these characteristics, specially one case of poor social support. The data collected show that the profile of the patient in whom the drug has been prescribed can be varied and broad.

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Lithium, a mood stabilizer, is a commonly prescribed and effective treatment for bipolar affective disorder. It´s excreted almost exclusively by the kidneys with a half-life primarily determined by renal function. Chronic intoxication results from an insidious accumulation of lithium in a chronically medicated patient (due to a reduction in renal function secondary to volume depletion, a new medication, et cetera). Patients often present with neurologic findings, including tremor, ataxia, dysarthria, confusion and neuromuscular excitability.

The objective of this report is to describe a clinical case of lithium neurotoxicity (myoclonus and encephalopathy), along with a review of the literature on the topic.

We describe a case of lithium neurotoxicity, along with a brief non-systematic review of the literature on lithium toxicity. We conducted a PubMed bibliographic search using keywords such as “lithium intoxication”, “lithium neurotoxicity”, “lithium encephalopathy” and “lithium intoxication treatment”.

A women aged 81 was brought to the emergency department by her daughter following 1 week of asthenia, diarrhoea, periods of confused speech and involuntary movements. In the previous week, the patient had been diagnosed with COVID-19. Her past medical history is significant for bipolar affective disorder, hypertension, diabetes mellitus, dyslipidemia and asthma. The patient has been treated with following drugs: lithium carbonate (no recent change of dose and previous serum levels around 1mmol/L), quetiapine, lisinopril, metformin, simvastatin, formoterol and budesonide. On the first examination, she had an exuberant multifocal myoclonus. Posteriorly, she became somnolent, with language impairment (verbal perseveration, echolalia) and dysarthria. Investigations revealed renal impairment (creatinine 1,5 mg/dL, blood urea nitrogen 42 mg/dL) and supratherapeutic lithium levels (lithium serum level 1,7 mmol/L). Computed tomography scan of the brain was negative for acute injuries. The electroencephalogram showed triphasic waves (1-1,5 Hz). Encephalopathy secondary to lithium intoxication was diagnosed (probably in the context of acute kidney injury precipitated by hypovolaemia – diarrhoea). Lithium was stopped and intravenous isotonic fluids were given. After 1 week, her myoclonus resolved and over the following week the other signs resolved as well. The patient was later discharged to her daughter’s home, with follow-up neurology and psychiatry visits.

Both reversible and irreversible neurotoxicity related to lithium have been reported, specially occurring alongside chronic intoxication. If not addressed, impaired consciousness can lead to coma and death. A high clinical suspicion is needed for prompt diagnosis and treatment (intravenous fluids and sometimes haemodialysis are warranted).

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Clozapine is an effective Atypical antipsychotic used in the treatment of resistant schizophrenia .However it can induce liver dysfunction from a simple transient asymptomatic cytolisis (30 to50 %) toa serious fulminant liver failure (0.001 %).

To show the heptotoxicity potential of Clozapine and adress the importance of monitoring the liver function tests in clozapine titration to prevent sever conditions

A case report of a fifty-year old Tunisian male patient diagnosed with resistant schizophrenia who developed a hepatototoxicity under a low dose of clozapine within five days of treatment .

Mr F is a 50 year old patient diagnosed with schizophrenia in 2018 . He had received various antypical and typical antipsychotic treatments including ( Haloperidol , Risperidone , Amisulpride , Olanzapine ) at effective doses and minimal periods of six weeks . He had no history of systemic diseases or substance use disorder . He smokes 10 cigarettes a day . He had a history of hepatotoxicity on olanzapine. These medications have failed to resolve the persecutory delusion and auditory hallucinations , and the trial of clozapine was institued . Baseline examination and laboratory tests were normal . The previous antipsychotic medication was not continued and a dose of 25 mg clozapine was administred . A marking drowsiness was present in the fisrt days , so we decided to keep the same dose . Five days later , he had high levels of Liver function test (LFT) : Elevated aspartate ( 5 times above normal) and alanine aminotransferase levels (4 times above normal ) , white blood cell count and bilirubine levels were normal . He had no fever or jaundice . The abdominal examination showed a mild sensiblity in the right upper quadrant . Clozapine was immediatly discontinuated . 24 hours later LFT continued to escalate to 5 times greater then normal . Then it decreased continueosly

Clozapine has a potential of hepatotoxicity even at lower dose . Screening liver function tests must be integrated in survey recommendations of clozapine treatment . Further researches must be conducted to understand the mechanism of this side effect in order to avoid sever conditions .

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Antipsychotic medications remain the mainstay of the treatment of various psychiatric disorders, particularly schizophrenia. However, this therapeutic class can induce a range of side effects. Although the treatment with second generation antipsychotics includes a lower risk for extrapyramidal symptoms as compared to first generation antipsychotics, there are numerous adverse events that can result from atypical antipsychotics. Since the introduction of clozapine, there has been increased awareness regarding antipsychotic-induced hematological side effects.

The objective of this case report is to highlight the importance of the management of antipsychotic-induced neutropenia.

We report a patient with history of schizophrenia who developed neutropenia induced by Haloperidol, Chlorpromazine, Olanzapine, Amisulpride and Aripiprazole.

We present a case of a 43-year-old male patient with a history of schizophrenia, admitted in our department for the management of a state of agitation in the context of a relapse of his condition. On admission, the patient experienced psychotic symptoms, including delusions and auditory hallucinations, in addition to negative symptoms, such as affective flattening, alogia, avolition and asociality. He was then started on 12 mg of Haloperidol and 200 mg of Chlorpromazine with a white blood cells count (WBC) of 5.98 x 109/L and absolute neutrophil count (ANC) of 2.52 x 109/L (WBC reference range: 4.0-10.0 x 109 /L; ANC reference range: 1.5-7.0 x 109 /L). The patient did not report adverse events on this medication.

15 days into hospitalization, a mild neutropenia was detected (WBC=3.92 x 109 /L and ANC=1.01 x 109 /L), leading to a discontinuation of the antipsychotic treatment. No signs of infection were found. After one month, the patient had a normal WBC and ANC. Aripiprazole was discussed as a first alternative and was begun at 5 mg/day and then at 10 mg/day. After one week of treatment with Aripiprazole, the patient’s WBC was normal, but the ANC decreased again leading to a moderate neutropenia (ANC=0.91x 109 /L). The antipsychotic treatment was once again discontinued and the hematological evaluation found no other identifiable cause. Afterwards, neither Olanzapine nor Amisulpride showed significant response to this adverse effect. Finally, the administration of Risperidone led to a positive outcome on the WBC and the ANC.

Awareness regarding the hematological side effects of antipsychotics should increase and clinical management of this type of adverse event should be a subject of interest among psychiatrists.

None Declared

Bipolar Affective Disorder(BAPD) is characterized by variations in mood from elation and/or irritability to depression.Valproic acid(VPA) is indicated for the treatment of acute manic episodes in BPAD.The use of VPA can be limited by either loss or lack of efficacy or by adverse drug reactions. Stevens-Johnson syndrome(SJS) toxic epidermal necrolysis(TEN) are the rare but fatal cutaneous adverse drug reactions for VPA.

We wanted to draw attention that drug induced bullous lesions which has been seen rarely in the literature caused by valproic acid in bipolar disorder.

We examined the side effects of valproic acid in one of our patients with bipolar affective disorder using our observations and laboratory tests.

A 41 year old man was admitted to the our hospital with complaints of decreased amount of sleep, increased amount of speech, skepticism,irritability and dysphoric mood.The patient who was followed up with a diagnosis of BPAD for about 10 months,attempted suicide by taking lithium 2 days before his hospitalization.Considering that it was a mixed episode and the prophylactic effect of lithium was insufficient,VPA 1000 mg/day and Risperidone 2 mg/day treatment were started.Risperidone was increased to 4 mg/day because psychotic symptoms persisted.Valproic acid dose was increased to 1000 to 1500mg/day after the Valproic acid blood level reached 55.28 in the follow-ups.After 5 days 2 bullous lesions developed on the lower extremity of the patient.Routine laboratory investigations were within normal limits.When we consult the patient with the dermatologist;the dermatologist recommended that the lesion be fixed drug eruption and that valproic acid should be discontinued if possible.It was thought that the lesions of the patient who did not have dermatological disorders and did not describe insect bites,might be due to valproic acid. In addition to all these,the patient’s mother had pemphigus vulgaris.The patient’s valproic acid drug was discontinued and lithium was started.Risperidone treatment was continued.In the follow-ups,the patient’s bullous lesions regressed and no new lesion formation was observed.

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The differential diagnosis of bullous lesions at first may appear overwhelming.In this case traumatic bulla,Pemphigus vulgaris,drug induced bulla,Fixed drug eruption,Steven Johnson Syndrome were among our prediagnosis.Cutaneous drug eruptions associated with VPA can range from maculopapular eruption to severe Stevens-Johnson syndrome or toxic epidermal necrolysis.We were worried that the patient had SJS, but it remained only bullous lesions.We could not biopsy the patient lesions to understand the underlying cause but development of bullous lesions with the initiation of valproate and subsequent remission of the lesions with the discontinuation of the drug and subsequent course clearly suggests a causal relation between valproate and skin lesions.

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A 28-year old male patient was admitted involuntarily to the 4th PICU of the Mental Health Hospital of Thessaloniki, due to severe psychotic symptoms and disorganised behaviour. Upon mental health examination the symptoms included auditory hallucinations, tangible speech, delusional ideas of somatic and persecutory type and significant neglect of his personal hygiene. The onset of his psychotic illness was 3 years prior, with two hospitalizations in the UK, and several unsuccessful attempts of outpatient monitoring.

The study of persistent hiccup as an adverse effect of antipsychotic medication.

Monitoring for adverse effects during admission.

On the 8th day of admission, oral olanzapine 10 mg was commenced at night. On the 9th day, olanzapine was increased to 20 mg per day. Discontinuation of intramuscular medication occurred on the 16th day. After presenting no clinical improvement for 27 days with the administration of olanzapine as monotherapy, amisulpride at 2ml per day was initiated alongside the Olanzapine. In the context of medication titration, amisulpride reached 8ml per day, equivalent to 800mg per day after 2 months of hospitalisation.

Apart from minor constipation, no other gastrointestinal health problems were reported in his records. The onset of the hiccups occurred along the dosages of 800mg/day of amisulpride and 20mg/day of olanzapine.

There was a satisfactory response to treatment evidenced by a 30% reduction on the Positive scale of the PANSS, however, the hiccups did not recede.

None Declared

Patients taking lithium complain of cognitive impairment. This was assumed to be real by expert clinicians for years until relatively recent objective neuropsychological studies have failed to verify much impairment.

Second and perhaps underemphasized side effect from lithium is sexual dysfunction.

The objective of this review is to highlight for the cognitive and sexual problems, which are two very important areas for discussion with patients. It should be brought up right when beginning to prescribe.

Data was obtained through an internet-based literature review, using the research platform PubMed and the World Health Organization website. Eight articles from the last five years were included.

Due to the lack of evidence in neuropsychological studies, what was considered to be impaired cognitive function in the past has been recently considered a loss of sharp thinking in manic states or mild persisting depressions.

About sexual dysfunction it is important eliminating other possible causes, lowering lithium dose, timing sex, and taking sildenafil and 240 mg/day of aspirin may help.

Cognitive impairment and sexual problems are two important subjects that involve the issues of dosing, of managing and dealing with people’s willingness to take lithium.

Providing psychoeducation about these possible effects can head off abrupt discontinuation impulses.

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Aripiprazole is the third generation Antipsychotic, and Dopamine serotonin system stabiliser.It is partial agonist at D2 and 5 HT1 A and antagonist at 5 HT2.Most commonly seen adverse effects are Akathesia, fatugue,insomnia and headache the major advanatage is less propensity for extrapyramidal side effects and lmetabolic side eefects.

To report a case of Schizophrenia treated with Aripiprazole 15mg/day developiing occular gyric crisis which was tratment resistant.

We administered Electroconvulsvive therapy, bidirectional brief pulse constant current 8 ECTS, under General anesthesia with medical fitness .

Patient Showed complete resolution of Dystonia after second ECTs and Showed improvment in Pyschosis Parameterd. Assessment using Naranjo Protocol made.

Electroconvulsive therapy therapy is viable alternative to manage Dystonia when medical treatment fails

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Aripiprazole is a third generation atypical antipsychotic and a dopamine serotonin system stabilizer, effective against positive and negative symptoms of schizophrenia. Within the group of atypical antipsychotics, aripiprazole shows a relatively benign safety profile (e.g. lower metabolic impact, mild effect on cardiovascular parameters), although the reported rate of extrapyramidal side effects is measurable.

Oculogyric crisis (OGC) is a rare movement disorder characterized by a prolongued involuntary upward deviation of the eyes, lasting minutes to hours. In most cases, OCG is a drug-induced adverse event with acute or tardive onset often attributable to a functional impairment of dopaminergic neurotransmission.

OGC is seldom reported in children and young adults during treatment with aripiprazole, althouh it is commonly used in youths.

We report a case of an aripiprazole-induced oculogyric crisis in a 19 year old girl who diagnosed with schizophrenia (paranoid).

There was a complete remission of the OGC’s following aripiprazole dose reduction, suggesting the clinical manifestation was a dose-dependent phenomenon.

The present report should raise awarness among clinicians for this relevant possible adverse event, that can happen also with the use of aripiprazol, not only with typical or more antidopaminergic antipsychotics. Future research in the field should emphasize neurobiological dysfunctions as the basis of EPS/OGC in patients.

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The decreased capacity of testing reality causes patients with psychosis consequences regarding their families, professional life, and social interactions, with an overall reduction in quality of life. In these cases, antipsychotic treatment is mandatory to recreate the patient’s connection with the environment. Second-generation antipsychotics (SGAs), particularly clozapine and olanzapine, can have severe metabolic side effects that impact body weight, insulin resistance, and glucose metabolism. The specific mechanism that determines such metabolic processes is not yet fully understood. Recent research has demonstrated that metformin may be utilized to regulate metabolic processes. The ultimate purpose of using this adjunctive therapy is to effectively control both physical and mental health difficulties among psychiatric patients.

The primary purpose of this report is to underline the importance of adverse metabolic reactions of antipsychotics and to study the effectiveness of metformin regarding this matter.

Our patient is a 33 years-old man who was diagnosed with schizoaffective disorder around the age of 32. He was initially treated with olanzapine; during the first year, he gained more than 20kg. Severe weight gain was a significant health factor that determined us to search for therapeutic alternatives. Metformin was added, monitoring BMI and abdominal circumference. Because of the severe body weight gain, switching from olanzapine to aripiprazole was attempted, but the psychiatric symptoms worsened. Paliperidone was considered and administered, concomitant with rising doses of metformin. Although an initial increase in body weight was documented when paliperidone was administered, his body weight deescalated significantly after metformin reached a therapeutic dose of 2000mg per day.

Metformin co-administered with antipsychotic medication helped to control the severe metabolic adverse effects in this case. Reaching a lower BMI index after adding metformin to paliperidone was a therapeutic goal and essential for the patient’s physical and psychological health.

Metformin is a complex treatment widely prescribed as an antidiabetic drug. Lately, attention has shifted towards its effects on controlling the adverse metabolic effects of antipsychotics. This case underlines the importance of the metabolic syndrome as an adverse reaction of the SGAs and presents the results of this treatment option for schizoaffective disorder treated with antipsychotics. Although the current recommendation is to switch to another antipsychotic with lower metabolic risk, the new drug may not control the psychiatric symptoms in all cases. Therefore, metformin is an adjuvant solution in situations where antipsychotic treatment can cause severe metabolic reactions with a significant impact on the patient’s physical health.

None Declared

Several studies have shown that ketamine, an NMDA receptor antagonist, represents a promising alternative in treating depression and suicide. The intranasal or intravenous use of ketamine, currently used, has limitations in terms of cost and complexity. The subcutaneous (SC) route may be an affordable alternative for the treatment of depression and suicidality.

To evaluate the response of SC ketamine (0,5 mg/kg) applications on depressive, anxiety, and suicide symptoms.

A patient with unipolar depression and suicide attempt was submitted to 3 sessions of SC ketamine (0,5 mg/kg). The applications had 2 days of intervals. Clinical evaluations were measured by BDI, BSI, and BAI. The vital signs were monitored under 2 hours after injections and the potential side effects.

Changes in measurement instruments according to applications can be seen in Tab 1:

The average measurements of vital signs during 2 hours of monitoring for each application can be seen in Tab 2:

The use of SC ketamine showed remission in BDI, BSI and BAI, respectively demonstrated safety in use.

None Declared

The use of selective serotonin reuptake inhibitors (SSRIs) has increased exponentially and worldwide in the last decade. Taking into account their tolerability and safety profile, they constitute the first line, in all age groups and in polimedicated population, for treatment of depressive, anxious, and phobic disorders, among others. Although safe, especially when compared to first generation antidepressants, they are not totally exempt of adverse effects, and may cause, especially in this context, some degree of cognitive impairment, which may or may not be completely reversible. On the other hand, and despite the controversy related to the subject, some studies suggest a possible protective effect of this pharmacologic class regard the development of cognitive disfunction, which, although not very consistent, should not be neglected.

To understand the cognitive impact of short- and long-term use of SSRIs, given the increasing use in an aging, polymedicated population.

Brief sistematic review of selected articles from Pubmed, Medline and Uptodate databases, with the keywords “SSRIs”, “cognitive”, “impairment”, “adverse effects”, “dementia”.

SSRIs are not entirely exempt from cognitive effects, despite their recognized safety profile. Some of the adverse effects typically related to the class, such as hyponatraemia, especially when insidious and silent course, as well as anticholinergic activity (typically associated with first generation antidepressants, but not exclusive) interfere with global functionality and may clinically present as mild cognitive impairment or even major neurocognitive disorders. Furthermore, given their potential to induce or inhibit the cytochrome P450 system, they are significantly implicated in pharmacokinetic drugs interactions that increase cognitive burden associated with other psychotropic drugs.

In the long term, and in certain patient populations, it has been hypothesized that they may exert some protective effect on physiological and pathological cognitive functions decline, by preventing neuronal death, acetylcholine decrease and amoyloidogenesis.

Despite their benign adverse effect profile, when compared with tricyclic antidepressants, SSRIs are not devoid of adverse effects on cognitive domains. However, and despite contradictory and inconsistent results, when well tolerated, SSRIs may confer benefits in terms of preserving global functionality, far beyond the affective symptoms resolution that motivated their introduction in the first place.

None Declared