Frontotemporal dementia(FTD) is the prevalent type of primary progressive dementia. Psychiatric symptoms can be seen in FTD. So it can imitate psychiatric disorders and be misdiagnosed. However, few studies have investigated the underlying cause of misdiagnosis.

The primary aim of this study was to identify the prior psychiatric diagnoses of patients before receiving a definitive diagnosis of FTD and the main reasons to cause diagnostic delay.

We screened through the records of patients who were admitted to our psychiatry outpatient or inpatient clinic from January 1st, 2018 to June 30th, 2021. The patients with FTD were included in our study.

Our sample consisted of 13 patients with FTD(mean age= 54.77 ± 12.22, 7 females). Psychiatric misdiagnoses were depression(n=6), psychosis(n=5), bipolar affective disorder (n=5), conversion disorder(n=4), and malingering(n=1). As we looked at the first symptoms of the patients, it was revealed that 9 of 12 patients presented with depressive symptoms or at least experienced a short depressive period at the beginning of their behavioral changes. Interestingly, 8 of 12 patients had given a history of stressful life events just before their complaints emerged, which was thought the main misdirector for physicians. The average delays in diagnosis were 14.58(±16.93) months in the psychiatry clinic, 5.66(±11.02) months in the neurology clinic in our hospital.

Our study suggests that the depressive episode preceding behavioral changes may be the prodromal stage for fully developed FTD. Moreover, the depressive episode and the history of stressful life events appear to mislead clinicians in diagnosing FTD.

No significant relationships.

Autoimmune encephalitis are inflammatory diseases of the CNS mediated by antibodies that attack neurotransmitter receptors or proteins on the surface of neurons, usually in the limbic system. The clinic is different according to the antineuronal Ac involved.

To make a correct differential diagnosis between autoimmune encephalitis and primary psychiatric pathologies that may be similar in symptoms through a complete study of the patient including anamnesis, physical examination, imaging tests, cerebrospinal fluid and serum studies.

Description of a clinical case. A 31-year-old female patient, with no previous history of interest, was brought to the emergency department for a suspected seizure. The previous days she had presented emotional lability, difficulty in concentration and reading, blurred vision, confusion and hemicranial headache. Two days later she returned to the emergency room for insomnia, dysarthria, difficulty in reading, comprehension, naming, and excessive rumination of her problems. Incoherent and repetitive language. The Emergency service requested to rule out a conversive disorder.

Neuropsychiatric manifestations (anxiety, depression, behavioral disturbances, insomnia, memory deficits, psychomotor agitation, mania, auditory and visual hallucinations, delusions) are the first symptom in 70% of autoimmune encephalitis due to anti-NMDA antibodies and usually respond poorly to psychiatric treatment, making the treatment of the primary cause necessary for the remission of these symptoms.

Given their increasing recognition and prevalence, autoimmune causes should always be taken into account in behavioral changes, cognitive or consciousness impairment of subacute installation, especially in young patients and once infectious, metabolic and vascular causes have been ruled out with an appropriate complementary study.

No significant relationships.

Frontotemporal dementia (FTD) is common in presenile population. The overlapping symptoms with other psychiatric disorders can lead to wrong/late diagnosis which cause delays/difficulties regarding case-management. Especially, long-standing and/or late-onset depression can descriptively envelop bvFTD (behavioral-variant) and leads to unnecessary treatments and increased distress. It’s important to implement a descriptive diagnostic algorithm which will help clinicians to distinguish the phenomenology of these disorders.

This presentation aims to call attention of the clinicians/researchers to an elaborated effort concerning differential diagnosis of two common disorders with overlapping features through a case-study of a 59-year-old male patient.

One case from an inpatient unit of a psychiatric clinic in Lower Saxony, Germany will be reported.

Case: The patient was referred to our acute-psychiatric-ward from the day-clinic-unit because of treatment-resistant, severe and long-lasting depressive symptoms. He was depressed, desperate, hopeless, listless and had suicidal thoughts. During the first days of treatment, symptoms like apathy, bad hygiene, weird eating-behavior, urinary incontinence, lack of empathy, language disorders and other behavioral symptoms were evident. Brain-MRI yielded frontotemporal lobar atrophy. Trail-Making-Test and Frontal-Assessment-Battery showed pronounced impairment of executive functions. Mini mental state examination and DemTect yielded light to moderate memory dysfunction. Diagnostic Criteria for Probable bvFTD (International-Consensus-Criteria) were fulfilled.

The diagnosis of bvFTD enabled a rapid assignment of a legal representative and relieved the long-lasting discomfort of the patient and his family that was caused by multiple unsuccessful treatment trials against depression. The differential diagnostic frame between bvFTD and depression will be discussed in view of the current literature.

No significant relationships.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized with ritualized behavior, difficulties in communication/ social interaction, restricted interests, and sensitivity to external stimuli. The ASD has gained attention in recent years, however it’s still difficult in geropsychiatric setting to identify high-functioning ASD, especially when patients’ coping mechanisms are successful. Not to determine high-functioning ASD structure in older age can lead to wrong diagnosis and inappropriate treatment trials.

The aim of this presentation is to emphasize the importance of the evaluation of ASD-structure in old-age-psychiatry through the case study of a 65-years-old man.

One case report from the inpatient unit of a psychiatric clinic in Lower Saxony, Germany will be presented.

Case: The patient was referred to our acute-psychiatric-ward due to delusional thoughts, depressive symptoms and lorazepam dependency. Delusional disorder was diagnosed in the outpatient-setting since he had interpreted some external stimuli in an eccentric way. During the therapeutic process, some features of high-functioning ASD such as social difficulties, dislike of change and repetitive/restrictive habits were prominent. Developmental history of the patient and the Autism-Spectrum-Quotient-50 also supported the clinical diagnosis of the ASD. Delusional disorder was excluded, and the therapy organized according to the structure characteristics of the high-functioning ASD which yielded to significant amelioration of depressive symptoms and increased perceived life quality of the patient.

Although coping mechanisms of the patients can be successful, identifying high-functioning ASD-structure even in an old-age can be quite helpful in diagnostic/therapeutic processes. An elaborate discussion of the subject through contemporary literature will be presented.

No significant relationships.

Bipolar disorder (BD) is considered a risk factor for developing Parkinson’s Disease (PD) because of an altered dopamine activity in both entities. Comorbidity may delay diagnosis and difficult therapeutic management.

To describe the case of a patient with both BD and PD and to determine the appropriate diagnostic and therapeutic approach for patients presenting both entities.

We present the case of a 58-year-old woman attended in our neurology unit due to the initial presence of visual hallucinations as a core symptom.

Psychotic symptoms as hallucinations and off-times, frequently observed in PD, may be misdiagnosed with a worsening of depressive polarity of BD. Thus, overlap between symptoms may lead to a challenging differential diagnosis. Moreover, there is no consensus about the therapeutic management of the comorbidity, due to the bidirectional worsening of symptoms when treatment is adjusted. In our case, a diagnosis of dopaminergic psychosis was made so antipsychotic treatment with quetiapine 50 mg/d was initiated. A worsening of symptoms was observed, presenting the patient a stuporous status, mutism and generalized rigidity. Neuroimaging and lumbar puncture were performed showing no alterations; electroencephalogram showed diffuse slowing. Final diagnosis was an off-episode of PD and a multifactorial encephalopathy resulting in visual hallucinations.

Coexistence of PD and BD may lead to a diagnostic and therapeutic delay and therefore a worse prognosis. Although these diseases are well-known, it is still challenging to manage patients presenting both entities. Further research is needed to clarify the proper diagnostic and therapeutic approach for these patients.

No significant relationships.

Autism spectrum disorders (ASD) is one of the most urgent problems of psychiatry because of their high prevalence, diagnostic difficulties as well as insufficient knowledge of the pathogenetic mechanisms.

To determine the number of inflammation markers in patients with various forms of ASD in links with features of a clinical condition for creating diagnostic criteria for differential diagnosis and improve reliability.

The clinical examination of patients (135 children with various ASD forms) was carried out by using psychometric scales (CARS, BFCRS, CGI-S). The activity of inflammation markers (LE and α1-PI) and the level of autoantibodies to S-100b and MBP were measured in plasma. Complex evaluation of immune system activation was also conducted, taking into consideration interactions of innate and adaptive immunity.

Non-psychotic ASD forms (Asperger’s syndrome and Kanner’s syndrome) were not accompanied by a change of the immunological indices in comparison with control. In psychotic ASD forms, a significant increase of the studied indices was revealed (р<0.05). Correlation between the complex evaluation of the immune system activation and the stage of the disease (r=0.49, р<0.05) was demonstrated. Also the significant correlations between the severity of autistic disorders according to CARS (r=0.48, p<0.05), catatonic disorders by BFCRS (r=0.42, p<0.05), and the assessment by CGI (r= 0.61, p<0.05) were observed.

The immune markers as well as their complex evaluation may be used as additional diagnostic criteria in the clinical examination for differential ASD diagnostics and assessment of the quality of remission, and also monitoring of the patient condition.

No significant relationships.

Dissociative seizures (DS) are classified as dissociative convulsions within the group of dissociative disorders. Although they share many features with epileptic seizures (ES), they are not a consequence of abnormal brain discharges and may be related to psychogenic causes. DS represent a common diagnostic and are often confounded with ES.

The aim of this study is to review the current evidence about the differential diagnosis between DS and ES.

We conducted a non-sytematic review on the topic, using Pubmed/Medline database.

Studies emphasize a correct diagnosis before treatment of seizures. DS and ES respond differently to anticonvulsant medication and early or incorrect prescription of can even exacerbate DS. Clinical features and a neuropsychiatric history can also help. The presence of a dissociative “stigmata”, such as unexplained sensory loss, may support a non-epileptic diagnosis. EEG videorecording method is the gold standard diagnosis for DS, however often displays rhythmic movement artifacts that may resemble seizure activity and confound the interpretation. The absence of ictal EEG discharges characteristic of epilepsy is a sign of DS. However, this may not be true for some partial ES, particularly those from temporal lobes, whom also tend to report shorter duration of seizures, whereas patients with DPD often describe experiences lasting for hours or longer.

Distinguish DS from ES can be challenging. However, there are features that can help in the differential diagnosis. A correct diagnosis is essential for an adequate therapeutic approach, better prognosis, reduction of medical costs and also a referral to the right medical specialty.

No significant relationships.

The identification of potential biomarkers is crucial to improve the management and treatment of mood disorders. Glycogen synthase kinase-3 (GSK-3) is a multifunctional enzyme with an important role in the etiology of mood disorders. Recent findings suggested GSK-3 as a putative biomarker in mood disorders.

The aims of the study are: - to evaluate GSK3 as potential biomarker for differential diagnosis (MDD and BD); - to analyze the regulation of GSK3 by psychopharmacological treatments.

Patients included fulfill the following criteria: (a) principal diagnosis of MDD or BD (DSM-5); (b) age ≥ 18 years; (c) drug-free for at least 4 weeks before the inclusion. For each patient included a healthy control is enrolled, matched by gender and age. All included subjects at the study entry point (t0) are assessed through: - semistructured clinical interview and clinical rating scales (Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale; Young Mania Rating Scale, Clinical Global Impression) - blood draw, to measure GSK-3 levels Patients with MDD or BD are assessed again after 1 week (T1) and after 2 month (T2) of specific pharmacological treatment.

So far, we enrolled 16 patients and 16 healthy controls. The enrollment is still ongoing.

We expect to find GSK-3 levels differently expressed between healthy controls, patients with DDM and patients with BD. This finding would be crucial as it could contribute to the improvement of differential diagnosis. Moreover, we expect to observe a change in GSK-3 levels after psychopharmacological treatments.

Capgras syndrome, where patients have the conviction that one or more close people have been replaced by a “double,” is the most prevalent delusional misidentification syndrome. It appears in psychiatric illness and organic brain damage. It seems to be due to damage of bifrontal and right limbic and temporal regions, mainly in the right hemisphere.

To review the pathologies associated to Capgras Syndrome and the relevance of the differential diagnosis

53-year-old female was admitted due to great sadness, crying, social withdrawal and severe paranoid concerns over the last month. Follow-up in Mental Health since 2014, because of anxious depression. After her mother’s death, she felt being followed because of old faults. Since then, low dosis of antipsychotics were used. Now she is afraid of being harmed in relation to petty thefts she committed over 15 years ago. In recent days, she has been noticing small details indicating that her family members have been impersonated by strangers, showing anguish regarding their whereabouts.

During her admission, high doses of antidepresants and paliperidone 6 mg/day were used with the complete disappearance of Capgras Syndrome and her anguish. Mild guilty thoughts were present after her discharge. That is why she was diagnosed with psychotic depression.

Capgras syndrome can be encountered in primary psychiatric diagnosis (particularly in schizophrenia and mood disorders) – where an organic element may exist in about a third of all cases – or secondary to organic disorders or medication-induced, through to overt organic brain damage, particularly in neurodegenerative disease.

No significant relationships.