Barış Önen Ünsalver

Psychiatric Morbidity and its Effect on the Quality of Life of Patients with Chronic Hepatitis B and Hepatitis C

Objective: The primary aim of our study was to determine the prevalence of psychiatric morbidity in a cohort of consecutive chronic hepatitis patients not receiving antiviral therapy. The secondary aim of our study was to determine if psychiatric morbidity, type of hepatitis, and the level of depression correlated with health-related quality of life (HRQL). Methods: The study was conducted in collaboration with Hepatology and Infectious Disease Clinics at three-major university hospitals. One hundred seven patients who met the criteria for being diagnosed with either chronic hepatitis B or C, had non-cirrhotic compensated liver disease, had not received antiviral treatment in the preceding 6 months, and had no accompanying physical illness were included in the study. The Structured Clinical Interview for DSM-IV Axis I Disorders, the Short Form — 36 for measuring HRQL, and semi-structured interviews for assessing psychosocial variables were used. Sixty-seven healthy adults formed the control group. Results: 43.9% of the patients had hepatitis B, 56.1% hepatitis C. A psychiatric diagnosis was made in 48.6%, of which 15% was depression. No significant difference was found in the rate of psychiatric diagnosis between hepatitis B and hepatitis C patients. Hepatitis B and C patients were found to vary significantly (p < 0.001) from the control group on all subcategories of quality of life criteria. Psychiatric morbidity (mainly depression) was the major variable on lowering HRQL (p = 0.000). Conclusions: Chronic hepatitis B and C patients presented a high rate of psychiatric disorder. HRQL was significantly decreased in patients with psychiatric morbidity.

Neural synchronization as a hypothetical explanation of the psychoanalytic unconscious

Cognitive scientists have tried to explain the neural mechanisms of unconscious mental states such as coma, epileptic seizures, and anesthesia-induced unconsciousness. However these types of unconscious states are different from the psychoanalytic unconscious. In this review, we aim to present our hypothesis about the neural correlates underlying psychoanalytic unconscious. To fulfill this aim, we firstly review the previous explanations about the neural correlates of conscious and unconscious mental states, such as brain oscillations, synchronicity of neural networks, and cognitive binding. By doing so, we hope to lay a neuroscientific ground for our hypothesis about neural correlates of psychoanalytic unconscious; parallel but unsynchronized neural networks between different layers of consciousness and unconsciousness. Next, we propose a neuroscientific mechanism about how the repressed mental events reach the conscious awareness; the lock of neural synchronization between two mental layers of conscious and unconscious. At the last section, we will discuss the data about schizophrenia as a clinical example of our proposed hypothesis.

The Soul, as an Uninhibited Mental Activity, is Reduced into Consciousness by Rules of Quantum Physics

This paper is an effort to describe, in neuroscientific terms, one of the most ambiguous concepts of the universe—the soul. Previous efforts to understand what the soul is and where it may exist have accepted the soul as a subjective and individual entity. We will make two additions to this view: (1) The soul is a result of uninhibited mental activity and lacks spatial and temporal information; (2) The soul is an undivided whole and, to become divided, the soul has to be reduced into unconscious and conscious mental events. This reduction process parallels the maturation of the frontal cortex and GABA becoming the main inhibitory neurotransmitter. As examples of uninhibited mental activity, we will discuss the perceptual differences of a newborn, individuals undergoing dissociation, and individuals induced by psychedelic drugs. Then, we will explain the similarities between the structure of the universe and the structure of the brain, and we propose that consideration of the rules of quantum physics is necessary to understand how the soul is reduced into consciousness.

Affect development as a need to preserve homeostasis

In this review, we aim to present our hypothesis about the neural development of affect. According to this view, affect develops at a multi-layered process, and as a mediator between drives, emotion and cognition. This development is parallel to the evolution of the brain from reptiles to mammals. There are five steps in this process: (1) Because of the various environmental challenges, changes in the autonomic nervous system occur and homeostasis becomes destabilized; (2) Drives arise from the destabilized homeostasis; (3) Drives trigger the neural basis of the basic emotional systems; (4) These basic emotions evolve into affect to find the particular object to invest the emotional energy; and (5) In the final stage, cognition is added to increase the possibility of identifying a particular object. In this paper, we will summarize the rationale behind this view, which is based on neuroscientific proofs, such as evolution of autonomic nervous system, neural basis the raw affective states, the interaction between affect and cognition, related brain areas, related neurotransmitters, as well as some clinical examples.

Polydipsia as a Precursor of Manic Episode in Bipolar Affective Disorder Patients with Alcohol Use Disorder

Bipolar affective disorder (BD) diagnosis and initiation of appropriate treatment are often delayed, and this is associated with poorer outcomes, such as rapid cycling or cognitive decline. Therefore, identifying certain warning signs of a probable successive episode during the inter-episode phase is important for early intervention. We present the retrospective data of three cases of BD. Our first case had a history of alcohol use disorder (AUD), where he drank in a dipsomaniac manner, and the other two cases had dipsomaniac alcohol use before their manic attacks, and none of them had any AUD after the mood episode was over. Two brothers also had hypertensive episodes during the manic attacks. None of the cases reported increased fluid intake when they were euthymic. We suggest that polydipsia in BD may be a warning sign of an upcoming manic episode, especially in those patients with AUD. Polydipsia in BD may be caused or facilitated by a combination of hyperdopaminergic activity, hypothalamic dysfunction, and dysregulated renin-angiotensin system. To be able to prevent new episodes, a patient’s drinking habits and change in fluid intake should be asked at every visit. Those patients with a history of alcohol abuse should especially be informed about polydipsia and manic episode association.

Major depressive disorder with religious struggle and completed suicide after hair transplantation

Objectives: Psychological outcomes of aesthetic surgical procedures like hair transplantation are mostly positive including decreased anxiety, depression and social phobia and increased general well-being, self-efficacy and self-esteem. However, some patients may suffer from post-surgical depression and post-surgical increased suicide rates have been reported for breast augmentation patients. Difficulty adapting to the new image, unfulfilled psychological needs expected to be met by the surgery, side effects of the surgery like tissue swelling or bruising, uncontrolled pain, presence of body dysmorphic disorder and previous history of mood disorder may be some of the risk factors for post-surgical depression. Methods: Here, we present a case without prior psychiatric history who developed major depressive disorder after hair transplantation and died of suicide. Results: He started experiencing religious struggle related to his decision about the hair transplant which he interpreted as acting against God’s will. While religious involvement has been reported to be a protective factor against depression, spiritual struggle, which includes religious guilt, has been described as an important risk factor for depression, hopelessness and suicidality which might explain the severity of depression in our patient. Conclusions: This case highlights the importance of a detailed psychiatric evaluation and exploration of religious concerns of any patient before any type of aesthetic surgery. Major depressive disorder is a treatable condition; however, mild depression can go unnoticed. Religious belief and related religious practices affect an individual’s personal health attitudes; therefore, we think that every physician is needed to explore the religious concerns of any patient during any medical examination or surgical procedure. Relevant religious authorities should be consulted when necessary.

Seasonal mood changes in patients with obsessive–compulsive disorder

Obsessive-compulsive disorder (OCD) is frequently associated with mood disorders. However, to date, the co-occurrence of OCD with seasonal affective disorder (SAD) has not been investigated. We have aimed to estimate the prevalence of seasonal mood changes in patients with OCD and explore the contribution of seasonality in mood to the severity of OCD. The Seasonal Pattern Assessment Questionnaire (SPAQ), the Yale-Brown Obsession and Compulsion Scale (Y-BOCS), the Hamilton Depression Rating Scale-17 Items (HDRS-17), and the Beck Anxiety Inventory (BAI) were administered to patients with OCD (n=104) and controls (n=125). The degree of seasonality was measured by the Global Seasonality Score (GSS) calculated from the SPAQ. SAD and subsyndromal seasonal affective disorder (S-SAD) were significantly more prevalent in patients with OCD (53%, n=55) than controls (25%, n=31). When patients were assessed in the season in which SAD occurs, depression and compulsions (but not obsessions, OCD or anxiety) were more severe than those assessed in a season during which SAD does not occur. SAD frequently co-occurs with OCD and, given this co-occurrence, depression symptoms in some patients with OCD might be expected to vary on a seasonal basis.

Repeated Transcranial Magnetic Stimulation as a Successful Augmentation Strategy in a Patient with First Episode Psychosis

Repeated transcranial magnetic stimulation (rTMS) is a non-invasive brain stimulation method that may be preferred as an augmentation strategy for psychiatric patients who may not have responded well enough to psychotropic drugs. In psychoses rTMS may act via changing cortical excitability, connectivity and plasticity. rTMS may induce transcallosal inhibition and antipsychotic drugs may extend the duration of this inhibition. We present a first episode psychosis patient initially unresponsive to antipsychotic treatment, in whom 20 sessions of right 1Hz rTMS augmentation resulted in clinical response and who remained in remission by the 8th month of treatment. We suggest that rTMS is a well-tolerated treatment that may not be reserved only for treatment resistant patients but may also be considered early on in the management of psychiatric disorders.

Persistent Lingual Dyskinesia and Protrusion Due To Clomipramine and Risperidone

A 41 year-old female patient presented to the psychiatry clinic with complaints of speaking difficulty and involuntary tongue movements (ITM). She was started on clomipramine 150 mg/ day 13 years ago and added risperidone 1 mg/day 2 years ago treatment for obsessive compulsive disorder according to DSM-V. ITM and protrusion (Figure 1A-1B) was began 1 year ago. Therefore risperidone was discontinued. Despite ITM was not decrease. Diazepam, clonazepam, aripiprazole and clozapine was ineffective for ITM. She had no family history of movement disorder. Neurological and systemic examination was normal. Cranial magnetic resonance imaging (MRI) and quantitative electroencephalography (QEEG) were done. No paroxysmal activity was found in QEEG. Magnetic resonance imaging (MRI) was normal. Examination of eyes did not show Keyser-Fleisher rings. Based on these findings her condition was diagnosed as drug induced persistent lingual dyskinesia. ITM was decrease after tetrabenazine 25 mg/day treatment.

Hyperamylasemia Related to Sertraline

To the Editor Elevation of serum amylase level is usually associated with pancreatitis,1) but 2% of cases are associated with medication. 2) Only 1 case of pancreatitis caused by sertraline has been reported.1) Although it has been reported that selective serotonin reuptake inhibitors may rarely cause pancreatitis,2) Elevated serum amylase levels associated with sertraline use in cases without pancreatitis has not been reported in the literature. To our knowledge, our case is the first report of hyperamylasemia related to sertraline. A 35-year-old male patient with the diagnosis of recurrent depression was followed for over 10 years. He had been taking sertraline 25–50 mg/d for two years. Although the patients biochemical test results were normal and he was clinically in remission, amylase levels started to increase slowly. At the twentieth month of treatment, her blood amylase level was 120 U/L, and 4 months later, it was 160 U/L (normal range, 29 to 115 U/L). There were no clinical or biochemical signs of pancreatitis. He did not have gallbladder stones and was not abusing alcohol. Sertraline was suspected to be the cause of increased amylase level. Sertraline was gradually discontinued over 2 months and was replaced with amitriptyline 50 mg/d. The amylase level started to decrease 20 days after discontinuation of sertraline, and slowly reached 90 U/L. However, his depression relapsed after discontinuation of sertraline. Lamotrigine 50 mg/d was added to the treatment regimen, and amitriptyline dosage was increased to 75 mg/d. In the third week of treatment, the patient was again in remission. Blood amylase level remained constant at 90 U/L. Asymptomatic hyperamylasemia can also occur without pancreatitis.3) However, in these cases, the amylase level remains consistently high. In our case, the amylase level returned to normal after discontinuation of sertraline. The reason for hyperamylasemia associated with sertraline is not known. Clinicians should be aware of the possibility that sertraline may cause hyperamylasemia. Sincerely,