Objective: Emotions are the indicators of mental wellbeing. In this paper, we present an interactive tool called SAEIT (Self-Assessment of Emotions by Interactive Tool) for recognition of six basic emotions which includes anger, disgust, fear, happy, sad and surprise based on the 2D Valence-Arousal emotional model. Method: The tool is developed using LabVIEW software and uses two parameters namely valence and arousal to identify the emotional status. This interactive tool enables the user to enter the valence-arousal parameters of their current affective state; the tool then determines the emotion being experienced based on these inputs. Experimental boundary conditions are used for designing the classifier rules. Further these conditions helps in the classification of emotions which includes quadrant I, II and III emotions of the 2D valence-arousal model. The user can also feed in the activity being performed at the time, which too will be recorded along with the date and time for further analysis. Application: The programmed interactive tool displays personalized messages or suggestions based on the mood of the user to help make better decisions in their present emotional state. Keywords: Emotional Status Recognition, Interactive Tool, LabVIEW, Valence-Arousal model, SAEIT
The biological basis of psychiatric disorders has been the focus of research in various studies across the world including India. In this selective overview we summarize findings of various EEG, neuro-imaging and blood related studies that have been reported in the Indian Journal of Psychiatry.
Prefrontal cortex deficits have been consistently demonstrated in schizophrenia. The orbitofrontal lobe (OFL), a critical component of the prefrontal cortex, subserves social and neuro-cognitive functions. While these functional impairments are established in schizophrenia, the OFL volume deficits have not been well studied, especially in antipsychotic-naïve patients.To study OFL volume deficits in antipsychotic-naïve schizophrenia patients in comparison with matched healthy controls using high-resolution 3-tesla (3T) magnetic resonance imaging (MRI).Fourteen antipsychotic-naïve schizophrenia patients (DSM-IV) and 14 age-, sex-, handedness- and education-matched healthy controls were scanned using 3T MRI. Psychopathology was assessed in the patient group using the scale for assessment of negative symptoms and the scale for assessment of positive symptoms (SAPS). The OFL volume was measured using Region of Interest (ROI)-based manual morphometry technique, with good inter-rater reliability (intra-class correlation coefficient = 0.98).Total OFL volume was significantly smaller in schizophrenia patients (43.3 ± 9.6 mL) in comparison with healthy controls (52.1 ± 12.2 mL) after controlling for the potential confounding effects of age, sex and intracranial volume (F = 5.3, P = .03). Duration of untreated psychosis did not correlate significantly with OFL volumes. There was a trend towards significant negative correlation between the left and total OFL volumes and SAPS scores (r = -0.49, P = .06).OFL volume deficits might underlie the pathogenesis of schizophrenia symptoms with possible neuro-developmental origins.
Sir, Treatment of bipolar depression in the elderly is challenging due to the presence of medical comorbidities and it is often resistant to treatment.[1] Modafinil with its novel mechanism of action, utilizing multiple neurotransmitter systems such as dopamine, hypocretin, histamine, epinephrine, gamma-aminobutyric acid, and glutamate, is a well-tolerated medication with minimum drug interactions.[2] Lately, studies evaluating the role of modafinil in the treatment of bipolar depression in the adult population have shown encouraging results.[3] However, its use in treatment of depression in elderly is yet to be explored. In this context we present the first case report of successful use of modafinil in an elderly woman with resistant bipolar depression. Mrs. A, a 61-year-old homemaker, presented to us with 30-year-long episodic illness with around 15 depressive and 3 hypomanic episodes and poor interepisodic functioning. She had received adequate trials of various combinations of mood stabilizers (lithium, valproate, and lamotrigine) and antidepressants (amitryptiline, imipramine, clomipramine, fluoxetine, fluvoxamine, paroxetine, escitalopram, pregabalin, prothiaden, venlafaxine, and reboxitin) and quetiapine with only partial improvement. She had never attained premorbid levels of functioning. For the past eight months, she had worsening of her symptoms-pervasive sad mood, crying spells, anhedonia, easy fatigability, decreased sleep and appetite, and features suggestive of apathy. She had history of hypertension and hypothyroidism for four years and was on treatment for the same. There was family history of hypothyroidism in two children. On physical examination she was overweight (BMI=26.6 kg/m2). Her blood pressure was controlled (116/82 mmHg) on a combination of losartan 50 mg/day and hydrochlorthiazide 12.5 mg/day. On mental status examination, she had psychomotor retardation, depressive cognitions, death wishes, depressed effect with impaired attention, and difficulty in new learning. She scored 31 on the Hamilton depression rating scale (HDRS) and 61 on the apathy evaluation scale.[4] Her thyroid function tests and serum vitamin B12 levels were normal. Magnetic resonance imaging revealed generalized atrophy predominantly temporal with leukoaraiosis. Atherosclerotic changes were noted in bilateral internal carotid arteries. In view of the above, she was diagnosed as having bipolar II disorder without full interepisodic recovery, current episode moderate depression. She was then started on modafinil, titrated to 50 mg/day. She has shown gradual improvement with the same and has reached premorbid levels of functioning. When last followed up, at the end of 16 weeks, she had a score of 8 on the HDRS and 31 on the apathy evaluation scale. The index patient had resistant bipolar depression with significant apathy which improved significantly after modafinil was started. Modafinil with its apparent two-pronged action on both depressive and apathetic symptoms, and lack of serious side effects,[3] is an important therapeutic option in this, otherwise difficult to treat, population. Indirect evidence implicates the dopaminergic system in the pathogenesis of apathy, and modafinil through its dopaminergic action is reported to be successful in treatment of apathy.[5] However, further systematic trials are needed to elucidate the mechanism of modafinil's antidepressant and antiapathy actions.
Sir, Cannabinoids modulate mood probably through serotonergic neurons in medial prefrontal cortex and cannabinoid receptor (CB1) receptor antagonists may reverse these effects.[1] Rimonabant, a CB1 receptor antagonist and an anti-obesity agent has been associated with depressive and anxiety symptoms in clinical trials[2] though was initially considered to be safe.[3] We report a patient with schizophrenia developing depression possibly due to rimonabant. Mr. A, 19-year-old male, presented to us in February 2008 with symptoms of delusions of persecution and reference, thought broadcast, 3rd person auditory hallucinations, alogia, anhedonia, amotivation since 2 years. He did not have history of mood symptoms or suicidal ideation. Using mini international neuropsychiatric inventory (MINI) and comprehensive clinical interview, he was diagnosed as having schizophrenia (DSM-IV). He was on treatment with risperidone 6 mg/day and trihexyphenidyl 4 mg and escitalopram 10 mg/day for treatment of negative symptoms since past one month and reported 60% improvement. On scale for assessment of negative symptoms (SANS), he had a score of 95 and a score of 36 on scale for assessment of positive symptoms (SAPS). His weight was 94.5 kgs, waist circumference 104 cms, and body-mass-index- 30.85 suggestive of obesity. On appetite questionnaire,[4] he had a score of 36. Investigations showed normal fasting glucose and lipid profile, except increased triglycerides (181.9 mg%) and total cholesterol (223 mg%). He was started on Rimonabant 20 mg/day along with dietary modifications and exercise, while other medications were continued. After 1 month, he had no positive psychotic symptoms (zero on SAPS), but continued to have negative symptoms (106 on SANS). He had 4.5 kg reduction in weight (weight- 90 kgs, BMI- 29.38) and 50% reduction in appetite (17 on appetite questionnaire). He complained of new onset pervasive sad mood, insomnia, feelings of worthlessness, psychomotor retardation, recurrent suicidal ideation, diminished ability to think in the past 2 weeks suggestive of major depressive episode (DSM IV). On Montgomery Asberg depression rating scale (MADRS), he had a score of 34. In view of new onset depressive symptoms, rimonabant was stopped, while rest of the medications continued. Within next 2 weeks, there was improvement in depressive symptoms (22 on MADRS). The temporal correlation between rimonabant initiation and onset of depressive symptoms and improvement of depressive symptoms on withdrawal of drug points towards possibility of depressive symptoms due to rimonabant. However, post-psychotic depression is a possibility. But rapid recovery as seen in this case is uncommon in post-psychotic depression.[5] New onset of sad mood and suicidal ideation described above are indicative of depression than continuation of negative symptoms. Though patient was on escitalopram 10 mg/day, dose may not have been sufficient to prevent depression of severe intensity as seen in earlier reports.[6] In conclusion, our reports suggest rimonabant can result in new onset depression in patients with schizophrenia and one has to be cautious in initiating rimonabant though there are studies that suggest the contrary.[7]
Atypical antipsychotics are known to be associated with electroencephalogram abnormalities. Olanzapine can lower seizure threshold and induce epileptiform discharges. However in patients on olanzapine for the treatment of a primary psychiatric disorder, clinical seizure is a rare occurence. We report the case of a 25-year-old man with a diagnosis of paranoid schizophrenia with obsessive-compulsive disorder of 8 years' duration who developed new-onset generalized tonic-clonic seizure with exposure to olanzapine. Electroencephalogram showed epileptiform discharges; results of computed tomographic scan and metabolic investigations were normal. His antipsychotic was changed to haloperidol, and the patient showed a significant improvement in psychotic symptoms with no recurrence of seizures and did not require anticonvulsant therapy. Olanzapine has a profile similar to that of clozapine and shares its seizure-inducing potential. Typical antipsychotics such as haloperidol might be a safer option for such patients.
Background: Thought disorder is considered to be central to the core disturbances in schizophrenia and was described by Goldstein as aberrant “concept formation.” Executive dysfunction is another core deficit in schizophrenia. With a greater emphasis on psychopathology in nosological systems, the classical thought disorder receives less prominence. The present study aimed to understand the association between classical thought disorder (aberrant concept formation and concrete abstraction) and executive dysfunction. Methods: Thirty patients with schizophrenia and thirty healthy subjects, matched on age, gender, education, and socioeconomic status, were screened using MINI 5.0, following which they were assessed on object sorting test (OST) and selected tests for executive functions (EFs). Results: Individuals with schizophrenia were found to have significantly decreased performance on all domains of EFs and OST. Total peculiar scores on OST were significantly associated with mental speed, focused attention, and divided attention. Total impoverished scores on OST was significantly associated with focused attention, sustained attention, planning, set shifting, perseveration, and concept formation. Conclusion: Several correlations, among performance on OST and neuropsychological tests, suggest that patterns of responses on OST can point to underlying executive dysfunction. Both thought disorder and executive dysfunction mirror similar constructs. This similarity represents a conceptual bridge between the classical and contemporary descriptions of the core deficits in schizophrenia.
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