Peripheric edema could be caused by various medical conditions as well as pharmacologic agents such as antihypertensives, nonsteroidal antiinflamatory drugs, endocrine agents and immunotherapies. Olanzapine is an atypical antipsychotic that is widely prescribed for the treatment of schizophrenia and bipolar affective disorder. Most common adverse reactions of olanzapine are weight gain, postural hypotension, constipation, dizziness, akathisia, sedation. Peripheral edema was reported as an infrequent side effect, which affected 3% of the olanzapine treated patients. In this report, we aim to draw attention of psychiatrists on this rare adverse effect by presenting a 56-year-old case, who applied to our hospital with severe depressive and obsessive-compulsive symptoms and hospitalized because of suicide risk. Before psychiatric admission, he wasn’t taking any medication. He was diagnosed as major depression with psychotic features and obsessive-compulsive disorder. He was started on olanzapine 10 mg/day, quetiapine 300 mg/day and fluoxetine 40 mg/day. Two weeks after initiation of olanzapine, he was found to have bilateral pedal edema without ulceration and temperature change but minimal redness was observed. He had no history suggestive of cardiac, renal and liver dysfunction or allergic reaction against to any drug that could explain his existing edema. Possible medical conditions which may cause edema were ruled out by laboratory tests and physical examination. Olanzapine was stopped immediately and the therapy was modified to risperidone 1 mg/day. After discontinuation of olanzapine, edema was gradually resolved within two weeks. Because olanzapine associated edema has been seen rarely, it could be overlooked by psychiatrists in comparison to its more common side effects. Although it shows self-limited and benign course, patients may feel discomfort and their compliance to treatment may decrease. Also, it may interfere with differential diagnosis of other medical conditions which may cause edema. In conclusion, we suggest that patients should be observed carefully for edema during olanzapine treatment.

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Cerebellum called as the “little brain” .The cerebellum regulates various functions like motor coordination, equilibrium and muscle tone because of its connections with other parts of the brain as well as other parts of the body. Whether the fastigial nucleus of the rat cerebellum plays any role in behavior, reference and working memory forms the focus of the present study. The fastigial nucleus as part of spino-cerebellum of Wistar albino rat was unilaterally (left side) destroyed by electrolytic lesion using stereotaxic procedures and the behavior, learning and memory were analyzed by using open field, elevated plus maze and eight arm radial mazes on 10th and also 15th day after the lesion along with controls as well as with sham operated animals. The alterations in behavior were only observed on the 10th day but not in 15th day. There was no alteration was observed in radial maze among the groups indicated that cerebellum has no role in memory process. The changes perceived in behavior on 10th day may be due the inflammation or reduced metabolism in the damaged areas followed which may recovered on 15th day as inflammation subsides and the metabolism is normalized. These results indicate that fastigial nucleus is not playing any role in either behavior or memory.

Several studies suggest that memory suppression in humans occur as an active process of executive control, mediated by regions of prefrontal cortex, which is a substrate for ovarian hormones. However the effect of ovarian hormones on this process is not known. In order to address this question, we utilized the quantitative analysis of ovarian hormones in combination with the procedure of a memory control model, the think (T) /no think (NT) paradigm in a within-subject design study. We compared the rate of memory control between the follicular (low estrogen and progesterone) and mid-luteal (high estrogen and progesterone) phases of regularly cycling healthy women. Our data demonstrate that during midluteal phase, 63.6 % of subjects are able to ‘suppress’ or actively forget (significantly less % recall below the baseline) previously learned word pairs in the ‘NT condition; i.e., not to think the target word associated with the cue word’. However during the follicular phase there was no effect of ‘NT condition’ on the active forgetting of word pairs below the baseline as assessed by the memory test applied after the T/NT procedure. Thus, our results indicate that ovarian hormones are associated with the process of memory control.

Agmatine may act as a neurotransmitter or neuromodulator. Behaviorally, agmatine exerts antidepressant-like effects. The enzyme agmatinase degrades and thereby inactivates agmatine. The gene coding for human agmatinase is located on chromosome 1p36, a gene locus which has been linked to bipolar disorder and major depression. However, the enzyme has not yet been studied in detail in the context of neuropsychiatric diseases. We analyzed agmatinase protein expression in postmortem hippocampi of individuals with affective disorders. Agmatinase protein was detected in a subset of interneurons in the hippocampus and other brain regions. In depressive patients the number and the numerical density of agmatinase-immunopositive cell bodies was strongly elevated in all regions under study (i.e. hippocampus, habenula, insular cortex and temporal cortex). Agmatine is naturally produced by the breakdown of arginine. The cellular uptake of L-arginine and other cationic amino acids (such as L-lysine and L-ornithine) is mainly mediated by cationic amino acid transporter (CAT) proteins. In patients with mood disorder there was a circumscribed decrease in the numerical density of hCAT1 immunoreactive neurons in the CA2 region of the hippocampus.

The glutamate hypothesis of schizophrenia based on the observations that administration of drugs that block N-methyl-D-aspartate (NMDA) glutamate receptors could induce schizophrenia-like symptoms. There are several evidences linking abnormal glutamatergic transmission to cognitive, negative, and positive symptoms of schizophrenia and the glutamatergic system is now a major focus for the development of new compounds in schizophrenia. The polyamines are omnipresent aliphatic molecules comprising putrescine, spermidine, spermine and agmatine. The polyamines and their biosynthetic enzymes are found throughout the body, including the central nervous system (CNS), where they display specific regional distributions in the CNS. The polyamines have an important role in the modulation of cell growth and on cell membrane functions. It was hypothesized that schizophrenia may be related to a general abnormality in neuronal membranes. Agmatine, a polyamine, selectively blocks the NMDA subclass of glutamate receptors in rat hippocampal neurons. There are also several evidences indicate that a relationship between polyamines and etiopathogenesis of schizophrenia. In this review, a new approach for understanding schizophrenia via NMDA receptors and their interaction with agmatine which is a biological active polyamine transmitter in brain is proposed.

Polyamines, including spermidine, spermine, and agmatine, serve several brain-specific functions. Polyamine transport mechanisms may account for the redistribution of these organic cations, which may also be synaptically released as neuromodulators or neurotransmitters, in the brain. Therefore, the localization of polyamine pathway enzymes, in addition to the localization and functional investigation of the polyamines itself, provides valuable insights regarding the identification of cell- and region-specific roles for polyamines, notably in the context of mental disorders and neurodegenerative diseases. Identified neuronal circuits are subject to physiological and pharmacological investigations. With this respect, we electrophysiologically studied the cerebellar cortex and the medial habenula, showing a prominent synaptic expression of spermidine synthase and agmatinase, respectively. In both areas, the relevant polyamines clearly influence the electrical activity. The medial habenula may be involved with the aetiology of major depressive disorder. In this context, the expression of agmatinase in other brain areas, e.g. the paraventricular thalamic nucleus, possibly also involved with depression, is discussed.

Blood injury injection phobia (BII) involves an intense fear of situations, in which an individual is directly or indirectly exposed to blood, injections or viewing injuries, along with a tendency to avoid these situations. BII phobia is highly prevalent in females as compared to males. It is virtually the only specific phobia and the only anxiety disorder, in which fainting occurs. Although fainting is much distressed to the BII phobic individuals, but it may have developed in the humans at the time when they needed it much as a survival mechanism. In this article we discuss how in the humans there may have developed the trait of BII phobia in the ancestors, including the variation in the symptoms among sexes. There are not studies which specifically examine the syncope related brain differences among genders. But there are other well defined studies which highlight marked differences among male and female brains. Considering this we also review some recent breakthrough discoveries showing differences in the brain of males and females at gene expression level which leads to the variation in brain and behaviour related problems among genders. There is an exigent need to understand the brain behavioral problems through multiple perspectives.

Rabies is a tropical zoonotic disease, transmitted to human being by carnivorous animals. Majority of human rabies cases were reported from Asia and African countries. India recorded more deaths from rabies than any other country in the world. There is no effective treatment for rabies; it can only be prevented by vaccination. It needs multiple levels of interventions at human and animal level. World Health Organization’s target is to eliminate the disease by 2020 in endemic South-East Asian countries which include India. Key challenges in control of rabies in India are lack of intersectoral coordination, weak surveillance system on rabies, inadequate rabies research and lack of sustainability. To conclude, breaking the rabies cycle in a sustained manner is necessary to eliminate rabies from this part of the world.