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Background:Vitamin B12 deficiency is a common condition causing neurologic, cognitive, psychiatric, and mood symptoms. With varied religious, ethnic, and socioeconomic heterogeneity among the people in India greatly influencing their dietary habits and with the high prevalence of Helicobacter pylori infection, Vitamin B12 deficiency is not uncommon, but is often under recognized due to the lack of classical symptomatic presentation.Materials and Methods:Retrospective study on Vitamin B12 deficiency with neuropsychiatric symptoms in patients who attended neurology, psychiatry, and geriatric OPDs for a period of 1 year in a specialized neuropsychiatric institute in South India.Results:Out of 259 patients who had Vitamin B12 deficiency (<220 pmol/L), 60 had neuropsychiatric symptoms. Among them the Vitamin B12 levels were <150 (severe), 150-200 (moderate), and 201-220 pmol/L (mild) in 19, 24, 17 patients, respectively. Twenty one were diagnosed with Posterior dementias, 20 with frontotemporal dementia, 7 with Schizophrenia, 4 each with Parkinson's disease and alcohol-dependent syndromes (ADS), 3 with bipolar affective disorder, and 1 with Creutzfeldt-Jakob disease. Eight patients also had hypothyroidism. First symptom of presentation was behavioral disturbances in 30 (50%), memory loss in 20 (33.9%), and sensorimotor and movement disorders in 9 (15.3%), and 56.7% were vegetarians while 43.3% were nonvegetarians. In our study, Vitamin B12 deficiency was more prevalent in elderly males (56.67%) and was associated with increased severity of behavioral disturbances (P = 0.043) which was the most common presentation. Memory loss was present in 16 (84.2%) patients of severe Vitamin B12 deficiency. Hindi mental status examination (HMSE) score was graded as <20, 20-24, 24-31 in 37 (61.7%), 10 (16.7%), and 13 (21.7%) patients, respectively. Cognitive decline in Vitamin B12 deficiency was significantly associated with increased serum cholesterol (P = 0.019) and was significantly prevalent in neurological disorders when compared with primary psychiatric illnesses (P = 0.001). Mean folate and mean homocysteine in our study was 11.7 ± 6.44 ng/ml and 17.77 ± 5.45 μmol/L, respectively. Eighty percent of the population had normal folate levels whereas mean homocysteine values were much higher than that of the western population (10-12 μmol/L).Conclusion:Vitamin B12 deficiency though common in India is often overlooked. It increases the load of cognitive decline and accentuates vascular risk factors in neuropsychiatric illnesses. Vitamin B12 deficiency also increases homocysteine levels contributing to the vascular comorbidity in cerebro and cardiovascular illnesses. So prevention, early detection, and management of this reversible Vitamin B12 deficiency state is of profound importance.

Background:Apraxia is a state of inability to carry out a learned motor act in the absence of motor, sensory or cerebellar defect on command processed through the Praxis circuit. Breakdown in default networking is one of the early dysfunction in cortical dementias and result in perplexity, awkwardness, omission, substitution errors, toying behavior and unrecognizable gestures in response to command with voluntary reflex dissociation where, when unobserved patient will carry out reflex movements normally. Awareness into the organicity of these phenomenas will help in early diagnosis, which will help in initiating appropriate treatment and slowing down the progression of the disease.Aims and Objectives:The aim was to look for the various kinds of apraxias in patients with dementia using appropriate simple tests.Patients and Methods:Three hundred patients satisfying Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for dementia were evaluated in detail with mandatory investigations for dementia followed by testing for ideational, ideomotor, limb-kinetic, buccopharyngeal, dressing apraxia, constructional apraxia and gait apraxias in addition to recording of rare apraxias when present.Results:Alzheimer's disease showed maximum association with apraxias in all the phases of the disease ideational, ideomotor, dressing and constructional apraxias early and buccopharyngeal and gait apraxia late. Frontotemporal lobe dementia showed buccopharyngeal and gait apraxias late into the disease. Cortical basal ganglionic degeneration showed limb apraxias and diffuse Lewy body disease showed more agnosias and less apraxias common apraxias seen was Ideational and Ideomotor.Conclusion:Recognition of the apraxias help in establishing organicity, categorization, caregiver education, early strategies for treatment, avoiding anti-psychotics and introducing disease modifying pharmacotherapeutic agents and also prognosticating.

Context:The diagnostic accuracy of the currently available tools carries poor sensitivity resulting in significant delay in specific diagnosis of cortical dementias. Considering the properties of default mode networking of the brain it is highly probable that specific changes may be seen in frontotemporal dementias (FTDs) and Alzheimer's disease sufficiently early.Aim:The aim of this study is to look for changes in Transcranial Magnetic Stimulation (TMS) in cortical dementia.Materials and Methods:Evaluated with a single pulse TMS with the figure of eight coil and recorded from right first dorsal interossei (FDI). Resting Motor Threshold (RMT) was estimated on the opposite motor cortex (T1). Second site of stimulation was cervical spine at C7-T2. Central motor conduction time (CMCT) is equal toT1-T2. Silent Period (SP) identified by applying TMS pulse to contracting FDI.Conclusions:RMT was reduced in seven out of eight Alzheimer's dementias. CMCT was in the upper limit of normal in both patients with FTD. The most consistent observation was that SP was reduced and there were escape discharges noticed during the SP suggesting increased cortical excitability and decreased cortical inhibition. This suggests probable early asymptomatic changes in the gamma-aminobutyric acid (GABA) nergic and cholinergic system is taking place. This if confirmed may give some insight into early diagnosis and therapeutic role of GABA agonists in these disorders.

Background:It was observed that a good number of patients presenting with psychiatric manifestations when investigated later because of unresponsiveness to treatment or late development of organic features turned out to be treatable limbic syndromes.Introduction:The aim of this study is to assess the patients presenting with new onset neuropsychiatric symptoms satisfying the criteria for probable limbic encephalitis.Patients and Methods:Patients referred to neurology department following a period of treatment for neuropsychiatric symptoms, which did not respond to conventional treatment were analyzed using Electroencephalography (EEG), magnetic resonance imaging, cerebrospinal fluid, screening for malignancy Vasculitic work-up, histopathology and autoantibody done when feasible.Results:There were 22 patients satisfying criteria for probable limbic encephalitis. Their mean age was 34.5 years. Symptoms varied from unexplained anxiety, panic and depression, lack of inhibition, wandering, incontinence, myoclonus, seizures and stroke like episodes. Three had systemic malignancy, 10 had chronic infection, one each with vasculitis, acute disseminated encephalomyelitis, Hashimoto encephalitis and two each with non-convulsive status, cryptogenic and Idiopathic inflammation.Conclusion:All patients who present with new onset neuropsychiatric symptoms need to be evaluated for sub-acute infections, inflammation, autoimmune limbic encephalitis and paraneoplastic syndrome. A repeated 20 minute EEG is a very effective screening tool to detect organicity.

Introduction:In frontotemporal dementia (FTD) and Alzheimer's disease (AD), central autonomic structures get affected early. An insight into autonomic functions in these patients is likely to be of diagnostic importance and thus help in prognosticating and also probably explain unexplained sudden death in some of these patients.Objectives:The objective of this study is to identify autonomic dysfunction prevailing in patients. Then, if there is dysfunction, is the pattern same or different in these two conditions. And if different it will serve as an additional biomarker for specific diagnosis.Patients and Methods:There were 25 patients and 25 controls and six patients and three controls in AD and FTD groups, respectively. The participants who were recruited were assessed for heart rate variability and conventional cardiac autonomic function testing. The parameters were analyzed using LabChart version 7 software and compared with control population using appropriate statistical methods using SPSS version 22 software.Results:The mean overall total power was low in the FTD group (P < 0.001), and there was significant reduction in the standard deviation of normal-to-normal intervals and root mean square of successive differences (P < 0.001) with elevated sympathovagal balance in the FTD group (P = 0.04). Patients with AD also showed sympathetic dominance, but there was in addition parasympathetic suppression unlike in the FTD group.Conclusion:This study reveals autonomic dysfunction in patients with FTD and AD. Both conditions show sympathetic dominance, probably consecutive to the involvement of central autonomic regulatory structures as a shared domain. It remains to be confirmed if these findings are the cause or effect of neurodegeneration and might open up newer territories of research based on the causal role of neurotransmitters in these regions and thus lead to novel therapeutic options such as yoga. The presence of parasympathetic suppression in AD in addition helps differentiate these two conditions.

Schwartz–Jampel syndrome is a very rare congenital myotonic syndrome with typical phenotypic and electrophysiological features. Diagnosis is made by awareness into the typical phenotypic characters.

Knowledge hiding is the deliberate concealment of knowledge when requested. This study underscores three divergent elements of the knowledge hiding process. First, it underlines both the distinct internal and external factors that trigger the knowledge hiding process. Second, it brings out the critical facilitators of knowledge hiding, which do have roots in both the internal and external factors but are inseparable and indistinguishable. Finally, this study brings out a conceptual framework that underscores the vital importance of neuroscience in establishing episodes of knowledge hiding. This final phase of the study categorically establishes the typical need for memory and the frontal lobe integrity in justifying any sequence of events or their combinations as an episode of knowledge hiding.