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Traumatic brain injury (TBI) occurs when a blow or jolt to the head or a penetrating injury results in damage to the brain. It is the most frequent cause of hospitalization in young people with a higher prevalence in men. TBI is the leading cause of disability and mortality between the ages 1 and 45. TBI can be caused either by the direct result of trauma or due to a complication of the primary injury. The most common etiological factors for TBI are falls, road traffic accidents, violent physical assaults, and injuries associated with athletic activities. Following TBI, significant neurologic complications may occur which include seizures, dementia, Alzheimer's disease, and cranial nerve injuries. In addition, people may suffer from various psychiatric complications such as depression, posttraumatic stress disorder, generalized anxiety disorder, obsessive-compulsive disorder, and other cognitive and behavioral sequel that might significantly increase the comorbidity of the victims. Considering all of the above complications, TBI is one of the significant public health burdens. Literature has shown that only about 25% of people achieve long-term functional independence following TBI. In this paper, we focused not only on the epidemiology but also the etiology, complications following TBI and understanding their underlying pathogenesis. Further, we focused on analyzing the options to improve the treatment and rehabilitation following TBI in future.

AimTo assess the relative efficacies of clozapine plus Electroconvulsive Therapy (ECT) compared against non-clozapine typical and atypical antipsychotics plus ECT for the treatment of “Treatment Resistant Schizophrenia” (TRS). Primarily to assess if clozapine delivers a significant improvement over other antipsychotics when combined with ECT.DesignMajor electronic databases were searched between 1990 and March 2017 for trials measuring the effects of either clozapine augmented ECT, other antipsychotic-augmented ECT, or both. After the systematic review of the data, a random-effects meta-analysis was conducted measuring the relative effect sizes of the different treatment regimens.Subjects1179 patients in 23 studies reporting the usage of ECT augmentation with antipsychotics. A total of 95 patients were tested with clozapine, and ECT (9 studies) and 1084 patients were tested with non-clozapine antipsychotics (14 studies) such as flupenthixol, chlorpromazine, risperidone, sulpiride, olanzapine, and loxapine with concurrent ECT treatment considered for systematic review. Of these, 13 studies reported pre and post-treatment scores were included in the meta-analysis.Main outcome measuresThe main outcome measure was the presence and degree of both positive and negative psychotic symptoms, as measured by either of two standardized clinician administered tests, the Brief Psychiatric Rating Scale (BPRS), and the Positive and Negative Symptom Scale (PANSS).ResultsThe comparison of the different antipsychotics established the supremacy of ECT-augmented clozapine treatment against other typical and atypical antipsychotics. The Forest Plot revealed that the overall standard mean difference was 0.891 for non-clozapine studies and 1.504 for clozapine studies, at a 95% interval. Furthermore, the heterogeneity plots showed that while clozapine studies showed no significant heterogeneity, non-clozapine studies showed an I2 statistic value at 42.19%, suggesting moderate heterogeneity. Lastly, publication bias showed asymmetrical plots and significant values of Kendal's tau and Egger's rank test.ConclusionECT augmentation technique was found to be effective in the reduction of psychometric scale scores, and the resulting improvement was significant. Clozapine maintained its stance as the most effective treatment for Treatment-Resistant Schizophrenia, followed by flupenthixol.

Background and Objectives Recent evidence has suggested that cannabis use precipitates cerebrovascular events. We investigated the relationship between cannabis use disorder (CUD) and hospitalization for epilepsy. Methods Nationwide inpatient sample (NIS) was analyzed from 2010 to 2014 for patients (age 15‐54) with a primary diagnosis of epilepsy (N = 657 072) and comparison was made between patients with ICD‐9 classification of CUD and without CUD. We utilized logistic regression to study the association (odds ratio [OR]) between CUD and epilepsy. Results The incidence of CUD in epilepsy patients was 5.77%, and patients with CUD had a threefold higher likelihood of emergency admissions. Patients with CUD were younger (25‐34 years), male and African American. In regression analysis, adjusted for confounders, cannabis (OR, 1.56), tobacco (OR, 1.20), and alcohol (OR, 1.63) use disorders were found to be associated with higher odds of epilepsy hospitalization, but lower odds with cocaine (OR, 0.953), amphetamine (OR, 0.893), and opioid (OR, 0.828) use disorders. Conclusions and Scientific Significance With the increasing prevalence of medical marijuana legalization, there is increased use of medicinal marijuana. Studies of cannabidiol and marijuana for epilepsy have been highly publicized, leading to its off‐label use for treatment. There is limited evidence to suggest that the cannabinoids may also induce a seizure. This study found that CUD is independently associated with a 56% increased likelihood of epilepsy hospitalization and this association persists even after adjusting for other substance use disorders and confounders. (Am J Addict 2019;28:353–360)

Tobacco smoking is the most preventable cause of morbidity and mortality. In just a few short years, electronic cigarettes (e-cigarettes) have become increasingly popular, especially for younger individuals. Many people believe that e-cigarettes are safe. The inhaled aerosols of e-cigarettes contain numerous potential toxicities, some of which could be dangerous for health with long-term use. The safety of prolonged aerosol exposure is not known. The use of e-cigarettes as a harm-reduction tool at stopping tobacco smoking is not uniformly successful. E-cigarettes may be safer than tobacco products, but repeated prolonged exposure to their aerosols has its own considerable potential risk. The long-term health consequences of their use remain to be established. Physicians should vigorously discourage the use of e-cigarettes and tobacco products, with special emphasis on abstinence for younger people and during pregnancy or lactation.

Depression is the most frequently seen neuropsychiatric manifestation in stroke patients. It hampers the ability to undergo therapy and impairs their functional outcome. Depression also increases the risk of suicide in stroke patients, therefore, increasing mortality. The etiology of post-stroke depression (PSD) is complex and reported to be multi-factorial in origin. It also depends on the size and location of the infarct. In addition, family history or prior history of depressive disorders makes them prone to be affected with depression following a stroke. In this article, we will mention various aspects of PSD, as well as the prevalence and the different screening assessment tools used in literature studies. Although there are many available testing tools, little consistency was seen in them being valid or reliable. We will also discuss the pathophysiology of depression in stroke patients with various available options for managing the condition. We will briefly review the use of alternative treatment such as Electroconvulsive therapy (ECT) and Transcranial Magnetic Stimulation (TMS) as well. However, we need further evidence-based research exploring the screening tool; i.e. universally acceptable for PSD and implementing an effective, non-invasive treatment modality impacting the prognosis. Also, we require further investigations to identify the role of antidepressants in the recovery of stroke patients. Keywords:Stroke, Post-stroke depression, Stroke location, Assessment and Treatment, Post-stroke Depression, Prevalence of PSD, Pathology in PSD, Mood disorders in PSD, Symptoms and diagnosis criteria in PSD, Assessment scales in PSD, Pharmacotherapy and other treatments in PSD, Depression in stroke survivors MethodologyA search for relevant published literature was performed using PubMed, Google Scholar. The keywords and phrases used included: Stroke lesion, post stroke depression, major depression, Post stroke symptoms, assessment and treatment. Other relevant studies were found by a review of the primary studies obtained in the search as well as reference tracing of selected articles. The inclusion and exclusion criteria were: Any articles that reported the symptomatology, pathophysiology, evaluation and treatment of post stroke depression. All research studies which were published in English language from Neuropsychiatry (London) (2017) 7(6) 907 Review Ali Mahmood Khan PrevalenceOn average for every 40 seconds, there is a stroke case in the United States -around 600.000 new stroke cases are evident every year [12,13]. Based on the literature studies, there is variability in data reported about PSD prevalence. These differences are usually due to the variations in criteria used to diagnose PSD and the difference in age of patients studied. The higher prevalence was seen in hospital-based settings rather than community-based settings [14].While several clinicians use DSM-III and DSM-IV criteria to reach the diagnosis of PSD, some use a different kind of scales or questionnaires. Also, different clin...

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