RESUMO
India has been a part of 5 major wars since its independence in 1947 and hosts over 212,413 refugees from Sri Lanka, Tibet and Bangladesh. So, a wide spectrum of trauma survivors, both civilian and military, live in this country and require mental healthcare. We discuss the psychological impact of armed conflict and how the country and culture tint it uniquely. We not only explore the current scene but the resources available and what can be done to make such vulnerable parts of the Indian population feel safer.
The spectrum of victims of armed conflict in India and the impact on their mental health.The current deficient governmental and non-governmental psychosocial support available.Recommendations for optimum management of these trauma victims through programmes and individual therapy.
Assuntos
Refugiados , Transtornos de Estresse Pós-Traumáticos , Humanos , Transtornos de Estresse Pós-Traumáticos/epidemiologia , Transtornos de Estresse Pós-Traumáticos/psicologia , Emoções , Refugiados/psicologia , Conflitos Armados , ÍndiaRESUMO
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect any part of the neuraxis. Many neurological conditions have been attributed to be caused by SARS-CoV-2, namely encephalopathy (acute necrotizing encephalopathy and encephalopathy with reversible splenial lesions), seizures, stroke, cranial nerve palsies, meningoencephalitis, acute disseminated encephalomyelitis (ADEM), transverse myelitis (long and short segment), Guillain-Barré syndrome (GBS) and its variants, polyneuritis cranialis, optic neuritis (ON), plexopathy, myasthenia gravis (MG), and myositis. The pathophysiology differs depending on the time frame of presentation. In patients with concomitant pulmonary disease, for instance, acute neurological illness appears to be caused by endotheliopathy and cytokine storm. Autoimmunity and molecular mimicry are causative for post-coronavirus disease 2019 (COVID-19)-sequelae. It has not yet been shown that the virus can penetrate the central nervous system (CNS) directly. This review aims to describe the disease and root pathogenic cause of the various neurological manifestations of COVID-19. We searched Pubmed/Medline and Google Scholar using the keywords "SARS-CoV-2" and "neurological illness" for articles published between January 2020 and November 2022. Then, we used the SWIFT-Review (Sciome LLC, North Carolina, United States), a text-mining workbench for systematic review, to classify the 1383 articles into MeSH hierarchical tree codes for articles on various parts of the nervous system, such as the CNS, peripheral nervous system, autonomic nervous system, neuromuscular junction, sensory system, and musculoskeletal system. Finally, we reviewed 152 articles in full text. SARS-CoV-2 RNA has been found in multiple brain areas without any histopathological changes. Despite the absence of in vivo virions or virus-infected cells, CNS inflammation has been reported, especially in the olfactory bulb and brain stem. SARS-CoV-2 genomes and proteins have been found in affected individuals' brain tissues, but corresponding neuropathologic changes are seldom found in these cases. Additionally, viral RNA can rarely be identified in neurological patients' CSF post hoc SARS-CoV-2 infection. Most patients with neurological symptoms do not have active viral replication in the nervous system and infrequently have typical clinical and laboratory characteristics of viral CNS infections. Endotheliopathy and the systemic inflammatory response to SARS-CoV-2 infection play a crucial role in developing neuro-COVID-19, with proinflammatory cytokine release mediating both pathological pathways. The systemic inflammatory mediators likely activate astrocytes and microglia across the blood-brain barrier, indirectly affecting CNS-specific immune activation and tissue injury. The management differs according to co-morbidities and the neurological disorder.
RESUMO
Mitochondrial DNA (mtDNA) is responsible for encoding 13 subunits of the respiratory chain. These subunits are crucial in providing reducing equivalents for the energy-intensive intracellular processes. Leber hereditary optic neuropathy (LHON) is a mitochondrial illness that causes carcinogenesis due to oxidative stress and painless loss of central vision as a result of selective degradation of retinal ganglion cells as well as their axons. We present a case of a 23-year-old male patient who was diagnosed with subacute LHON. The mutation in our patient was found in a less commonly mutated exon sequence of MT-NDL4, which codes for NADH (nicotinamide adenine dinucleotide hydrogen, reduced) dehydrogenase subunit 4L. The MT-ND4L exon is located immediately upstream of the MTD4 exon on the human mtDNA. The take-home message is to always perform a comprehensive mitochondrial genome analysis for identifying rare mutations when LHON is suspected.
RESUMO
COVID-19 occurs due to infection by the SARS-CoV-2 virus (severe acute respiratory syndrome coronavirus 2), which has caused havoc globally. It presents with a wide range of symptoms, mainly respiratory symptoms, but with time various neurological manifestations of the disease have also been noted, like myelitis. This case report aims to shed light on COVID-19-associated myelitis so that potential neurological complications of COVID-19 can be identified and treated timely. We report a case of a 41-year-old male who presented with weakness of all limbs with urinary complaints. He also had a cough and sore throat for the past few days. The MRI scan of the spine showed long segment myelitis in the cervical cord extending from the cervicomedullary junction to the upper end of the C4 vertebral body. COVID-19 myelitis is a rare but severe complication of COVID-19 infection and needs to be discussed.
RESUMO
Background In this study, we aimed to describe eight cases of dengue encephalitis along with their magnetic resonance imaging (MRI) findings. Dengue encephalitis is caused by an arbovirus that has four strains DENV1-DENV4. The dengue virus is usually non-neurotropic but DENV2 & DENV3 are neurotropic. Dengue encephalitis is characterized by headaches, seizures, and altered consciousness. Methodology At our facility, we performed 3T MRI on eight suspected cases of dengue encephalitis using the criteria established by Varatharaj et al. We were able to diagnose dengue encephalitis based on the proposed criteria which included symptoms, serology, cerebrospinal fluid (CSF) analysis results, MRI findings, and routine blood laboratory workup in dengue encephalitis. Because numerous brain regions are potentially impacted in severe cases of dengue encephalitis, an MRI of the brain can reveal the severity of the condition. In deteriorating situations, it may detect whether or not further regions are being impacted. Hence, MRI should be done in all suspected cases of dengue encephalitis. Results The changes observed on MRI of the eight cases were in the supra-tentorium (deep periventricular white matter, subcortical white matter, and deep gray matter of the brain, which includes basal ganglia and thalami), infra-tentorium (cerebellar white matter and brainstem, which includes pons), and occasionally in cortical gray matter. The MRI showed mild-to-moderate hyperintensities on T2-weighted images and fluid-attenuated inversion recovery sequence (FLAIR); diffusion restriction is seen on diffusion-weighted images. The neurological clinical features included non-localizing signs and symptoms such as altered mental status, headache with vomiting, and fever. Conclusions The commonly affected areas of the brain in dengue encephalitis are the basal ganglia, thalamus, brainstem, cerebellum, cortical white matter, periventricular white matter, and cortical gray matter, which are all hyperintense on T2-weighted images and FLAIR. The lesions are iso or hypointense on T1-weighted images and micro-hemorrhages appear as blooming on susceptibility-weighted MRI. MRI is a crucial initial investigation in suspected cases of dengue encephalitis and known cases of dengue fever experiencing worsening neurological conditions.
RESUMO
The ataxia telangiectasia mutant (ATM) protein is a sensor and signal transducer that amplifies and communicates signals of DNA damage further to the mediators of cell cycle arrest, apoptosis, and senescence (p16, p19, p21, BAX etc.) which is modified by the strength of the cellular stress. They are able to act as recognition and signaling proteins because of their kinase activity. Classic ataxia telangiectasia is associated with homozygous mutations of the ATM gene, the complete absence of its kinase activity and/or deleterious ATM gene mutations such as truncation/nonsense mutations, loss of function mutation, non-conservative substitutions, frameshift, and deletions. On the other hand, variant ataxia-telangiectasia (A-T) is associated with the presence of residual kinase activity. We report a six-year-old male patient who presented to us with abnormal neck movements as his initial complaint. ATM gene analysis showed a rare pathogenic variant of the ATM gene. The variant was a homozygous nonsense mutation in exon 2 of the ATM gene that resulted in the formation of a stop codon and premature truncation of the protein at codon 23 in exon 2 (p.Arg23Ter). In conclusion, we report a case of an unusual presentation of classic A-T. We should pursue a long-term follow-up and maintain a low threshold for performing pedigree analysis and genetic testing in pediatric patients with movement disorders. In resource-limited settings where kinase enzyme assays are not universally available to patients, web-based mutation prediction tools may be beneficial to predict the deleterious effects of the mutation.