#https://lupinepublishers.com/neurology-brain-disorders-journal/ | Explore Tumblr posts and blogs

lupinepublishers · 4 years ago

Text

Lupine Publishers| Association of Prx Gene Expression with the Gingival Phenotype.

Keywords

Gingival phenotype; Prx; Periodontal surgery; Transcription factor

Introduction

In addition to their role in development Prx genes have important roles in cell proliferation and migration [1]. Smooth muscle cells transfected with rat Prx1 showed increased proliferation [1]. Moreover, treatment of fibroblasts in vitro with morpholino oligos designed to specifically inhibit Prx1 and Prx2 protein expression resulted in downregulation of Tenascin-C expression and reduction in cell migration towards fibronectin [1]. Specifically, the healing process after surgical manipulation in the oral mucosa, is determined in a high degree by the gingival phenotype. Assuming that the gingival phenotype might be regulated by gene expression, the aim of our study was to investigate if there is an association between the presence and the levels of Prx1 and Prx2 mRNA and the phenotype of human gingivae.

Materials and Methods

Subjects included in the study: Twenty two patients in need of crown lengthening were included in the study, ten with thick and twelve with thin gingival phenotype. The assessment of the gingival phenotype was done based on the clinical characteristics of the gingiva. Surgical Procedures: All surgeries were performed by postgraduate students at the Department of Periodontology and Biology of Dental Implants at the Aristotle University of Thessaloniki. All patients were required to sign a consent form before. Tissue samples: Connective tissue fragments 1mm x 1mm were collected from the buccal flap during the surgical procedure and immediately placed in sterile tubes containing 1mL of RNA later (Sigma). Samples were maintained in RNA later at -80°C until further processing. RNA isolation-Reverse Transcription: Total RNA was isolated from tissue samples using the NucleoSpin RNA Kit (Macherey Nagel) following the manufacturer’s protocol. The concentration and quality of RNA in each sample was determined using a SmartSpec Plus spectrophotometer (Biorad). 200ng of RNA were reversed transcribed to cDNA using the PrimeScript II 1st strand cDNA synthesis kit (Takara) using oligo-dT primer. cDNA samples were stored at -20°C until further processing.

PCR Analysis for Prx1 and Prx2 mRNA Expression: The presence and levels of Prx1 and Prx2 mRNA expression were examined by semiquantitative PCR analysis. Two microliters of the cDNA were directly used as a template for the PCR in a total reaction volume of 25μL. The reaction mixture contained 12.5μL OneTaq Hot Start 2x Master Mix with standard buffer (New England Biolabs), 1μL of each primer (10μM), 2μL cDNA template, and PCR grade water. For detecting the presence of Prx1 primers Prx1F 5’-TCCCTCCTCAAATCCTAC-3’ and Prx1R 5’-ACTATATTCCTTGGCCTTC-3’ [2] were used.

For Prx2 detection primers Prx2F 5’-AGCACAGTGCCACCCTACA-3’ and Prx2R 5’-CTTGGCAGGCTCTTCCACC-3’ [2]. Expression of Gadph was used as an endogenous control. The primers for Gadph detection were: Forward 5’-TGG TAT CGT GGA AGG ACT CATGAC-3’ and Reverse: 5′-ATG CCA GTG AGC TTC CCGTTC AG-3′ [3].

PCR conditions were as follows: initial denaturation for 5 minutes at 94°C, then 25 cycles of denaturation at 94°C for 30s, annealing at 48°C for Prx1, 52°C for Prx2 and 48°C for Gadph for 30s, extension for 45s at 68°C and final extension at 68°C for 5 min. PCR products were visualized in a 2% agarose gel using Midori green Advance (Nippon Genetics) DNA/RNA stain and a FastGene LED Transilluminator (Nippon). Semi-quantification of the PCR products was done by using the ImageJ (https://imagej.nih.gov/) analysis program. All experiments were repeated twice to ensure statistical accuracy.

Statistical analysis: The differences between thin and thick phenotypes were analyzed using t-test. Inter-group differences were analyzed by t-test and Mann-Whitney test for independent samples. A p- value <0.05 was considered statistically significant.

Results

PCR Analysis for Prx1 mRNA Expression: PCR analysis showed Prx1 mRNA expression in higher levels in thick gingival phenotypes compared to thin. In addition, both Prx1a and Prx1b alternatively spliced isoforms were detected and Prx1a was more abundant in most of the samples compared to Prx1b. In thin gingival phenotypes Prx1a was either expressed in different levels or completely absent, fact that indicates that thin gingival phenotype might be regulated by other genes’ expression (Figure 1).

PCR Analysis for Prx2 mRNA Expression: PCR analysis showed that Prx2 mRNA expression was absent in thick gingival phenotypes except for one sample. On the contrary, Prx2 was highly expressed in all samples with thin gingival phenotype (Figure 2).

Discussion

Recent studies determine the gingival phenotype based only on clinical characteristics of the gingiva. Placing the periodontal probe in the gingival sulcus can give the appearance of transparency of the gingiva and this biotype is characterized as ‘thin’. If the gingiva is not transparent when placing the probe, the gingiva is characterized as ‘thick’ [4,5]. In this study we aimed to associate the expression of Prx genes with the gingival phenotype. Our results indicate that Prx2 is expressed in thin phenotypes, whereas Prx1 is expressed in thick phenotypes. It is well established that Prx genes play an important role in craniofacial development. Our study indicates that Prx genes are not only expressed in tissues of ectomesenchymal origin, but they might also play an important role in determining the gingival phenotype at a molecular level. It is interesting t that Prx2 was almost exclusively expressed in thin phenotypes and in the same samples Prx1 was absent, implying opposing roles of the two genes in adult gingival tissues. Overall, our study indicates a strong association of Prx1 and Prx2 gene expression with the gingival phenotype. It is possible that Prx gene expression can be used as a molecular screening test to define more accurately the gingival phenotype.

Acknowledgment

Apostolos S. Angelidis, D.V.M., M.P.V.M., Ph.D. Laboratory of Milk Hygiene and Technology Department of Food Hygiene and Technology School of Veterinary Medicine Aristotle University of Thessaloniki, Greece

#For more information #https://lupinepublishers.com/dental-and-oral-health-journal/archive.php #Please Click here #https://lupinepublishers.com/neurology-brain-disorders-journal/#lupine Publishers #MODERN APPROACHES IN DENTISTRY AND ORAL HEALTH CARE #Dental Health

4 notes · View notes

lupinepublishers-ojnbd · 4 years ago

Text

Lupine Publishers| Sleep is for Life: an Essential Part of Everyday Life

Lupine Publishers| Journal of Neurology and Brain Disorders

Abstract

Sleep is essential for basic survival as well as for optimal physical and cognitive performance in both human beings and animals. Sleep is a normal human function that is detrimental to sustaining life yet; individuals are affected differently by their sleep schedule. However, the community at large often underestimates sleep and its importance, therefore leading people to not be as concerned with a proper night’s sleep, thereby preventing them from performing at peak efficiency. Sleep plays a vital role in learning and when a person fails to obtain enough sleep the night prior, neurons in the brain might not fire properly, the body becomes out of synch, and it can even lead to accidental physical injuries. As many studies have been conducted, the majority have seemed to come to similar conclusions: a lack of sleep can have detrimental side effects on the human mind and body and by regularly obtaining enough sleep each night; a person can function more efficiently.

Introduction

Go to

Sleep is one of the great unsolved mysteries of biology. Actually a large part of the population spends one third of his life asleep, it is therefore not surprising that this phenomenon has always been a great fascination for humanity. It is an important physiological process responsible for the physical, mental and emotional health of a living being. A good sleep is one of the most satisfying human experiences with a role to play in maintaining a good mood and cognitive acuity as well as in promoting physiologic balance and resilience [1]. Sleep is a regular physiological state of natural life and is observed in majority of organisms [2]. Sleep is a naturally persistent reversible state of rest state characterized by reduced or absence of consciousness, suspended sensory activity, and inactivity of voluntary muscles. Sleep is a heightened anabolic state, accentuating the growth and rejuvenation of the immune, nervous, skeletal and muscular systems [3]. It is generated by complex but specific brain neuronal circuitry and heavily influenced by various factors such as biological rhythms, hormonal changes and environmental factors [4,5]. Sleep is an essential element of the human condition, which allows us to perform critical daily functions at peak optimization when obtaining in the correct amount. Sleep is important because it has a determining role in mental and physical health, along with quality of life [6,7]. Sleep, a complex phenomenon, is not merely the result of physical fatigue or decrease in activity; instead it is a complicated behavioural state requiring the integration of several neuronal processes [8].

Sleep Stages

Sleep is a reversible, physiological state with reduced motility. It is subdivided into REM sleep (rapid eye movement sleep, paradoxical sleep, active sleep, D sleep or deep sleep, REMS), and NREM sleep (SWS or slow wave sleep, non-REM sleep, NREMS). REMS is characterized by muscle atonia, activation of several brain areas, including the cortex and physically occurring eye movements, muscle twitches and changes in pulse rate, blood pressure and respiration. NREMS is characterized by body rest [9].

Functions of Sleep

Sleep is a global state, the control mechanisms of which are manifested at every level of biological organization: from genes and intracellular mechanisms to networks of cell populations, and to all central neuronal systems that control movement, arousal, autonomic functions, behaviour and cognition [10]. Sleep boosts up the immune functions has a role in brain maturation and helps in energy conservation. [11,12].Sleep contributes to memory consolidation possibly by enhancing synaptic plasticity [13]. Xie and colleagues reported that during sleep, waste products of brain metabolism are removed from the interstitial space among brain cells where they accumulate this is due to change in the brain’s extracellular space between sleep and waking states [14]. In sleep, metabolic rates decrease and reactive oxygen species generation is reduced allowing restorative processes to take over. It is theorized that sleep helps facilitate the synthesis of molecules that help repair and protect the brain from these harmful elements generated during waking [15].

Though sleep is essential for life, it is difficult to enumerate its functions. Sleep is needed to regenerate certain parts of the body, mainly the brain, so that it may continue to function optimally. One of the important functions of sleep is to promote synaptic plasticity and neuronal recovery for proper brain functioning. Memory consolidation, brain growth and repair are other functions proposed for sleep [16,17]. Various Behavioural and electrophysiological studies have revealed that sleep plays a crucial role in long-term memory storage [18].

It is stated that sleep is essential for restoration and recovery. Energy conservation is one function that is proposed for sleep. It is thought that sleep may help the body conserve energy and other resources that the immune system needs to mount an attack on diseases. Sleep may help to discharge emotions through dreaming [17]. Many experiments have shown that we retain newly acquired knowledge or a newly learned skill more effectively the day after a good night’s sleep and because the hippocampus is known to be heavily involved in encoding memories, REM sleep may thus contribute to learning and memory [19]. The amygdala– hippocampus–medial prefrontal cortex network involved in emotional processing, fear memory and valence consolidation shows strongest activity during REM sleep [20].

Summary

Although sleep occupies approximately a third of the human lifespan, the amount of time humans spend awake has increased over the years. Many neurological diseases from Alzheimer’s to stroke and dementia are associated with sleep disturbances. Lack of sleep could have a causal role, by allowing the byproducts to build up and cause brain damage. Sleep is one of the important needs like oxygen and nutrition for survival. Sleep is a basic drive of nature. Sufficient sleep helps us think more clearly, complete complex tasks better and more consistently and enjoy everyday life more fully. “You probably develop damage if you don’t get your sleep.”

“Sleep that knits up the ravelled sleave of care, The death of each day’s life, sore labour’s bath, Balm of hurt minds, great Nature’s second course, Chief nourisher in life’s feast.”

For more Lupine Publishers Open Access Journals Please visit our website: https://lupinepublishers.us/

For more Open Access Journal of Neurology & Neurosurgery articles Please Click Here:

https://lupinepublishers.com/neurology-brain-disorders-journal/

#Neurology and Brain Disorders #neurology #Neuroscience #neuro #brain development #brain disorders #journal of neuroscience #Lupinepublishers #Lupine publishers #Lupine Publishers Group

2 notes · View notes

lupine-publishers-lojpcr · 4 years ago

Text

Lupine Publishers | A De-Novo SCN2A Mutation Identified in a Chinese Patient With Epilepsy: A Case Report

Lupine Publishers | LOJ Pharmacology & Clinical Research

Abstract

Objective: To investigate the genetic causes of epilepsy in a 5-year-old Chinese female patient.

Methods: Clinical diagnosis and next-generation sequencing.

Results: The patient carries a de-novo heterozygous missense mutation (c.3686 A>T p.Asp1229Val) in the SCN2A gene. This mutation was evaluated as a pathogenic mutation based on the standards and guidelines of ACMG (American College of Medical Genetics and Genomics) and clinical research publications.

Conclusion: The de-novo heterozygous mutation (c.3686 A>T p.Asp1229Val) in the SCN2A gene is the genetic cause of the epilepsy for the patient. So far, this mutation of SCN2A gene is the first reported in the worldwide overall populations.

Keywords: Chinese; Epilepsy; SCN2A gene

Abbreviations: Whole Exome Sequencing (WES); Sanger sequencing; American College of Medical Genetics and Genomics (ACMG)

Introduction

The SCN2A gene encodes the voltage-gated sodium channel Na(v)1.2, which plays an important role in the initiation and conduction of action potentials. SCN2A is expressed in axon initiation segments and at nodes of Ranvier in myelinated nerve fibers during early development, and is later expressed in unmyelinated axons [1]. Mutations in the SCN2A gene, cause a variety of neuropsychiatric syndromes with different severity ranging from self-limiting epilepsies with early onset to developmental and epileptic encephalopathy with early or late onset and intellectual disability (ID), as well as ID or autism without seizures [2-4]. So far, more than 700 mutations in SCN2A were reported to be associated with epilepy [5]. The aim of the present study was to detect and report genetic causes of a 5-year-old Chinese female patient with epilepsy. The patient was found to have a de-nove mutation (c.3686 A>T p.Asp1229Val) in the SCN2A gene that has not reported in the previous studies.

Materials and Methods

Clinical diagnosis

A 5-year-old female Chinese patient who was born with no family history of seizures or other types of neurological diseases, has experienced epileptic spasms since she was 1.5 years old. The patient had fallen down while she was walking, and her head contacted the ground, but she did not loss consciousness at the time. On the same day, the patient began to nod her head continuously, with each occurance lasting approximately several seconds in length. Since then, her head nods occurred in clusters daily, and up to 30 to 40 times a day at the worst cases. The patient was carried to the hospital and was diagnosed with infantile spasms. Her symptoms of head nodding was relieved after treatment with intravenous immunoglobulin (pH4), Sodium valproate oral solution and Topiramate. The patient took Sodium valproate oral solution and Topiramate after her discharge from the hospital. However, she still had the head nods which occurred at random intervals. After she turned 2-years-old, the head nods did not occur again, but she began to have epilepsy symptoms such as loss of consciousness, twitching of the limbs, spitting out white foam et al. The epilepsy happened approximately once a month and lasted approximately 1 to 2 minutes in length at each occurence. The patient visited the hospital again and the Clonazepam was added to her medications [6]. Her symptoms of epilepsy were being controlled well and did not happen within a 8 month period. However, in April of 2019, when the patient was 5 years old, her head nods occurred again without any obvious causes. This time, the head nods happened in the early morning, and 4～5 times everyday. The patient was admitted to our hospital (the Second Hospital of Shanxi Medical University). The following tests were performed for the patient: physical examinations, brain MRI, and electroencephalogram.

Molecular test

In order to study the cause of the disease, whole exome sequencing was performed for the patient. Furthermore, Sanger sequencing was used to verify the variant for the patient and her parents. Sequencing data was analyzed by using numerous bioinformatics’ softwares, the pathogenicity of the mutation was evaluated based on the standards and guidelines of ACMG (American College of Medical Genetics and Genomics), Clinvar database, OMIM (Online Mendelian Inheritance in Man), HGMD (Human Gene Mutation Database), and clinical research papers published in scientific journals.

Results and Analysis

Clinical data analysis

The patient was admitted to our hospital in April of 2019. The patient appeared normal under physical examinations. She has a clear mind, but only can pronunce simple words. She had poor orientation, cognition, memory, calculation, and attention span. Brain MRI showed that the symmetrical brain hemispheres on both sides, and the structures of gray and white matter were normal. No other abnormalities were found in the brain parenchyma (Figure 1). The electroencephalogram of the patient showed that the slowwave activity were in the awake period (Figure 2A). Total epileptic discharge during sleep period (Figures 2B & 2C). The patient was given intravenous human immunoglobulin and Dexamethasone for immunotherapy. The medications she has had were also adjusted to Levetiracetam tablets, Clonazepam, Topiramate, and Sodium valproate oral liquid. No recurrence of the head nods after 3 month of the treatment. Figure 2D showed that no obvious abnormal discharge was found in the patient’s return visit on Oct. 2020.

Molecular biological data analysis

In order to identify the causes of the patient’s seizures, we conducted Whole Exome Sequencing (WES) based on Nextgeneration sequencing for the patient. a heterozygous missense mutation in SCN2A gene (c.3686 A>T p.Asp1229Val) reference transcript, NM_001040143) was detected in the patient. This variant was further confirmed by Sanger Sequencing, and not detected in either of the healthy parents, which indicated that this variant was de novo (Figure 3A). No other pathogenic variants were detected in more than approximately 800 genes that were defined by the OMIM database as related with epilepsy syndromes for this patient (Figures 3B & 3C). The mutation c.3686 A>T (p.Asp1229Val) either not being recorded in any clincial disease-related database (Clinvar and HGMD), nor in Human genome databases (1000 Genome and Genome mutation frequency database). The function prediction databases (SIFT and polyphen, etc.) predicted this mutation to be damaging. This variant was evaluated as a pathogenic mutation based on the standards and guidelines of ACMG.

Discussion

Pathogenic variants in SCN2A are reported in a spectrum of neurodevelopmental disorders including developmental and epileptic encephalopathies, benign familial neonatal-infantile seizures, episodic ataxia, and autism spectrum disorder and intellectual disability with and without seizures [1]. More than 1000 mutaions of SCN1A gene were reported in the Clinvar database, including deletion, duplication, indel, insertion and single nucleotide types. Around 70% of those variations was evaluated as responsible for the occurences of Benign familial infantile seizures or early infantile epileptic encephalopathy 11. The single nucleotide mutations were the most frequently reported mutations and were 84% in the total mutation types. However, only about 8.5% of the single nucleotide mutations were due to de-nove mutations in the SCN2A gene. Comparing with the 65% of the de-novo rate in the SCN1A gene, the rate of de-novo in the SCN2A gene is significantly lower [6]. We evaluated WES data from 332 Chinese patients with epilepsy and identified the one de-nove missense mutation in the SCN2A in this patient and the mutation was evaluated as the cause of the disease. Generally, the de-novo mutations of SCN2A gene often lead to severe phenotype with developmental delay [3]. The patient in our case reported here is only 5 years old, but she had epilepsy syndromes for more than three years and had more severe symptoms such as poor orientation, cognition, memory, calculation, and attention et al. The mutation of the SCN2A gene we detected (c.3686 A>T p.Asp1229Val) has not been recorded in the Clinvar database as of today [6]. Our report provided further evidence for the cause of epilepsy from a genetic level. We predict the result will be immediately useful for the clinical interpretation of SCN2A variants, and also provides deeper insights for SCN2A mutations associated with the broad clinical spectrum of seizures.

Declarations

The experimental protocol was established, according to the ethical guidelines of the Helsinki Declaration and was approved by the Human Ethics Committee of the Second Hospital of Shanxi Medical University. Written informed consent was obtained from individual or guardian participants. This study was supported in the part by grants from the Epilepsy Research Fund (UCB No. 2014007) from China antiepileptic Association.

https://lupinepublishers.com/pharmacology-clinical-research-journal/fulltext/a-de-novo-scn2a-mutation-identified-in-a-chinese-patient-with-epilepsy-a-case-report.ID.000139.php

https://lupinepublishers.com/pharmacology-clinical-research-journal/pdf/LOJPCR.MS.ID.000139.pdf

For more Lupine Publishers Open Access Journals Please visit our website: https://lupinepublishersgroup.com/ For more Pharmacology & Clinical Research Please Click Here: https://lupinepublishers.com/pharmacology-clinical-research-journal/ To Know more Open Access Publishers Click on Lupine Publishers

Follow on Linkedin : https://www.linkedin.com/company/lupinepublishers Follow on Twitter : https://twitter.com/lupine_online

#Lupinepublishers #Lupine Publishers Group #lupine publishers indexing Journals

0 notes

lupine-publishers-rrhoaj · 4 years ago

Text

Lupine Publishers|Neurosarcoidosis: A Review of the State of Art

Lupine Publishers | Journal of Health Research and Reviews

Abstract

Neurosarcoidosis is a rare disease, difficult to diagnose. A correct diagnostic approach should include a multidisciplinary assessment involving physicians, radiologists and pathologists. Corticosteroids are the first-line treatment for neurosarcoidosis, followed by steroid-sparing immunosuppressants.

Keywords: Sarcoidosis; Neurosarcoidosis; Central Nervous System Diseases; Peripheral Nervous System Diseases

Introduction

Sarcoidosis is a chronic disease with a highest annual incidence among African-American females (39.1/100,000) and males (29.8/100,000), followed by Caucasian females (12.1/100,000) [1]. Although sarcoidosis continues to be considered as an idiopathic disease, there is an increasing evidence of a genetic predisposition that associated with several environmental factors that act as trigger agents (e.g. mycobacteria, viruses, neoplasms and inorganic compounds as aluminum) contributes to the development of the disease [2]. Lungs and intrathoracic lymph nodes are the most frequently affected sites, but sarcoidosis can also involve the heart, skin, joints, gastrointestinal tract and nervous system.

Neurosarcoidosis

The involvement of the central and peripheral nervous system (neurosarcoidosis) is rare, clinically happening in about 5-10% of patients with sarcoidosis, with an average age of onset around 33-41 years [1]. Because of the rarity of this entity and the nonspecificity of its clinical and radiological findings, there is surely a high percentage of poorly diagnosed cases, mainly in an initial approach, as the neurological involvement can be found in up to 25% of autopsies from patients with sarcoidosis [1,2]. Non-specific symptoms such as fatigue, headache, cognitive dysfunction and mood disorders are frequent in cerebral neurosarcoidosis, but the clinical picture is usually dominated by cranial neuropathy or aseptic basilar meningitis. The damage of the optic nerve, the most frequently affected followed by the facial nerve, is associated with a poor prognosis in terms of visual recovery [3]. Spinal neurosarcoidosis can be divided into intramedullary and extramedullary involvement (leptomeningeal, extradural, vertebral and disc involvement); paresthesia and weakness of the lower extremities are the main symptoms, although it often presents as symmetric sensory motor polyneuropathy. Rarely, cases of sudden paraplegia can occur, along with bowel and bladder dysfunction [3].

Diagnosis

The Zajicek criteria are the mostly adopted classification system for neurosarcoidosis established in 1999 and later revised. The other set of criteria belong to WASOG (World Association of Sarcoidosis and Other Granulomatous Disorders), updated in 2014. The specificity and sensitivity of these two options are unknown [4]. A definite diagnosis of neurosarcoidosis can only be established with a positive biopsy of the affected nervous system, frequently considered impossible or too invasive; for this reason, the biopsy is usually performed outside the central nervous system, in a peripheral nerve or another affected and more accessible organ (as neurosarcoidosis frequently coexists with other organ involvement). None of the serum biomarkers used nowadays have been accepted as the one that stablishes the diagnosis, including the angiotensin converting enzyme (ACE) or the serum soluble activity of the interleukin-2 receptor (sIL2 receptor) [1].

Levels of ACE in cerebrospinal fluid (CSF) have a low sensitivity (between 24-55%), but may raise the suspicion of neurosarcoidosis due to its high specificity (around 94%). It seems that there is no correlation between serum and CSF levels of ACE and serum levels do not correlate with the degree of clinical activity [5]. Image findings should not be considered alone for the diagnosis of neurosarcoidosis, but always included in an appropriate diagnostic algorithm. Magnetic resonance imaging (MRI) is the preferred imaging technique because it provides the best definition for brain and spinal cord disease [3,4]. Meningeal involvement can appear as nodular or diffuse enhancement on contrast-enhanced T1- weighted images, mainly in the basilar meninges, as opposed to intraparenchymal lesions that manifest as multiple small, nonenhancing periventricular or subcortical white matter lesions, with high signal on T2-weighted images [3]. Fluorodeoxyglucose positron emission tomography (FDG-PET) can reveal areas of hypermetabolism that correspond to active lesions in asymptomatic sites, which can be used to identify suitable sites to do a biopsy, although there is a lack of evidence regarding the use of FDG-PET and its usefulness in neurosarcoidosis [4]. Histopathologically, neurosarcoidosis is characterized by the presence of noncaseating epithelioid granulomas, the same lesions as those found elsewhere in the body in systemic disease. These granulomas although not specific for sarcoidosis, are valuable diagnostic clues [1]. The differential diagnosis includes: tuberculosis, especially in endemic areas, other infections like histoplasmosis, aspergillosis and cryptococcosis, but also granulomatosis with polyangiitis [6].

Treatment

There are no international guidelines to treat neurosarcoidosis and randomized clinical trials are lacking to make treatment recommendations. Taking this into consideration, there is a general consensus that corticosteroids should be the first line of treatment, as the majority of patients improve with only glucocorticoids [1,3,7]. If the symptoms are severe, with involvement of the central nervous system, a short course of intravenous steroids is usually given, up to 1g of methylprednisolone a day for 3-5 days. Subsequently, or if the clinical symptoms are less severe, oral steroids can be administered (e.g. prednisone 40-80mg, around 1mg/kg/day), with gradually descending pattern until the lowest effective or maintenance dose (around 10mg/day). Relapse often occurs after the dose of glucocorticoids is tapered down; if the required maintenance dose is more than 10 mg a day, or if clinical response is insufficient, it is recommended to add a steroid-sparing immunomodulatory agent. The evidence is in favor of methotrexate (between 10-25mg once a week), but other immunosuppressant drugs can be considered, such as azathioprine (at 2mg/kg/day, maximum 200mg/day) [1,3,7]. In severe resistant or refractory cases, cyclophosphamide is classically used (500-1000mg iv every 2-4 weeks, or at a dose of 0.5g/m2 of body surface area every 4 weeks).

Anti- TNF-alpha agents are becoming strongly recommended because of the increasing evidence of rapid reversal of clinical and radiologic features with these agents, especially infliximab (intravenously at a dose of 3-5mg/kg at weeks 0,2 and 6, with intervals of 4-6 weeks thereafter); some groups are already considering this treatment option before cyclophosphamide [3,7]. Patients treated with long-term infliximab could develop anti-infliximab antibodies that will lead to treatment failure. To avoid this, concomitant methotrexate is recommended, as an immunomodulatory agent. When to stop the treatment remains controversial [7]. Surgery is generally limited to the diagnostic biopsy rather than to the therapeutic use. Cranial mass lesions could benefit from radiation therapy, although this is not recommended as standard treatment [3].

Prognosis

There is no cure, but optimal immunosuppressive therapy can achieve clinical remission in approximately two thirds of cases, along with variable improvement in imaging findings. Despite the use of new therapies, close to one third of patients remain stable, deteriorate or die [3,8].

Conclusion

The optimal diagnostic approach to neurosarcoidosis should include a multidisciplinary team with physicians, radiologists and pathologists. Corticosteroids are the first-line of treatment, followed by steroid-sparing immunomodulatory agents. There is increasingly more evidence considering anti-TNF-alpha agents as the therapeutic of choice for severe resistant or refractory cases. When clinical deterioration progresses despite intensive immunosuppression treatment, an alternative diagnosis should always be ruled out. New therapeutic approaches are expected in the upcoming years.

For more Lupine Publishers Open Access Journals Please visit our website: http://lupinepublishers.us/ For more Research and Reviews on Healthcare articles Please Click Here: https://lupinepublishers.com/research-and-reviews-journal/ To Know More About Open Access Publishers Please Click on Lupine Publishers Follow on Linkedin : https://www.linkedin.com/company/lupinepublishers Follow on Twitter : https://twitter.com/lupine_online

#Lupinepublishers #Lupine publishers #Lupine Publishers Group

0 notes

lupine-publishers-ctbb · 5 years ago

Text

Some Simple Mathematical Models in Epilepsy

Lupine Publishers- Biostatistics and Biometrics Open Access Journal

Abstract

Epilepsy is a chronic disorder of the brain that affects people of all ages. Here epileptic seizures equations are related to the telegraph equation.

Introduction

Some Basic Facts about Epilepsy

Epilepsy is a chronic disorder of the brain that affects people of all ages. Approximately 50 million people worldwide have epilepsy, making it one of the most common neurological diseases globally. People with epilepsy respond to treatment approximately 70% of the time. About three fourths of people with epilepsy living in lowand middle- income countries do not get the treatment they need. Therefore, using different approaches to study epilepsy is useful [1].

2.2. Telegraph Equation in Epilepsy

Telegraph equation [2,3] is a generalization of diffusion equation where the standard diffusion equation depends on the continuity equation and Fick’s law

Where,

j is the diffusing object (e. g. technology, concept, etc...),

c is the distribution function of this object and

D is the diffusion constant.

The resulting standard diffusion equation is

where is the second order differentiation w. r. t. position x.

A basic weakness of this equation is that the flux j reacts simultaneously to the gradient of c and consequently an unbounded propagation speed is assumed. To solve this problem Fick’s law is replaced by

where T is a time constant which measures the memory or delay effect. Thus, one gets the telegraph equation:

Applying this equation to the case

and making the identifications

one regains equations 1-4 in [4] where t0 is small and we made the expansion

These equations are used to explain dynamical properties of epileptic seizures.

For more Lupine Publishers Open Access Journals Please visit our website:

https://lupinepublishers.us/

For more Bio statistics and Bio metrics Open Access Journal articles Please Click Here: https://lupinepublishers.com/biostatistics-biometrics-journal/

To Know More About Open Access Publishers Please Click on Lupine Publishers

#Lupinepublishers #Lupine Publishers Group #lupine publishers #Journal of Biometrics #Lupine Publishers Review on Biostatistics and Biometrics Journal

0 notes

narcissistpsychopath-abuse · 6 years ago

Link

Sam Vaknin,

Member of the Editorial Board Scholarly Journal of Psychology and Behavioral Sciences

https://lupinepublishers.com/psychology-behavioral-science-journal/editorial-committee.php

Membership in Editorial Boards

http://www.narcissistic-abuse.com/mediakit.html

Editor in Chief of Journal of Psychology and Psychiatry Studies (Certificate of Editorship)

Member of the Editorial Board of International Journal of Psychological Research and Reviews (IJPRR) (Certificate of Editorship)

Member of the Editorial Board of Archives of Psychiatry and Behavioral Sciences

Member of the Editorial Board Scholarly Journal of Psychology and Behavioral Sciences

Member of the Editorial Board of Psychology and Psychological Research International Journal (PPRIJ)

Member of the Editorial Board of Journal of Clinical Review & Case Reports

Associate Editor of International Journal of Arts and Humanities

Member of the Editorial Board of Psychology Research

Member of the Editorial Board of Clinical Depression

Member of the Editorial Board of Asclepius Medical Case Reports

Member of the Editorial Board of Psychology and Psychotherapy: Research Study

Member of the Editorial Board of EC Psychology and Psychiatry

Member of the Editorial Board of Journal of Neurology, Psychiatry, and Brain Research

Member of the Editorial Board of Global Journal of Addiction and Rehabilitation Medicine

Member of the Editorial Board of Research Journal of Sports and Health Psychology

Member of the Editorial Board of Bipolar Disorder (Open Access)

0 notes

lupinepublishers · 4 years ago

Text

Lupine Publishers|Mental Illness at Work – Forms of Managerial Intervention

Abstract

Mental illness is still a gray area at most Austrian companies and remains associated with various stigmas, even though nearly one in every 10 days of sick leave is due to mental illness. This causes the phenomenon of presenteeism, and it also results in a considerable cost for the business and the economy as well as losses in productivity. Numbers of sick days taken due to mental illness are growing significantly, and this trend can only be counteracted with a corporate culture of openness, education, and destigmatization, and by taking the appropriate measures in all aspects of prevention. Both companies and politicians are therefore called upon to become proactive by creating the appropriate framework.

Keywords: Mental Illness; Early Intervention; Presenteeism; Awareness; Destigmatization; Workplace

Introduction

Since the mid-1990s, statistics produced by the Austrian association of social insurance providers have shown a clear trend with a high growth rate: While the number of absences caused by other significant illness groups such as injuries, cardiovascular disease, and respiratory, muscular and skeletal disease has declined slightly, the number of sick days caused by mental illness has almost tripled over the same period (Figure 1). However, the actual significance of these mental health problems for the overall health of the labor force is difficult to estimate on the basis of these statistics. It is clear that over this period doctors have been more prepared to attribute health problems to mental causes. But it is safe to assume that numerous cases of sick leave, some of which are caused by poor mental health, continue to be attributed to other illness groups due to the symptoms present when the diagnosis is made. For example, complaints such as allergies, stomach ache, and circulation problems can be caused by stress and psychological strain without the resulting cases of sick leave being attributed to mental health problems.

Figure 1: Development of mental illness (source: Austrian association of social insurance providers).

The major significance of mental stress and illness in the working environment can be confirmed with other sources. Studies have repeatedly shown that depression, stress, and anxiety are among the health problems most frequently cited by employees in relation to their job. The OECD estimates that in its member states between 20 and 25% of the working-age population are affected by clinical mental health issues. Around 5% have serious mental disorders, while the remaining 15% have minor to moderate disorders [1]. The average duration of sick leave taken by individual employees as a result of mental illness is 34.6 days per incident – nearly four times as long as for somatic illnesses, which on average across all illness groups result in just 9.6 sick days per incident (Figure 2) [2]. But how can this huge increase in illnesses and sick leave be explained? Has mental stress at work increased in recent years? Have employees become less resilient? Is it that we can now talk more openly about mental disorders, so that we are finally seeing the true extent of the burden of disease? Are we better at diagnosing mental health problems than we were before?. All these reasons play their part to a certain extent.

Figure 2: Average length of sick leave, “Somatic versus mental”.

Spiraling Costs

As the data shown above make clear, psychiatric illness has become a major cost factor for businesses and the Austrian economy as a whole. And the pension statistics also reveal some extremely alarming figures: the 2019 annual report produced by the Austrian pension insurance institution shows that 6.6% of working-age people in Austria are disabled or unable to work. The largest cause of early retirement is mental illness (43.8%), a long way clear of the next-highest causes – musculoskeletal conditions (17.4%) and nervous system disorders (7.9%) – while 66.1% of people claiming rehabilitation allowance were doing so as a result of mental illness [3] (Figures 3-5). Taking into account the fact that disorders are frequently under-diagnosed and misdiagnosed for a variety of reasons, the increase in absences from work as a result of mental health problems is even bigger than shown by the statistics.

Presenteeism and Absenteeism

In addition to longer periods of absence and incapacity for work, there is the problem of reduced productivity and performance from those employees who frequently come into work when they are ill. This phenomenon is known as “presenteeism”. Employees suffering from depression, for example, make more mistakes at work and do not work as quickly as their healthy colleagues. Typical symptoms of this illness, such as impaired concentration and ability to retain information, negatively impact performance, and sufferers also tend to withdraw socially from their working environment, which can add to the strain on the rest of their team. By contrast to presenteeism, there is the problem known as absenteeism, which refers to feigning illness when the person is in fact fully able to work. Presenteeism and absenteeism are also called “motivated absence”, and just like absences caused by health issues they have a harmful short and long-term impact both economically and socially. The 2018 Austrian workplace absence report, which focused on this issue, concluded that both absenteeism and presenteeism can be influenced by personality traits [see below], but also that workplace and organizational factors (such as corporate culture and leadership) and structural factors (such as workplace safety) play a role [4].

The 2018 Workplace Absence Report Identified the Following Primary Risk Factors for Presenteeism at a Personal Level

a) Problems setting personal boundaries b) A strong feeling of loyalty towards managers and colleagues c) A sense of obligation towards customers/clients d) Work that can only be performed by the individual in question, e.g. in the case of staff shortages or a high level of specialization. e) A strong sense of camaraderie within teams, e.g. when working on projects with tight deadlines [4].

The Report Identified the Following Risk Factors at an Organizational or Structural Level

a) Poor leadership and corporate culture, e.g. when there is little respect, trust, or support between management and employees, or when employees are suspected of not having genuine reasons for absences, b) High working demands with inadequate support [4].

In the workplace absence report, presenteeism and absenteeism were measured on the basis of self-reporting collected by surveys. The available survey data clearly show that they are issues of considerable importance for the Austrian economy. Data from the 2014 Austrian Health Survey, alongside analysis carried out by the Upper Austrian Chamber of Labour in its Work Climate Index and Employee Health Monitor for the period between 2008 and 2017, show that over the course of a year around half of Austrian employees display presenteeism [4].

Across All Sectors, those Who Displayed Presenteeism gave the Following Reasons

a) A sense of obligation towards colleagues (60%), b) Lack of a substitute (33%) c) Worry about work that would otherwise not be done (35%), d) Fear of negative consequences (16%), e) Either having themselves had previous problems at work relating to sick leave or knowing that someone else at the company/organization had these problems (around 15%).

However, the 2018 workplace absence report noted considerable differences between the sectors and the qualifying groups [4].

Economic Impact of Mental Illness in Austria and Europe

A report produced by the OECD and the European Commission (Health at a Glance: Europe 2018) revealed that mental illnesses such as depression, anxiety and alcohol/drug addiction affect more than one in six EU citizens. In addition to the impact on citizens’ wellbeing, the OECD estimates that the total cost is over 600 billion euros – or more than 4% of GDP – across the 28 EU countries. A large part of this cost can be attributed to lower employment rates and reduced productivity from people with mental illness (1.6% of GDP or 260 billion euros) and to higher social insurance spending (1.2% of GDP or 170 billion euros), while the rest is accounted for by direct spending on healthcare provision (1.3% of GDP or 190 billion euros) [5]. Millions of people would benefit from earlier diagnosis and treatment of mental illness. The study showed that in Austria the cost is 4.33% of GDP (thus amounting to 15 billion euros), somewhat higher than the European average [5]. The high cost of mental illness for patients, families, employers and the wider economy has also been highlighted by the British publication “Mental Health in the Workplace” [6]. It is therefore little surprise that improving mental health at work has become a key strategic focus. This increased interest has led to new reviews of the evidence base in relation to common mental disorders and to the introduction of policies aimed at boosting mental health and wellbeing in the workplace.

In particular, it has been argued that employers should provide safe and supportive working environments and improve work organization – though this can be difficult in practice. One reason is that mental illness continues to be viewed as an individual’s problem, with the associated stigma, and another is that people confronted with these problems in the workplace (e.g. senior managers, line managers, and HR specialists) often lack the necessary skills to handle them. In addition, access to professional occupational health services is frequently inadequate, especially for employees at SMEs [6].

Managerial Measures to Combat Mental Illness

Effective prevention of mental disorders in employees can only be successful if it is adopted as a corporate goal and if a solution-oriented approach to improve mental health is agreed in consultation with all employees. A crucial aspect of this is companywide support in removing the taboo surrounding this issue, alongside the provision of information and guidance for managers and employees [7].

Destigmatization and Raising Awareness of Mental Illness

There remains a stigma around being mentally ill. Inadequate knowledge about mental illness and the associated stigmas have harmful consequences on the mental health of those affected.

There are three Main Forms of Stigma

a) Public stigmatization: Discrimination by work colleagues, managers, and the population as a whole on the basis of mental illness. b) Self-stigmatization: The person affected internalizes these negative perceptions. c) Structural discrimination: Mental illness is not allocated the same resources by health and pension insurance providers as somatic illnesses.

Prejudices and stereotypes remain widespread: Those suffering from mental illness are considered dangerous, unpredictable, incurable, and even likely to display violent behavior. It is also incorrectly assumed that there is a clear boundary between being mentally healthy and mentally ill, when in fact, mental health is constantly in a state of flux. The preconception that those affected are at fault for their own suffering leads to a lack of understanding and can even cause hostile reactions, and those who are mentally ill are often treated with fear or simply avoided. On top of this, a vague (but very common) sense of “being normal” remains a barrier to opening up about mental health.

These Forms of Stigmatization have the Following Consequences

a) Those affected become withdrawn within their team, b) They and their families suffer from a lower sense of self-worth, c) They begin to feel guilt and shame, d) They only begin psychiatric/psychotherapeutic therapy belatedly or not at all, as they don’t want to be labeled as “mentally ill” by undergoing this therapy, e) In a worst case scenario, suicide is seen as the last and only “way out”.

These factors make clear the importance of raising awareness of the nature and context of mental illness, particularly in a business environment [8].

Awareness Campaigns at Work

One of the key steps that can be taken to improve people’s basic understanding of this issue are awareness campaigns on the facts and figures, available treatments, and wider context surrounding mental illness in today’s workplace. These should aim to involve all employees, no matter where they are in the company hierarchy, and can for example be conducted through “Mental Health Awareness Days” or employee events.

It is Recommended that the Following Messages (Among Others) be Conveyed to Employees

a) One in three Austrians will suffer from mental illness at some point in their life (“It can happen to anyone”). b) Mental illness can be treated effectively. c) Seeking professional help is no reason to feel ashamed (“the sooner the better”). d) There are treatments available and people to talk to in a psychosocial network (“Where can I turn to if I need help?”).

There are lots of creative ways to design destigmatization campaigns using a variety of media. For example, the content can consist of videos of those affected (whether employees or senior managers) talking about their experience of mental illness and how they returned to work. The key message to convey is: “If only I’d done something about it earlier, I’d have made things a lot easier for myself!”. This testimony, alongside informational material and e-learning tools, can help improve general awareness of mental illness.

The Following were Identified as Essential Requirements for Good Work [9]

a. A secure job with a secure income (92%) b. Meaningful, varied work (85%) c. The social aspect of work (84%) d. Health and safety (74%) e. Scope for influence and freedom to act (71%) f. Opportunities for development (66%) g. High-quality management (66%)

The INQA Study Showed that in Many Sectors Work Conditions were No Better Than “Average”, Meaning that there is Room for Improvement in Various Respects. As a Result of the Study, The Following Approaches can be Recommended to Help Prevent Mental Disorders

a. A respectful, supportive management style, b. A corporate culture explicitly aimed at improving mental health in its mission statement, c. Steps to protect employees with an evaluation of the risk of mental stress factors, d. Measures to promote a positive work atmosphere, e. Opportunities for personal development, f. Sufficient potential to have an influence in order to identify more strongly with the company, g. Policies to enable a good work-life balance, h. Establishing a culture based on trust, i. Work perceived as being meaningful and varied.

Behavioral prevention strategies provide opportunities to improve health skills, such as learning about personal stress and time management, resilience training, and mindfulness-based interventions [8]. However, few well-designed evaluation studies have been carried out on resilience training and mindfulnessbased interventions in a professional environment [10]. Primary preventive measures are in principle always to be welcomed, but the real challenge for companies and managers is reacting promptly and appropriately to specific cases, i.e. employees who are already showing the first signs of possible mental illness.

Secondary prevention (early intervention)

A survey of 312 psychiatrists in Germany showed that around 26% of all mental illnesses are primarily caused by stressful circumstances at work – and that figure is growing [11]. This makes early intervention especially important, alongside the primary preventive steps mentioned above. Mental illness develops over a long period of time, which should provide a sufficiently large window of opportunity to intervene early and effectively. However, this requires a certain level of sensitivity on the part of business management to notice the behavioral changes and drop in performance of an affected employee that indicate undue levels of mental stress.

Early Warning Signs Include

a. Chronic irritability, frequent conflicts with colleagues, b. Withdrawal from the team, resigned behavior, c. Drops in performance at work, frequent excuses for incomplete work, d. Crying without an obvious reason.

These are just some examples of behavior that may indicate the onset of mental illness. Business managers should not just look away when a case begins to develop. Instead, they should show concern for their employee’s welfare by talking to them in private at an early stage and, if required, telling them about the available treatments. Occupational health care professionals have a major role to play as the interface between the workplace and psychosocial treatment services. Targeted management training workshops providing basic skills for responding to mental illness and practice-based training for handling these sensitive conversations using tried-andtrusted guidelines have been proven to work very well at a number of companies.

It is recommended to refrain from giving well-intentioned but inexpert advice such as “Take a few days off”. Neither should (suspected) diagnoses or recommended treatments be expressed, as this is not the responsibility of business managers. Of prime importance in the company’s interest is that the performance of the employee in question return to normal levels. Good managers should have the appropriate skills to handle sensitive conversations, such as active listening, displaying sympathy, and focusing on the key issues arising from the conversations. By meeting their duty of care, and by informing employees confidentially of the professional treatment available (if appropriate), managers can avoid long periods of presenteeism with reduced performance and long absences on sick leave. It does not need to be explained that this goes hand in hand with an enormous potential to save money, and that a clearly defined policy will benefit both management and the team (Figure 7).

Tertiary Prevention (Rehabilitation)

In addition to the pre-existing rehabilitation services for mental illness, the introduction of a law in Austria regulating part-time work during reintegration (known as WIETZ) [12] on 1 July 2017 represented another major step forward in tertiary prevention. It gives employees the opportunity to ease themselves back into working routines when returning from lengthy sick leave absences. After long-term sick leave (defined as at least six weeks), working hours can be reduced by up to 50% when returning to a professional environment before gradually being increased until the employee can perform at full capacity. WIETZ stipulates that this readjustment period can last between one and six months, though if required it can be extended by a further three months. In addition to receiving proportionate pay from their employer, the employee also receives a reintegration allowance funded by health insurance.

Although WIETZ does not obligate employers in Austria to offer a Company Integration Management (CIM) program, companies in Germany have been legally required to do so since 2004 (CIM in section 167 subsection 2 of Volume 9 of the German Social Insurance Code). German employers must offer a CIM program to all employees who within one year are unable to work for an uninterrupted period of longer than six weeks, or who are repeatedly unable to work. As this legal requirement results in clear structural benefits for the implementation and procedure of a CIM program, 18 companies in Upper Austria, with 24,000 employees in total, have agreed to voluntarily adopt this requirement in line with the German model (CIM Network Austria) [13]. A large study and research report (known as EIBE 2) conducted on behalf of the German Federal Ministry of Labour and Social Affairs has also made a compelling case for the economic and business benefits of a CIM program, demonstrating a Return on Investment (ROI) of 1:4.81. In other words, each euro invested leads to a future saving of 4.81 euros [14].

CIM is a key tool for preventing employee absence due to sick leave, which is particularly important when there is a shortage of specialists in the workforce, so it pays off for an employer to offer CIM to its employees. And for the employees themselves, CIM (which is always voluntary) can help prevent unemployment or the need to draw an incapacity pension [15] (Figure 8). In this context, mention should also be made of a synthesis of systematic reviews of databases from between 2000 and 2012 to determine the level of evidence for mental health interventions in the workplace. The search resulted in 3363 titles, of which 14 were eventually found to meet the inclusion criteria and were summarized in the synthesis. The synthesis reported on workplace mental health interventions that impacted absenteeism, productivity, and financial outcomes. It concluded that there is positive evidence for the effectiveness of workplace mental health interventions (in particular multicomponent mental health and/or psychosocial interventions and exposure in vivo containing interventions for particular anxiety disorders). The authors also stated, however, that due to the complexity of the issue further research was required in order to provide clear guidance for business managers on the best workplace mental health interventions.

The Role of Psychiatrists in Reintegration

As psychiatrists, we can make our patients aware that WIETZ can help. The occupational health care professional is their first port of call at work, and they can work with the patient to develop a reintegration plan. If the company does not have an occupational health care professional, patients can use the “fit2work” program (Figure 9).

Example of Successful Reintegration

A manager from the IT sector with diagnosed moderate depression and burnout syndrome was on sick leave for three months, during which time he was treated as an outpatient at our hospital with both drug therapies and additive non-drug therapies. Although his concentration levels and resilience in particular remained limited, he was informed at an early stage of the possibility of part-time work as part of his reintegration. After consulting with contact persons at his company, such as the occupational health care professional and his HR manager, the company approved this step and agreed a period of part-time work of five months to aid his reintegration. This meant he could be eased back in by gradually increasing his workload, which proved to be extremely beneficial for his rehabilitation. On the patient’s request, the company was also able to involve the HR manager to discuss various strategies for tailoring his workload to his levels of resilience. Reintegration was viewed as a process which required continuous monitoring and support. To this end, short weekly feedback conversations were arranged with the HR manager over the first few months to review the effectiveness of the agreed steps. The employee is now fully recovered and performing at normal levels.

#For more Information #https://lupinepublishers.com/neurology-brain-disorders-journal/archive.php #please click here #https://lupinepublishers.com/neurology-brain-disorders-journal/#lupine Publishers #Online Journal of Neurology and Brain Disorders #Rehabilitation

4 notes · View notes

lupinepublishers · 4 years ago

Text

Lupine Publishers|Mental Illness at Work – Forms of Managerial Intervention

Keywords: Mental Illness; Early Intervention; Presenteeism; Awareness; Destigmatization; Workplace

Introduction

Spiraling Costs

Presenteeism and Absenteeism

The 2018 Workplace Absence Report Identified the Following Primary Risk Factors for Presenteeism at a Personal Level

The Report Identified the Following Risk Factors at an Organizational or Structural Level

Across All Sectors, those Who Displayed Presenteeism gave the Following Reasons

However, the 2018 workplace absence report noted considerable differences between the sectors and the qualifying groups [4].

Economic Impact of Mental Illness in Austria and Europe

Managerial Measures to Combat Mental Illness

Go to

Destigmatization and Raising Awareness of Mental Illness

There remains a stigma around being mentally ill. Inadequate knowledge about mental illness and the associated stigmas have harmful consequences on the mental health of those affected.

There are three Main Forms of Stigma

These Forms of Stigmatization have the Following Consequences

These factors make clear the importance of raising awareness of the nature and context of mental illness, particularly in a business environment [8].

Awareness Campaigns at Work

It is Recommended that the Following Messages (Among Others) be Conveyed to Employees

The Following were Identified as Essential Requirements for Good Work [9]

Secondary prevention (early intervention)

Early Warning Signs Include

Tertiary Prevention (Rehabilitation)

The Role of Psychiatrists in Reintegration

Example of Successful Reintegration

#For more Information #https://lupinepublishers.com/neurology-brain-disorders-journal/#Please click here #https://lupinepublishers.com/neurology-brain-disorders-journal/archive.php #lupine publishers #Online Journal of Neurology and Brain Disorders #Mental Illness

4 notes · View notes

lupinepublishers · 4 years ago

Text

Lupine Publishers|Fibrinogen and/or Fibrin as a Cause of Neuroinflammation

Opinion

Involvement of fibrinogen(Fg) and fibrin during various pathologies associated with neuroinflammatory diseases associated with memory reduction are well known. Elevated level of Fg, called hyperfibrinogenemia (HFg) (e.g. ≥ 4±0.1 mg/ml of plasma during inflammation vs.~2±0.1 mg/ml of normal plasma [1]), accompanies inflammatory diseases such as stroke [2,3], hypertension [1,4], diabetes [5] and traumatic brain injury (TBI) [6-9]. Blood level of Fg increases during inflammation in general [10]. HFg is considered not only a marker of inflammation [11] but also a cause of inflammatory responses [12-16]. Gradual extravascular deposition of Fg in the brain accelerates neurovascular damage and promotes neuroinflammation [17,18]. It has been shown that Fg is associated with an increased risk of dementia and AD [19]. Derivative of Fg, fibrin have been found postmortem in the brains of patients with TBI [18,20,8], Alzheimer’s Disease (AD) [21], and multiple sclerosis (MS) [22]. Elevated blood levels of Fg (HFg) are found to be associated with increased risk of AD, cognitive decline, and dementia [19,23]. Furthermore, formations of plaques containing Fg/fibrin were found in inflammatory neurodegenerative diseases associated with memory reduction such as AD [24], MS [25], and TBI [26]. Strong association of Fg/fibrin with amyloid beta (Aβ) peptide was linked to severity of AD [24]. In fact, it has been shown that Aβ mediates formation of clots with abnormal structure and resistance to fibrinolysis [27]. This can be a possible mechanism for Fg-Aβ complex and subsequent plaque formation that is highly resistant to degradation. Although Fg/fibrin [28] and Aβ [29,30] containing plaque formations are the hallmark of AD [28,31,24], some studies indicate that content of Aβ has limited effect on memory [32,33]. These results suggest that formation of Fg-Aβ complex can have a greater effect on loss of memory than deposition of Fg or Aβ alone. Thus, although Aβ is known to be associated with AD [24], a greater role of cellular prion protein (PrPC) in memory reduction has been shown [32,33]. There are data indicating that PrPC is involved in TBI-associated memory reduction [34]. We have recently shown that Fg can specifically associate with its receptor PrPC on the surface of astrocyte [35,36] and others have found that Fg interacts with non-digestive PrPSc [37]. Our data showed that Fg can form a complex with PrPC in extravascular space during mild-to-moderate TBI [9]. As for the functional effects, it has been indicated that Fg that escaped from ruptured brain vessels causes astrocyte scar formation [38] and axonal damage [39]. Our data showed that Fg, which was transcytosed through endothelial cells (ECs) of non-damaged cerebral microvessels deposited in vasculo-astrocyte interfaces [40]. We found that Fg can activate astrocytes [40,41,35]. Furthermore, these effects of extravasated Fg were associated with neurodegeneration [40] and memory reduction during TBI [9,40,42]. All these data indicate an undoubtful role of Fg in inflammatory neurodegenerative diseases associated with memory impairment. However, blood-clotting proteins generate thrombin, which catalyzes the conversion of Fg (factor I) - a soluble plasma protein - into long, sticky threads of insoluble fibrin (factor Ia). Thrombin is a serine protease that is generated by proteolytic cleavage of its inactive precursor, prothrombin. Neurons and glial cells can release prothrombin and thrombin [43]. Therefore, extravasated Fg that is immobilized in extravascular space, eventually, will be converted to fibrin. In literature, the terms Fg and fibrin are often used interchangeably that creates a confusion: it becomes unclear if effects are caused by soluble Fg or its hardened, insoluble derivative – fibrin (a monomer). It has been shown that Fg does not cross blood brain barrier (BBB) in the normal brain of young mice [44]. However, our data showed that at higher (4 mg/ml) than physiological blood level, Fg not only increases EC layer permeability to albumin but itself moves through the endothelium [13]. Furthermore, we found that cerebrovascular permeability was increased in acute conditions of a HFg [12]. Similarly, cerebrovascular permeability was increased in transgenic mice exhibiting inherent HFg [45]. Using our dualtracer probing method, we found that HFg-induced cerebrovascular protein crossing occurred mainly via transcellular pathway [46,45]. Effects of HFg on formation of caveolae and caveolar transcytosis in vitro [47], and an increased cerebrovascular permeability mainly via caveolar transcytosis have been shown [45,48,46]. All these data indicate that, most likely, blood soluble protein - Fg and not its insoluble derivative fibrin, crosses walls of small cerebral vessels during various neuroinflammatory pathologies accompanied with HFg. Crossing the walls of unruptured cerebral microvessels for fibrin that is characterized with high aggregative properties and lesser flexibility is very unlikely. While in the extravascular space, Fg interacts with its receptors intercellular adhesion molecule 1 (ICAM-1) and PrPC [49-51] on the surface of astrocytes [35]. It is possible that Fg can reach neurons and on their surface interact with its receptors - ICAM-1 and PrPC. Thus, these interactions will most likely lead to formation of Fg-PrPC complexes. As Fg is immobilized in extravascular space, it becomes an easy target for thrombin that is released from neurons and glial cells [43]. The rate of plasma Fg (0.1 mg/ml) polymerization is about 23±2 x10-5sec-1, while release of fibrinopeptides A and B from it via enzymatic (thrombin-catalyzed cleavage) step may take from 40 to 120 min [52], maybe even faster. As a consequence of Fg’s conversion to fibrin in Fg-PrPC complex, a highly resistant to enzymatic degradation, fibrin-PrPC complex will be formed. All further effects, including possible formation plaques, would be a result of specific properties of fibrin deposited in the brain extravascular space. Therefore, in our opinion, we need to be careful in describing effects of Fg, when in blood, crosses the vascular wall, deposits in extravascular space and forms complexes with other proteins, and fibrin (which can be formed in blood but least likely to extravasate) that is formed in extravascular space and by creating undegradable protein complexes (and possibly plaques) leads to memory reduction.

Keywords: Memory impairment; Neurodegeneration

Acknowledgement

This work was supported in part by funding from the National Institutes of Health - HL-146832.

#For more information #https://lupinepublishers.com/neurology-brain-disorders-journal/archive.php #please click here https://lupinepublishers.com/neurology-brain-disorders-journal/#lupine publishers #Online Journal of Neurology and Brain Disorders #Brain Disorder

2 notes · View notes

lupinepublishers · 6 years ago

Text

Lupine Publishers - Journal of Neurology & Neurosurgery

Ictal Asystole after Meningioma Resection: Case Report by Adeel Ilyas

We report the first-ever case of left fronto temporal-onset seizures causing ictal a systole, within 24 hours of a left sphenoid wing meningioma resection. It reinforces the importance of close monitoring of neurosurgical patients with continuous EEG. Autonomic dysfunction in various forms, affecting the cardiovascular, respiratory, gastrointestinal and other systems, is commonly associated with seizures. Seizures frequently affect the heart rate and rhythm, often in a transient manner. An increase in heart rate is very common with various kinds of seizures, but ictal bradycardia and a systole are much less common [1]. Symptomatic ictal Brady arrhythmias occur in less than 0.5% of epilepsy patients, and the overwhelming majority have been reported in association with temporal lobe epilepsy. The common presentation is a patient who has complex partial seizures with or without secondary generalizations, who develops ictal a systole and syncope. It has been suggested that this is a seizure self-termination mechanism [2].We report here a case of a woman with new onset seizures caused by a meningioma, who had episodes of ictal a systole following tumor resection. To our knowledge, this is the first-ever report of ictal a systole that began after tumor resection - most cases in the literature noted this in the setting of long-standing temporal lobe epilepsy. While illustrating the importance of the central autonomic network in cardiac function, it also emphasizes the need for neurosurgical patients to be closely monitored following their procedure. To know more please click on below link https://lupinepublishers.com/neurology-brain-disorders-journal/fulltext/ictal-asystole-after-meningioma-resection-case-report.ID.000102.php

For more Lupine Publishers Open Access Journals Please visit our website: https://lupinepublishersgroup.com/ For more Open Access Journal on Neurology articles Please Click Here: https://lupinepublishers.com/neurology-brain-disorders-journal/

To Know More About Open Access Publishers Please Click on Lupine Publishers

#Lupine Publishers #Lupine Publishers Group #lupine publishers indexing Journals #lupine publishers indexing list #Neurology Journal

16 notes · View notes

lupinepublishers-ojnbd · 5 years ago

Text

Lupine Publishers| Ictal Asystole after Meningioma Resection: Case Report

Lupine Publishers|Open Access Journal of Neurology & Neurosurgery

Abstract

Keywords: Seizure; A systole; Meningioma; Case report

Introduction

Autonomic dysfunction in various forms, affecting the cardiovascular, respiratory, gastrointestinal and other systems, is commonly associated with seizures. Seizures frequently affect the heart rate and rhythm, often in a transient manner. An increase in heart rate is very common with various kinds of seizures, but ictal bradycardia and a systole are much less common [1]. Symptomatic ictal Brady arrhythmias occur in less than 0.5% of epilepsy patients, and the overwhelming majority have been reported in association with temporal lobe epilepsy. The common presentation is a patient who has complex partial seizures with or without secondary generalizations, who develops ictal a systole and syncope. It has been suggested that this is a seizure self-termination mechanism [2].

We report here a case of a woman with new onset seizures caused by a meningioma, who had episodes of ictal a systole following tumor resection. To our knowledge, this is the first-ever report of ictal a systole that began after tumor resection - most cases in the literature noted this in the setting of long-standing temporal lobe epilepsy. While illustrating the importance of the central autonomic network in cardiac function, it also emphasizes the need for neurosurgical patients to be closely monitored following their procedure.

Case Report

A 69-year old female with diabetes mellitus with a newly- diagnosed left sphenoid wing meningioma was admitted to our hospital for resection. The meningioma had been diagnosed after she had developed new-onset seizures a month prior to admission. She had been started on levetiracetam for seizure prophylaxis. Her admission labs were significant for elevated glucose, and mild hyponatremia of 128mill moles per liter, that corrected to 135mmol/L when adjusted for elevated glucose level.

After an uneventful left craniotomy and mass removal, she remained in the intensive care unit for monitoring. Late in the evening on the day of her surgery, she had an episode of bradycardia progressing to loss of pulse, for which cardiopulmonary resuscitation with chest compressions was initiated. However, she regained spontaneous circulation quickly. She was showing some confusion and altered speech, and therefore had a long-term EEG placed to rule out seizure. The EEG was significantly asymmetric, with attenuation, slowing, and rare trains of epileptiform activity over the left hemisphere. She had another episode of loss of pulse, requiring cardiopulmonary resuscitation through chest compressions, with the spontaneous return of circulation within 1 minute. EEG revealed subtle left frontal seizure preceding the asystole that quickly spread to the contra lateral hemisphere. Subtle left arm and head jerking were the only other clinical correlate. Diffuse EEG suppression followed the a systole.

She was started on a dopamine infusion, but the next morning she had two more episodes of asystole lasting 15 and 10 seconds in rapid succession. There was EEG evidence of left fronto temporal onset seizures with rapid progression to involve the contra lateral side preceding this asystolic event. There was also evidence for fontal rhythmic intermittent delta activity (FIRDA) on the left, a nonspecific finding that might indicate increased intracranial pressure or other frontal dysfunction. A temporary transvenous pacemaker was implanted. She had an episode of supra ventricular tachycardia, but remained otherwise stable.

Figure 1: (A) Standard scalp EEG sampled at 500 Hz, time compressed at 2mm/sec and viewed with filter 1-70 Hz. The red circle denotes onset of a partial seizure in the left temporal region. The blue circle highlights asystole lasting 56 seconds. (B) Single lead EKG demonstrating bradyarrythmia leading to asystole. (C) left temporal chain electrodes demoinstarting seizure onset. (D) Time compressed FFT (1-40Hz) - left hemisphere over right hemisphere. The black circle highlights the abrupt flattening of EEG following asystole.

Increasing the daily levetiracetam dose and correction of hyponatremia with hypertonic saline led to the cessation of epileptiform discharges on the EEG. However, her affect remained flat, and the decision was made to taper the levetiracetam and start oxcarbazepine. Her seizures remained under control, and no further brad arrhythmias were noted, leading to the removal of the temporary pacemaker five days after it was inserted. The patient was discharged to a rehabilitation facility and remained stable at follow-up (Figure 1).

Discussion

The cause of ictal Brady arrhythmias is debated. There does not seem to be any evidence for primary cardiac conduction defects. It has been suggested that the fact that there are delays between seizure onset and a systole that the pathology involves activation of certain brain regions [2]. It is known that there is a central autonomic network in the brain, of which the insula is a part, and stimulation of areas within it can trigger parasympathetic outflow changes. Catenoix et al. [3] stimulated the insula in human subjects, causing high-frequency discharges there, which were followed by a systole after 2 seconds. A direct postganglionic effect on the heart is possible, which may tend to synchronize autonomic input to the heart with epileptic activity [4].

The insula is a deep structure, and scalp correlate to an insular seizure is likely to be a frontal or a temporal ictal discharge. In our case, subtle but unequivocal left frontotemporal rhythmicity preceded the a systole in both events. It was otherwise absent from the record. It is feasible to postulate that left frontal seizures originating from a known lesion reached the insula, and caused cardiac pause and/or a systolic arrest.

There are some studies which suggest that autonomic control, especially as mediated by the insula, shows hemispheric lateralization, with the right hemisphere predominantly modulating sympathetic tone, and the left hemisphere parasympathetic tone [5]. However, studies on ictal arrhythmias have not been consistent in their findings concerning lateralization [2]. Therefore, the question of what makes certain epilepsy patients prone to Brady arrhythmias and a systole, as opposed to tachy arrhythmias, remains open.

Conclusion

This first report of ictal a systole following meningioma resection reinforces the need for close monitoring of neurosurgical patients, especially with EEG, and being alert to the possibility of a systole and syncope in those with fronto temporal seizures. The brain-heart connection as represented by the central autonomic network's influence on cardiac function needs to be further investigated.

For more Lupine Publishers Open Access Journals Please visit our website: https://lupinepublishers.us/

For more Open Access Journal on Online Journal of Neurology and Neurosurgery articles Please Click Here: https://lupinepublishers.com/neurology-brain-disorders-journal

To Know More About Open Access Publishers Please Click on Lupine Publishers

#Lupine Publishers #Lupine Publishers Group #lupinepublishers #Lupine Publishers Indexing Sites #Lupine Publishers Indexing Journals #open access

7 notes · View notes

lupinepublishers-ojnbd · 5 years ago

Text

Lupine Publishers| Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) Syndrome: A Case Report

Lupine Publishers | Journal of Neurology and Brain Disorders

Abstract

Cerebral autosomal dominant arteriopathy with sub cortical infarcts and leukoencephalopathy (CADASIL) is a rare autosomal dominant genetic disease. A35 year old women presented with progressive loss of memory left sided weakness and hemiplegic and non insulin dependent diabetes mellitus with characteristic MRI findings is reported due to its rarity.

Keywords: CADASIL Small vessel disease; Cognitive impairment

Introduction

Cerebral small vessel disease (SVD) is increasingly being recognized as the cause of stroke, impaired cognitive function and mood disorders in geriatric age group. Commonly SVD is sporadic due to old age and high blood pressure, but occasionally SVD has a monogenic cause. The best known among these is cerebral autosomal dominant arteriopathy with sub cortical infarcts and leuko encephalopathy(CADASIL), a rare type of autosomal dominant cerebral angiopathy. It causes recurrent sub cortical ischemic events and vascular dementia which appear as diffuse white matter abnormality on neuro imaging. It involves mainly the small cerebral vessels; histopathology reveals non-atherosclerotic and non-amyloidal angiopathy. [1] The 1st case of aforementioned symptoms was reported 30 years ago in a Swedish family [2] and the term CADASIL was coined in early 1990's [3] Since then CADASIL has been diagnosed in number of families and ethnic groups all over the world.

The prevalence of the condition varies between 2 and 5 in 100,000. Clinically the condition manifests in early or middle adulthood with variety of complaints ranging from migraine, with or without aura, which occur in 30-40% individual, mood disorders, usually depression seen in 30 % people, along with recurrent ischemic events, transient or permanent, accompanied by progressive cognitive impairment leading to dementia and premature death [4-5].

Case Report

This 35 years old married female patient was brought to the psychiatry outpatient department by her family members with the complaint of gradual decline of memory, difficulty in walking due to residual left sided motor weakness and co morbid Non Insulin dependent Diabetes Mellitus. There was no history of hypertension, depression or psychosis or impaired pain sensation. No history of seizures. EEG done earlier did not reveal any abnormality. There was past history of two episodes of CVA in last 5 years. Family history was not significant for headache but there was history of premature death of uncles. Physical examination showed thin built poorly nourished lady. There was no pallor, cyanosis, icterus, edema or generalized lymphadenopathy. Systemic examination of central nervous system revealed grade 3 motor weakness in left upper and lower limbs. Cranial nerves and fundi were normal. There were no sensory deficits or cerebellar signs. Examination of other systems was normal. Score on Mini Mental Status Examination was 12 out of 20. Relevant investigations including hemoglobin, blood sugar, HbA1c, liver function tests, SGOT, SGPT, alkaline phosphatase, blood urea, serum creatinine, were within normal limits. CT Scan brain showed a lacunar infarct in left external capsular region and age inappropriate diffuse cerebral atrophy. MRI of brain revealed diffuse cerebral atrophy with prominent sulcal spaces with periventricular and subcortical arteriosclerotic white matter changes. Small areas of acute to sub acute infarct in rest of the bilateral parietal and frontal lobes support diagnosis of CADASIL Syndrome.

Discussion

CADASIL gene was first identified on the chromosome 19 in the year 1996 [6] Subsequent studies revealed the mutation of NOTCH3 gene on chromosome 19q12. This gene codes for transmembrane receptor protein which is located on surface of smooth muscle cell which surrounds arteries. When pathological NOTCH3 receptor protein got accumulated in cerebral arteries it resulted in varied symptoms of CADAIL [7].

Patient with CADASIL can present with a variety of psychiatric manifestation in 20-41% of cases. The psychiatric manifestations range from agoraphobia, psychoses, personality disorders, alcohol and substance use disorders, adjustment disorder to episodic mood disturbances and bipolar affective disorder [4,8].

CADASIL should be suspected in individual with history of transient ischemic attacks, migraine, severe mood disturbances or late onset affective disorder with headache and neurological symptoms [8-9]. MRI studies shows hyper-intense lesion and ischemic lesion in Basal Ganglia and frontal location of white matter is associated with mood disturbances in patient of CADASIL [10-11].

To conclude it is advisable to do MRI brain in patients presenting with late onset Psychiatric Disturbances and a diagnosis of CADASIL should be considered as a possible differential diagnosis whenever a marked leukoencephalopathy is reported [12].

https://lupinepublishers.com/neurology-brain-disorders-journal/fulltext/cerebral-autosomal-dominant-arteriopathy-with-sub-ortical-infarcts-and-leukoen-cephalopathy-syndrome-a-case-report.ID.000101.php

For more Journal of Neurology and Brain Disorders articles Please Click Here: https://lupinepublishers.com/neurology-brain-disorders-journal/

To Know More About Open Access Publishers Please Click on Lupine Publishers

Follow on Linkedin : https://www.linkedin.com/company/lupinepublishers

Follow on Twitter : https://twitter.com/lupine_online

#Lupine Publishers #lupine publishers group #Lupine Indexing Journals #open access publishers

2 notes · View notes

lupinepublishers-ojnbd · 5 years ago

Text

Lupine Publishers|Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) Syndrome: A Case Report

Lupine Publishers|Open Access Journal of Neurology & Neurosurgery

Abstract

Keywords: CADASIL Small vessel disease; Cognitive impairment

Introduction

Case Report

Discussion

For more Lupine Publishers Open Access Journals Please visit our website:

https://lupinepublishers.us/

For more Open Access Journal of Neurology & Neurosurgery articles Please Click Here:

https://lupinepublishers.com/neurology-brain-disorders-journal/

To Know More About Open Access Publishers Please Click on Lupine Publishers

https://lupinepublishers.com

#Lupine Publishers #Lupine Publishers Group #Lupinepublishers

2 notes · View notes

lupinepublishers-ojnbd · 5 years ago

Text

Lupine Publishers|Seizure and Psychosis

Lupine Publishers | Journal of Neurology and Brain Disorders

Abstract

Go to

Seizures are due to abnormal excessive and synchronous neuronal activity in the brain [1]. Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness, to shaking movements involving only part of the body with variable levels of consciousness, to a subtle momentary loss of awareness. Up to 10% of people have at least one epileptic seizure in their lifetime out of which 50% have a recurrence [2].

Introduction

Go toAim

To differentiate between different types of psychosis following epilepsy.

Methods

A prospective study was conducted including 1000 consecutive patients with seizure disorder irrespective of the seizure type and cause and followed up between 2010 to 2017. The clinical profile of patients with seizures with respect to age, sex, aetiology of seizure, neurological status, seizure type, investigations, prescription pattern of Anti-Epileptic drugs and response to treatment was analysed.

Results

Out of a total of 1000 patients, 59% of the population had focal seizures and 41% had generalised seizures, 66% were found to have an idiopathic onset, followed by neurocysticercosis, tuberculosis, vascular, post infective, post traumatic and congenital having 16%, 8%, 3%,3% and 2% of the cases respectively. In the study 45.77% of patients with focal seizures remained uncontrolled while 46.35% and 20% of tonic clonic and myoclonic seizures remained uncontrolled. A total of 430 patients were prescribed monotherapy while 460 were on two and 110 on 3 or more drugs. Thirty-eight patients had associated psychosis, 20 patients having postictal psychosis, 12 having brief psychosis out which 3 were chronic (lasting more than 6 months) and 6 having inter-ictal psychosis.

Case Vignette

Go to

A 79-yr old male known to have diabetes and hypertension was admitted with complaints of progressively increasing irritability, alteration in behaviour, forgetfulness and intermittent episodes of disorientation since last 2 weeks. His blood investigations showed hyponatremia of 118meq/L, rest of the blood investigations were within normal limits. Gradual hyponatremia correction was done over 2 days but there was no clinical improvement in the patients’ clinical condition. Neuroimaging and CSF evaluation showed mild elevation in protein (58mg/dl) with normal csf glucose, viral markers and autoimmune antibody panels. Possibility of psychosis due to prolonged hospitalisation was also considered and was started on haloperidol and quitiapine but did not cause any clinical benefit. His EEG showed attenuation of alpha rhythm corresponding to age. He was started on Inj Lamotrigine 100 mg IV BD following which he showed improvement in the orientation and irritability over the next two days and was finally diagnosed as chronic ictal psychosis.

Case II

Go to

68-year-old lady admitted in an ICU at a hospital elsewhere 5 days back with accelerated hypertension, developed irritability, disorientation and loss of bowel and bladder control upon discharge the following day. Her blood investigations were normal including ammonia and liver function tests. Her MRI brain and CSF were within normal limits, EEG showed generalised slowing of theta- delta range. On day two an occasional jerky movement was noted over the face and started on Inj Lacosamide 100 mg IV BD, she showed dramatic improvement after 12 hours, being able to eat solid food herself and walk independently by the evening. She was diagnosed to have brief psychosis with seizures.

Discussion

Go to

The association between epilepsy and psychosis has attracted the interest of neurologists and psychiatrists alike for many years. While much of this interest has concerned the chronic psychosis. The categorization of these brief psychotic syndromes has traditionally been according to their temporal relationship to the seizures, as ictal, postictal, and inter-ictal.

Psychosis: A psychiatric disorder characterized by delusions, hallucinations, disorganized speech or thought, and/or grossly disorganized or catatonic behaviour.

Brief Psychosis: Psychosis that lasts more than a day but generally less than 1 month. Some epilepsy-related brief psychoses may last up to 2–3 months. Psychoses lasting more than 6 months are chronic, and those lasting more than 3 months are tending to chronicity.

Postictal Psychosis: Psychosis that follows immediately after 1 or generally multiple seizures, but certainly within 1 week of the last seizure.

Inter-Ictal Psychosis: Psychosis that develops when the patient with epilepsy has not had a seizure for more than 1 week or is unrelated to the any recent increase in seizure activity [3]. Psychosis may range from acute to subacute in presentation with clinical presentation ranging from mild disorientation to complete lack of awareness, being mute and unresponsive, frank catatonia, irritability and mania. Treatment would include primary biofeedback and behavioural therapy with pharmacotherapy mainly with atypical antipsychotics like quetiapine, olanzapine, aripiprazole. Initially to be started at a lower dosage of olanzapine 2.5 mg daily to 5 mg twice daily.

Conclusion

Go to

Though psychosis immediately following the episodes of seizures is most commonly encountered, chronic psychosis up to 6 months post the episode or those without any prior event are also present and should not be considered unrelated to the primary aetiology. Often it is encountered that a patient may present with psychosis and create a diagnostic dilemma due to long standing psychosis in a seizure disorder patient or psychosis presenting initially in a patient not having a prior history of evident seizures.

For more Lupine Publishers Open Access Journals Please visit our website:

https://lupinepublishersgroup.com/

For more Open Access of Journal of Neurology and Brain Disorders articles Please Click Here:

https://lupinepublishers.com/neurology-brain-disorders-journal/

To Know More About Open Access Publishers Please Click on Lupine Publishers

#Lupine Publishers #Lupine Publishers Group #Lupinepublishers #Lupine Publishers Indexing Sites #Lupine Publishers Indexing Journals

2 notes · View notes