Koji Ohira*

Laboratory of Nutritional Brain Science, Department of Food Science and Nutrition, Mukogawa Women’s University, Nishinomiya, Japan

It is widely accepted that new neurons are generated throughout life, which is called adult neurogenesis, in limited regions of the adult mammalian brain, such as the hippocampal dentate gyrus and subventricular zone. In these regions, neural stem cells (NSCs) and neural progenitor cells (NPCs) have been reported to proliferate and produce postmitotic neurons. Adult neurogenesis in these regions is influenced by various factors. For examples, antidepressant treatments, learning and memory, and environmental enrichment prompt to increase generation and survival of new neurons. Moreover, pathological processes, such as neuroinflammation, stroke or epilepsy, are able to induce proliferation and differentiation of NSCs and NPCs. In contrast, down-regulation of adult neurogenesis is associated with alcohol abuse, high stress level, some drugs, such as cytostatics, COX-2 inhibitors, and opioides. Recently, adult neurogenesis in the cerebral cortex is becoming clear gradually, and cortical NSCs and NPCs are identified in a few mammals. However, it remains largely unknown what factors can regulate adult neurogenesis in the cerebral cortex. This review focuses on the effects of regulating factors on cortical adult neurogenesis, such as brain damages, aging and certain drugs, and we discuss implications of cortical adult neurogenesis for brain diseases and damages.

DOI: 10.29245/2572.942X/2018/4.1192 View / Download Pdf

Mostafa A. Rabie, Mai A. Abd El Fattah, Noha N. Nassar, Dalaal M. Abdallah, Hanan S. El-Abhar*

Department of Pharmacology and Toxicology Faculty of Pharmacy, Cairo University, Cairo, Egypt

The current review sheds light on the importance of the cerebral renin angiotensin system (RAS) in Parkinson’s disease (PD), as a neurodegenerative disorder. Local RAS has been identified in the nigrostriatal pathway and plays a pivotal role in the progression of PD via binding to the upregulated angiotensin II type-1 receptor (AT-1R). Activation of AT-1R induces an oxidative stress neuroinflammatory status that results in further deterioration of dopaminergic neurons. Mas receptor (MasR) together with AT-2R, are considered major components of RAS protective arm, which mediates actions opposing AT-1R activation. Accordingly, angiotensin converting enzyme-2 (ACE-2)/Angiotensin 1-7 (Ang 1-7)/MasR axis has been emerged as a novel therapeutic target to ameliorate the devastating effects of Ang II/AT-1R cue in a 6-hydroxydopamine (OHDA) lesioned PD model. Stimulation of MasR via its physiological ligand Ang 1-7 attenuated 6-OHDA induced neurotoxicity as evidenced by the improved motor performance and coordination along with the preservation of the dopaminergic neurons. Via enhanced MasR/PI3K/Akt/ CREB/BDNF/TrKB neurogenesis cascade, besides both antioxidants and anti-inflammation mechanisms, Ang 1-7 proved its therapeutic benefits in PD, partly through MasR, to open up a new avenue for treatment.

DOI: 10.29245/2572.942X/2018/4.1208 View / Download Pdf

Cuneyt Tetikkurt*

Department of Pulmonary Medicine, Cerrahpasa Medical Faculty, Istanbul University, Turkey

Neurosarcoidosis is a multisystemic disease that involves the the brain, spinal cord, meninges, cranial, or the peripheral nerves. As sarcoidosis is a multiorgan granulomatosis, neurological features may represent the systemic effects of sarcoidosis in other organs or neurosarcoidosis. For the diagnosis of neurosarcoidosis, consistent histological changes in neurologic tissues should occur with systemic involvement in other organs, essentially in the lungs, lymph nodes, skin, or eyes. The prevalance of neurosarcoidosis is difficult to establish because most patients are either asymptomatic, have minor undiagnosed neurologic symptoms, incidence of neurosarcoidosis is variable, and different clinical criteria are used for the identification of neurologic involvement. Neurosarcoidosis occurs in approximately 5 percent of the sarcoidosis patients while postmortem studies reveal that 10 percent of the sarcoidosis cases have neurologic disease. Furthermore, less than 1 percent of sarcoidosis patients may present with isolated neurosarcoidosis. Because of diverse clinical appearence, lack of specific laboratory or radiogic findings, and difficulty to obtain neural tissue biopsy the diagnosis of neurosarcoidosis poses a challenge for the clinician. The prognosis of neurologic involvement is another difficult aspect to predict. Identification of neurosarcoidosis constitutes one of the most crucial aspects of sarcoidosis as the delayed diagnosis may lead to an unfavorable prognostic outcome for the patient.

DOI: 10.29245/2572.942X/2018/4.1190 View / Download Pdf

Claire-Marie Rangon*

Head of Scientific Auriculotherapy Diploma, Faculty of Medicine, University of Paris-Saclay, 94276 Le Kremlin-Bicêtre, France

The ears are a potential gateway to the brain, mainly through their innervation. Transcutaneous stimulation of the vagus (tVNS) and trigeminal (TNS) nerves at the auricles is gaining ground in the field of non-invasive brain therapeutics.

The concept of Auricular Neuromodulation (AN), described in the article « Auricular Neuromodulation: The emerging concept beyond the stimulation of vagus and trigeminal nerves”1 is particularly interesting for neurologists, and might even help researchers to unravel fundamental mechanisms of brain functioning.

DOI: 10.29245/2572.942X/2018/4.1200 View / Download Pdf

Conrad E. Johanson1*, Nancy L. Johanson2

1Department of Neurosurgery, Alpert Medical School at Brown University, Providence, RI, 02903 USA

2408 Autumn Trail, Georgetown, TX 78626, USA

The choroid plexus (CP) of the blood-cerebrospinal fluid barrier (BCSFB) impacts CSF homeostasis, brain diseases, and neuromedical translation. CP executes neuroendocrine, excretory, and neuroimmune actions. BCSFB diversely manages brain-spinal cord fluid environments, giving rise to a wide pathophysiology spectrum. Newly-discovered choroidal phenomena include integration of circadian clock signals, immune interaction with gut microbiotica, and expression of receptors to taste CSF composition. BCSFB tight junctions and transcellular mechanisms differ from blood-brain barrier (BBB) counterparts, variably regulating pathogen and leukocyte access to the CSF-brain nexus. This review highlights microbial agents, substrates and autoantigens using CP epithelial membranes to penetrate CSF and periventricular regions. Lipopolysaccharide (LPS) is analyzed as a barrier-damaging agent and neuroinflammation promoter. Transducing LPS- and toll-like receptor activity produce CP-CSF cytokines in sickness behavior and virulent sepsis-associated encephalopathy. Agents/systems that counter oxidative activity such as matrix metalloproteinase 8 inhibitors and Nrf2 activators (bile acids and isothiocyanates) show promise as neural and CP protectants. One review theme emphasizes CP’s preponderant role in initiating central diseases, and their remediation. In view of BCSFB permeability alterations and epithelial transformation, we discuss systemic lupus erythematosus, N-methyl D-aspartate-associated autoencephalitis, helicobacter disruption of BCSFB, toll-like receptor 2 stimulation in CP (neuroinflammation), the CP gateway for trypanosomes, and APOE-linked cholesterol transport into CSF. Another section treats concurrent involvement of BCSFB-BBB alterations in helminthic meningitis, forebrain ischemia, acute hyperthermia, leptin resistance/obesity, diabetes mellitus, and Alzheimer-type neurodegeneration. Barrier impairment is analyzed by injury type, time course, therapeutic strategies, and translational neuromedicine principles. The restorative power of BCSFB-transported growth factors, hormones and medicinal agents is emphasized for strengthening CP-CSF homeostatic mechanisms in seizures, stroke and Parkinsonism. A worthy therapeutic aim is to attenuate CNS disorders triggered by BCSFB malfunction, using CSF-delivered therapeutic agents for promoting neural viability.

DOI: 10.29245/2572.942X/2018/4.1194 View / Download Pdf

Brian E. Engdahl1-4, Lisa M. James1,2,4,5, Ryan D. Miller1, Arthur C. Leuthold1,2, Scott M. Lewis1,6, Adam F. Carpenter1,6, Apostolos P. Georgopoulos1,2,4-6*

1Brain Sciences Center, Department of Veterans Affairs Health Care System, Minneapolis, Minnesota, USA

2Department of Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota, USA

3Department of Psychology, University of Minnesota, Minneapolis, Minnesota, USA

4Center for Cognitive Sciences, University of Minnesota, Minneapolis, Minnesota, USA

5Department of Psychiatry, University of Minnesota Medical School, Minneapolis, Minnesota, USA

6Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota, USA

GWI has affected a substantial number of Gulf War (GW) veterans. The disease involves several organ systems among which the brain is most prominent. Neurological, cognitive and mood-related (NCM) symptoms frequently dominate and are at the root of chronic ill-health and disability in veterans suffering from GWI. In addition, such symptoms frequently co-occur with diagnosable mental health disorders, predominantly posttraumatic stress disorder (PTSD). Here we investigated the possibility that increased GWI severity leads, above a threshold, to a diagnosable mental health disorder (excluding psychosis). For this purpose, we used, in separate analyses, symptom severity scores and resting-state brain functional connectivity patterns, as determined by magnetoencephalography (MEG). Two-hundred-thirty GW-era veterans participated in this study. They completed diagnostic interviews to establish the presence of GWI and assess mental health status. This distinguished 3 groups: healthy controls (N = 41), veterans with GWI and no mental illness (GWI group, N = 91), and veterans with both GWI and mental health disorder (GWI+MH, N = 98). For each veteran, symptom severity scores in the 6 GWI domains (fatigue, pain, NCM, skin, gastrointestinal, respiratory) were available as well as 9 summary measures of the distribution of Synchronous Neural Interactions (SNI) derived from the MEG recordings. We tested the hypothesis that, in the presence of GWI, the appearance of a diagnosable mental health disorder may depend on GWI symptom severity. For that purpose, we performed a logistic regression on the GWI population, where the presence (or absence) of the MH disorder was the dependent variable and the age- and gender-adjusted GWI severity in the 6-symptom domains were the predictors. The outcome was the probability that a participant will have MH disorder or not. Similarly, we tested the hypothesis that the presence of the MH disorder can be predicted by the SNI distribution patterns by performing a second logistic regression as above but with the 9 SNI measures as predictors. We found GWI symptom severity differed significantly across groups (GWI+MH > GWI > Control). SNI distributions of the GWI group also differed significantly from the other groups in a systematic hemispheric pattern, such that the presence of GWI involved predominantly the left hemisphere, and presence of mental health disorders involved, in addition, the right hemisphere. Both logistic regressions yielded highly significant outcomes, demonstrating that both GWI symptom severity and SNI distribution measures can predict the presence of MH disorder in GWI. Remarkably, the prediction probabilities for MH presence derived from the symptom-based and SNI-based logistic regressions were positively and highly statistically significantly correlated. Taken together, both objective (neural) and subjective (symptoms) indices suggest that GWI is distinct from healthy controls and varies in severity in a continuum that leads, at the higher end, to a diagnosable MH disorder. The positive correlation between the GWI symptom-based and brain-based predicted classifications provides a key link between GWI symptom severity and synchronous neural interactions in the context of mental illness.

DOI: 10.29245/2572.942X/2018/4.1198 View / Download Pdf

Sara R. Roig1, Irene Estadella1, Sergi Cirera-Rocosa1, María Navarro-Pérez1, Antonio Felipe1*

1Molecular Physiology Laboratory, Dpt. de Bioquímica i Biomedicina Molecular, Institut de Biomedicina (IBUB), Universitat de Barcelona, Av. Diagonal 643, E-08028 Barcelona, Spain

Microglial cells are responsible for brain immunosurveillance. These cells maintain brain homeostasis, phagocytose cellular debris, present antigens to T-lymphocytes and secrete cytokines and chemokines. Upon activation, microglia can polarize into two different phenotypes in particular environments: the classical M1 proinflammatory state and the alternative M2 anti-inflammatory state. Chronically activated M1 microglial cells are involved in neuroinflammation in various brain diseases. In multiple sclerosis, Alzheimer’s disease, Parkinson’s disease and neuropathic pain, brain inflammation is involved in initiation and pathological progression, which is partially mediated by activated microglia. Molecular studies revealed that expression of the voltage-gated potassium channel Kv1.3 is a M1 phenotypic feature. Indeed, an increase in Kv1.3 expression and function was detected in chronically activated microglial cells in patients. Therefore, recent works evaluated Kv1.3-targeted therapies for neuroimmune diseases and showed encouraging results. Inhibition of Kv1.3 activity led to amelioration of some pathology-related features in brain diseases. This review summarizes the latest findings concerning microglial function in neuroinflammatory processes, focusing on the involvement of Kv1.3 and highlighting this channel as a promising therapeutic target.

DOI: 10.29245/2572.942X/2018/4.1191 View / Download Pdf

Bilal El Waly1, Myriam Cayre1, Pascale Durbec1*

1Aix Marseille University, CNRS, IBDM-UMR 7288, Case 907, Parc Scientifique de Luminy, campus de Luminy, 13288 Marseille, Cedex 09, France

DOI: 10.29245/2572.942X/2018/4.1196 View / Download Pdf

Ani Amar*

Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Israel

Heart failure is characterized as any heart condition resulting from impairment of the heart’s ability to pump blood, with high prevalence in both aged and diseased hearts. Numerous population-based studies have shown that, in patients with impaired left ventricular systolic function, additional structural and functional cardiovascular abnormalities are often found, making it difficult to understand the underlying pathophysiological processes. Advances in experimental and modeling tools have led to the identification of many cellular mechanisms that contribute to cardiac failure. Still, the mechanism by which cardiac myofiber adaptation ultimately leads to failure remains unclear. Several human cell, tissue, and organ models are used to model heart failure. In this mini review, several available human models are summarized with a focus on the simulation of cellular remodeling: from membrane excitation at the level of the single cell to contraction of the ventricle.

DOI: 10.29245/2572.942X/2018/4.1186 View / Download Pdf

Cristine Betzer1,2, Poul Henning Jensen1,2*

1Danish Research Institute of Translational Neuroscience - DANDRITE, Aarhus University, Denmark

2Department of Biomedicine, Aarhus University, Denmark

DOI: 10.29245/2572.942X/2018/4.1197 View / Download Pdf

Yannick Kronimus, Richard Dodel*, Sascha Neumann

Department of Geriatrics, University Duisburg-Essen, Germaniastrasse 1-3, 45356 Essen, Germany

Accumulation and aggregation of Beta-Amyloid (Aβ) and Alpha-Synuclein (α-Syn) are considered as central or even causative for the development of Alzheimer’s (AD) and Parkinson’s disease (PD). Therefore, the regulation of these proteins seems to be an essential aspect for prevention and is of central interest in current research aiming to find therapeutic approaches. The human immunological repertoire already contains such a regulatory system. Naturally occurring autoantibodies (nAbs) against the proteins Aβ (nAbs-Aβ) and α-Syn (nAbs-α-Syn) are part of the innate immune system and modulate the metabolism of their specific antigens including protein clearance and inhibition of aggregation. Thus, many researchers hypothesize that in the course of AD and PD, quantitative alterations of nAbs-Aβ and nAbs-α-Syn arise resulting in impaired proteastasis. Such alterations would represent promising, reliable biomarkers and indicate potential approaches for therapeutic strategies. Hence, it is not surprising that many studies dealing with nAbs-Aβ and nAbs-α-Syn titers in AD and PD patients in comparison to control participants are available in the literature. In this mini review, we summarize the current evidence. Furthermore, we critically discuss problems and future requirements for nAbs quantification when a clinical application is the overriding goal.

DOI: 10.29245/2572.942X/2018/4.1189 View / Download Pdf

Valeria Belleudi1, Nera Agabiti1*, Marina Davoli1, Danilo Fusco1

1Department of Epidemiology, Lazio Regional Health Service, Via Cristoforo Colombo, 112, 00147 Rome, Italy

DOI: 10.29245/2572.942X/2018/3.1195 View / Download Pdf

Kathleen Monahan, D.S.W., L.C.S.W., L.M.F.T.

Associate Professor Director, Trauma Specialization Stony Brook School of Social Welfare 101 Nicolls Road Health Sciences Center, Level 2 Stony Brook, NY, USA

Intimate Partner Violence (IPV) remains at epidemic proportions in the United States. Traumatic Brain Injury (TBI) as an outcome of IPV is now being investigated by researchers, particularly long-term sequelae. This review addresses underreporting and lack of treatment, and the physical and psychological impact for victims of IPV who have received a TBI. Recent research has begun to investigate professional sports players who experience repeated concussions and their at-risk status for Chronic Traumatic Encephalopathy (CTE). Women who are in abusive relationships for long periods of time may also incur repeated blows to the head. Researching the at-risk status for CTE is a much needed line of inquiry for this underserved population.

DOI: 10.29245/2572.942X/2018/3.1181 View / Download Pdf

Gerhard Ransmayr

Dept. of Neurology 2, Kepler University Hospital, Krankenhausstr 9, A-4020 Linz, Austria

DOI: 10.29245/2572.942X/2018/3.1184 View / Download Pdf

Apostolos P. Georgopoulos1,2*, Effie-Photini C. Tsilibary1,2, Eric P. Souto1, Lisa M. James1,2, Brian E. Engdahl1,2, Angeliki Georgopoulos3

1Brain Sciences Center, Department of Veterans Affairs Health Care System, Minneapolis, Minnesota

2Department of Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota

3Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota

Gulf War Illness (GWI) is a chronic debilitating disease of unknown etiology that affects the brain and has afflicted many veterans of the 1990-91 Gulf War (GW). Here we tested the hypothesis that brain damage may be caused by circulating harmful substances to which GW veterans were exposed but which could not be eliminated due to lack of specific immunity. We assessed the effects of serum from GWI patients on function and morphology of brain cultures in vitro, including cultures of embryonic mouse brain and neuroblastoma N2A line. Blood serum from GWI and healthy GW veterans was added, alone and in combination, to the culture and its effects on the function and morphology of the culture assessed. Neural network function was assessed using electrophysiological recordings from multielectrode arrays in mouse brain cultures, whereas morphological assessments (neural growth and cell apoptosis) were done in neuroblastoma cultures. In contrast to healthy serum, the addition of GWI serum disrupted neural network communication and caused reduced cell growth and increased apoptosis. All of these detrimental effects were prevented or ameliorated by the concomitant addition of serum from healthy GW veterans. These findings indicate that GWI serum contains neuropathogenic factors that can be neutralized by healthy serum. We hypothesize that these factors are persistent antigens circulating in GWI blood that can be neutralized, possibly by specific antibodies present in the healthy serum, as proposed earlier1.

DOI: 10.29245/2572.942X/2018/2.1177 View / Download Pdf

Elke Kalbe1*, Ann-Kristin Folkerts1

1 Medical Psychology | Neuropsychology and Gender Studies & Center for Neuropsychological Diagnostics and Intervention (CeNDI), University Hospital Cologne, Kerpenerstraße 62, 50937 Cologne, Germany

While it is undeniable that cognitive stimulation (CS) is effective in patients with dementia, there is still a lack of understanding of the underlying mechanisms of the effects, and questions like “Who benefits?” or “Which factors determine the benefits?” are not yet answered. Therefore, this commentary gives an overview of different aspects (e.g., sociodemographic factors, disease characteristics, living setting) that need to be considered while doing research on CS to understand their impact on CS effects. It is also necessary to examine the effects of CS in real-life settings (e.g., geriatric hospitals) with mixed samples (e.g., patients with different severity of dementia). Additionally, important factors for future studies on CS in dementia (e.g., reporting according to the CONSORT guidelines, more health-economics studies) are outlined.

DOI: 10.29245/2572.942X/2018/2.1175 View / Download Pdf

M Mirzaei1,2,3 *, V B Gupta4, V K Gupta2

1Department of Molecular Sciences, Macquarie University, Sydney, NSW, Australia

2Department of Clinical Medicine, Macquarie University, Sydney, NSW, Australia

3Australian Proteome Analysis Facility, Macquarie University, Sydney, NSW, Australia

4School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia

DOI: 10.29245/2572.942X/2018/2.1173 View / Download Pdf

Septimiu Tudor Bucurescu

Neurology at Vital-Klinik, Bad Driburg, Germany

In this paper we describe the case of a Guillain-Barré syndrome patient who was diagnosed with an active yersiniosis and past chlamydiosis. We also discuss the diagnosis, therapy and recovery prognosis of patients with Guillain-Barré syndrome.

DOI: 10.29245/2572.942X/2018/2.1156 View / Download Pdf

Wolf-Dieter Heiss, MD

1Max Planck Institute for Metabolism Research, Cologne, Germany

The diagnosis of cerebral small vessel disease (SVD) is difficult because there is no consensus on clinical criteria and therefore, imaging is important for diagnosis. Most patients undergo brain imaging by computed tomography (CT), which is able to detect ischemic strokes, hemorrhages and brain atrophy and may also indicate white matter changes. Magnetic resonance imaging (MRI) remains the key neuroimaging modality and is preferred to CT in vascular cognitive impairment (VCI) because it has higher sensitivity and specificity for detecting pathological changes. These modalities for imaging morphology permit to detect vascular lesions traditionally attributed to VCI in subcortical areas of the brain, single infarction or lacunes in strategic areas (thalamus or angular gyrus), or large cortical-subcortical lesions reaching a critical threshold of tissue loss. In SVD multiple punctuate or confluent lesions can be seen in the white matter by MRI and were called leukoaraiosis. Another major neuroimaging finding of small vessel disease in VCI are microhemorrhages. However, while CT and MRI are able to detect morphologic lesions, these modalities cannot determine functional consequences of the underlying pathological changes.

Positron emission tomography (PET) can support the clinical diagnosis by visualizing cerebral functions in typically affected brain regions. In SVD, Fluor-Deoxy-Glucose (FDG)-PET can clearly differentiate scattered areas of focal cortical and subcortical hypometabolism that differ from the typical metabolic pattern seen in Alzheimer Dementia (AD) with marked hypometabolism affecting the association areas. Additional PET tracers can further support the diagnosis of a type of dementia and also yield information on the underlying pathophysiology.

DOI: 10.29245/2572.942X/2018/2.1171 View / Download Pdf

Hanna Kalamarz-Kubiak

Department of Genetics and Marine Biotechnology, Institute of Oceanology, Polish Academy of Sciences, Sopot, Poland

DOI: 10.29245/2572.942X/2017/1.1172 View / Download Pdf

Lucia Mendoza-Viveros1,2, Karl Obrietan3, Hai-Ying M. Cheng1,2*

1Department of Biology, University of Toronto Mississauga, Mississauga, ON, L5L 1C6, Canada

2Department of Cell and Systems Biology, University of Toronto, Toronto, ON, M5S 3G3, Canada

3Department of Neuroscience, Ohio State University, Columbus, OH, 43210, USA

Daily rhythms in behavior and physiology are coordinated by an endogenous clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. This central pacemaker also relays day length information to allow for seasonal adaptation, a process for which melatonin signaling is essential. How the SCN encodes day length is not fully understood. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by directing target mRNAs for degradation or translational repression. The miR-132/212 cluster plays a key role in facilitating neuronal plasticity, and miR-132 has been shown previously to modulate resetting of the central clock. A recent study from our group showed that miR-132/212 in mice is required for optimal adaptation to seasons and non-24-hour light/dark cycles through regulation of its target gene, methyl CpG-binding protein (MeCP2), in the SCN and dendritic spine density of SCN neurons. Furthermore, in the seasonal rodent Mesocricetus auratus (Syrian hamster), adaptation to short photoperiods is accompanied by structural plasticity in the SCN independently of melatonin signaling, thus further supporting a key role for SCN structural and, in turn, functional plasticity in the coding of day length. In this commentary, we discuss our recent findings in context of what is known about day length encoding by the SCN, and propose future directions.

DOI: 10.29245/2572.942X/2017/1.1169 View / Download Pdf

Gizem Yalcin

Department of Medical Biology, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey

Sirtuins are highly conserved NAD+-dependent enzymes connected to an increasing set of biological processes. These enzymes have attracted major interest because of their roles in age-related diseases. Sirtuins are implicated in various biological pathways related to stress response, mitochondrial dysfunction, oxidative stress, protein aggregation and inflammatory processes that are intertwined with age-related neurodegenerative diseases.

DOI: 10.29245/2572.942X/2017/1.1168 View / Download Pdf

Nathan Collins MD, Jeffrey Sager MD

Santa Barbara Cottage Hospital Department of Internal Medicine Santa Barbara, CA, USA

Acute laryngeal dystonia (ALD) is a drug-induced dystonic reaction that can lead to acute respiratory failure and is potentially life-threatening if unrecognized. It was first reported in 1978 when two individuals were noticed to develop difficulty breathing after administration of haloperidol. Multiple cases have since been reported with the use of first generation antipsychotics (FGAs) and more recently second-generation antipsychotics (SGAs). Acute dystonic reactions (ADRs) have an occurrence rate of 3%-10%, but may occur more frequently with high potency antipsychotics. Younger age and male sex appear to be the most common risk factors, although a variety of metabolic abnormalities and illnesses have also been associated with ALD as well. The diagnosis of ALD can go unrecognized as other causes of acute respiratory failure are often explored prior to ALD. The exact mechanism for ALD remains unclear, yet evidence has shown a strong correlation with extrapyramidal symptoms (EPS) and dopamine receptor blockade. Recognition and appropriate management of ALD can prevent significant morbidity and mortality.

DOI: 10.29245/2572.942X/2017/1.1167 View / Download Pdf

Khan MI1*

1Orthopedic & Hand surgery, Beverly Hills, CA, USA

DOI: 10.29245/2572.942X/2017/1.1165 View / Download Pdf

Torsak Tippairote1, Dunyaporn Trachootham2*

1BBH Hospital, Bangkok, Thailand

2Institute of Nutrition, Mahidol University, Nakhon Pathom, Thailand

Zinc status is an important modifiable factor in Attention Deficit and Hyperactive Disorders (ADHD) and Autistic Spectrum Disorders (ASD), the two most common neurodevelopmental disorders. Many studies reported low serum or plasma zinc level in children with these conditions. While hair zinc level can be obtained non-invasively in young children, the reports of the hair zinc levels in ASD and ADHD children were varied. ASD children were reported to have lower than or indifferent level of hair zinc from that of healthy children. In ADHD children, hair zinc levels were reported as either lower or higher than their healthy control groups. Many factors interplayed and affected measurement of hair zinc level. Until more standardized method has been established, currently the zinc level in hair samples may be used as screening or supporting evidence. Other functional zinc markers such as serum zinc concentrations, dietary zinc intakes, and percentage of stunting rate, are still needed to assess the zinc status in susceptible children.

DOI: 10.29245/2572.942X/2017/10.1158 View / Download Pdf