Relevant bibliographies by topics / Anti-GAD

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Anti-GAD'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2025

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Journal articles on the topic "Anti-GAD"

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Obaid, Reem M., Sabah N. Alwachi, and Munthir Mustafa. "Early Detection of T1DM Using Anti- GAD and Anti-Insulin Antibodies." Greener Journal of Biological Sciences 4, no. 3 (2014): 86–91. https://doi.org/10.15580/gjbs.2014.3.012114052.

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Markers have been described in type1 diabetes, a number of specific and non- specific antigens have been identified. The major auto-antigens involved in the destructive process of beta-cells leading to the development of type 1 diabetes are insulin hormone and glutamic acid decarboxylase (GAD).  This study was conducted to find the relationship between antibodies for this antigens and T1DM which can be used for the early detection of T1DM in normal Iraqi patients. The study was carried out on 80 samples (50 men and 30 women) with age ranged from (20– 60 years old), they are divided
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Reem, M. Obaid, N. Alwachi Sabah, and Mustafa Munthir. "Early Detection of T1DM Using Anti- GAD and Anti-Insulin Antibodies." Greener Journal of Biological Sciences 4, no. 3 (2014): 086–91. http://dx.doi.org/10.15580/gjbs.2014.3.012114052.

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Gul, Kamile, Ihsan Ustun, Yusuf Aydin, et al. "Autoimmune thyroid disease in patients with anti-GAD positive type 1 diabetes mellitus." Open Medicine 4, no. 4 (2009): 415–22. http://dx.doi.org/10.2478/s11536-009-0080-z.

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AbstractThe aim of the study was to determine the frequency and titers of anti-thyroid peroxidase (Anti-TPO), anti-thyroglobulin (Anti-TG), and anti-glutamic acid decarboxylase (Anti-GAD) antibodies in Turkish patients with type 1 diabetes mellitus (DM), and to compare the frequency of anti-TPO and anti-TG titers in the presence or absence of anti-GAD. A total of 104 patients including 56 males and 48 females with type 1 DM and their age-, gender-, and body mass index-matched control group, including 31 males and 27 females, 58 cases in total with an age range of 15-50 years, were recruited in
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Seneviratne, Sinali O., Katherine A. Buzzard, Belinda Cruse, and Mastura Monif. "Cerebellar Ataxia Followed by Stiff Person Syndrome in a Patient with Anti-GAD Antibodies." Case Reports in Immunology 2020 (February 8, 2020): 1–4. http://dx.doi.org/10.1155/2020/8454532.

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Anti-GAD antibody syndrome is a result of the production of antibodies against glutamic acid decarboxylase (GAD), the main enzyme responsible for the production of gamma-aminobutyric acid (GABA). Several neurological manifestations including cerebellar ataxia and stiff person syndrome have been reported in association with anti-GAD antibodies. In this paper, we present a case of a young woman with anti-GAD antibodies who initially presented with cerebellar ataxia followed by stiff person syndrome three and a half years later. Having both cerebellar ataxia and stiff person syndrome is a rare oc
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Belém, Abel Dantas, Thaís de Maria Frota Vasconcelos, Rafael César dos Anjos de Paula, et al. "Stiff-Eye Syndrome—Anti-GAD Ataxia Presenting with Isolated Ophthalmoplegia: A Case Report." Brain Sciences 11, no. 7 (2021): 932. http://dx.doi.org/10.3390/brainsci11070932.

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Anti-GAD ataxia is one of the most common forms of immune-mediated cerebellar ataxias. Many neurological syndromes have been reported in association with anti-GAD. Ophthalmoparesis has been described in stiff person syndrome. We report a case of anti-GAD ataxia presenting initially with isolated ophthalmoplegia and showing complete resolution after immunotherapy. A 26-year-old male patient presented with ophthalmoparesis characterized by tonic upwards deviation of the right eye. In the following month, he developed progressive ataxia with anti-GAD titers of 1972 UI/mL. After treatment with met
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Wardhani, Puspa, S. Darmadi, M. Faizi, and Netty Harjantien. "DETEKSI ANTI GLUTAMIC ACID DECARBOXILASE/TYROSINE PHOSPHATASE (ANTI GAD/IA2) PADA PENDERITA DM TIPE 1 ANAK." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 14, no. 2 (2018): 83. http://dx.doi.org/10.24293/ijcpml.v14i2.907.

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Our study evaluated anti GAD/IA2 levels in Type 1 DM patients in Dr. Soetomo Hospital Surabaya. We conducted cross sectionalstudy, involving Type 1 DM patients that already been established (C-Peptide bellow normal). Patient’s age range was from 2.8 yearsold to 17 years old, so they were regarded as children. We used anti GAD/IA2 reagents from Euroimmun wich had basic principal EIA.Twelve patients was involved in this study. The average level of anti GAD/IA2 was 210.37 IU/mL. The Average level of anti GAD/IA2was higher in female than male patients (227.38 IU/mL dan 162 IU/mL). All patients had
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Dade, Maëlle, Giulia Berzero, Cristina Izquierdo, et al. "Neurological Syndromes Associated with Anti-GAD Antibodies." International Journal of Molecular Sciences 21, no. 10 (2020): 3701. http://dx.doi.org/10.3390/ijms21103701.

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Glutamic acid decarboxylase (GAD) is an intracellular enzyme whose physiologic function is the decarboxylation of glutamate to gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter within the central nervous system. GAD antibodies (Ab) have been associated with multiple neurological syndromes, including stiff-person syndrome, cerebellar ataxia, and limbic encephalitis, which are all considered to result from reduced GABAergic transmission. The pathogenic role of GAD Ab is still debated, and some evidence suggests that GAD autoimmunity might primarily be cell-mediated. Diagnosis
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Frerker, Bernd, Marco Rohde, Steffen Müller, Christian G. Bien, Rüdiger Köhling, and Timo Kirschstein. "Distinct Effects of Stereotactically Injected Human Cerebrospinal Fluid Containing Glutamic Acid Decarboxylase Antibodies into the Hippocampus of Rats on the Development of Spontaneous Epileptic Activity." Brain Sciences 10, no. 2 (2020): 123. http://dx.doi.org/10.3390/brainsci10020123.

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Background: The conversion of glutamic acid into γ-aminobutyric acid (GABA) is catalyzed by the glutamic acid decarboxylase (GAD). Antibodies against this enzyme have been described in neurological disorders, but the pathophysiological role of these antibodies is still poorly understood. We hypothesized that anti-GAD autoantibodies could diminish the GABA content in the slice and facilitate epileptic activity. Methods: Cerebrospinal fluids (CSF) from two patients containing anti-GAD (A and B) were injected into the rat hippocampus in vivo. Hippocampal slices were prepared for electrophysiologi
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Tsiortou, Popianna, Harry Alexopoulos, and Marinos C. Dalakas. "GAD antibody-spectrum disorders: progress in clinical phenotypes, immunopathogenesis and therapeutic interventions." Therapeutic Advances in Neurological Disorders 14 (January 2021): 175628642110034. http://dx.doi.org/10.1177/17562864211003486.

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Antibodies against glutamic acid decarboxylase (GAD), originally linked to stiff person syndrome (SPS), now denote the “ GAD antibody-spectrum disorders” ( GAD-SD) that also include autoimmune epilepsy, limbic encephalitis, cerebellar ataxia and nystagmus with overlapping symptomatology highlighting autoimmune neuronal excitability disorders. The reasons for the clinical heterogeneity among GAD-antibody associated syndromes remain still unsettled, implicating variable susceptibility of GABAergic neurons to anti-GAD or other still unidentified autoantibodies. Although anti-GAD antibody titers d
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Kareem, Saad Abdul, Bharadwaj Adithya Sateesh, Lars J. Berg, Girma Ayele, Betelehem Atalay, and Miriam Michael. "Stiff Person with Anti-GAD Antibodies." Case Reports in Clinical Medicine 12, no. 06 (2023): 168–73. http://dx.doi.org/10.4236/crcm.2023.126023.

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Dissertations / Theses on the topic "Anti-GAD"

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Saiz, Hinajeros Albert. "Espectro de enfermedades neurológicas asociadas a anticuerpos anti-glutamato decarboxilasa (GAD)." Doctoral thesis, Universitat de Barcelona, 1998. http://hdl.handle.net/10803/2235.

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El GAD (glutamato decarboxilasa) es la enzima que cataliza la síntesis del neurotransmisor inhibitorio ácido gamma-aminobutírico (GABA) a partir del glutamato. El GAD se expresa selectivamente en los botones sinápticos de las neuronas GABA-érgicas. Fuera del sistema nervioso se encuentra en altas concentraciones en las células beta de los islotes pancreáticos, sin que existan diferencias entre el GAD de las células pancreáticas o del sistema nervioso.<br/><br/>La repuesta inmune contra el GAD se ha relacionado con la patogenia de dos enfermedades humanas: el síndrome de la persona rígida ("Sti
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Holfelder, Christina Ingrid. "Effects of the glutamic acid decarboxylase (GAD) inhibitor semicarbazide and anti-GAD autoantibodies-containing immunoglobulin G on neuronal network activity within the motor cortex." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-123547.

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Maraschin, Jorge de Faria. "Acurácia diagnóstica do anticorpo anti-descarboxilase do ácido glutâmico (ANTI-GAD) como marcador de auto-imunidade no diabete melito." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2007. http://hdl.handle.net/10183/13426.

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A correta classificação do tipo de DM leva mais precocemente ao tratamento adequado e atualmente é dividida em 4 categorias: DM tipo 1, DM tipo 2, Outros tipos e Diabete Gestacional. O DM tipo 1 é geralmente auto-imune, surge em geral antes dos 20 anos de idade e é dependente de insulina para impedir a cetoacidose. O DM tipo 2 é responsável por mais de 90% dos casos, acontece em geral após os 45 anos, com história familiar e associado à síndrome metabólica. Na categoria “outros tipos”, o Maturity Onset Diabetes of the Young (MODY) é um subtipo que inicia abaixo dos 25 anos, não-dependente de i
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Holfelder, Christina Ingrid [Verfasser]. "Effects of the glutamic acid decarboxylase (GAD) inhibitor semicarbazide and anti-GAD autoantibodies-containing immunoglobulin G on neuronal network activity within the motor cortex / vorgelegt von Christina Ingrid Holfelder." 2010. http://d-nb.info/1009568817/34.

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Books on the topic "Anti-GAD"

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Newsome, Scott D. Other Proven and Putative Autoimmune Disorders of the CNS. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0092.

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Antiglutamic acid decarboxylase (GAD)-associated disorders are a group of rare neuroimmunological disorders that encompass an expanding spectrum of neurological syndromes. The pathophysiology of these disorders is not well understood, although the presence of very high levels of antibodies to GAD is indicative of immunological dysfunction. The most well-known disease within this class of disorders is stiff-person syndrome (SPS), which often manifests as painful spasms, stiffness/rigidity in axial and limb musculature, and increased lumbar lordosis. Other anti-GAD-associated disorders include i
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Book chapters on the topic "Anti-GAD"

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Walker, Helen, Ashwani Jha, Paul Holmes, Thomasin Andrews, Michael Kopelman, and Mervi Pitkanen. "Case Study: Anti-GAD Encephalitis." In Neuropsychiatry Case Studies. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42190-2_33.

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Nakamura, Shigenobu, Hidekazu Kamei, and Yasuyo Mimori. "Anti-GAD Antibody in Various Neurological Diseases." In GABA: Receptors, Transporters and Metabolism. Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8990-2_6.

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Miller, Aaron E., Tracy M. DeAngelis, Michelle Fabian, and Ilana Katz Sand. "Gad-Awful Spasms." In Neuroimmunology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190693190.003.0019.

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Stiff person syndrome (SPS) is a rare autoimmune neurological disease that causes progressive, fluctuating, painful muscle rigidity and spasms, generally beginning in the axial muscles, truncal region, and progressing to proximal musculature. A hyperlordotic posture is considered an early clinical hallmark of the condition. The most common pathological correlate is with anti-glutamic acid decarboxylase (GAD) 65 antibodies, but several other associated antibodies have been identified There is a clinical spectrum of disease with variants including stiff leg syndrome, progressive encephalomyeliti
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Zuckerman-Levin, Nehama, Oz Mordechai, and Naim Shehadeh. "Case 48: Glycogenic Hepatopathy in an Adolescent with Type 1 Diabetes." In Diabetes Case Studies: Real Problems, Practical Solutions. American Diabetes Association, 2015. http://dx.doi.org/10.2337/9781580405713.48.

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A 13-year-old adolescent with type 1 diabetes (T1D) was admitted to the hospital with fatigue, vomiting, and weight loss. He was a second twin, born after an uneventful pregnancy, with a birth weight of 1,900 g. His family history included a twin brother with bronchial asthma, and a grandmother with type 2 diabetes (T2D). T1D was diagnosed at the age of 9 years. No diabetic ketoacidosis (DKA) was noted at diagnosis. He had positive anti-GAD and anti-islet cell antibodies (ICA). He used an insulin pump for 2 years, but because of recurrent severe hypoglycemic episodes, his treatment was changed
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Verma, Ritika, Kiet Huynh, Rajani Gundluru, Michael Gardner, and James Sowers. "Case 12: Acromegaly Presenting With Diabetic Ketoacidosis." In Diabetes In Practice: Case Studies with Commentary. American Diabetes Association, 2021. http://dx.doi.org/10.2337/9781580407663.12.

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We present a 31-year-old male without any comorbidities who presented to the emergency room (ER) with a 2-week history of polyuria, polydipsia, constipation, and fatigue. He also reported a weight loss of 40 lb over the last 3 months. During the interview, he mentioned having oily skin and acne all of his life. He denied palpitations, hyperhidrosis, or difficulty with sexual activity. Physical exam was striking for frontal bossing, prognathism, hypertrichosis, and large hands and feet, suggesting acromegaly. No acanthosis nigricans or acrochordons was noted. Initial lab work revealed the follo
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Amiel, Stephanie A. "Clinical features of type 1 diabetes mellitus." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1311.

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As described in Chapter 13.2.3, type 1 diabetes results from the destruction of the glucose-responsive, insulin-secreting β‎ cells of the pancreatic islets. Its principal clinical features reflect significant insulin deficiency. In general, the β‎ cell damage is immune mediated and other clinical features occur related to other autoimmune processes. Although typically considered to have a short prodrome, in research studies biochemical evidence of impaired glucose metabolism has been detected years before diagnosis, in the form of mild elevation of blood glucose. It is likely that the clinical
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Conference papers on the topic "Anti-GAD"

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CARVALHO, ANDRÉIA MARIA DOS SANTOS, VICTOR JOSÉ CAMPELO VILANOVA, JONH HEBERTHON DE SOUZA ARAÚJO, MARIA JULIA OLIVEIRA DE MOURA, CRISTINA REIS DE SOUSA BRITO ROCHA, and TIBERIO SILVA BORGES DOS SANTOS. "POLINEUROPATIA ASSOCIADA À ATAXIA E ANTI-GAD: UM RELATO DE CASO." In ANAIS DO VI CONGRESSO MéDICO ACADêMICO BRASILEIRO/ XIV CONGRESSO NORDESTINO MéDICO ACADêMICO/ XXX CONGRESSO MéDICO ACADêMICO DO PIAUí. Galoa, 2024. https://doi.org/10.17648/comapi-2024-196173.

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Gurian, Jordana Gaudie, Maria Ondina Machado Diniz, Amanda Nascimento Bispo, Aline Boaventura Ferreira, Fernando Elias Borges, and Ane Cristina Dunck. "Case report: stiff Person syndrome." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.346.

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Introduction: The rigid person syndrome is rare, characterized by blockade of the GAD enzyme, responsible for inhibiting muscle contraction. Although it is not mandatory for the diagnosis, most patients are positive for Anti-GAD. Objectives: To report a case of rigid person syndrome seen at Hospital Geral de Goiânia. Methods: Information was obtained through clinical follow-up in a neurology ward and outpatient clinic. Results: Patient, female, 32 years old, complaining of paresthesia ascending to upper limbs, worsening over a period of six months with paresis with gait impairment, increased t
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Yagnik, Deepti, Josephine Chan, Ben McGettigan, Andrew Laycock, and Allycia MacDonald. "3121 New onset refractory epilepsy (NORSE) secondary to anti-glutamic acid decarboxylase (anti-GAD) and anti-Hu antibodies related paraneoplastic encephalitis from lymphocyte-rich thymoma." In ANZAN Annual Scientific Meeting 2024 Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/bmjno-2024-anzan.110.

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Rao, Meghana, Katy Helms, and Araya Puwanant. "Late-Onset Cerebellar Ataxia Associated with Anti-GAD Autoantibodies: A Rare and Puzzling Disease (P4-5.013)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000204188.

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Correia Monteiro, Jean Michell, Mateus Cavarzan Lopes, Heitor Furlan Giordano, Diogo Souza Domiciano, and Samuel Katsuyuki Shinjo. "Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome associated with anti-GAD antibody-related limbic encephalitis." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1909.

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Domingos, Francine de Paula Roberto, Sayuri Aparecida Hirayama, Rafael de Almeida, et al. "Atypical presentation of Stiff Person syndrome: case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.490.

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Introduction: Stiff Person syndrome (SPS) is a rare, immune-mediated neurological disease related to several antibodies, the most obvious being Antiglutamic acid decarboxilase (GAD). This case intends to show atypical clinical presentation of Stiff Person Syndrome, in which the patient started with ataxia and gait alteration, evolving with dimidiated spasms. Case report: L.S.M, male, 58 years old, denied previous comorbidities, smoking and alcoholism. He woke up with vertigo, associated with dysarthria and ataxia in the left side of the body. Two weeks after the onset of symptoms, he evolved w
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Malagutti, Beatriz Cocato, Lucas da Silva Oliveira, Matheus Spilari, Victoria Lot Avezum Mestriner, and Helen Maia Tavares de Andrade. "Stiff Person syndrome and lumbosacral plexopathy post COVID-19." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.537.

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Introduction: Coronavirus diasease 2019 (COVID-19) has been associated with inflammatory, ischemic and autoimmune neurological complications. We report a case of Stiff Person Syndrome (SPS) as an autoimmune neurological complication in COVID-19, an association still rare in the literature. Case report: A 45-year-old woman, presented with back pain of strong intensity with irradiation to the left lower limb, associated with painful muscle contracture and weakness in the same limb with progressive worsening in two days. Neurological examination revealed strength grade II, hyporeflexia, tactile a
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Damasceno Júnior, Eustáquio Costa, Isabella Sabião Borges, João Victor Aguiar Moreira, et al. "Successful treatment with rituximab in a refractory Stiffperson syndrome (SPS)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.507.

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Background: SPS is a disorder consisting of rigidity of axial muscles with painful spasms. More than 80 % of SPS patients have high titer antibodies against glutamic acid decarboxylase (GAD). The use of rituximab for the treatment of SPS is a recent therapeutical approach showing promising results. We present a case of SPS treated with rituximab, showing a good and safe response. Case: A 38-year-old female patient presented with a history of rigidity of abdominal and paravertebral muscles associated with painful spasms in lower back region, increased tonus, lumbar lordosis, frequent falls and
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Tolentino, VRS, IO Santos, AR Ianicelli, et al. "INTERFERENTE ANALÍTICO NA DOSAGEM SÉRICA DE INSULINA: UM RELATO DE CASO." In Resumos do 55º Congresso Brasileiro de Patologia Clínica/Medicina Laboratorial. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s2.9788.

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Objetivo: A insulina é um hormônio produzido pelas células β do pâncreas, cuja principal função é regular a glicemia. Sua dosagem está indicada para avaliar a secreção e/ou resistência insulínica ou investigar síndromes hipoglicêmicas. Normalmente, é dosada por ensaio imunométrico quimio ou eletroquimioluminescente, porém, esses métodos podem sofrer influência de vários interferentes. Neste relato, descrevemos a investigação laboratorial de um resultado espúrio de insulina, não condizente com o quadro clínico. Método: Paciente do sexo feminino, 53 anos, apresentou, em agosto de 2022, glicemia
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Oliveira, Daniel Alves de, Arthur Cesário de Holanda, Vitor Maia Arca, Marcos Eugênio Ramalho Bezerra, and Renata Amaral Andrade. "Fluctuating spastic paraparesis with “owls sign” in spine MRI: a diagnostic challenge." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.775.

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Case presentation: A 42-year-old female patient, with no previous comorbidities, complained of tremors and gait disturbance that had started two years before. She mentioned that her legs had fluctuating moving difficulties, associated with pain. At her first evaluation at clinical onset, the case was interpreted as episodic myoclonus, and clonazepam was prescribed with partial improvement. In the initial physical examination, it was observed pathologic glabellar reflex, bilateral hyperreflexia in the lower limbs, and bilateral foot and knee clonus, with no findings in tonus or muscle weakness.
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