scholarly journals Autoimmune Neurogenic Dysphagia

Dysphagia ◽  
2021 ◽  
Author(s):  
Panos Stathopoulos ◽  
Marinos C. Dalakas
Keyword(s):  
Acute Onset ◽  
Neurogenic Dysphagia ◽  
Acetyl Choline ◽  
Gastrointestinal Dysmotility ◽  
Common Causes ◽  
Bulbar Onset ◽  
Spectrum Disorders ◽  
Treatable Condition ◽  
Prompt Diagnosis ◽  
Progressive Dysphagia

AbstractAutoimmune neurogenic dysphagia refers to manifestation of dysphagia due to autoimmune diseases affecting muscle, neuromuscular junction, nerves, roots, brainstem, or cortex. Dysphagia is either part of the evolving clinical symptomatology of an underlying neurological autoimmunity or occurs as a sole manifestation, acutely or insidiously. This opinion article reviews the autoimmune neurological causes of dysphagia, highlights clinical clues and laboratory testing that facilitate early diagnosis, especially when dysphagia is the presenting symptom, and outlines the most effective immunotherapeutic approaches. Dysphagia is common in inflammatory myopathies, most prominently in inclusion body myositis, and is frequent in myasthenia gravis, occurring early in bulbar-onset disease or during the course of progressive, generalized disease. Acute-onset dysphagia is often seen in Guillain–Barre syndrome variants and slowly progressive dysphagia in paraneoplastic neuropathies highlighted by the presence of specific autoantibodies. The most common causes of CNS autoimmune dysphagia are demyelinating and inflammatory lesions in the brainstem, occurring in patients with multiple sclerosis and neuromyelitis optica spectrum disorders. Less common, but often overlooked, is dysphagia in stiff-person syndrome especially in conjunction with cerebellar ataxia and high anti-GAD autoantibodies, and in gastrointestinal dysmotility syndromes associated with autoantibodies against the ganglionic acetyl-choline receptor. In the setting of many neurological autoimmunities, acute-onset or progressive dysphagia is a potentially treatable condition, requiring increased awareness for prompt diagnosis and early immunotherapy initiation.

Acute myocardial infarction in the neonatal period

2002 ◽  
Vol 12 (4) ◽  
pp. 411-413 ◽  
Author(s):  
S. Jothi Murugan ◽  
James Gnanapragasam ◽  
Joseph Vettukattil
Keyword(s):  
Myocardial Infarction ◽  
Left Coronary Artery ◽  
Neonatal Period ◽  
Acute Onset ◽  
Cardiac Centre ◽  
Electrocardiographic Changes ◽  
Echocardiographic Assessment ◽  
High Index Of Suspicion ◽  
Treatable Condition ◽  
Fatal Myocardial Infarction

AbstractWe describe two neonates presenting with myocardial infarction, due to two different aetiologies of this extremely rare but potentially treatable condition, and discuss the management. One neonate had myocardial infarction complicating enteroviral myocarditis and recovered completely. The second had fatal myocardial infarction due to thrombosis of the left coronary artery. Although rare, the attending paediatrician should have a high index of suspicion when evaluating a neonate with acute onset of collapse. Electrocardiographic changes are diagnostic, but further echocardiographic assessment and prompt management at a tertiary cardiac centre are advised.

Infranuclear Ophthalmoplegia

2019 ◽  
pp. 127-132
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak
Keyword(s):  
Differential Diagnosis ◽  
Muscular Dystrophy ◽  
Acute Onset ◽  
Progressive External Ophthalmoplegia ◽  
Oculopharyngeal Muscular Dystrophy ◽  
Chronic Progressive External Ophthalmoplegia ◽  
Fisher Syndrome ◽  
Ocular Myasthenia ◽  
Common Causes ◽  
The Common

Infranuclear ophthalmoplegia is characterized by global weakness of the extraocular and levator muscles. It has a broad differential diagnosis that varies depending on the tempo of onset. In this chapter, we begin by describing how to differentiate nuclear-infranuclear ophthalmoplegia from supranuclear ophthalmoplegia at the bedside. We next list the common causes of acute onset infranuclear ophthalmoplegia, which include Miller Fisher syndrome, Guillain-Barré syndrome, stroke, and ocular myasthenia. We then list the common causes of chronic progressive infranuclear ophthalmoplegia, which include mitochondrial disorders, oculopharyngeal muscular dystrophy, and myotonic dystrophy. We discuss the clinical features and diagnostic workup of chronic progressive external ophthalmoplegia due to mitochondrial disease. Lastly, we briefly discuss the management of ptosis and diplopia in the setting of chronic progressive external ophthalmoplegia.

scholarly journals P-Chloroaniline Poisoning Causing Methemoglobinemia: A Case Report and Review of the Literature

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Anna Sarah Messmer ◽  
Christian Hans Nickel ◽  
Dirk Bareiss
Keyword(s):  
Case Report ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Peripheral Oxygen Saturation ◽  
Arterial Blood Gas ◽  
Oxygen Administration ◽  
Arterial Blood ◽  
Arterial Blood Gas Analysis ◽  
Common Causes ◽  
Treatable Condition

Background. Methemoglobin (MetHb) most commonly results from exposure to an oxidizing chemical but may also arise from genetic, dietary, or even idiopathic etiologies.P-chloroaniline (PCA) was one of the first substances described in the context of acquired methemoglobinemia.Case Report. We report the case of a cyanotic chemistry worker who presented to our emergency department (ED) after working with PCA. His peripheral oxygen saturation (SpO2) measured by pulse oximetry was at 81% and remained on that level despite oxygen administration (100% oxygenation via nonrebreather mask). His MetHb level was measured at 42.8% in arterial blood gas analysis. After treatment with intravenous methylene blue cyanosis resolved and the patient was discharged after 36 hours of observation.Conclusion. Acquired methemoglobinemia is a treatable condition, which may cause significant morbidity and mortality. The knowledge about the most common causes, fast diagnostic, and proper treatment is crucial.

Testicular Torsion

1994 ◽  
Vol 15 (11) ◽  
pp. 455-456
Keyword(s):  
Physical Examination ◽  
Testicular Torsion ◽  
Neonatal Period ◽  
Acute Onset ◽  
Nausea And Vomiting ◽  
Surgical Exploration ◽  
Urethral Discharge ◽  
Testicular Pain ◽  
Prompt Diagnosis ◽  
Careful History

Testicular torsion is a surgical emergency having an incidence that is probably underestimated at 1 in 4000 males. While torsion may occur at any age, its peak incidence is in adolescence (12 to 18 years) and the neonatal period. A prompt diagnosis is necessary to optimize the chance for testicular salvage by surgical exploration via detorsion and bilateral orchidopexy. A careful history and physical examination should lead to the diagnosis of testicular torsion. Adolescents often present having the acute onset of lateralized scrotal or testicular pain that is intense, unaffected by position, and associated with nausea and vomiting. There are no associated voiding complaints, urethral discharge, or fever.

scholarly journals A Diagnostically Challenging Case of Febrile Ulceronecrotic Mucha-Habermann Disease in an Adult Female Successfully Treated with Methotrexate and Cyclosporine

2021 ◽  
pp. 12-17
Author(s):  
Tracy Ngo ◽  
Claudia Hossain ◽  
Jason Cohen ◽  
Beth McLellan ◽  
Rachel Blasiak ◽  
...  
Keyword(s):  
Clinical Presentation ◽  
Acute Onset ◽  
Methotrexate Therapy ◽  
Diagnostic Challenge ◽  
Fatal Disease ◽  
Pityriasis Lichenoides ◽  
Cyclosporine Therapy ◽  
Intravenous Vitamin ◽  
Variable Presentation ◽  
Prompt Diagnosis

Febrile ulceronecrotic Mucha-Habermann disease (FUMHD) is a rare and severe variant of pityriasis lichenoides et varioliformis acuta (PLEVA) characterized by intermittent pyrexia, acute onset of generalized ulceronecrotic lesions, and histopathology suggestive of PLEVA. Prompt diagnosis and treatment are necessary to halt the progression of this potentially fatal disease; however, the widely variable presentation of FUMHD in addition to its rarity poses a diagnostic challenge. We report the case of a previously healthy 43-year-old woman who presented to the emergency department with 1 month of generalized rash and intermittent fevers. Her only reported new exposure were elective intravenous vitamin infusions received at a medi-spa 1 week prior to onset of lesions. Initial evaluations were inconclusive, and confluent ulceronecrotic, hemorrhagic lesions appeared on approximately 90% of her body despite steroid, antibiotic, and cyclosporine therapy. Repeat histopathology was consistent with PLEVA, and in the context of her clinical presentation she was diagnosed with FUMHD. The patient rapidly attained remission with methotrexate therapy but sustained residual scarring.

scholarly journals Anemia That Presented with Desaturation: A Focus on Core Concepts

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Lakshmi Shobhavat ◽  
Antonio D’Costa ◽  
Karthik Shroff
Keyword(s):  
Blood Smear ◽  
Intensive Care Admission ◽  
Case Presentation ◽  
Threatening Condition ◽  
Core Concepts ◽  
Life Threatening ◽  
History Of ◽  
The Common ◽  
Treatable Condition ◽  
Prompt Diagnosis

Background. Methemoglobinemia is a potentially life-threatening condition which presents with cyanosis and characteristic “chocolate-coloured blood.” Although a co-oximetry would give a prompt diagnosis, there have been multiple reports of misdiagnosing this treatable condition—from being diagnosed as sepsis to asthma and even being operated for “ruptured ectopic pregnancy.” Here, we report a case which presented without the classical signs of poisoning and methemoglobinemia—without vomiting, cyanosis, or chocolate-coloured blood. We also discuss the common misconceptions regarding anemia physiology and the pitfalls in diagnosing this condition and warn the reader regarding the reflexive use of antidotes like methylene blue. Case Presentation. A well-grown 3-year old boy presented with an acute history of irritability, cola-coloured urine, and desaturation on examination. The child was pale, with tachypnoea and in failure. Blood smear was suggestive of severe hemolytic anemia. Methemoglobinemia was diagnosed on co-oximetry. By focussing on physiologic principles of management rather than a specific antidote, the child was discharged home, well and active within 3 days of intensive care admission.

scholarly journals Switching antipsychotics: Results of 16-month non-interventional, prospective, observational clinical research of inpatients with schizophrenia spectrum disorders

2017 ◽  
Vol 67 (1) ◽  
pp. 99-112
Author(s):  
Cvetka Bačar Bole ◽  
Mitja Pišlar ◽  
Metka Šen ◽  
Rok Tavčar ◽  
Aleš Mrhar
Keyword(s):  
Clinical Practice ◽  
Psychiatric Hospital ◽  
Adverse Reactions ◽  
Treatment Strategies ◽  
Schizophrenia Spectrum Disorders ◽  
Schizophrenia Spectrum ◽  
Switching Patterns ◽  
Common Causes ◽  
Spectrum Disorders ◽  
Switching Strategies

AbstractThe study aims to identify prescribing and switching patterns of antipsychotics in clinical practice. A 16-month, prospective study was conducted at the Psychiatric Hospital Idrija, Slovenia. Inpatients (N = 311) with schizophrenia spectrum disorders were observed. The causes for switching antipsychotics and switching strategies were analyzed. Analyzing a total of 3954 prescriptions, the collected data confirmed that treatment strategies in this psychiatric hospital are very complex. It was found that 37 percent of inpatients had at least one switch. Moreover, switches that included three or more antipsychotics were detected. The most common causes for switching antipsychotics were adverse reactions and inefficacy or lack of efficacy. Among switching options, abrupt switch was recorded several times. As some patients are receiving several antipsychotics at the same time, it is possible that unusual switching occurs in clinical practice. It seems that the choice of switching strategy is also affected by the cause and urgency for switching an antipsychotic.

Interstitial lung disease (ILD)

2021 ◽  
pp. 299-312
Author(s):  
Terry Robinson ◽  
Jane Scullion
Keyword(s):  
Respiratory Failure ◽  
Interstitial Lung Disease ◽  
Lung Diseases ◽  
Clinical Findings ◽  
Acute Onset ◽  
Interstitial Lung Diseases ◽  
Disease Entity ◽  
Common Causes ◽  
Single Disease Entity ◽  
Radiographic Changes

The interstitial lung diseases (ILDs), are an extensive range of lung diseases, rather than a single disease entity. These diseases are often grouped together because they have similarities in clinical presentation, radiographic changes, physiological features, and symptoms. Despite their similarities, these diseases have a variety of aetiologies, treatments, and prognoses. The rate of onset of symptoms is very variable. Some patients present with long-standing radiological symptoms, often found opportunistically. Other patients present with acute onset symptoms, rapidly developing respiratory failure and ultimately progressing to death. This chapter covers the presentation, clinical findings, diagnosis, common causes, and associated investigations. Common ILDs are also described.

A Case of Syncope and Impaired Micturition

2018 ◽  
pp. 195-200
Author(s):  
Aaron E. Miller ◽  
Tracy M. DeAngelis ◽  
Michelle Fabian ◽  
Ilana Katz Sand
Keyword(s):  
Differential Diagnosis ◽  
Plasma Exchange ◽  
Antibody Level ◽  
Symptom Severity ◽  
Metabolic Disorders ◽  
Acute Onset ◽  
Neurological Symptoms ◽  
Acetyl Choline ◽  
Immunosuppressive Medications ◽  
Symptoms And Signs

Panautonomic failure is manifested by a variety of symptoms indicating dysfunction of the sympathetic, parasympathetic, and enteric autonomic systems. An acute onset of this syndrome, in the absence of other systemic illness or neurological symptoms and signs, indicates autoimmune autonomic ganglionopathy (AAG), in which symptoms are causally related to the presence of antibodies to ganglionic nicotinic acetyl choline receptors. Differential diagnosis consists principally of toxic/metabolic disorders and other autoimmune illnesses, most notably Sjögren’s syndrome. Antibodies to ganglionic nicotinic acetyl choline receptors are present in 50–60% of cases, and, unlike in some other antibody-mediated disorders, symptom severity is related to the antibody level. Paroxysmal coughing spells are a feature of the illness in Japanese, but not Western, patients. Corticosteroids are generally ineffective when used alone, but may provide better response when used in combination with IVIg or plasma exchange. Other immunosuppressive medications are often required.

scholarly journals Intestinal lesions in dogs with acute hemorrhagic diarrhea syndrome associated with netF-positive Clostridium perfringens type A

2018 ◽  
Vol 30 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Miriam Leipig-Rudolph ◽  
Kathrin Busch ◽  
John F. Prescott ◽  
Iman Mehdizadeh Gohari ◽  
Christian M. Leutenegger ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Significant Proportion ◽  
Type A ◽  
Acute Onset ◽  
Gram Positive Bacteria ◽  
Intestinal Lesions ◽  
Common Causes ◽  
Acute Necrotizing ◽  
Diarrhea Syndrome ◽  
Clostridium Spp

Acute hemorrhagic diarrhea syndrome (AHDS), formerly named canine hemorrhagic gastroenteritis, is one of the most common causes of acute hemorrhagic diarrhea in dogs, and is characterized by acute onset of diarrhea, vomiting, and hemoconcentration. To date, histologic examinations have been limited to postmortem specimens of only a few dogs with AHDS. Thus, the aim of our study was to describe in detail the distribution, character, and grade of microscopic lesions, and to investigate the etiology of AHDS. Our study comprised 10 dogs with AHDS and 9 control dogs of various breeds, age, and sex. Endoscopic biopsies of the gastrointestinal tract were taken and examined histologically (H&E, Giemsa), immunohistochemically ( Clostridium spp., parvovirus), and bacteriologically. The main findings were acute necrotizing and neutrophilic enterocolitis (9 of 10) with histologic detection of clostridia-like, gram-positive bacteria on the necrotic mucosal surface (9 of 10). Clostridium perfringens isolated from the duodenum was identified as type A (5 of 5) by multiplex PCR (5 of 5). In addition, each of the 5 genotyped isolates encoded the pore-forming toxin netF. Clostridium spp. (not C. perfringens) were cultured from duodenal biopsies in 2 of 9 control dogs. These findings suggest that the pore-forming netF toxin is responsible for the necrotizing lesions in the intestines of a significant proportion of dogs with AHDS. Given that the stomach was not involved in the process, the term “acute hemorrhagic diarrhea syndrome” seems more appropriate than the frequently used term “hemorrhagic gastroenteritis.”

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