Tracing Spasmodic Dysphonia: the source of Ludwig Traube’s priority

Objectives: Since the mid-20th century, one citation is given historical priority as the first description of Spasmodic Dysphonia (SD): Ludwig Traube’s 1871 case of the “spastic form of nervous hoarseness”. Our objective is to understand how this case serves as the foundation of understanding laryngeal movement disorders. Methods: The original German paper was located and translated. Bibliographical and bibliometric methods are used to determine the citation history of this original source over the past 140 years. Results: Although secondary citations in contemporary publications typically credit Traube for establishing the clinical entity SD, his case does not conform to currently accepted diagnostic features. Citation patterns indicate the source of Traube’s priority is publications by Arnold and Luchsinger, mid-20th century ENT clinician, particularly their influential 1965 textbook used to train US and UK clinicians on voice disorders for several generations. Conclusions: Sometimes secondary citations in medical literature lead to the inadvertent perpetuation of factual misrepresentation. The clinical picture of Traube’s original case does not represent what clinicians would recognize as SD today. The rich 19th century literature on voice disorders is a valuable resource for present day clinicians

Morell Mackenzie’s contribution to the description of spasmodic dysphonia

Objectives: Since the middle of the 20th century most discussions of Spasmodic Dysphonia reference a paper by Ludwig Traube published in1871 as the first historical citation, crediting him with priority for this clinical syndrome. However, our recent research has determined that the original observation by Traube was published in 1864 and does not in fact describe what is currently recognized as SD. It appears that many clinics throughout Europe and North America were investigating and publishing observations on a range of voice disorders.. Methods: The wider context of work on laryngeal disorders in the 1860s-1870s is considered. One of Traube’s contemporaries, Morell Mackenzie made significant contributions to the understanding of laryngeal movement disorder and its consequences for the voice. These will be examined to gain a clearer focus on the characterization of this disorder. Results: The clinical descriptions published by Morrell Mackenzie in the 1860s provide details which conform quite closely to our current day understanding of SD. Conclusions: The citation of Traube’s “hysterical” patient links to mid-20th century views of the functional nature of SD and the utility of psychiatric treatment. The description presented by Mackenzie is consistent with current views of SD as a movement disorder

Redirected nuclear glutamate dehydrogenase supplies Tet3 with alpha-ketoglutarate in neurons

Tet3 is the main alpha -ketoglutarate (alpha KG)-dependent dioxygenase in neurons that converts 5-methyl-dC into 5-hydroxymethyl-dC and further on to 5-formyl- and 5-carboxy-dC. Neurons possess high levels of 5-hydroxymethyl-dC that further increase during neural activity to establish transcriptional plasticity required for learning and memory functions. How alpha KG, which is mainly generated in mitochondria as an intermediate of the tricarboxylic acid cycle, is made available in the nucleus has remained an unresolved question in the connection between metabolism and epigenetics. We show that in neurons the mitochondrial enzyme glutamate dehydrogenase, which converts glutamate into alpha KG in an NAD(+)-dependent manner, is redirected to the nucleus by the alpha KG-consumer protein Tet3, suggesting on-site production of alpha KG. Further, glutamate dehydrogenase has a stimulatory effect on Tet3 demethylation activity in neurons, and neuronal activation increases the levels of alpha KG. Overall, the glutamate dehydrogenase-Tet3 interaction might have a role in epigenetic changes during neural plasticity. alpha -ketoglutarate (alpha KG) is an intermediate in the tricarboxylic acid cycle that is required in the nucleus for genomic DNA demethylation by Tet3. Here, the authors show that the enzyme glutamate dehydrogenase, which converts glutamate to alpha KG, is redirected from the mitochondria to the nucleus.Proteomic

Mental Health and School Functioning for Girls in the Child Welfare System : the Mediating Role of Future Orientation and School Engagement

This study investigated the association between mental health problems and academic and behavioral school functioning for adolescent girls in the child welfare system and determined whether school engagement and future orientation meditated the relationship. Participants were 231 girls aged between 12 and 19 who had been involved with the child welfare system. Results indicated that 39% of girls reported depressive symptoms in the clinical range and 54% reported posttraumatic symptoms in the clinical range. The most common school functioning problems reported were failing a class (41%) and physical fights with other students (35%). Participants reported a mean number of 1.7 school functioning problems. Higher levels of depression and PTSD were significantly associated with more school functioning problems. School engagement fully mediated the relationship between depression and school functioning and between PTSD and school functioning, both models controlling for age, race, and placement stability. Future orientation was not significantly associated with school functioning problems at the bivariate level. Findings suggest that school engagement is a potentially modifiable target for interventions aiming to ameliorate the negative influence of mental health problems on school functioning for adolescent girls with histories of abuse or neglect

A Controversy That Has Been Tough to Swallow: Is the Treatment of Achalasia Now Digested?

Esophageal achalasia is a rare neurodegenerative disease of the esophagus and the lower esophageal sphincter that presents within a spectrum of disease severity related to progressive pathological changes, most commonly resulting in dysphagia. The pathophysiology of achalasia is still incompletely understood, but recent evidence suggests that degeneration of the postganglionic inhibitory nerves of the myenteric plexus could be due to an infectious or autoimmune mechanism, and nitric oxide is the neurotransmitter affected. Current treatment of achalasia is directed at palliation of symptoms. Therapies include pharmacological therapy, endoscopic injection of botulinum toxin, endoscopic dilation, and surgery. Until the late 1980s, endoscopic dilation was the first line of therapy. The advent of safe and effective minimally invasive surgical techniques in the early 1990s paved the way for the introduction of laparoscopic myotomy. This review will discuss the most up-to-date information regarding the pathophysiology, diagnosis, and treatment of achalasia, including a historical perspective. The laparoscopic Heller myotomy with partial fundoplication performed at an experienced center is currently the first line of therapy because it offers a low complication rate, the most durable symptom relief, and the lowest incidence of postoperative gastroesophageal reflux