Abnormal Posturing

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Susan R. Orenstein - One of the best experts on this subject based on the ideXlab platform.

  • Sandifer Syndrome Posturing: Relation to Abdominal Wall Contractions, Gastroesophageal Reflux, and Fundoplication
    Digestive Diseases and Sciences, 2006
    Co-Authors: Eric A. Frankel, Theresa M. Shalaby, Susan R. Orenstein
    Abstract:

    Sandifer syndrome designates Abnormal Posturing in patients with gastroesophageal reflux. To explore its mechanisms via examining relationships among Sandifer syndrome Posturing, abdominal wall contractions, and reflux episodes, we studied an affected child in detail. The study utilized esophageal pHmetry, surface electromyography, and split-screen videography. The multichannel physiologic study demonstrated association of rectus abdominis contraction with onset of reflux episodes ( P < 0.001) and association of reflux episodes with Sandifer syndrome Posturing. This child’s subsequent course confirmed his diagnosis and suggested mechanisms of the association of reflux and Sandifer syndrome. We conclude that abdominal wall contractions may induce reflux episodes. Sandifer syndrome may be due to gastroesophageal reflux even without hiatal hernia, macroscopic esophagitis, or reflux symptoms. Despite the absence of more typical reflux symptoms and failure to respond to very aggressive medical therapy, Sandifer syndrome may resolve after fundoplication.

Eric A. Frankel - One of the best experts on this subject based on the ideXlab platform.

  • Sandifer Syndrome Posturing: Relation to Abdominal Wall Contractions, Gastroesophageal Reflux, and Fundoplication
    Digestive Diseases and Sciences, 2006
    Co-Authors: Eric A. Frankel, Theresa M. Shalaby, Susan R. Orenstein
    Abstract:

    Sandifer syndrome designates Abnormal Posturing in patients with gastroesophageal reflux. To explore its mechanisms via examining relationships among Sandifer syndrome Posturing, abdominal wall contractions, and reflux episodes, we studied an affected child in detail. The study utilized esophageal pHmetry, surface electromyography, and split-screen videography. The multichannel physiologic study demonstrated association of rectus abdominis contraction with onset of reflux episodes ( P < 0.001) and association of reflux episodes with Sandifer syndrome Posturing. This child’s subsequent course confirmed his diagnosis and suggested mechanisms of the association of reflux and Sandifer syndrome. We conclude that abdominal wall contractions may induce reflux episodes. Sandifer syndrome may be due to gastroesophageal reflux even without hiatal hernia, macroscopic esophagitis, or reflux symptoms. Despite the absence of more typical reflux symptoms and failure to respond to very aggressive medical therapy, Sandifer syndrome may resolve after fundoplication.

Theresa M. Shalaby - One of the best experts on this subject based on the ideXlab platform.

  • Sandifer Syndrome Posturing: Relation to Abdominal Wall Contractions, Gastroesophageal Reflux, and Fundoplication
    Digestive Diseases and Sciences, 2006
    Co-Authors: Eric A. Frankel, Theresa M. Shalaby, Susan R. Orenstein
    Abstract:

    Sandifer syndrome designates Abnormal Posturing in patients with gastroesophageal reflux. To explore its mechanisms via examining relationships among Sandifer syndrome Posturing, abdominal wall contractions, and reflux episodes, we studied an affected child in detail. The study utilized esophageal pHmetry, surface electromyography, and split-screen videography. The multichannel physiologic study demonstrated association of rectus abdominis contraction with onset of reflux episodes ( P < 0.001) and association of reflux episodes with Sandifer syndrome Posturing. This child’s subsequent course confirmed his diagnosis and suggested mechanisms of the association of reflux and Sandifer syndrome. We conclude that abdominal wall contractions may induce reflux episodes. Sandifer syndrome may be due to gastroesophageal reflux even without hiatal hernia, macroscopic esophagitis, or reflux symptoms. Despite the absence of more typical reflux symptoms and failure to respond to very aggressive medical therapy, Sandifer syndrome may resolve after fundoplication.

Hyder A. Jinnah - One of the best experts on this subject based on the ideXlab platform.

  • New approaches to discovering drugs that treat dystonia.
    Expert Opinion on Drug Discovery, 2019
    Co-Authors: Sarah Pirio Richardson, Hyder A. Jinnah
    Abstract:

    ABSTRACTIntroduction: Dystonia consists of involuntary movements, Abnormal Posturing, and pain. In adults, dystonia presents in a particular region of the body and causes significant disability due...

  • the basal ganglia and cerebellum interact in the expression of dystonic movement
    Brain, 2008
    Co-Authors: Vladimir Neychev, Vanyo Mitev, Ellen J. Hess, Hyder A. Jinnah
    Abstract:

    Dystonia is a neurological disorder characterized by excessive involuntary muscle contractions that lead to twisting movements or Abnormal Posturing. Traditional views place responsibility for dystonia with dysfunction of basal ganglia circuits, yet recent evidence has pointed towards cerebellar circuits as well. In the current studies we used two strategies to explore the hypothesis that the expression of dystonic movements depends on influences from a motor network that includes both the basal ganglia and cerebellum. The first strategy was to evaluate the consequences of subthreshold lesions of the striatum in two different animal models where dystonic movements are thought to originate from Abnormal cerebellar function. The second strategy employed microdialysis to search for changes in striatal dopamine release in these two animal models where the cerebellum has been already implicated. One of the animal models involved tottering mice, which exhibit paroxysmal dystonia due to an inherited defect affecting calcium channels. In keeping with prior results implicating the cerebellum in this model, surgical removal of the cerebellum eliminated their dystonic attacks. In contrast, subclinical lesions of the striatum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exaggerated their dystonic attacks. Microdialysis of the striatum revealed dystonic attacks in tottering mice to be associated with a significant reduction in extracellular striatal dopamine. The other animal model involved the induction of dystonia via pharmacological excitation of the cerebellar cortex by local application of kainic acid in normal mice. In this model the site of stimulation determines the origin of dystonia in the cerebellum. However, subclinical striatal lesions with either 6OHDA or QA again exaggerated their generalized dystonia. When dystonic movements were triggered by pharmacological stimulation of the cerebellum, microdialysis revealed significant reductions in striatal dopamine release. These results demonstrate important functional relationships between cerebellar and basal ganglia circuits in two different animal models of dystonia. They suggest that expression of dystonic movements depends on influences from both basal ganglia and cerebellum in both models. These results support the hypothesis that dystonia may result from disruption of a motor network involving both the basal ganglia and cerebellum, rather than isolated dysfunction of only one motor system.

Vladimir Neychev - One of the best experts on this subject based on the ideXlab platform.

  • the basal ganglia and cerebellum interact in the expression of dystonic movement
    Brain, 2008
    Co-Authors: Vladimir Neychev, Vanyo Mitev, Ellen J. Hess, Hyder A. Jinnah
    Abstract:

    Dystonia is a neurological disorder characterized by excessive involuntary muscle contractions that lead to twisting movements or Abnormal Posturing. Traditional views place responsibility for dystonia with dysfunction of basal ganglia circuits, yet recent evidence has pointed towards cerebellar circuits as well. In the current studies we used two strategies to explore the hypothesis that the expression of dystonic movements depends on influences from a motor network that includes both the basal ganglia and cerebellum. The first strategy was to evaluate the consequences of subthreshold lesions of the striatum in two different animal models where dystonic movements are thought to originate from Abnormal cerebellar function. The second strategy employed microdialysis to search for changes in striatal dopamine release in these two animal models where the cerebellum has been already implicated. One of the animal models involved tottering mice, which exhibit paroxysmal dystonia due to an inherited defect affecting calcium channels. In keeping with prior results implicating the cerebellum in this model, surgical removal of the cerebellum eliminated their dystonic attacks. In contrast, subclinical lesions of the striatum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exaggerated their dystonic attacks. Microdialysis of the striatum revealed dystonic attacks in tottering mice to be associated with a significant reduction in extracellular striatal dopamine. The other animal model involved the induction of dystonia via pharmacological excitation of the cerebellar cortex by local application of kainic acid in normal mice. In this model the site of stimulation determines the origin of dystonia in the cerebellum. However, subclinical striatal lesions with either 6OHDA or QA again exaggerated their generalized dystonia. When dystonic movements were triggered by pharmacological stimulation of the cerebellum, microdialysis revealed significant reductions in striatal dopamine release. These results demonstrate important functional relationships between cerebellar and basal ganglia circuits in two different animal models of dystonia. They suggest that expression of dystonic movements depends on influences from both basal ganglia and cerebellum in both models. These results support the hypothesis that dystonia may result from disruption of a motor network involving both the basal ganglia and cerebellum, rather than isolated dysfunction of only one motor system.