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Lateral Canal Paroxysmal Positional Vertigo Revisited
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| Zeitschriftentitel: | Annals of the New York Academy of Sciences |
|---|---|
| Personen und Körperschaften: | , , |
| In: | Annals of the New York Academy of Sciences, 1164, 2009, 1, S. 316-323 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Nuti, Daniele Mandalà, Marco Salerni, Lorenzo Nuti, Daniele Mandalà, Marco Salerni, Lorenzo |
|---|---|
| author |
Nuti, Daniele Mandalà, Marco Salerni, Lorenzo |
| spellingShingle |
Nuti, Daniele Mandalà, Marco Salerni, Lorenzo Annals of the New York Academy of Sciences Lateral Canal Paroxysmal Positional Vertigo Revisited History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
| author_sort |
nuti, daniele |
| spelling |
Nuti, Daniele Mandalà, Marco Salerni, Lorenzo 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1111/j.1749-6632.2008.03720.x <jats:p>The first reports of an involvement of the lateral canal (LC) in paroxysmal positional vertigo (PPV), were published in 1985, by Luciano Cipparrone <jats:italic>et al.</jats:italic>, from Italy and Joseph McClure from Canada. The increasing interest of otolaryngologists and neurologists has led to a progressive advance in the knowledge of this labyrinthine disorder regarding its epidemiological, physiopathological, clinical, and therapeutic aspects. According to the most recent data, LC–benign PPV accounts for 17% of all PPV patients, regardless of gender and between the two labyrinths. The LC–PPV syndrome is characterized by intense positional vertigo and direction‐changing geotropic horizontal nystagmus, both caused by rotation of the head in the supine position. Less frequently, it presents with apogeotropic nystagmus. In some patients nystagmus is also detectable in the sitting position, mimicking a spontaneous nystagmus. In most cases nystagmus is caused by displaced otoconia floating in the semicircular canal. The pathological side, which must be identified for successful treatment, is usually indicated by nystagmus intensity: the more intense positional nystagmus beats toward the affected ear. In a few cases, where there is no difference in nystgmus intensity, other indicators are necessary to determine the pathological side. Vestibular neuritis and posterior fossa lesions should be considered in the differential diagnosis. Treatment of LC–PPV relies on some physical maneuvers, the objective of which is to allow the otoconial debris to exit from the LC by centrifugal inertia and/or by gravitation.</jats:p> Lateral Canal Paroxysmal Positional Vertigo Revisited Annals of the New York Academy of Sciences |
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| title |
Lateral Canal Paroxysmal Positional Vertigo Revisited |
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Lateral Canal Paroxysmal Positional Vertigo Revisited |
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Lateral Canal Paroxysmal Positional Vertigo Revisited |
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Lateral Canal Paroxysmal Positional Vertigo Revisited |
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Lateral Canal Paroxysmal Positional Vertigo Revisited |
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Lateral Canal Paroxysmal Positional Vertigo Revisited |
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lateral canal paroxysmal positional vertigo revisited |
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History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
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http://dx.doi.org/10.1111/j.1749-6632.2008.03720.x |
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2009 |
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316-323 |
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<jats:p>The first reports of an involvement of the lateral canal (LC) in paroxysmal positional vertigo (PPV), were published in 1985, by Luciano Cipparrone <jats:italic>et al.</jats:italic>, from Italy and Joseph McClure from Canada. The increasing interest of otolaryngologists and neurologists has led to a progressive advance in the knowledge of this labyrinthine disorder regarding its epidemiological, physiopathological, clinical, and therapeutic aspects. According to the most recent data, LC–benign PPV accounts for 17% of all PPV patients, regardless of gender and between the two labyrinths. The LC–PPV syndrome is characterized by intense positional vertigo and direction‐changing geotropic horizontal nystagmus, both caused by rotation of the head in the supine position. Less frequently, it presents with apogeotropic nystagmus. In some patients nystagmus is also detectable in the sitting position, mimicking a spontaneous nystagmus. In most cases nystagmus is caused by displaced otoconia floating in the semicircular canal. The pathological side, which must be identified for successful treatment, is usually indicated by nystagmus intensity: the more intense positional nystagmus beats toward the affected ear. In a few cases, where there is no difference in nystgmus intensity, other indicators are necessary to determine the pathological side. Vestibular neuritis and posterior fossa lesions should be considered in the differential diagnosis. Treatment of LC–PPV relies on some physical maneuvers, the objective of which is to allow the otoconial debris to exit from the LC by centrifugal inertia and/or by gravitation.</jats:p> |
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| description | <jats:p>The first reports of an involvement of the lateral canal (LC) in paroxysmal positional vertigo (PPV), were published in 1985, by Luciano Cipparrone <jats:italic>et al.</jats:italic>, from Italy and Joseph McClure from Canada. The increasing interest of otolaryngologists and neurologists has led to a progressive advance in the knowledge of this labyrinthine disorder regarding its epidemiological, physiopathological, clinical, and therapeutic aspects. According to the most recent data, LC–benign PPV accounts for 17% of all PPV patients, regardless of gender and between the two labyrinths. The LC–PPV syndrome is characterized by intense positional vertigo and direction‐changing geotropic horizontal nystagmus, both caused by rotation of the head in the supine position. Less frequently, it presents with apogeotropic nystagmus. In some patients nystagmus is also detectable in the sitting position, mimicking a spontaneous nystagmus. In most cases nystagmus is caused by displaced otoconia floating in the semicircular canal. The pathological side, which must be identified for successful treatment, is usually indicated by nystagmus intensity: the more intense positional nystagmus beats toward the affected ear. In a few cases, where there is no difference in nystgmus intensity, other indicators are necessary to determine the pathological side. Vestibular neuritis and posterior fossa lesions should be considered in the differential diagnosis. Treatment of LC–PPV relies on some physical maneuvers, the objective of which is to allow the otoconial debris to exit from the LC by centrifugal inertia and/or by gravitation.</jats:p> |
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| spelling | Nuti, Daniele Mandalà, Marco Salerni, Lorenzo 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1111/j.1749-6632.2008.03720.x <jats:p>The first reports of an involvement of the lateral canal (LC) in paroxysmal positional vertigo (PPV), were published in 1985, by Luciano Cipparrone <jats:italic>et al.</jats:italic>, from Italy and Joseph McClure from Canada. The increasing interest of otolaryngologists and neurologists has led to a progressive advance in the knowledge of this labyrinthine disorder regarding its epidemiological, physiopathological, clinical, and therapeutic aspects. According to the most recent data, LC–benign PPV accounts for 17% of all PPV patients, regardless of gender and between the two labyrinths. The LC–PPV syndrome is characterized by intense positional vertigo and direction‐changing geotropic horizontal nystagmus, both caused by rotation of the head in the supine position. Less frequently, it presents with apogeotropic nystagmus. In some patients nystagmus is also detectable in the sitting position, mimicking a spontaneous nystagmus. In most cases nystagmus is caused by displaced otoconia floating in the semicircular canal. The pathological side, which must be identified for successful treatment, is usually indicated by nystagmus intensity: the more intense positional nystagmus beats toward the affected ear. In a few cases, where there is no difference in nystgmus intensity, other indicators are necessary to determine the pathological side. Vestibular neuritis and posterior fossa lesions should be considered in the differential diagnosis. Treatment of LC–PPV relies on some physical maneuvers, the objective of which is to allow the otoconial debris to exit from the LC by centrifugal inertia and/or by gravitation.</jats:p> Lateral Canal Paroxysmal Positional Vertigo Revisited Annals of the New York Academy of Sciences |
| spellingShingle | Nuti, Daniele, Mandalà, Marco, Salerni, Lorenzo, Annals of the New York Academy of Sciences, Lateral Canal Paroxysmal Positional Vertigo Revisited, History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
| title | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| title_full | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| title_fullStr | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| title_full_unstemmed | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| title_short | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| title_sort | lateral canal paroxysmal positional vertigo revisited |
| title_unstemmed | Lateral Canal Paroxysmal Positional Vertigo Revisited |
| topic | History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
| url | http://dx.doi.org/10.1111/j.1749-6632.2008.03720.x |