Pathology, Classification, and Treatment of Syringomyelia

Milhorat, Thomas H.; Fox, Andrew; Todor, D. Roxanne

doi:10.1007/978-4-431-67893-9_2

Cited by 7 publications

(5 citation statements)

References 35 publications

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“…Such names have resulted in confusion and in 2006 an international veterinary working group, invited by the UK Cavalier Club, were briefed to agree a name in order to dispel confusion ( 24 ). The suffix “like” was added to the human condition Chiari-I malformation because dogs do not have cerebellar tonsils and the severity of the condition is not dependent on the size of the cerebellar herniation ( 25 ). Although the working group agreed the acronym as CM/SM for Chiari-like malformation and secondary syringomyelia, CLM has been used as an acronym for CM in some research articles to distinguish it from the corresponding human condition.…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, the description of Chiari malformation in humans has morphed over time and includes CM Type 0 with normally placed cerebellar tonsils ( 21 , 30 ). The human classification of SM has also changed over time ( 25 , 31 ) with advanced imaging techniques applied to CSF circulation and it is possible that further phenotypic variations for both SM and CM may be revealed.…”

Section: Introductionmentioning

confidence: 99%

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Morphogenesis of Canine Chiari Malformation and Secondary Syringomyelia: Disorders of Cerebrospinal Fluid Circulation

2018

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Chiari-like Malformation (CM) and secondary syringomyelia (SM), as well as their analogous human conditions, is a complex developmental condition associated with pain and accompanying welfare concerns. CM/SM is diagnosed ever more frequently, thanks in part to the increased availability of magnetic resonance imaging in veterinary medicine. Research over the last two decades has focused primarily on its pathophysiology relating to overcrowding of the cranial caudal fossa. More recent characterizations of CM/SM include brachycephaly with osseous reduction and neural parenchymal displacement involving the entire brain and craniocervical junction to include rostral flattening, olfactory bulb rotation, increased height of the cranium, reduced cranial base with spheno-occipital synchondrosis angulation, reduced supraoccipital and interparietal crest and rostral displacement of the axis and atlas with increased odontoid angulation. The most shared manifestation of CM is the development of fluid-filled pockets (syrinx, syringes) in the spinal cord that can be readily quantified. Dogs with symptomatic CM without SM have a reduced basioccipital bone, compensatory increased cranial fossa height with displaced parenchyma whereby the cerebellum is invaginated beneath the occipital lobes but without compromising cerebrospinal fluid channels enough to cause SM. Thus, broadly defined, CM might be described as any distortion of the skull and craniocervical junction which compromises the neural parenchyma and cerebrospinal fluid circulation causing pain and/or SM. The etiology of CM is multifactorial, potentially including genetically-influenced, breed-specific abnormalities in both skeletal and neural components. Since causation between specific morphologic changes and SM or clinical signs is unproven, CM might be more appropriately considered as a brachycephalic obstructive CSF channel syndrome (BOCCS) rather than a single malformation. Understanding the normal development of the brain, skull and craniocervical junction is fundamental to identifying deviations which predispose to CM/SM. Here we review its anatomical, embryological, bio-mechanical, and genetic underpinnings to update the profession's understanding of this condition and meaningfully inform future research to diminish its welfare impact.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Morphogenesis of Canine Chiari Malformation and Secondary Syringomyelia: Disorders of Cerebrospinal Fluid Circulation

2018

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“…There is no history of the spinal cord damage. So we suppose the origin of central canal dilation is slightly narrow of vertebral canal, and this cavity can be classified as noncommunicating central canal dilation [13]. Also we suppose that such small cavity does not have a contribution in clinical manifestation.…”

Section: Discussionmentioning

confidence: 95%

Clinical cases of amyotrophic lateral sclerosis with atypical onset concurrent with hydromyelia

Богданов¹,

Менделевич²,

Khabibrakhmanov³

et al. 2020

Preprint

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“…Therefore, we hypothesize that a slightly narrow vertebral canal is the cause of the central canal dilation, and this cavity can be classified as noncommunicating central canal dilation. 13 Moreover, such small cavity does not have a contribution in clinical manifestation. During 2014-2019, the cavity remained same size, despite the dramatic clinical deterioration in the last 2 years.…”

Section: Discussionmentioning

confidence: 99%