Hydrodynamic mechanism of syringomyelia: its relationship to myelocele

Wj, Gardner

doi:10.1136/jnnp.28.3.247

Cited by 594 publications

(213 citation statements)

References 15 publications

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“…SYRINGOMYELIA as a late sequel to traumatic paraplegia and tetraplegia has been described by Bastian (1876), Strumpell (1880), Holmes (1915), Freeman (1959), Finckle (1960), Barnett, Bottrell, Jousse and Wynn-Jones (1966), Gardner (1973), Barnett, Foster and Hudgson (1973), Shannon,Symon,Logue,Cull,Kang and Kendall (198 1). Barnett et al (1966) found a clinical picture suggesting syrinx formation in 10 patients out of a total of 59 1 paraplegic patients admitted to Lyndhurst Lodge between 1945 and 1966 but were only able to confirm this at operation in one patient.…”

Section: Introductionmentioning

confidence: 95%

Post-traumatic syringomyelia

Vernon

Silver²,

Ohry

1982

Spinal Cord

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Abstract. A description is given of the syndrome of post-traumatic syringomyelia amongst patients with traumatic spinal injuries seen at the National Spinal Injuries Centre. The diagnosis was made on clinical grounds. It was confirmed wherever possible by neuroradiology prior to surgery; one case was confirmed only at post mortem. The incidence of the condition was found to be in keeping with other large series but, in contrast, no difference was found between the time of onset after injury between complete and incomplete lesions of the spinal cord. The commonest manifestation was pain, followed by sensory loss and rarely motor weakness. In the majority of patients the condition eventually became bilateral and in a significant number the lesion ascended to involve the trigeminal territory. The natural history of the condition was followed, and in all cases the condition gradually progressed. The pathogenesis of the condition is briefly discussed in view of the findings.

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Section: Introductionmentioning

confidence: 95%

Post-traumatic syringomyelia

Vernon

Silver²,

Ohry

1982

Spinal Cord

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“…The studies by Gardner and Williams studies [4,5] and Aboulker's theory [1] do not seem applicable to this lesion. We prefer to agree with the hypothesis of Sigal et al [13] who suggest that the dilatation could be the result of a lack of communication between the ventriculus terminalis and the central canal of the spinal cord.…”

Section: Introductionmentioning

confidence: 99%

Symptomatic cystic dilatation of V ventricle: Case report and review of the literature

1997

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“…In cases of cavitation with underlying adhesive arach noiditis a circulatory impairment of the spinal cord was considered as a possible pathogenetic mechanism. A greater role than that of thickening of the vessel walls causing diminution of the blood supply (Tauber & Langworthy, 1935;Lubin, 1940;McLaurin et al, 1954), may be played by impaired venous drainage (venostasis) from the cord with resulting ischaemia (Stevenson, cited by Nelson, 1943)· Appleby et al (1969) postulated an association between hydromyelia and adhesive arachnoiditis around the outflow foramina of the 4th ventricle and generally at the foramen magnum to be caused by Gardner's (1965) hydrodynamic mechanism (pulsatile CSF pressure from the ventricular system into central canal -communicating syringomyelia).…”

Section: Discussionmentioning

confidence: 99%