Flaccid paraplegia: a feature of spinal cord lesions in Holmes-Adie syndrome and tabes dorsalis.

Swash, Michael; Earl, C J

doi:10.1136/jnnp.38.4.317

Cited by 6 publications

(3 citation statements)

References 25 publications

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“…In a minority of cases, flaccidity persists chronically after occurrence of a central lesion, e.g., with some spinal cord infarcts25, 132, 193 or cerebral lesions 177. Persistent flaccidity is often associated with a greater degree of paresis and poorer outcome,36, 79, 82, 133, 177, 197, 221 although this is not always the case 159, 201. Occasionally, a secondary reduction of spasticity is also observed months after spinal cord injury, which may suggest secondary impairment or degeneration of premotor neuronal circuits or of motor neurons 108…”

Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

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Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

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Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

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“…3,4 Other forms of spinal cord involvement in syphilis have also been described. 5,6 We describe the magnetic resonance imaging (MRI) findings in a patient with tabes dorsalis. These neuroimaging abnormalities have not yet been described in the literature to our knowledge.…”

Section: Introductionmentioning

confidence: 99%

Magnetic resonance imaging of the spinal cord in a man with tabes dorsalis

Pandey

2011

The Journal of Spinal Cord Medicine

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Background: Tabes dorsalis is a late manifestation of untreated syphilis that is characterized by ataxia, lancinating pains, and urinary incontinence. A form of tertiary syphilis or neurosyphilis, it is the result of slow, progressive degeneration of the nerve cells in the spinal cord. Method: Case report. Findings: A 39-year-old man presented with tingling paresthesia in the lower limbs, difficulty in walking, and loss of vision. Magnetic resonance imaging (MRI) of the dorsal spine showed intramedullary hyperintensity and cord atrophy, similar to changes seen in subacute combined degeneration. MRI features of tabes dorsalis have not been described previously to the best of our knowledge. Conclusion: MRI findings in this patient with tabes dorsalis were similar to those seen in subacute combined degeneration, which is characterized predominantly by cord atrophy and intramedullary hyperintensities.

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“…These authors also reported on the histology of the rest of the nervous system, suggesting that the areflexia was due to selective degeneration of neurones in the dorsal root ganglia, possibly supplying the muscle spindles. The pathophysiology of the reflex changes is discussed in Harriman and Garland (1968) and Swash and Earl (1975).…”

Section: Discussionmentioning

confidence: 99%

The Holmes‐Adie Syndrome—A Report of Three Cases and Observations on its Natural History

Talbot¹

1981

Int J Clinical Practice

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Three cases of the Holmes-Adie Syndrome are described, demonstrating facets of the natural history of the disorder. Confusion with neuro-syphilis is mentioned as is the aetiology of the condition. A note of recent developments is added. SUMMARYA case of acute intestinal obstruction due to appendicitis occurring in complete malrotation of the midgut is reported. Malrotation causing symptoms in adults is unusual, but most cases described have had a long history of undiagnosed pain extending back to childhood.

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Flaccid paraplegia: a feature of spinal cord lesions in Holmes-Adie syndrome and tabes dorsalis.

Cited by 6 publications

References 25 publications

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

Magnetic resonance imaging of the spinal cord in a man with tabes dorsalis

The Holmes‐Adie Syndrome—A Report of Three Cases and Observations on its Natural History

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