Delayed radiation myelopathy in man

Jellinger, K. A.; Sturm, Klaus

doi:10.1016/0022-510x(71)90174-2

Cited by 110 publications

(38 citation statements)

References 36 publications

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“…[3][4][5][6][7][8][9][10][11] One of them is demyelination (mainly related to the loss of oligodendrocytes and glial progenitor cells), which causes consecutive axonal loss, gliosis and astrocytosis (Type 1 lesion). Vascular (Type 2) lesions include endothelial cell damage in all vessels, preferentially in arterioles and venules, 11 but also in capillaries, accompanied by a chronic inflammatory reaction involving mononuclears (lymphocytes, mainly T cells, macrophages and microglia) and often fibrinoid necrosis of the vascular wall (radiation vasculitis).…”

Section: Discussionmentioning

confidence: 99%

“…Type 3 lesions involve the simultaneous occurrence of the above-mentioned two types of injuries. Besides white matter reactions, grey matter sequelae (neuronal degeneration, chromatolysis, and a coarse tigroid appearance of the Nissl substance) may also occur in the anterior and posterior horns of the spinal cord, [4][5][6][7]11,13 but the grey matter per se is less radiosensitive than the white matter. [4][5][6]11 Tables 1 and 2 present data on 17 cases of Type 1 lesions and 10 cases of Type 2 injuries, collected from the English literature.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6]11 Tables 1 and 2 present data on 17 cases of Type 1 lesions and 10 cases of Type 2 injuries, collected from the English literature. [4][5][6]9,12,[17][18][19][20][21][22][23][24][25][26] The Type 2 lesions were further subclassified on the basis of the delivered dose, as cases with doses in the conventional therapeutic range (six cases) and those with an accidental, extremely high overdosage (four cases).…”

Section: Discussionmentioning

confidence: 99%

“…This rare complication of radiotherapy can affect the white and grey matter structures separately or in combination. [3][4][5][6][7][8][9][10][11] The clinical picture of predominantly white matter injury (demyelination and vascular injury) consists of spastic motor sequelae, and sensory and vegetative deficits. Radiation myelopathy may also manifest itself less frequently as grey matter damage, that is, the destruction of neurones.…”

Section: Introductionmentioning

confidence: 99%

“…The most marked damage generally involves the large motor neurones of the anterior horns, resulting in consecutive flaccid paresis. [4][5][6][7][11][12][13] Radiation myelopathy usually runs a chronic, progressive, irreversible and relentless clinical course, with only rare recovery from established motor sequelae. A thorough literature search unearthed only seven welldocumented published cases of remission.…”

Section: Introductionmentioning

confidence: 99%

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Autopsy verifies demyelination and lack of vascular damage in partially reversible radiation myelopathy

Lengyel

Rékó²,

Majtenyi³

et al. 2003

Spinal Cord

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Study design: Case report of recovering radiation myelopathy. Objective: To present autopsy and functional imaging findings on a unique case of slowly recovering radiation myelopathy with the aim of the clarification of the underlying mechanism. Patient: The cervical spinal cord and the distal part of the medulla oblongata of a 36-year-old thyroid cancer patient had been incorrectly irradiated with a total dose of 61 Gy and a fraction size of 3.4 Gy (J Neurol Sci 1999; 163:39-43), resulting in incomplete cervical transection with a 5-month latency period following the termination of radiotherapy. This was followed by a 9.5-year spontaneous improvement until her demise, during which the check-ups were supplemented by positron emission tomography (PET) investigations; these indicated increased Results: Autopsy revealed demyelination (with axonal loss) and neuronal damage in the cervical spinal cord and the distal part of the medulla oblongata. In the same region, only minimal vascular injury (thickening of some of the capillary walls) was detected, but not cell proliferation or chronic inflammation. Bilateral, secondary pyramidal tract degeneration caudal to the irradiated segment was observed. The PET and autopsy findings, although separated by 2 years, are consistent. Conclusions: The pathological state of the spinal cord revealed by the autopsy is concordant with the incomplete cervical transection, implying that the functional recovery is supported by a process that probably differs from the restoration of the mechanism destroyed by the radiotherapy. For the restoration of the function, we suggest an altered conduction mechanism of the action potential, involving an increased number of sodium channels along the demyelinated segments of the injured axons, which is fully congruent with the PET findings.

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