Ultrastructural changes in the rat spinal cord after temporary occlusion of the thoracic aorta

Schneider, Hans-Jochen; Dralle, J.

doi:10.1007/bf00688078

Cited by 19 publications

(1 citation statement)

References 33 publications

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“…The post-mortem examination of the monkeys who were not paralysed, revealed that in four of the eight monkeys there were small areas of cellular destruction in the grey matter, particularly at the base of the anterior horns. Van Harreveld and Khattab 12 and Schneider and Dralle 13 have shown early sensitivity to ischaemia of the interneurones in layer VIII. Azzarelli and Roessmann 6 and Gilles and Nag 14 found a neural loss at the base of the anterior horns in the spinal cords of patients who died after hypovolemia or hypoxia.…”

Section: Discussionmentioning

confidence: 98%

Ischaemic myelopathy following aortic surgery or traumatic laceration of the aorta

et al. 1998

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Paraplegia is one of the major complications following repair of aortic aneurysms or congenital malformations and from trauma of the aorta. In a series of 12 surviving patients we describe the clinical features as well as the evolution and pathophysiology of ischaemic lesions of the spinal cord. The clinical characteristics: loss of tendon re¯exes, preservation of light touch sensation and bladder function, and the special topography of pin prick impairment, suggest involvement of the central grey matter. This lesion of the grey matter is incomplete in most of the patients and tends to extend for 2 ± 10 segments. In some cases it can extend downward to the conus resulting in complete¯accid paraplegia. On follow-up we have observed limited improvement in most cases. No patient has recovered fully. Except in cases of traumatic laceration, where symptoms existed before surgery, paraplegia followed surgical repair in all other cases. Ischaemia can be related to the duration and the site of crossclamping of the aorta. Clamping above the left subclavian artery and/or a ligation of the intercostal arteries without previous visualisation of the spinal cord arteries can be dangerous. Other factors such as the phenomena of revascularisation and the presence of free radicals are discussed. These could explain delayed postischaemic spinal cord hypoperfusion.

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Section: Discussionmentioning

confidence: 98%

Ischaemic myelopathy following aortic surgery or traumatic laceration of the aorta

et al. 1998

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Peripheral nerve ischemia: Part 2. Accumulation of organelles

Korthals

Wı́sniewski

1978

Annals of Neurology

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Following simultaneous ligation of the aorta and femoral artery in the cat, organelles accumulated in distal portions of the sciatic nerve and in lower portions of the tibial and peroneal nerves. The accumulations were located in the proximal and distal ends of the nerve infarction and delineated the borders of the necrotic area. Topographical analysis of the necrosis and organelle accumulations following ligation of these main arteries showed the larger nerve fascicles to be more sensitive to ischemia than the smaller ones. The center of a nerve fascicle was more sensitive than the periphery. The organelles accumulated in ischemic nerves during the first hours after arterial ligation, presumably as a result of lack of energy for fast axoplasmic transport. Later accumulations reflected mechanical block of axoplasmic transport due to focal necrosis of the nerve. The content of organelle accumulations was similar to that found in lesions resulting from transection except for the presence of 60 to 70 A filaments at the distal end of the infarction.

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Delayed paralysis of the deltoids due to selective anterior horn necrosis in a patient with traumatic tetraplegia

Foo

Sarkarati

Rossier

et al. 1979

Annals of Neurology

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In spinal cord studies of patients with traumatic paraplegia, one sometimes observes a second lesion apparently not related to fracture-dislocation of the spine. We report a case that is particularly interesting in terms of clinicopathological correlations.A 49-year-old man sustained multiple injuries in an automobile accident and was immediately unconscious. At the emergency room he had 3 cardiac arrest but was successfully resuscitated. On the second and fourth days after injury he had two short episodes of cardiac asystole which responded to atropine. Four days after the accident the patient was lethargic but arousable. Pain and touch were absent below C6 bilaterally. Muscle strength in the upper extremities was preserved but the hands were paralyzed; Necrosi.c of the central part of the anterior horns at C5 (arrows). Note the symmetry of the lesion. (Luxol-fast blue.)the paralyzed lower extremities were flaccid. Roentgenograms of the cervical spine showed fractures of the C7 laminae and of the C4, C5, and C6 spinous processes. O n the tenth day after injury the patient showed decreased strength in both deltoid muscles. Two days later, both deltoid muscles had absent function whereas biceps and triceps functions were present. The neurological state remained otherwise unchanged. The patient died of pneumonia on the twentieth day following injury.Autopsy of the spinal cord showed massive necrosis at C8-TI. In view of the bilateral loss of the deltoids with preservation of the biceps, attention was paid to C5. The spinal cord between the C4 and C6 roots was cut into four slices which were embedded separately. Macroscopically, the C5 level appeared normal except for a slight depression in the anterior horns in the second and third slices. Histologically, the three upper slices showed neuronal depopulation and chromatolysis of the surviving motor neurons, progressing to frank central necrosis of the anterior horns with accumulation of lipid macrophages (Figure). The lower slice was normal except for early wallerian degeneration in the posterior columns. The anterior spinal artery and its sulcal branches were normal. Above C5, at C6 and C7, and below T I , the cord was normal except for early wallerian degeneration. The brain was normal.The selective necrosis of the anterior horns at C5 with sparing of two segments above the site of the major traumatic injury at C8-T1 accounts for a clinical finding difficult to explain during life, i.e., sparing of the biceps with complete loss of the deltoids occurring ten days after injury. The innervation of the deltoid is located at a somewhat higher level in the cord compared with the biceps, and sparing of the lower part of C5 and of C6 thus accounts for relative preservation of the biceps in this patient. Selective necrosis of the anterior horns is a pathological entity distinct from central spinal cord necrosis. Central cord necrosis is a common occurrence in spinal cord injury, probably due to stretching of the horizontally oriented blood vessels in anteroposterior compre...

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Ultrastructural changes in the rat spinal cord after temporary occlusion of the thoracic aorta

Cited by 19 publications

References 33 publications

Ischaemic myelopathy following aortic surgery or traumatic laceration of the aorta

Ischaemic myelopathy following aortic surgery or traumatic laceration of the aorta

Peripheral nerve ischemia: Part 2. Accumulation of organelles

Delayed paralysis of the deltoids due to selective anterior horn necrosis in a patient with traumatic tetraplegia

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