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PubMed1987

Cervical disc prolapse in the elderly: an easily overlooked, reversible cause of spinal cord compression.

It is important to distinguish cord compression due to cervical disc prolapse, which has a very favourable prognosis following surgery, from that due to cervical spondylosis. In the elderly the occurrence of cervical disc prolapse as a cause of spinal compression may be under-recognised because symptoms are too readily attributed to long standing degenerative changes on plain cervical X-rays. The difficulty of making an accurate diagnosis is complicated further in the elderly by the prevalence of other diseases which may mask the symptoms of cord compression. We report our experience with 19 patients over 60 who underwent anterior cervical discectomy for myelopathy due to intervertebral disc prolapse. There was generally a short history of walking difficulty, but the presence of 'numb clumsy hands', perhaps due to selective posterior column impairment, was often a more disabling complaint. Neck pain and disturbances of micturition were unusual. The prognosis after disc excision can be excellent. In this series all the severely disabled patients returned to an independent existence. Overall 16/19 patients made an excellent or good recovery.

Aged↗
PubMed1976

Angiographic changes following acute spinal cord compression: an experimental study in monkeys.

Acute paraplegia was produced in monkeys by abruptly inflating a balloon catheter within the epidural space. The arteriographic and epidural venous changes following such trauma were serially evaluated. Spinal-cord arteriograms following cord injury remained normal during an acute (four-hour) follow-up. Serial epidural venograms demonstrated obstruction of epidural veins within four hours at the site of contusion in less than half of the animals studied. Neither spinal arteries nor epidural showed consistent diagnostic changes following trauma due to acute epidural compression.

Acute Disease↗
PubMed2006

Mouse spinal cord compression injury is reduced by either activation of the adenosine A2A receptor on bone marrow-derived cells or deletion of the A2A receptor on non-bone marrow-derived cells.

Activation of the adenosine A(2A) receptor (A(2A)R) at the time of reperfusion has been shown to reduce ischemia-reperfusion injury in peripheral tissues and spinal cord. In this study we show that treating mice with the A(2A)R agonist, 4-{3-[6-amino-9-(5-cyclopropylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-piperidine-1-carboxylic acid methyl ester for four days beginning before or just after the onset of reperfusion after compression-induced spinal cord injury rapidly (within 1 day) and persistently (>42 days) reduces locomotor dysfunction and spinal cord demyelination. Protection is abolished in knockout/wild type bone marrow chimera mice selectively lacking the A(2A)R only on bone marrow-derived cells but retaining receptors on other tissues including blood vessels. Paradoxically, reduced spinal cord injury is also noted in A(2A)R -/- mice, and in wild type/knockout bone marrow chimera mice selectively lacking the A(2A)R on non-bone marrow-derived cells, or in mice treated with the A(2A) antagonist, 4-(2-[7-amino-2-[2-furyl][1,2,4]triazolo[2,3-a][1,3,5]triazin-5-yl-amino]ethyl)phenol. The greatest protection is seen in knockout/wild type bone marrow chimera mice treated with 4-{3-[6-amino-9-(5-cyclopropylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-piperidine-1-carboxylic acid methyl ester, i.e. by activating the A(2A)R in mice expressing the receptor only in bone marrow-derived cells. The data suggest that inflammatory bone marrow-derived cells are the primary targets of A(2A) agonist-mediated protection. We conclude that A(2A) agonists or other interventions that inhibit inflammation during and after spinal cord ischemia may be effective in reducing spinal cord injury in patients, but excessive or prolonged stimulation of the A(2A)R may be counterproductive. It may be possible to devise strategies to produce optimal spinal cord protection by exploiting temporal differences in A(2A)R-mediated responses.

Adenosine A2 Receptor Agonists↗