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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Anterior spinal artery syndrome: Weakness below the level of the lesion.Flaccid/areflexic acutely, progressing to spastic weakness: Sensory loss below the level of the lesion.Loss of pain, temperature, light touch.Preserved discriminating touch, vibration, proprioception.
Spinal CordAnatomical and Physiological Features
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Anterior spinal artery syndrome occurs when there is critical ischaemia of the anterior two-thirds of the spinal cord which leads to (i) paraplegia as a result of damage to corticospinal and vestibulospinal tracts; (ii) loss of pain, pressure and deep touch mediated by the spinothalamic tract and (iii) the preservation of light touch, proprioception and vibration sense which are mediated by the intact posterior (dorsal) columns which are supplied by the posterior spinal arteries.
Examine the lower limbs
Published in Hani TS Benamer, Neurology for MRCP PACES, 2019
Q: What are the main causes of spastic paraparesis? Multiple sclerosis in young patients.Cervical spondylotic myelopathy in middle-aged and elderly patients.Spinal trauma.Spinal tumours (primary or metastatic).Vascular causes, such as spinal arteriovenous malformation and spinal ischaemia (anterior spinal artery syndrome).
Feasibility, safety, and functional outcomes using the neurological controlled Hybrid Assistive Limb exoskeleton (HAL®) following acute incomplete and complete spinal cord injury – Results of 50 patients
Published in The Journal of Spinal Cord Medicine, 2023
Mirko Aach, Thomas Armin Schildhauer, Amrei Zieriacks, Oliver Jansen, Martin Weßling, Alexis Brinkemper, Dennis Grasmücke
Fifty patients with acute incomplete and complete SCI (14 females, 36 males) participated in this prospective study. All patients were in the acute phase of SCI. In all patients, the time interval between SCI and the onset of HAL® training was less than one year (mean time 117.98 ± 95.82 days; range 4–327 days). All patients were classified prior to training according to the American Spinal Injury Association Impairment Scale (AIS). SCI lesions were located between C4 and L4 (AIS A-D). Sixteen subjects suffered from tetraplegia, and 34 from paraplegia. Three patients were classified as AIS grade A with no motor sensory function in the sacral segments S4/S5, but with zones of partial preservation (ZPP) below the lesion level. 30 patients were categorized as AIS grade C. Seventeen patients were classified as AIS grade D. No subject was classified as AIS grade B. Thirty-nine of the subjects had suffered traumatic spinal cord injuries. In four patients, massively prolapsed intervertebral discs caused incomplete paraplegia and in one patient, an epidural abscess with spondylodiscitis caused the SCI. In one patient, intramedullary cavernoma, and in another patient, anterior spinal artery syndrome caused the spinal cord lesion. One patient suffered from tuberculosis with osteolysis of the vertebra T7-T10. In one patient, a tumor infiltrated the spinal canal, one patient suffered cervical spinal canal stenosis and cervical myelopathy and in one patient, ischemic myelopathy caused the spinal cord lesion. Mean age ± SD at the time of enrollment was 43.88 ± 15.0 years (range, 18–72 years).
Is the anterior spinal artery occluded in severe cervical compressive myelopathy?
Published in The Journal of Spinal Cord Medicine, 2021
In our series, no ASA occlusion was found in 11 CCM patients with spinal canal sagittal diameter compression more than 80% and with hyperintensity on T2-weighted MR images. This finding indicates that the spinal cord more easily experiences compression than the ASA in its anterior surface. These negative findings are similar to our report that ASA rupture is not commonly observed in acute blunt cervical spinal cord injury,4 in CCM patients with spinal canal sagittal diameter compression less than 80%,2 and in cervical spondylotic amyotrophy and CCM patients with the “snake-eye” MRI sign.5 These results are helpful for understanding the large difference in incidence between CCM and anterior spinal artery syndrome (ASAS), which is caused by occlusion or hypoperfusion of the ASA and results in spinal cord infarction.
The comparison of recovery patterns between ischemic spinal cord injury and traumatic spinal cord injury from acute to chronic phase
Published in The Journal of Spinal Cord Medicine, 2021
Jin Young Ko, Hyunsu Choi, Jee Hyun Suh, Kyung Seok Park, Joon Woo Lee, Ju Seok Ryu
Ischemic spinal cord injury (ISCI), also called spinal cord infarction, usually develops from acute occlusion of anterior and posterior spinal arteries, and account for 0.3–1% of all infarctions.1,2 Although ISCI is frequently caused by complications of aortic surgery, many of them occur spontaneously in clinical settings.3–5 ISCI is characterized by sudden onset and rapid progression of symptoms. Clinical manifestation of ISCI is defined by the vascular territory of the artery involved. Anterior spinal artery syndrome is characterized by severe sharp pain, paralysis, loss of sphincter control, and deficit of thermal sense with relative preservation of position and vibratory sense. Conversely, posterior spinal artery syndrome is characterized by a significant loss of proprioception and vibratory sense and less severe weakness.6