Spinal cord stroke
[6] Preventions of the disease include decreasing the risk factors and maintaining enough spinal cord perfusion pressure during and after the operation.
The process of diagnosing the ischemic and hemorrhagic spinal cord stroke includes applying different MRI protocols and CT scan.
[1][5] Abrupt onset of pain at the back or neck marks the location of ischaemia or hemorrhage at the beginning, which radiates as the damage intensifies.
[9][10] Temporary paresis in limbs may occur days before the onset of spinal ischaemic stroke, though the relationship remains unclear.
[9][10] Infarction occurs predominantly in arteries, and the watershed region, which refers thoracic spinal cord here, is highly susceptible to ischaemic attack.
[4] Patients with a male gender, younger age, lower body mass index, hypertension, diabetes mellitus, renal insufficiency and chronic obstructive pulmonary disease are predisposed to higher risks of severe spinal cord stroke.
[5] In central spinal cord syndrome, impairment of motor function in the upper body is considerably more severe than that of lower body, which is related to hyperextension of corticospinal tracts and spinocerebellar tract in cervical spinal cord, accompanied by dysfunction in urinary bladder and sensational loss at a varying degree.
[6] Prolonged compression on the blood network by vertebral diseases such as cervical spondylosis and protruded intervertebral disks can be attributed to acute ischaemia in spinal cord, yet the correlation is uncertain.
Decreasing blood flow hampers oxygen and glucose delivery to neurones, causing a huge decline in ATP production and failure of calcium pump.
[15] The rising intracellular calcium level activates a series of enzymes like phospholipase A2 (PLA2), COX-2, calcineurin, calpain, mitogen-activated protein kinase, nitric oxide synthase, matrix metalloproteinases (MMPs) to produce proinflammatory and proapoptotic chemicals.
[15] Meanwhile, glutamate is released to extracellular space and binds to its excitatory receptors, further exacerbating calcium influx and a cascade of events involving mitochondrial, cell membrane damage, and production of reactive oxygen species.
[12] It aims to maintain enough spinal cord perfusion pressure, and make serial neurologic assessments to detect the disease.
[10] Doctor will first assess the clinical symptoms of the patient, such as paralysis, sensory loss and urinary and bowel dysfunction, to determine whether it is possible for the spinal stroke.
[21] Given the rarity and heterogeneity of spinal cord stroke, symptomatic treatment of associated complications is applied, which is based on patients' own circumstances.
Although some literature suggest that thrombolysis could be the treatment for ischaemic spinal stroke, the associated risks are unknown due to the scarce data.
Several case studies show a substantial link between the time from bleeding to surgical decompression and neurological outcome, with the greatest results coming from individuals who had surgery within 12 hours after symptom onset.
Although the mortality rate after spinal cord ischaemia is relatively high (23%), 58% of the survivors were ambulating with or without gait assistance at their final follow-up appointment.
