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| Discussion |
Case Report:
A 65-year-old man, known hypertensive, came with a history of sudden onset of quadriplegia after an episode of hypertensive crisis which was treated with nitroglycerine. There was no history of fever or trauma.
On examination, the patient was in hypotension and had flaccid paralysis of all four limbs with loss of bowel and bladder control. Deep tendon reflexes were absent and there was no Babinski's response. There was complete loss of pain and temperature sensation with relative preservation of light touch, position and vibration sense. Clinically, the quadriplegia was localized to the C4 level presumed to be of vascular origin.
An MRI of the cervicodorsal spine revealed a band like hyperintense signal within the cervical cord from C3 to D1 involving the anterior two - thirds of the cord. A sharp demarcation was seen between the involved anterior two- third of the cord & the uninvolved posterior one - third which was normal. Mild expansion of the cervical cord without any post contrast enhancement was also seen.
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Fig. 1a |
Fig. 1b |
Fig 1a: Sagittal T1WI of cervicodorsal cord show cord enlargement due to edema.
Fig 1b: Sagittal T2WI showing hyperintense signal extending from C3 to D1 involving central gray matter.
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Fig. 2a |
Fig. 2b |
Fig 2a: Axial T2WI reveals hyperintense signal in anterior 2/3 rd of spinal cord.
Fig 2b: Axial post contrast T1WI reveals no abnormal enhancement of the cord
Screening of the brain reveals multiple old infarcts in the basal ganglia & right cerebellar hemisphere, along with a few bilateral lacunar infarcts in the frontal & parietal white matter.
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Fig. 3a |
Fig. 3b |
Fig 3a & 3b: Axial T2WI showing old infarcts in the basal ganglia & right cerebellar hemisphere.
DIAGNOSIS:
Spinal cord infarct.
The patient succumbed to sudden cardio-respiratory arrest during his course in ward. At autopsy, there was ischemic necrosis cervico dorsal cord.
Although frequently devastating, spinal cord ischemia is an uncommon cause of
myelopathy and often remains undiagnosed as acute myelopathy of unknown origin. Spontaneous anterior spinal cord infarction primarily affects individuals with severe arthrosclerotic disease or aortic dissection. Other etiologies include aortic aneurysm, syphilis, vasculitis, emboli from disc herniation, hypotension, hematological disorders, pregnancy, diabetes, trauma and aortic repair.
Spontaneous aortic dissection is the most common cause and is responsible for about 2% of cases.
The blood supply to the spinal cord is from three arteries: a single anterior spinal artery and two posterior spinal arteries. The anterior spinal artery arises from a confluence of branches of both vertebral arteries just before they join to become the basilar artery. The anterior spinal artery supplies the anterior two thirds of the spinal cord. There are two posterior spinal arteries, which also arise from the vertebral arteries. In addition, at multiple levels there are feeding arteries that arise from the aorta, called radicular arteries, which also supply the spinal cord with collateral circulation. The largest of the radicular arteries is the arteria radicularis magna also referred to as the great radicular artery of Adamkiewicz.The radicular artery of Adamkiewicz arises at approximately the T10-T12 area and supplies the lower thoracic and lumbar cord. However, despite this large artery, the upper thoracic region and thoracolumbar junction do not have as reliable a collateral blood supply as the remainder of the cord and as such are more common sites of spinal cord infarcts. Additional impairment of hypogastric blood flow with eventual interruption of the greater radicular artery has also been reported to be critical in the development of spinal cord ischemia. Therefore, this anterior arterial system, crucial for spinal cord supply, is vulnerable to hypoperfusion.
The classical presentation of acute spinal cord ischemia syndrome is sudden onset of flaccid para or quadriparesis with or without burning pain. Dissociated sensory loss with preserved touch, vibration, and position sense is common.
MRI findings in spinal cord ischemia are independent of the etiology of the infarction. T1W images may be normal or may show a bulky cord. Areas of intramedullary cord signal abnormality are seen best on T2W images. Signal changes often involve only the central gray matter structures, though in more severely affected patients, they are present throughout the entire cross section of the cord. Enhancement of gray matter may be seen on postcontrast images during subacute stage. Similar MRI findings may also be seen in transverse myelitis, demyelination, intrinsic cord tumors, and inflammation, but the abrupt onset of clinical symptoms and the predilection for the central gray matter are findings that help in arriving at a diagnosis of spinal cord ischemia. T2W images may also show the associated vertebral body changes. Vertebral body infarction accompanies spinal cord infarction only if the arterial occlusion is proximal to the vessels supplying the vertebral body. Several months after infarction, the spinal cord may become atrophic.
Spinal cord infarct may be hemorrhagic as well, in which case the presence of an underlying vascular malformation should be considered. A simultaneous spinal MR angiography examination or subsequent spinal angiography may be considered in this situation. The treatment of cord infarct includes anticoagulation, steroids and treatment of the cause.
In our case nitroglycerine induced sudden hypotension was the cause for spinal cord infarction.