Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of angiodysgenetic myelomalacia are presented. Both patients had progressive weakness and sensory deficits in the lower extremities and vascular malformations of their spinal cords. The lesions were located on the dorsum of the spinal cord and the dorso-spinal roots. We believe the symptoms that developed later in life were due to spinal cord ischemia resulting from late degenerative changes in the vessels of the malformation and an ever increasing spinal "steal".
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PMID:Vascular malformations of the spinal cord (angiodysgenetic myelomalacia): a critique on its pathogenesis. 42 76

Seven patients who received epidural anesthesia for gynecological (5 cases), cosmetic (1 case) or general surgery (1 case) developed spinal arachnoiditis leading to subarachnoid cyst in all 7 and cord cavitation in 5. MRI was useful to show the subarachnoid and intramedullary cysts, as well as to monitor lesion extent and progress. Associated MRI findings were a Chiari anomaly in one case, a tethered cord in another and spinal cord atrophy in a third. One patient refused surgery but improved spontaneously while the other six were treated by a shunting procedure, with a satisfactory outcome in three. Meningeal inflammation may have left scars which later induced ischemia and subsequent cavitation. Alternatively, CSF circulation blockade may have dilated the central spinal canal causing ischemia by compression, followed by myelomalacia and cavitation. Careful handling of this procedure is urged in order to avoid such severe complications.
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PMID:[Spinal arachnoiditis as a complication of peridural anesthesia]. 799 43

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.
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PMID:Intravascular cartilaginous emboli in the spinal cord of turkeys. 964 39

We report the case of a 20-year-old male driver who suffered from a trauma to the cervical vertebral column in a head-on collision with a tree. The injuries included subluxation of the 2nd and 3rd cervical vertebrae and fracture of the odontoid process of the axis with ventrally directed displacement of the proximal fragment and dorsally directed displacement of the distal fragment. Already at admission to hospital a space-occupying spinal subdural hematoma was diagnosed. Clinically, paraplegia was diagnosed with progressive loss of consciousness. Pneumonia led to death 40 days after the accident. Autopsy disclosed a total myelomalacia of the cervical spinal cord obviously resulting from an ischemia caused by a traumatic lesion of the dorsal truncus arteriosus spinalis as well as a compression by the spinal subdural hematoma.
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PMID:Traumatic induced total myelomalacia of the cervical spinal cord associated with a space-occupying subdural hematoma. 1058 May 57

Intramedullary signal change (ISC) is a non-specific finding that is frequently observed on magnetic resonance imaging (MRI) examinations of the canine spinal cord. ISC can represent a variety of primary pathological processes such as neoplasms or myelitides or secondary changes such as edema, cysts, gliosis, or myelomalacia. An unusual phenotype of ISC is the "snake-eye" myelopathy (SEM), which refers to bilaterally symmetric T2 hyperintensities preferentially affecting the ventral horn gray matter on transverse MR images, which resemble a pair of snake's eyes. The pathophysiology of SEM is poorly understood in humans, and this imaging finding may be associated with cervical spondylotic myelopathy, spinal cord ischemia, ossification of the posterior longitudinal ligament, amyotrophic lateral sclerosis, and Hirayama disease. Here we describe four dogs with cervical MRI examinations consistent with an SEM-like phenotype. All dogs initially presented with a central cord syndrome or tetraparesis referable to a C6-T2 neuroanatomic localization, which was attributed to disc-associated spinal cord compression in three cases, while one dog had the SEM-like phenotype with no identifiable etiology. Once the SEM-like phenotype was present on MRI examinations, dogs demonstrated insidious clinical deterioration despite therapeutic interventions. Deterioration was characterized by lower motor neuron weakness and neurogenic muscle atrophy progressing to paralysis in the thoracic limbs, while neurological functions caudal to the level of the SEM-like lesion remained largely preserved for months to years thereafter. Neuropathological features of the SEM-like phenotype include multisegmental cavitations and poliomyelomalacia of laminae VI-IX of the caudal cervical spinal cord, although the lesion evolved into pan-necrosis of gray matter with extension into the adjacent white matter in one case with an 8 years history of progressive disease. Although the pathophysiology of SEM remains unknown, the topographical distribution and appearance of lesions is suggestive of a vascular disorder. As the SEM-like phenotype was uniformly characterized by longitudinally and circumferentially extensive neuronal necrosis, results of this small case series indicate that dogs with clinical signs of central cord syndrome and the SEM-like phenotype involving the cervicothoracic intumescence on MR examinations have a poor prognosis for the preservation or recovery of thoracic limb motor function.
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PMID:Canine Snake-Eye Myelopathy: Clinical, Magnetic Resonance Imaging, and Pathologic Findings in Four Cases. 3133 55

White cord syndrome (WCS) is a rare case of severe neurological deterioration after surgical decompression for cervical myelopathy. It was proposed to be secondary to an ischemia/reperfusion injury. An association of WCS with a hypoxic brain injury (HBI) has not been documented. A 63-year-old man presented to us with progressive symptoms of cervical myelopathy. Computed tomography scan and magnetic resonance imaging (MRI) scan findings were suggestive of an ossified posterior longitudinal ligament with cord atrophy and myelomalacia changes. He was managed surgically by decompression and fusion through a posterior approach. During the surgery, there was a sudden loss of neuromonitoring signals after laminectomy, and wake-up assessment revealed neurological deterioration. Immediate postoperative imaging revealed adequately placed screws and adequate cord decompression. A high dose of intravenous steroids was given. Repeat MRI scan on the 3rd postoperative day suggested cord edema over a large area on T2-weighted images. He was diagnosed as WCS and managed conservatively. He had persistent abdominal distension postoperatively, and a diagnostic endoscopy was advised. At the start of the procedure, the patient had a sudden-onset loss of consciousness. Electrocardiogram suggested bradyarrhythmias with hypotension. The patient was resuscitated, intubated, and shifted to intensive care unit. He was diagnosed to have a HBI. He was managed with multidisciplinary rehabilitation and discharged at 4 months' postoperatively with stable vitals. There was no improvement in the neurology or his consciousness. Spine surgeons have to be aware of this potentially disastrous complication of WCS. One should take adequate postoperative care to avoid preventable complications like HBI associated with it.
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PMID:"White Cord Syndrome" of Acute Tetraplegia after Posterior Cervical Decompression and Resulting Hypoxic Brain Injury. 3314 48